PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
2616041-2	1989	The activities of MAO-A and MAO-B were estimated radiochemically, in-vitro, in human hippocampus and rat striatum in the presence of various concentrations of THA with [2-14C]hydroxytryptamine binoxalate (100 microM) and beta-[ethyl-14C]phenylethylamine hydrochloride (20 microM) as substrates for the respective enzyme form.	Tacrine	159-162	monoamine oxidase B	Homo sapiens	28-33
2616041-2	1989	The activities of MAO-A and MAO-B were estimated radiochemically, in-vitro, in human hippocampus and rat striatum in the presence of various concentrations of THA with [2-14C]hydroxytryptamine binoxalate (100 microM) and beta-[ethyl-14C]phenylethylamine hydrochloride (20 microM) as substrates for the respective enzyme form.	[2-14c]hydroxytryptamine binoxalate	168-203	monoamine oxidase B	Homo sapiens	28-33
2616041-2	1989	The activities of MAO-A and MAO-B were estimated radiochemically, in-vitro, in human hippocampus and rat striatum in the presence of various concentrations of THA with [2-14C]hydroxytryptamine binoxalate (100 microM) and beta-[ethyl-14C]phenylethylamine hydrochloride (20 microM) as substrates for the respective enzyme form.	beta-[ethyl-14c]phenylethylamine hydrochloride	221-267	monoamine oxidase B	Homo sapiens	28-33
2809594-6	1989	The corresponding pyridinium species of MPTP and several of the MPTP analogs inhibited MAO-A competitively with Ki values at micromolar concentrations; in contrast the pyridinium species inhibited MAO-B competitively at considerably higher concentrations (i.e., 100 microM or greater Ki values).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	40-44	monoamine oxidase B	Homo sapiens	197-202
2809594-6	1989	The corresponding pyridinium species of MPTP and several of the MPTP analogs inhibited MAO-A competitively with Ki values at micromolar concentrations; in contrast the pyridinium species inhibited MAO-B competitively at considerably higher concentrations (i.e., 100 microM or greater Ki values).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	64-68	monoamine oxidase B	Homo sapiens	197-202
2809594-6	1989	The corresponding pyridinium species of MPTP and several of the MPTP analogs inhibited MAO-A competitively with Ki values at micromolar concentrations; in contrast the pyridinium species inhibited MAO-B competitively at considerably higher concentrations (i.e., 100 microM or greater Ki values).	pyridine	168-178	monoamine oxidase B	Homo sapiens	197-202
2809594-7	1989	The data provide information concerning the structural requirements for the oxidation of tetrahydropyridines by MAO-A and MAO-B and the inhibition of these enzymes by pyridiniums.	Pyrrolidines	89-108	monoamine oxidase B	Homo sapiens	122-127
2509446-1	1989	The rate of benzylamine utilization by monoamine oxidase (MAO)-B from human blood platelets was 2-4 times higher than that for octopamine.	benzylamine	12-23	monoamine oxidase B	Homo sapiens	39-64
2809594-1	1989	Twenty analogs of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were tested for their capacity to be oxidized by pure monoamine oxidase-A (MAO-A) prepared from human placenta and pure monoamine oxidase-B (MAO-B) prepared from beef liver.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	18-62	monoamine oxidase B	Homo sapiens	190-209
2809594-1	1989	Twenty analogs of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were tested for their capacity to be oxidized by pure monoamine oxidase-A (MAO-A) prepared from human placenta and pure monoamine oxidase-B (MAO-B) prepared from beef liver.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	18-62	monoamine oxidase B	Homo sapiens	211-216
2809594-2	1989	Several of the MPTP analogs were very good substrates for MAO-A, for MAO-B, or for both and had low Km values and high turnover numbers.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	15-19	monoamine oxidase B	Homo sapiens	69-74
2809594-3	1989	These values were similar to or even better than those of kynuramine and benzylamine, good substrates for MAO-A and MAO-B, respectively.	Kynuramine	58-68	monoamine oxidase B	Homo sapiens	116-121
2809594-3	1989	These values were similar to or even better than those of kynuramine and benzylamine, good substrates for MAO-A and MAO-B, respectively.	benzylamine	73-84	monoamine oxidase B	Homo sapiens	116-121
2809594-4	1989	MPTP had relatively low Km values for oxidation by both MAO-A and MAO-B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	66-71
2809594-5	1989	In contrast, the turnover number for MPTP oxidation by MAO-B was considerably higher than the value for MAO-A.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	37-41	monoamine oxidase B	Homo sapiens	55-60
2809594-6	1989	The corresponding pyridinium species of MPTP and several of the MPTP analogs inhibited MAO-A competitively with Ki values at micromolar concentrations; in contrast the pyridinium species inhibited MAO-B competitively at considerably higher concentrations (i.e., 100 microM or greater Ki values).	pyridine	18-28	monoamine oxidase B	Homo sapiens	197-202
2509446-2	1989	Both activities were inhibited 100% by 10(-7) M deprenyl (a specific MAO-B inhibitor) and were not affected by clorgyline (a specific MAO-A inhibitor) or by polyclonal antibodies to MAO-A.	Selegiline	48-56	monoamine oxidase B	Homo sapiens	69-74
2509446-3	1989	The preincubation of platelet MAO-B with purified MAO-A from mitochondrial membranes of human placenta resulted in appearance of excess octopamine activity.	Octopamine	136-146	monoamine oxidase B	Homo sapiens	30-35
2769256-0	1989	The novel neuropsychotropic agent milacemide is a specific enzyme-activated inhibitor of brain monoamine oxidase B.	milacemide	34-44	monoamine oxidase B	Homo sapiens	95-114
2769256-7	1989	The selective inhibitory effect of milacemide for MAO-B in vivo is confirmed by its potentiation of phenylethylamine-induced stereotyped behavior, whereas vasopressor responses to tyramine were not affected.	milacemide	35-45	monoamine oxidase B	Homo sapiens	50-55
2769256-2	1989	Under the in vitro conditions used in the present study, milacemide acts as an enzyme-activated, partially reversible inhibitor of MAO-B.	milacemide	57-67	monoamine oxidase B	Homo sapiens	131-136
2503040-4	1989	The presence of MAO-B was corroborated by the inhibition of PEA oxidation with nanomolar deprenyl concentrations and by inhibition of TYR oxidation with high clorgyline concentrations, as well as by the simple sigmoid curve obtained in both cases.	Selegiline	89-97	monoamine oxidase B	Homo sapiens	16-21
2769256-4	1989	The inhibitory activity of milacemide is significantly greater for MAO-B.	milacemide	27-37	monoamine oxidase B	Homo sapiens	67-72
2769256-6	1989	In contrast to the irreversible inhibitory action of L-deprenyl, the recovery of MAO-B activity in vivo after milacemide administration is significantly faster, a result suggesting that it is a partially reversible inhibitor.	milacemide	110-120	monoamine oxidase B	Homo sapiens	81-86
2503040-4	1989	The presence of MAO-B was corroborated by the inhibition of PEA oxidation with nanomolar deprenyl concentrations and by inhibition of TYR oxidation with high clorgyline concentrations, as well as by the simple sigmoid curve obtained in both cases.	Tyramine	134-137	monoamine oxidase B	Homo sapiens	16-21
2503040-4	1989	The presence of MAO-B was corroborated by the inhibition of PEA oxidation with nanomolar deprenyl concentrations and by inhibition of TYR oxidation with high clorgyline concentrations, as well as by the simple sigmoid curve obtained in both cases.	Clorgyline	158-168	monoamine oxidase B	Homo sapiens	16-21
2503040-8	1989	MAO-B was titrated with [3H]pargyline in order to find out the number of active sites.	[3h]pargyline	24-37	monoamine oxidase B	Homo sapiens	0-5
2753987-2	1989	MPTP is first metabolized to 1-methyl-4-phenylpyridine (MPP+), a primary neurotoxin, by monoamine oxidase B (MAO-B) and then taken up into dopaminergic neurons through the dopamine reuptake system.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	88-107
2788162-0	1989	Deuterium isotope effect measurements on the interactions of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine with monoamine oxidase B.	Deuterium	0-9	monoamine oxidase B	Homo sapiens	126-145
2788162-0	1989	Deuterium isotope effect measurements on the interactions of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine with monoamine oxidase B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	76-120	monoamine oxidase B	Homo sapiens	126-145
2788162-1	1989	Kinetic deuterium isotope effects for the noncompetitive, intermolecular monoamine oxidase B-catalyzed oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the corresponding 1-methyl-4-phenyl-2,3-dihydropyridinium species MPDP+ were found to be 3.55 on Vmax and 8.01 on Vmax/Km with MPTP-6,6-d2 as the deuterated substrate.	Deuterium	8-17	monoamine oxidase B	Homo sapiens	73-92
2788162-1	1989	Kinetic deuterium isotope effects for the noncompetitive, intermolecular monoamine oxidase B-catalyzed oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the corresponding 1-methyl-4-phenyl-2,3-dihydropyridinium species MPDP+ were found to be 3.55 on Vmax and 8.01 on Vmax/Km with MPTP-6,6-d2 as the deuterated substrate.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	116-160	monoamine oxidase B	Homo sapiens	73-92
2788162-1	1989	Kinetic deuterium isotope effects for the noncompetitive, intermolecular monoamine oxidase B-catalyzed oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the corresponding 1-methyl-4-phenyl-2,3-dihydropyridinium species MPDP+ were found to be 3.55 on Vmax and 8.01 on Vmax/Km with MPTP-6,6-d2 as the deuterated substrate.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	162-166	monoamine oxidase B	Homo sapiens	73-92
2788162-1	1989	Kinetic deuterium isotope effects for the noncompetitive, intermolecular monoamine oxidase B-catalyzed oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the corresponding 1-methyl-4-phenyl-2,3-dihydropyridinium species MPDP+ were found to be 3.55 on Vmax and 8.01 on Vmax/Km with MPTP-6,6-d2 as the deuterated substrate.	1-methyl-4-phenyl-2,3-dihydropyridinium	189-228	monoamine oxidase B	Homo sapiens	73-92
2788162-1	1989	Kinetic deuterium isotope effects for the noncompetitive, intermolecular monoamine oxidase B-catalyzed oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the corresponding 1-methyl-4-phenyl-2,3-dihydropyridinium species MPDP+ were found to be 3.55 on Vmax and 8.01 on Vmax/Km with MPTP-6,6-d2 as the deuterated substrate.	1-methyl-4-phenyl-2,3-dihydropyridinium	237-242	monoamine oxidase B	Homo sapiens	73-92
2788162-1	1989	Kinetic deuterium isotope effects for the noncompetitive, intermolecular monoamine oxidase B-catalyzed oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the corresponding 1-methyl-4-phenyl-2,3-dihydropyridinium species MPDP+ were found to be 3.55 on Vmax and 8.01 on Vmax/Km with MPTP-6,6-d2 as the deuterated substrate.	mptp-6,6-d2	298-309	monoamine oxidase B	Homo sapiens	73-92
2788162-4	1989	These results indicate that the monoamine oxidase B-catalyzed oxidation of this substrate may not proceed via a reaction pathway involving alpha-carbon deprotonation of an aminium radical intermediate.	Carbon	145-151	monoamine oxidase B	Homo sapiens	32-51
2788162-4	1989	These results indicate that the monoamine oxidase B-catalyzed oxidation of this substrate may not proceed via a reaction pathway involving alpha-carbon deprotonation of an aminium radical intermediate.	aminium	172-179	monoamine oxidase B	Homo sapiens	32-51
2788162-5	1989	Isotope effect measurements also established that the rate of inactivation of monoamine oxidase B by MPTP is unaffected by replacement of the C-6 methylene protons with deuterons, but is retarded by replacement of the C-2 methylene protons (DKi = 1.9).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	101-105	monoamine oxidase B	Homo sapiens	78-97
2788162-5	1989	Isotope effect measurements also established that the rate of inactivation of monoamine oxidase B by MPTP is unaffected by replacement of the C-6 methylene protons with deuterons, but is retarded by replacement of the C-2 methylene protons (DKi = 1.9).	Deuterium	169-178	monoamine oxidase B	Homo sapiens	78-97
2788162-6	1989	The mechanism-based inactivation of monoamine oxidase B by MPTP, therefore, is likely to mediated by a species derived from the enzyme-generated 2,3-dihydropyridinium oxidation product.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	59-63	monoamine oxidase B	Homo sapiens	36-55
2788162-6	1989	The mechanism-based inactivation of monoamine oxidase B by MPTP, therefore, is likely to mediated by a species derived from the enzyme-generated 2,3-dihydropyridinium oxidation product.	2,3-dihydropyridinium	145-166	monoamine oxidase B	Homo sapiens	36-55
2764901-0	1989	Monoamine oxidase A from human placenta and monoamine oxidase B from bovine liver both have one FAD per subunit.	Flavin-Adenine Dinucleotide	96-99	monoamine oxidase B	Homo sapiens	44-63
2760262-1	1989	The present study, using a diaminobenzidine (DAB)-coupled peroxidation method, examined the distribution and morphological characteristics of neuronal structures containing type B monoamine oxidase (MAO-B) in the cat hypothalamus.	3,3'-Diaminobenzidine	45-48	monoamine oxidase B	Homo sapiens	199-204
2753987-2	1989	MPTP is first metabolized to 1-methyl-4-phenylpyridine (MPP+), a primary neurotoxin, by monoamine oxidase B (MAO-B) and then taken up into dopaminergic neurons through the dopamine reuptake system.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	109-114
2753987-2	1989	MPTP is first metabolized to 1-methyl-4-phenylpyridine (MPP+), a primary neurotoxin, by monoamine oxidase B (MAO-B) and then taken up into dopaminergic neurons through the dopamine reuptake system.	1-Methyl-4-phenylpyridinium	29-54	monoamine oxidase B	Homo sapiens	88-107
2753987-2	1989	MPTP is first metabolized to 1-methyl-4-phenylpyridine (MPP+), a primary neurotoxin, by monoamine oxidase B (MAO-B) and then taken up into dopaminergic neurons through the dopamine reuptake system.	1-Methyl-4-phenylpyridinium	29-54	monoamine oxidase B	Homo sapiens	109-114
2753987-2	1989	MPTP is first metabolized to 1-methyl-4-phenylpyridine (MPP+), a primary neurotoxin, by monoamine oxidase B (MAO-B) and then taken up into dopaminergic neurons through the dopamine reuptake system.	mangion-purified polysaccharide (Candida albicans)	56-60	monoamine oxidase B	Homo sapiens	88-107
2753987-2	1989	MPTP is first metabolized to 1-methyl-4-phenylpyridine (MPP+), a primary neurotoxin, by monoamine oxidase B (MAO-B) and then taken up into dopaminergic neurons through the dopamine reuptake system.	mangion-purified polysaccharide (Candida albicans)	56-60	monoamine oxidase B	Homo sapiens	109-114
2753987-2	1989	MPTP is first metabolized to 1-methyl-4-phenylpyridine (MPP+), a primary neurotoxin, by monoamine oxidase B (MAO-B) and then taken up into dopaminergic neurons through the dopamine reuptake system.	Dopamine	139-147	monoamine oxidase B	Homo sapiens	109-114
2496202-6	1989	In contrast, the expressed MAO B prefers phenylethylamine as a substrate and is sensitive to the inhibitor deprenyl.	Selegiline	107-115	monoamine oxidase B	Homo sapiens	27-32
2788253-3	1989	Furthermore, tetrahydroisoquinoline, which has been reported to be present in human brain, and N-methyltetrahydroisoquinoline were found to be MAO-B substrates, being oxidized at about 3% the rate of MPTP.	1,2,3,4-tetrahydroisoquinoline	13-35	monoamine oxidase B	Homo sapiens	143-148
2788253-3	1989	Furthermore, tetrahydroisoquinoline, which has been reported to be present in human brain, and N-methyltetrahydroisoquinoline were found to be MAO-B substrates, being oxidized at about 3% the rate of MPTP.	n-methyltetrahydroisoquinoline	95-125	monoamine oxidase B	Homo sapiens	143-148
2788253-3	1989	Furthermore, tetrahydroisoquinoline, which has been reported to be present in human brain, and N-methyltetrahydroisoquinoline were found to be MAO-B substrates, being oxidized at about 3% the rate of MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	200-204	monoamine oxidase B	Homo sapiens	143-148
2501102-1	1989	L-Deprenyl is an inhibitor of monoamine oxidase B and dopamine uptake.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	30-49
2496202-6	1989	In contrast, the expressed MAO B prefers phenylethylamine as a substrate and is sensitive to the inhibitor deprenyl.	Phenethylamines	41-57	monoamine oxidase B	Homo sapiens	27-32
2501102-2	1989	Chronic L-deprenyl (10 mg/kg i.p., twice weekly for 4 weeks) was shown to inhibit monoamine oxidase B activity by 89%, and also to induce an up-regulation of the [3H]mazindol binding site associated with the striatal dopamine uptake carrier.	Selegiline	8-18	monoamine oxidase B	Homo sapiens	82-101
2543694-2	1989	MPTP is metabolized to 1-methyl-4-phenylpyridine (MPP+), which is a primary neurotoxin, by monoamine oxidase B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	91-110
2744079-0	1989	[3H]Ro 19-6327: a reversible ligand and affinity labelling probe for monoamine oxidase-B.	Tritium	1-3	monoamine oxidase B	Homo sapiens	69-88
2744079-2	1989	This compound is a novel, time-dependent inhibitor of monoamine oxidase type B (MAO-B) and is structurally closely related to [3H]Ro 16-6491.	Tritium	127-129	monoamine oxidase B	Homo sapiens	54-78
2744079-2	1989	This compound is a novel, time-dependent inhibitor of monoamine oxidase type B (MAO-B) and is structurally closely related to [3H]Ro 16-6491.	Tritium	127-129	monoamine oxidase B	Homo sapiens	80-85
2744079-5	1989	The dissociation rate was markedly decreased (t1/2 = greater than 24h) at 0 degrees C. MAO-B, but not MAO-A inhibitors, effectively prevented the binding of [3H]Ro 19-6327.	Tritium	158-160	monoamine oxidase B	Homo sapiens	87-92
2744079-6	1989	Like [3H]Ro 16-6491, [3H]Ro 19-6327 is recognized as a substrate by MAO-B, being eventually deaminated by the enzyme.	Tritium	6-8	monoamine oxidase B	Homo sapiens	68-73
2744079-6	1989	Like [3H]Ro 16-6491, [3H]Ro 19-6327 is recognized as a substrate by MAO-B, being eventually deaminated by the enzyme.	Tritium	22-24	monoamine oxidase B	Homo sapiens	68-73
2744079-7	1989	Since the deaminated aldehyde derivative of Ro 19-6327 did not inhibit MAO-B, a still unidentified reversible adduct, formed at the MAO-B active site, might explain the high potency and selectivity of [3H]Ro 19-6327.	Tritium	202-204	monoamine oxidase B	Homo sapiens	132-137
2744079-10	1989	The presence of unlabelled MAO-B inhibitors in the incubation mixture prevented the covalent incorporation of [3H]Ro 19-6327.	Tritium	111-113	monoamine oxidase B	Homo sapiens	27-32
2744079-11	1989	The irreversible MAO-B inhibitor, [3H] pargyline, labelled a protein with a molecular weight identical to the protein labelled by [3H]Ro 19-6327.	Tritium	35-37	monoamine oxidase B	Homo sapiens	17-22
2469451-3	1989	The investigation was thereafter continued in an open fashion by administering a single 10 mg dose of the MAO-B inhibitor deprenyl to the same subjects.	Selegiline	122-130	monoamine oxidase B	Homo sapiens	106-111
2469451-7	1989	In contrast, deprenyl, in a dose which almost totally inhibited MAO-B activity in blood platelets, did not appreciably affect the plasma concentrations of DHPG or DOPAC.	Selegiline	13-21	monoamine oxidase B	Homo sapiens	64-69
2469451-13	1989	Monoamine oxidase type B activity in blood platelets was slightly (less than 30%) and transiently inhibited after moclobemide.	Moclobemide	114-125	monoamine oxidase B	Homo sapiens	0-24
2543694-2	1989	MPTP is metabolized to 1-methyl-4-phenylpyridine (MPP+), which is a primary neurotoxin, by monoamine oxidase B.	1-Methyl-4-phenylpyridinium	23-48	monoamine oxidase B	Homo sapiens	91-110
2543694-2	1989	MPTP is metabolized to 1-methyl-4-phenylpyridine (MPP+), which is a primary neurotoxin, by monoamine oxidase B.	mangion-purified polysaccharide (Candida albicans)	50-54	monoamine oxidase B	Homo sapiens	91-110
2618592-2	1989	DA is a good substrate for MAO-B and selegiline enhances DA-transmission and improves akinesia of Parkinson"s disease (PD) by selective MAO-B blockade.	Dopamine	0-2	monoamine oxidase B	Homo sapiens	27-32
2694735-4	1989	In addition to these two major medications the essential therapeutic additives such as the decarboxylase inhibitor benserazide, the monoamineoxidase B inhibitor deprenyl and the dopamine receptor agonist lisuride should be used for the fine adjustment of the individual patient.	Selegiline	161-169	monoamine oxidase B	Homo sapiens	132-150
2515715-1	1989	Selegiline is a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B).	Selegiline	0-10	monoamine oxidase B	Homo sapiens	53-77
2515715-1	1989	Selegiline is a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B).	Selegiline	0-10	monoamine oxidase B	Homo sapiens	79-84
2515726-3	1989	It is the L-form of selegiline that is an active MAO-B inhibitor, the D-(+)-form being 25 times less active.	Selegiline	20-30	monoamine oxidase B	Homo sapiens	49-54
2618592-2	1989	DA is a good substrate for MAO-B and selegiline enhances DA-transmission and improves akinesia of Parkinson"s disease (PD) by selective MAO-B blockade.	Dopamine	0-2	monoamine oxidase B	Homo sapiens	136-141
2618592-2	1989	DA is a good substrate for MAO-B and selegiline enhances DA-transmission and improves akinesia of Parkinson"s disease (PD) by selective MAO-B blockade.	Selegiline	37-47	monoamine oxidase B	Homo sapiens	136-141
2618592-6	1989	In addition, synthesis of hydrogen peroxide generated via MAO-B is blocked by selegiline.	Hydrogen Peroxide	26-43	monoamine oxidase B	Homo sapiens	58-63
2618592-6	1989	In addition, synthesis of hydrogen peroxide generated via MAO-B is blocked by selegiline.	Selegiline	78-88	monoamine oxidase B	Homo sapiens	58-63
2618592-9	1989	As conclusion, selegiline is a safe inhibitor of MAO-B that reduces neurotoxicity possibly triggering PD.	Selegiline	15-25	monoamine oxidase B	Homo sapiens	49-54
2618593-6	1989	Indeed H2O2 derived from MAO B reaction and autooxidation of dopamine to melanin in the SN can drive the iron dependent Fenton reaction.	Hydrogen Peroxide	7-11	monoamine oxidase B	Homo sapiens	25-30
2618593-6	1989	Indeed H2O2 derived from MAO B reaction and autooxidation of dopamine to melanin in the SN can drive the iron dependent Fenton reaction.	Iron	105-109	monoamine oxidase B	Homo sapiens	25-30
2618594-9	1989	11C-L-selegiline and its "inactive" D-form have been used in clinical PET-studies aimed to evaluate the enzyme MAO-B.	11c-l-selegiline	0-16	monoamine oxidase B	Homo sapiens	111-116
2501449-0	1989	Localization of monoamine oxidase B in human brain by autoradiographical use of 11C-labelled L-deprenyl.	Carbon-11	80-83	monoamine oxidase B	Homo sapiens	16-35
2501449-0	1989	Localization of monoamine oxidase B in human brain by autoradiographical use of 11C-labelled L-deprenyl.	Selegiline	93-103	monoamine oxidase B	Homo sapiens	16-35
2501449-1	1989	11C-labelled L-deprenyl in vitro autoradiography was used to study the regional distribution of MAO-B in human brain.	Carbon-11	0-3	monoamine oxidase B	Homo sapiens	96-101
2501449-1	1989	11C-labelled L-deprenyl in vitro autoradiography was used to study the regional distribution of MAO-B in human brain.	Selegiline	13-23	monoamine oxidase B	Homo sapiens	96-101
2783611-7	1989	The moderate MAO-B inhibition measured after moclobemide intake in human platelets indicates that only minor amounts of Ro 16-6491 are formed in humans.	Moclobemide	45-56	monoamine oxidase B	Homo sapiens	13-18
2601584-0	1989	The effect of debrisoquin on MAO A and MAO B activities.	Debrisoquin	14-25	monoamine oxidase B	Homo sapiens	39-44
2601584-1	1989	To examine the mode of action of debrisoquin (DEB), we studied the effect of this drug in vitro on MAO A and MAO B enzyme activities.	Debrisoquin	33-44	monoamine oxidase B	Homo sapiens	109-114
3242595-0	1988	Inactivation of monoamine oxidase A by the monoamine oxidase B inactivators 1-phenylcyclopropylamine, 1-benzylcyclopropylamine, and N-cyclopropyl-alpha-methylbenzylamine.	1-phenylcyclopropylamine	76-100	monoamine oxidase B	Homo sapiens	43-62
2677243-4	1989	The efficacy of specific MAO inhibitors such as moclobemide (MAO-A) and deprenyl (MAO-B) are yet to be investigated.	Selegiline	72-80	monoamine oxidase B	Homo sapiens	82-87
2622533-3	1989	While dopaminergic neurons of the substantia nigra revealed no staining for monoamine oxidase, noradrenergic neurons of the locus coeruleus stained positively with the monoamine oxidase-A substrate serotonin, and serotonergic neurons of the raphe nuclei were stained by the monoamine oxidase-B substrate beta-phenylethylamine.	Serotonin	198-207	monoamine oxidase B	Homo sapiens	274-293
2568664-2	1989	It is now apparent that MAO-B is capable of oxidizing inert non-polar amines such as MPTP (N-methyl-4-phenyl-1,2,3,6, tetrahydropyridine) and milacemide (2-n-pentylaminoacetamide) into neuroactive substances giving rise to Parkinson inducing dopaminergic neurotoxin, MPP+ and inhibitory amino acid neurotransmitter, glycine respectively.	Amines	70-76	monoamine oxidase B	Homo sapiens	24-29
2568664-2	1989	It is now apparent that MAO-B is capable of oxidizing inert non-polar amines such as MPTP (N-methyl-4-phenyl-1,2,3,6, tetrahydropyridine) and milacemide (2-n-pentylaminoacetamide) into neuroactive substances giving rise to Parkinson inducing dopaminergic neurotoxin, MPP+ and inhibitory amino acid neurotransmitter, glycine respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	85-89	monoamine oxidase B	Homo sapiens	24-29
2568664-2	1989	It is now apparent that MAO-B is capable of oxidizing inert non-polar amines such as MPTP (N-methyl-4-phenyl-1,2,3,6, tetrahydropyridine) and milacemide (2-n-pentylaminoacetamide) into neuroactive substances giving rise to Parkinson inducing dopaminergic neurotoxin, MPP+ and inhibitory amino acid neurotransmitter, glycine respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	91-136	monoamine oxidase B	Homo sapiens	24-29
2568664-2	1989	It is now apparent that MAO-B is capable of oxidizing inert non-polar amines such as MPTP (N-methyl-4-phenyl-1,2,3,6, tetrahydropyridine) and milacemide (2-n-pentylaminoacetamide) into neuroactive substances giving rise to Parkinson inducing dopaminergic neurotoxin, MPP+ and inhibitory amino acid neurotransmitter, glycine respectively.	milacemide	142-152	monoamine oxidase B	Homo sapiens	24-29
2568664-2	1989	It is now apparent that MAO-B is capable of oxidizing inert non-polar amines such as MPTP (N-methyl-4-phenyl-1,2,3,6, tetrahydropyridine) and milacemide (2-n-pentylaminoacetamide) into neuroactive substances giving rise to Parkinson inducing dopaminergic neurotoxin, MPP+ and inhibitory amino acid neurotransmitter, glycine respectively.	milacemide	154-178	monoamine oxidase B	Homo sapiens	24-29
2568664-2	1989	It is now apparent that MAO-B is capable of oxidizing inert non-polar amines such as MPTP (N-methyl-4-phenyl-1,2,3,6, tetrahydropyridine) and milacemide (2-n-pentylaminoacetamide) into neuroactive substances giving rise to Parkinson inducing dopaminergic neurotoxin, MPP+ and inhibitory amino acid neurotransmitter, glycine respectively.	mangion-purified polysaccharide (Candida albicans)	267-271	monoamine oxidase B	Homo sapiens	24-29
2568664-2	1989	It is now apparent that MAO-B is capable of oxidizing inert non-polar amines such as MPTP (N-methyl-4-phenyl-1,2,3,6, tetrahydropyridine) and milacemide (2-n-pentylaminoacetamide) into neuroactive substances giving rise to Parkinson inducing dopaminergic neurotoxin, MPP+ and inhibitory amino acid neurotransmitter, glycine respectively.	Glycine	316-323	monoamine oxidase B	Homo sapiens	24-29
3068045-8	1988	Neurotoxicity of MPTP has been attributed to the formation of MPP+ by MAO-B, for the first step at least.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	17-21	monoamine oxidase B	Homo sapiens	70-75
3242595-0	1988	Inactivation of monoamine oxidase A by the monoamine oxidase B inactivators 1-phenylcyclopropylamine, 1-benzylcyclopropylamine, and N-cyclopropyl-alpha-methylbenzylamine.	1-benzylcyclopropylamine	102-126	monoamine oxidase B	Homo sapiens	43-62
3242595-0	1988	Inactivation of monoamine oxidase A by the monoamine oxidase B inactivators 1-phenylcyclopropylamine, 1-benzylcyclopropylamine, and N-cyclopropyl-alpha-methylbenzylamine.	N-(1-methyl)cyclopropylbenzylamine	132-169	monoamine oxidase B	Homo sapiens	43-62
3242595-9	1988	The results with 1-PCPA indicate that the active site topographies of MAO A and MAO B are different.	1-phenylcyclopropylamine	17-23	monoamine oxidase B	Homo sapiens	80-85
3242595-10	1988	The ability of N-C alpha MBA to undergo attachment to a cysteine residue in both MAO A and MAO B may lead the way toward peptide mapping of the two isozymes in order to determine differences in their primary structures.	Cysteine	56-64	monoamine oxidase B	Homo sapiens	91-96
3397993-0	1988	Stereoisomers of allenic amines as inactivators of monoamine oxidase type B.	allenic amines	17-31	monoamine oxidase B	Homo sapiens	51-75
3139834-2	1988	L-N-[11C-methyl]Deprenyl ([11C]L-deprenyl), a suicide inactivator of monoamine oxidase (MAO) type B, has been developed as a radiotracer for mapping MAO B in the living human and animal brain.	l-n-[11c-methyl]deprenyl	0-24	monoamine oxidase B	Homo sapiens	69-99
3139834-2	1988	L-N-[11C-methyl]Deprenyl ([11C]L-deprenyl), a suicide inactivator of monoamine oxidase (MAO) type B, has been developed as a radiotracer for mapping MAO B in the living human and animal brain.	l-n-[11c-methyl]deprenyl	0-24	monoamine oxidase B	Homo sapiens	149-154
3139834-2	1988	L-N-[11C-methyl]Deprenyl ([11C]L-deprenyl), a suicide inactivator of monoamine oxidase (MAO) type B, has been developed as a radiotracer for mapping MAO B in the living human and animal brain.	[11c]l-deprenyl	26-41	monoamine oxidase B	Homo sapiens	69-99
3139834-2	1988	L-N-[11C-methyl]Deprenyl ([11C]L-deprenyl), a suicide inactivator of monoamine oxidase (MAO) type B, has been developed as a radiotracer for mapping MAO B in the living human and animal brain.	[11c]l-deprenyl	26-41	monoamine oxidase B	Homo sapiens	149-154
3397993-2	1988	The kinetics of inactivation of mitochondrial monoamine oxidase type B (MAO-B) by a series of 18 stereoisomers of tertiary alpha-allenic amines have been investigated in detail.	alpha-allenic amines	123-143	monoamine oxidase B	Homo sapiens	46-70
3397993-2	1988	The kinetics of inactivation of mitochondrial monoamine oxidase type B (MAO-B) by a series of 18 stereoisomers of tertiary alpha-allenic amines have been investigated in detail.	alpha-allenic amines	123-143	monoamine oxidase B	Homo sapiens	72-77
3397993-6	1988	The stereoselectivity of MAO-B was examined further with a series of reversible aralkylamine inhibitors; thus (R)-1,2,3,4-tetrahydro-1-naphthylamine was determined to be 150-fold more potent than its enantiomer.	aralkylamine	80-92	monoamine oxidase B	Homo sapiens	25-30
3397993-6	1988	The stereoselectivity of MAO-B was examined further with a series of reversible aralkylamine inhibitors; thus (R)-1,2,3,4-tetrahydro-1-naphthylamine was determined to be 150-fold more potent than its enantiomer.	1-aminotetralin	110-148	monoamine oxidase B	Homo sapiens	25-30
3138141-2	1988	This effect was significantly reduced by the selective inhibition of monoamine oxidase B by 1-deprenyl (2.0 mg/kg).	1-deprenyl	92-102	monoamine oxidase B	Homo sapiens	69-88
3137566-4	1988	However, the neurotoxicity of these two analogs can be prevented by pretreatment with a combination of deprenyl and the selective MAO-A inhibitor clorgyline at doses that are sufficient to almost completely inhibit both MAO-B and MAO-A activities.	Clorgyline	146-156	monoamine oxidase B	Homo sapiens	220-225
3392550-4	1988	Isatin is a potent inhibitor of MAO, particularly of MAO B (IC50, 3 microM), and also binds to central benzodiazepine receptors (IC50 against clonazepam, 123 microM).	Isatin	0-6	monoamine oxidase B	Homo sapiens	53-58
3138141-4	1988	These results suggest that, in the brain, milacemide is oxidized to glycine and that this reaction is mediated primarily by monoamine oxidase B.	milacemide	42-52	monoamine oxidase B	Homo sapiens	124-143
3138141-4	1988	These results suggest that, in the brain, milacemide is oxidized to glycine and that this reaction is mediated primarily by monoamine oxidase B.	Glycine	68-75	monoamine oxidase B	Homo sapiens	124-143
3399053-6	1988	The major accumulation of monoamine oxidase B-positive neurons was observed in the same regions in which monoamine oxidase B is found to co-localize with serotonin in monkey tissues, including the nucleus raphe dorsalis and the nucleus centralis superior.	Serotonin	154-163	monoamine oxidase B	Homo sapiens	26-45
3399053-6	1988	The major accumulation of monoamine oxidase B-positive neurons was observed in the same regions in which monoamine oxidase B is found to co-localize with serotonin in monkey tissues, including the nucleus raphe dorsalis and the nucleus centralis superior.	Serotonin	154-163	monoamine oxidase B	Homo sapiens	105-124
3258018-1	1988	We synthesized a number of fluorinated analogs of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and tested their suitability as substrates for monoamine oxidase B in vitro and their dopaminergic neurotoxicity in vivo.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	50-94	monoamine oxidase B	Homo sapiens	150-169
3258018-1	1988	We synthesized a number of fluorinated analogs of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and tested their suitability as substrates for monoamine oxidase B in vitro and their dopaminergic neurotoxicity in vivo.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	96-100	monoamine oxidase B	Homo sapiens	150-169
3346666-0	1988	Formation of the neurotransmitter glycine from the anticonvulsant milacemide is mediated by brain monoamine oxidase B.	Glycine	34-41	monoamine oxidase B	Homo sapiens	98-117
3126263-0	1988	[3H]Ro 16-6491, a selective probe for affinity labelling of monoamine oxidase type B in human brain and platelet membranes.	Tritium	1-3	monoamine oxidase B	Homo sapiens	60-84
3126263-1	1988	[3H]Ro 16-6491 [N-(2-aminoethyl)-p-chlorobenzamide HCl], a reversible "mechanism-based" inhibitor of monoamine oxidase (MAO) type B, binds selectively and with high affinity to the active site of MAO-B in brain and platelet membranes.	Tritium	1-3	monoamine oxidase B	Homo sapiens	101-131
3126263-1	1988	[3H]Ro 16-6491 [N-(2-aminoethyl)-p-chlorobenzamide HCl], a reversible "mechanism-based" inhibitor of monoamine oxidase (MAO) type B, binds selectively and with high affinity to the active site of MAO-B in brain and platelet membranes.	Tritium	1-3	monoamine oxidase B	Homo sapiens	196-201
3126263-1	1988	[3H]Ro 16-6491 [N-(2-aminoethyl)-p-chlorobenzamide HCl], a reversible "mechanism-based" inhibitor of monoamine oxidase (MAO) type B, binds selectively and with high affinity to the active site of MAO-B in brain and platelet membranes.	n-(2-aminoethyl)-p-chlorobenzamide hcl	16-54	monoamine oxidase B	Homo sapiens	101-131
3126263-1	1988	[3H]Ro 16-6491 [N-(2-aminoethyl)-p-chlorobenzamide HCl], a reversible "mechanism-based" inhibitor of monoamine oxidase (MAO) type B, binds selectively and with high affinity to the active site of MAO-B in brain and platelet membranes.	n-(2-aminoethyl)-p-chlorobenzamide hcl	16-54	monoamine oxidase B	Homo sapiens	196-201
3126263-5	1988	The presence of the irreversible MAO-B inhibitor l-deprenyl completely abolished the irreversible labelling of the membranes by [3H]Ro 16-6491.	Selegiline	49-59	monoamine oxidase B	Homo sapiens	33-38
3346666-0	1988	Formation of the neurotransmitter glycine from the anticonvulsant milacemide is mediated by brain monoamine oxidase B.	milacemide	66-76	monoamine oxidase B	Homo sapiens	98-117
3285599-3	1988	The occurrence of long-term complications such as fluctuations of mobility (on/off phenomena) and dyskinesias caused the use of lower levodopa doses and the simultaneous application of other antiparkinson drugs, e. g. anticholinergics, amantadines, dopamine agonists and MAO-B-inhibitors.	Levodopa	134-142	monoamine oxidase B	Homo sapiens	271-276
3346666-4	1988	The apparent Km (30-90 microM) for milacemide oxidation by mitochondrial MAO-B preparations is significantly lower than that for milacemide oxidation by mitochondrial MAO-A (approximately 1,300 microM).	milacemide	35-45	monoamine oxidase B	Homo sapiens	73-78
3346666-4	1988	The apparent Km (30-90 microM) for milacemide oxidation by mitochondrial MAO-B preparations is significantly lower than that for milacemide oxidation by mitochondrial MAO-A (approximately 1,300 microM).	milacemide	129-139	monoamine oxidase B	Homo sapiens	73-78
3346666-5	1988	In vitro MAO-B (l-deprenyl and AGN 1135) rather than MAO-A (clorgyline) selectively inhibited the oxidation of milacemide.	Selegiline	16-26	monoamine oxidase B	Homo sapiens	9-14
3346666-5	1988	In vitro MAO-B (l-deprenyl and AGN 1135) rather than MAO-A (clorgyline) selectively inhibited the oxidation of milacemide.	Silver	31-34	monoamine oxidase B	Homo sapiens	9-14
3346666-5	1988	In vitro MAO-B (l-deprenyl and AGN 1135) rather than MAO-A (clorgyline) selectively inhibited the oxidation of milacemide.	milacemide	111-121	monoamine oxidase B	Homo sapiens	9-14
3346666-9	1988	The present data therefore demonstrate that milacemide is a substrate for brain MAO-B, and its conversion to glycinamide, further transformed to the inhibitory neurotransmitter, glycine, mediated by this enzyme may contribute to its pharmacological activities.	milacemide	44-54	monoamine oxidase B	Homo sapiens	80-85
3346666-9	1988	The present data therefore demonstrate that milacemide is a substrate for brain MAO-B, and its conversion to glycinamide, further transformed to the inhibitory neurotransmitter, glycine, mediated by this enzyme may contribute to its pharmacological activities.	glycine amide	109-120	monoamine oxidase B	Homo sapiens	80-85
3346666-9	1988	The present data therefore demonstrate that milacemide is a substrate for brain MAO-B, and its conversion to glycinamide, further transformed to the inhibitory neurotransmitter, glycine, mediated by this enzyme may contribute to its pharmacological activities.	Glycine	178-185	monoamine oxidase B	Homo sapiens	80-85
3126263-5	1988	The presence of the irreversible MAO-B inhibitor l-deprenyl completely abolished the irreversible labelling of the membranes by [3H]Ro 16-6491.	Tritium	129-131	monoamine oxidase B	Homo sapiens	33-38
3126263-5	1988	The presence of the irreversible MAO-B inhibitor l-deprenyl completely abolished the irreversible labelling of the membranes by [3H]Ro 16-6491.	Ro 16-6491	132-142	monoamine oxidase B	Homo sapiens	33-38
3126263-6	1988	The selective inactivation of MAO-B, e.g., by l-deprenyl prevented the covalent incorporation of [3H]Ro 16-6491 whereas selective inhibition of the MAO-A by clorgyline was without effect.	Selegiline	46-56	monoamine oxidase B	Homo sapiens	30-35
3126263-6	1988	The selective inactivation of MAO-B, e.g., by l-deprenyl prevented the covalent incorporation of [3H]Ro 16-6491 whereas selective inhibition of the MAO-A by clorgyline was without effect.	Tritium	98-100	monoamine oxidase B	Homo sapiens	30-35
3126263-6	1988	The selective inactivation of MAO-B, e.g., by l-deprenyl prevented the covalent incorporation of [3H]Ro 16-6491 whereas selective inhibition of the MAO-A by clorgyline was without effect.	Ro 16-6491	101-111	monoamine oxidase B	Homo sapiens	30-35
3126263-6	1988	The selective inactivation of MAO-B, e.g., by l-deprenyl prevented the covalent incorporation of [3H]Ro 16-6491 whereas selective inhibition of the MAO-A by clorgyline was without effect.	Clorgyline	157-167	monoamine oxidase B	Homo sapiens	30-35
3126263-7	1988	The covalent linkage to membranes of unlabelled Ro 16-6491 and Ro 19-6327 (a selective and reversible MAO-B inhibitor closely related to Ro 16-6491) after the addition of NaBH3CN at pH 4.5 irreversibly inactivated MAO-B activity whereas MAO-A activity was unaffected.	Ro 16-6491	48-58	monoamine oxidase B	Homo sapiens	102-107
3126263-7	1988	The covalent linkage to membranes of unlabelled Ro 16-6491 and Ro 19-6327 (a selective and reversible MAO-B inhibitor closely related to Ro 16-6491) after the addition of NaBH3CN at pH 4.5 irreversibly inactivated MAO-B activity whereas MAO-A activity was unaffected.	Ro 16-6491	48-58	monoamine oxidase B	Homo sapiens	214-219
3126263-7	1988	The covalent linkage to membranes of unlabelled Ro 16-6491 and Ro 19-6327 (a selective and reversible MAO-B inhibitor closely related to Ro 16-6491) after the addition of NaBH3CN at pH 4.5 irreversibly inactivated MAO-B activity whereas MAO-A activity was unaffected.	lazabemide	63-73	monoamine oxidase B	Homo sapiens	102-107
3126263-7	1988	The covalent linkage to membranes of unlabelled Ro 16-6491 and Ro 19-6327 (a selective and reversible MAO-B inhibitor closely related to Ro 16-6491) after the addition of NaBH3CN at pH 4.5 irreversibly inactivated MAO-B activity whereas MAO-A activity was unaffected.	lazabemide	63-73	monoamine oxidase B	Homo sapiens	214-219
3126263-7	1988	The covalent linkage to membranes of unlabelled Ro 16-6491 and Ro 19-6327 (a selective and reversible MAO-B inhibitor closely related to Ro 16-6491) after the addition of NaBH3CN at pH 4.5 irreversibly inactivated MAO-B activity whereas MAO-A activity was unaffected.	Ro 16-6491	137-147	monoamine oxidase B	Homo sapiens	102-107
3126263-7	1988	The covalent linkage to membranes of unlabelled Ro 16-6491 and Ro 19-6327 (a selective and reversible MAO-B inhibitor closely related to Ro 16-6491) after the addition of NaBH3CN at pH 4.5 irreversibly inactivated MAO-B activity whereas MAO-A activity was unaffected.	sodium cyanoborohydride	171-178	monoamine oxidase B	Homo sapiens	102-107
3126263-9	1988	Our results indicate that the polypeptide that is covalently labelled by [3H]Ro 16-6491 corresponds to one of the two MAO-B subunits.	Tritium	74-76	monoamine oxidase B	Homo sapiens	118-123
3127050-1	1988	Deprenyl, a selective inhibitor of monoamine oxidase, type B, which is free of the "tyramine effect," may ameliorate symptom fluctuations in advanced Parkinson"s disease (PD).	Selegiline	0-8	monoamine oxidase B	Homo sapiens	35-60
2451963-11	1988	Selective inhibition of MAO-B with selegiline (10 mg kg-1, i.p.)	Selegiline	35-45	monoamine oxidase B	Homo sapiens	24-29
2963592-6	1988	Preincubation of hepatocytes with inhibitors of monoamine oxidase type B, but not A, protected the cells from MPTP-induced cytotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	110-114	monoamine oxidase B	Homo sapiens	48-72
2963592-7	1988	Moreover, the monoamine oxidase B inhibitor, pargyline, prevented the rise in cytosolic free Ca2+ concentration and partially protected the plasma membrane Ca2+-ATPase from inhibition by MPTP.	Pargyline	45-54	monoamine oxidase B	Homo sapiens	14-33
2963592-7	1988	Moreover, the monoamine oxidase B inhibitor, pargyline, prevented the rise in cytosolic free Ca2+ concentration and partially protected the plasma membrane Ca2+-ATPase from inhibition by MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	187-191	monoamine oxidase B	Homo sapiens	14-33
3335842-3	1988	BP-N-methylbutylamine had a much higher affinity to MAO-A than an amine substrate, kynuramine, and it was a more potent inhibitor of MAO-A than of MAO-B.	Bifemelane	0-21	monoamine oxidase B	Homo sapiens	147-152
3129982-3	1988	Mechanisms of bioactivation by MAO-B of MPTP to MPP+, concentration of MPP+ in neurons with a catecholamine uptake system, and vulnerability to cellular toxic effects of MPP+ are the basis for the specificity of MPTP targeting of nigrostriatal dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	40-44	monoamine oxidase B	Homo sapiens	31-36
3129982-3	1988	Mechanisms of bioactivation by MAO-B of MPTP to MPP+, concentration of MPP+ in neurons with a catecholamine uptake system, and vulnerability to cellular toxic effects of MPP+ are the basis for the specificity of MPTP targeting of nigrostriatal dopaminergic neurons.	mangion-purified polysaccharide (Candida albicans)	48-52	monoamine oxidase B	Homo sapiens	31-36
3129982-3	1988	Mechanisms of bioactivation by MAO-B of MPTP to MPP+, concentration of MPP+ in neurons with a catecholamine uptake system, and vulnerability to cellular toxic effects of MPP+ are the basis for the specificity of MPTP targeting of nigrostriatal dopaminergic neurons.	Catecholamines	94-107	monoamine oxidase B	Homo sapiens	31-36
3129982-3	1988	Mechanisms of bioactivation by MAO-B of MPTP to MPP+, concentration of MPP+ in neurons with a catecholamine uptake system, and vulnerability to cellular toxic effects of MPP+ are the basis for the specificity of MPTP targeting of nigrostriatal dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	212-216	monoamine oxidase B	Homo sapiens	31-36
3258013-1	1988	Monoamine oxidase-B (MAO-B) has been determined to be the enzyme responsible for the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into its toxic metabolite 1-methyl-4-phenylpyridine ion (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	99-143	monoamine oxidase B	Homo sapiens	0-19
3258013-1	1988	Monoamine oxidase-B (MAO-B) has been determined to be the enzyme responsible for the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into its toxic metabolite 1-methyl-4-phenylpyridine ion (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	99-143	monoamine oxidase B	Homo sapiens	21-26
3258013-1	1988	Monoamine oxidase-B (MAO-B) has been determined to be the enzyme responsible for the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into its toxic metabolite 1-methyl-4-phenylpyridine ion (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	145-149	monoamine oxidase B	Homo sapiens	0-19
3335842-3	1988	BP-N-methylbutylamine had a much higher affinity to MAO-A than an amine substrate, kynuramine, and it was a more potent inhibitor of MAO-A than of MAO-B.	Amines	16-21	monoamine oxidase B	Homo sapiens	147-152
3258013-1	1988	Monoamine oxidase-B (MAO-B) has been determined to be the enzyme responsible for the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into its toxic metabolite 1-methyl-4-phenylpyridine ion (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	145-149	monoamine oxidase B	Homo sapiens	21-26
3258013-1	1988	Monoamine oxidase-B (MAO-B) has been determined to be the enzyme responsible for the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into its toxic metabolite 1-methyl-4-phenylpyridine ion (MPP+).	1-Methyl-4-phenylpyridinium	177-202	monoamine oxidase B	Homo sapiens	0-19
3045798-3	1988	The most selective MAO-A inhibitors are moclobemide and brofaromine, with ratios between their MAO-A and MAO-B inhibiting potency (estimated in in vitro assays) of 1: greater than or equal to 1000 and 1:500, respectively, whereas the least selective drug is cimoxatone with a ratio of 1:66.	brofaromine	56-67	monoamine oxidase B	Homo sapiens	105-110
3258013-1	1988	Monoamine oxidase-B (MAO-B) has been determined to be the enzyme responsible for the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into its toxic metabolite 1-methyl-4-phenylpyridine ion (MPP+).	1-Methyl-4-phenylpyridinium	177-202	monoamine oxidase B	Homo sapiens	21-26
3258013-1	1988	Monoamine oxidase-B (MAO-B) has been determined to be the enzyme responsible for the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into its toxic metabolite 1-methyl-4-phenylpyridine ion (MPP+).	mangion-purified polysaccharide (Candida albicans)	208-211	monoamine oxidase B	Homo sapiens	0-19
3258013-1	1988	Monoamine oxidase-B (MAO-B) has been determined to be the enzyme responsible for the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into its toxic metabolite 1-methyl-4-phenylpyridine ion (MPP+).	mangion-purified polysaccharide (Candida albicans)	208-211	monoamine oxidase B	Homo sapiens	21-26
3145523-1	1988	Blood pressure and heart rate responses to oral tyramine have been measured in healthy volunteers before and after administration of the selective monoamine oxidase B inhibitor selegiline at high dosage (30 mg/day).	Selegiline	177-187	monoamine oxidase B	Homo sapiens	147-166
3266532-3	1988	Brain selectivity would overcome the risk of tyramine interactions which have been shown to occur with selective MAO-A but not MAO-B inhibitors.	Tyramine	45-53	monoamine oxidase B	Homo sapiens	127-132
3305061-0	1987	Immunohistochemical localization of monoamine oxidase-B in the cat brain: clues to understanding N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	97-141	monoamine oxidase B	Homo sapiens	36-55
3247497-6	1988	MAO-A and MAO-B of human liver mitochondria were also inhibited by L-DOPA (Ki = 152 microM and 275 microM, respectively).	Levodopa	67-73	monoamine oxidase B	Homo sapiens	10-15
3120270-5	1987	Selegiline, as well as causing MAO-B inhibition, is interconverted to amphetamine.	Amphetamine	70-81	monoamine oxidase B	Homo sapiens	31-36
3118881-0	1987	[13N]-beta-phenethylamine ([13N]PEA): a prototype tracer for measurement of MAO-B activity in heart.	Nitrogen-13	1-4	monoamine oxidase B	Homo sapiens	76-81
3118881-0	1987	[13N]-beta-phenethylamine ([13N]PEA): a prototype tracer for measurement of MAO-B activity in heart.	phenethylamine	6-25	monoamine oxidase B	Homo sapiens	76-81
3118881-0	1987	[13N]-beta-phenethylamine ([13N]PEA): a prototype tracer for measurement of MAO-B activity in heart.	Nitrogen-13	28-31	monoamine oxidase B	Homo sapiens	76-81
3118881-2	1987	After intravenous administration, [13N]PEA was deaminated by MAO-B.	Nitrogen-13	35-38	monoamine oxidase B	Homo sapiens	61-66
3118881-5	1987	The radioactivity in the heart 15 min after administration was reduced in a dose-dependent manner by pretreatment with a specific MAO-B inhibitor, l-deprenyl, but not with a specific MAO-A inhibitor, clorgyline.	Selegiline	147-157	monoamine oxidase B	Homo sapiens	130-135
3118881-9	1987	These results indicate that [13N]PEA derivatives ([13N]PEA and [13N]d2PEA) can be useful radiotracers for noninvasive measurements of MAO-B activity in the human heart.	Nitrogen-13	29-32	monoamine oxidase B	Homo sapiens	134-139
3118881-9	1987	These results indicate that [13N]PEA derivatives ([13N]PEA and [13N]d2PEA) can be useful radiotracers for noninvasive measurements of MAO-B activity in the human heart.	Nitrogen-13	51-54	monoamine oxidase B	Homo sapiens	134-139
3118881-9	1987	These results indicate that [13N]PEA derivatives ([13N]PEA and [13N]d2PEA) can be useful radiotracers for noninvasive measurements of MAO-B activity in the human heart.	Nitrogen-13	51-54	monoamine oxidase B	Homo sapiens	134-139
3305061-0	1987	Immunohistochemical localization of monoamine oxidase-B in the cat brain: clues to understanding N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	143-147	monoamine oxidase B	Homo sapiens	36-55
3116977-7	1987	Significantly lower MAO B activities were observed in hypertensive patients both in men (19.25 +/- 2.20, n = 8 versus 24.35 +/- 2.22, n = 14, desaminated beta-phenyl-ethylamine/10(9) platelets/hour, x +/- SEM, p less than 0.05) and in women (23.92 +/- 2.74, n = 10 versus 35.76 +/- 2.35, n = 21, p less than 0.01) when compared to normotensive controls of the same sex.	phenethylamine	154-176	monoamine oxidase B	Homo sapiens	20-25
3315149-5	1987	Firm supportive evidence is obtained from the monoamine oxidase B inhibitor experience which demonstrated a block of the toxicity of MPTP in animals and probable prolongation of the course of human Parkinson"s disease.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	133-137	monoamine oxidase B	Homo sapiens	46-65
3315149-6	1987	The scientific data available is inconclusive but there is significant hope of retarding progressive catecholaminergic neuron degenerative changes by augmenting the free radical scavenging system with antioxidants (such as Vitamin E) and slowing catecholamine oxidation by monoamine oxidase B inhibition.	Catecholamines	101-114	monoamine oxidase B	Homo sapiens	273-292
3110375-3	1987	This influx constant was used as a measure of functional enzyme activity for sequential determinations of MAO-B recovery following a single high dose of unlabeled L-deprenyl.	Selegiline	163-173	monoamine oxidase B	Homo sapiens	106-111
3114597-7	1987	An atypical irreversible MAO-B selective inhibitor, selegiline (deprenyl) does not exhibit an adverse reaction on the ingestion of amine-containing foods.	Selegiline	52-62	monoamine oxidase B	Homo sapiens	25-30
3114597-7	1987	An atypical irreversible MAO-B selective inhibitor, selegiline (deprenyl) does not exhibit an adverse reaction on the ingestion of amine-containing foods.	Selegiline	64-72	monoamine oxidase B	Homo sapiens	25-30
3116977-8	1987	Recent in vitro studies have suggested that a reduction in platelet MAO B activity may be induced by an alteration in the phospholipidic and/or calcium environment of the enzyme.	Calcium	144-151	monoamine oxidase B	Homo sapiens	68-73
3495646-0	1987	Kinetics of [11C]N,N-dimethylphenylethylamine in mice and humans: potential for measurement of brain MAO-B activity.	Carbon-11	13-16	monoamine oxidase B	Homo sapiens	101-106
2884568-2	1987	MPTP is metabolized by monoamine oxidase Type B to 1-methyl-4-phenylpyridine (MPP+), which is selectively accumulated by high-affinity uptake mechanisms into dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	23-47
2884568-2	1987	MPTP is metabolized by monoamine oxidase Type B to 1-methyl-4-phenylpyridine (MPP+), which is selectively accumulated by high-affinity uptake mechanisms into dopaminergic neurons.	1-Methyl-4-phenylpyridinium	51-76	monoamine oxidase B	Homo sapiens	23-47
2884568-2	1987	MPTP is metabolized by monoamine oxidase Type B to 1-methyl-4-phenylpyridine (MPP+), which is selectively accumulated by high-affinity uptake mechanisms into dopaminergic neurons.	mangion-purified polysaccharide (Candida albicans)	78-82	monoamine oxidase B	Homo sapiens	23-47
3107514-12	1987	The greater effect of low-dose L-deprenyl therapy suggests that it is the inhibition of MAO-B, and not MAO-A, that may be important in the behavioral effects of L-deprenyl administration to patients with DAT.	Selegiline	31-41	monoamine oxidase B	Homo sapiens	88-93
3495757-1	1987	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is oxidised to a neurotoxic metabolite by monoamine oxidase B (MAO B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-44	monoamine oxidase B	Homo sapiens	94-113
3495757-1	1987	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is oxidised to a neurotoxic metabolite by monoamine oxidase B (MAO B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-44	monoamine oxidase B	Homo sapiens	115-120
3495757-1	1987	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is oxidised to a neurotoxic metabolite by monoamine oxidase B (MAO B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	46-50	monoamine oxidase B	Homo sapiens	94-113
3495757-1	1987	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is oxidised to a neurotoxic metabolite by monoamine oxidase B (MAO B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	46-50	monoamine oxidase B	Homo sapiens	115-120
3107514-12	1987	The greater effect of low-dose L-deprenyl therapy suggests that it is the inhibition of MAO-B, and not MAO-A, that may be important in the behavioral effects of L-deprenyl administration to patients with DAT.	Selegiline	161-171	monoamine oxidase B	Homo sapiens	88-93
3821373-2	1987	Quinoline had a higher affinity for MAO than kynuramine.	quinoline	0-9	monoamine oxidase B	Homo sapiens	36-39
3566791-0	1987	Photoaffinity labeling of beef liver monoamine oxidase-B by 4-fluoro-3-nitrophenyl azide.	4-fluoro-3-nitrophenyl azide	60-88	monoamine oxidase B	Homo sapiens	37-56
3566791-1	1987	4-Fluoro-3-nitrophenyl azide (FNPA) competitively inhibited beef liver monoamine oxidase-B (MAO-B) in the dark (Ki = 2.8 microM).	4-fluoro-3-nitrophenyl azide	0-28	monoamine oxidase B	Homo sapiens	71-90
3566791-1	1987	4-Fluoro-3-nitrophenyl azide (FNPA) competitively inhibited beef liver monoamine oxidase-B (MAO-B) in the dark (Ki = 2.8 microM).	4-fluoro-3-nitrophenyl azide	0-28	monoamine oxidase B	Homo sapiens	92-97
3566791-1	1987	4-Fluoro-3-nitrophenyl azide (FNPA) competitively inhibited beef liver monoamine oxidase-B (MAO-B) in the dark (Ki = 2.8 microM).	4-fluoro-3-nitrophenyl azide	30-34	monoamine oxidase B	Homo sapiens	71-90
3821373-3	1987	MAO-A in human brain synaptosomal mitochondria was also competitively inhibited by quinoline, while type B MAO (MAO-B) was reversibly and non-competitively inhibited by quinoline.	quinoline	83-92	monoamine oxidase B	Homo sapiens	0-3
3566791-1	1987	4-Fluoro-3-nitrophenyl azide (FNPA) competitively inhibited beef liver monoamine oxidase-B (MAO-B) in the dark (Ki = 2.8 microM).	4-fluoro-3-nitrophenyl azide	30-34	monoamine oxidase B	Homo sapiens	92-97
3566791-5	1987	When [3H]FNPA was photoirradiated with the purified MAO-B, a single radioactive band associated with MAO-B was observed by sodium dodecyl sulfate polyacrylamide gel electrophoresis.	Tritium	6-8	monoamine oxidase B	Homo sapiens	52-57
3821373-3	1987	MAO-A in human brain synaptosomal mitochondria was also competitively inhibited by quinoline, while type B MAO (MAO-B) was reversibly and non-competitively inhibited by quinoline.	quinoline	169-178	monoamine oxidase B	Homo sapiens	0-3
3566791-5	1987	When [3H]FNPA was photoirradiated with the purified MAO-B, a single radioactive band associated with MAO-B was observed by sodium dodecyl sulfate polyacrylamide gel electrophoresis.	Tritium	6-8	monoamine oxidase B	Homo sapiens	101-106
3821373-3	1987	MAO-A in human brain synaptosomal mitochondria was also competitively inhibited by quinoline, while type B MAO (MAO-B) was reversibly and non-competitively inhibited by quinoline.	quinoline	169-178	monoamine oxidase B	Homo sapiens	112-117
3566791-5	1987	When [3H]FNPA was photoirradiated with the purified MAO-B, a single radioactive band associated with MAO-B was observed by sodium dodecyl sulfate polyacrylamide gel electrophoresis.	Sodium Dodecyl Sulfate	123-145	monoamine oxidase B	Homo sapiens	52-57
3566791-5	1987	When [3H]FNPA was photoirradiated with the purified MAO-B, a single radioactive band associated with MAO-B was observed by sodium dodecyl sulfate polyacrylamide gel electrophoresis.	Sodium Dodecyl Sulfate	123-145	monoamine oxidase B	Homo sapiens	101-106
3806102-5	1987	MAO-B in human brain synaptosomes and liver mitochondria was found to be inhibited by N-MIQ, but the inhibition proved to be noncompetitive.	N-methylisoquinolinium	86-91	monoamine oxidase B	Homo sapiens	0-5
3566791-5	1987	When [3H]FNPA was photoirradiated with the purified MAO-B, a single radioactive band associated with MAO-B was observed by sodium dodecyl sulfate polyacrylamide gel electrophoresis.	polyacrylamide	146-160	monoamine oxidase B	Homo sapiens	52-57
3566791-5	1987	When [3H]FNPA was photoirradiated with the purified MAO-B, a single radioactive band associated with MAO-B was observed by sodium dodecyl sulfate polyacrylamide gel electrophoresis.	polyacrylamide	146-160	monoamine oxidase B	Homo sapiens	101-106
3566791-6	1987	The photo-dependent incorporation could be protected by phenylethylamine, the substrate for MAO-B, in a concentration-dependent manner.	Phenethylamines	56-72	monoamine oxidase B	Homo sapiens	92-97
3566791-7	1987	Complete tryptic-chymotryptic digestion of [3H]FNPA-labeled MAO-B resulted in three radioactive peaks on Sephadex G-25 column chromatography.	Tritium	44-46	monoamine oxidase B	Homo sapiens	60-65
3566791-7	1987	Complete tryptic-chymotryptic digestion of [3H]FNPA-labeled MAO-B resulted in three radioactive peaks on Sephadex G-25 column chromatography.	sephadex	105-113	monoamine oxidase B	Homo sapiens	60-65
3566791-8	1987	With the same digestion and separation procedures, only one major radioactive peak was observed for the [3H]pargyline-labeled MAO-B, and its elution volume was different from that of [3H]FNPA-labeled peptides.	Tritium	105-107	monoamine oxidase B	Homo sapiens	126-131
3566791-8	1987	With the same digestion and separation procedures, only one major radioactive peak was observed for the [3H]pargyline-labeled MAO-B, and its elution volume was different from that of [3H]FNPA-labeled peptides.	Pargyline	108-117	monoamine oxidase B	Homo sapiens	126-131
3566791-9	1987	These results suggest that, upon photolysis, FNPA may incorporate into a region in the active site of MAO-B which may be different from the pargyline binding site--the FAD prosthetic group of the enzyme.	Pargyline	140-149	monoamine oxidase B	Homo sapiens	102-107
3566791-9	1987	These results suggest that, upon photolysis, FNPA may incorporate into a region in the active site of MAO-B which may be different from the pargyline binding site--the FAD prosthetic group of the enzyme.	Flavin-Adenine Dinucleotide	168-171	monoamine oxidase B	Homo sapiens	102-107
3806102-6	1987	The inhibition of MAO-B by N-MIQ was completely reversible by dialysis of the incubation mixture.	N-methylisoquinolinium	27-32	monoamine oxidase B	Homo sapiens	18-23
3494215-1	1987	1-Methyl-4-phenylpyridine (MPP+) is now confirmed to be one of the oxidative products of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by type B monoamine oxidase (MAO-B) and is considered to cause a parkinsonism-like syndrome.	1-Methyl-4-phenylpyridinium	0-25	monoamine oxidase B	Homo sapiens	170-175
2952905-1	1987	Quinolinic acid (QUIN), a well-known excitotoxin, was found to inhibit type B monoamine oxidase (MAO-B) in human brain synaptosomal mitochondria.	Quinolinic Acid	0-15	monoamine oxidase B	Homo sapiens	97-102
2952905-1	1987	Quinolinic acid (QUIN), a well-known excitotoxin, was found to inhibit type B monoamine oxidase (MAO-B) in human brain synaptosomal mitochondria.	Quinolinic Acid	17-21	monoamine oxidase B	Homo sapiens	97-102
2952905-2	1987	By kinetic analysis, the inhibition of MAO-B activity by QUIN was competitive with the substrate, kynuramine.	Quinolinic Acid	57-61	monoamine oxidase B	Homo sapiens	39-44
2952905-2	1987	By kinetic analysis, the inhibition of MAO-B activity by QUIN was competitive with the substrate, kynuramine.	Kynuramine	98-108	monoamine oxidase B	Homo sapiens	39-44
2952905-4	1987	The selective inhibition of MAO-B by QUIN was confirmed using human liver mitochondria; only MAO-B was inhibited by QUIN and MAO-A was not inhibited.	Quinolinic Acid	37-41	monoamine oxidase B	Homo sapiens	28-33
2952905-4	1987	The selective inhibition of MAO-B by QUIN was confirmed using human liver mitochondria; only MAO-B was inhibited by QUIN and MAO-A was not inhibited.	Quinolinic Acid	116-120	monoamine oxidase B	Homo sapiens	93-98
2952905-6	1987	Among compounds structurally related to QUIN, 4-pyrimidine carboxaldehyde was the most potent substrate-competitive inhibitor of MAO-B, while 3-hydroxyanthranilic acid and xanthrenic acid, other metabolites of tryptophan, inhibited MAO non-competitively with the substrate.	Quinolinic Acid	40-44	monoamine oxidase B	Homo sapiens	129-134
2952905-6	1987	Among compounds structurally related to QUIN, 4-pyrimidine carboxaldehyde was the most potent substrate-competitive inhibitor of MAO-B, while 3-hydroxyanthranilic acid and xanthrenic acid, other metabolites of tryptophan, inhibited MAO non-competitively with the substrate.	4-pyrimidine carboxaldehyde	46-73	monoamine oxidase B	Homo sapiens	129-134
2952905-6	1987	Among compounds structurally related to QUIN, 4-pyrimidine carboxaldehyde was the most potent substrate-competitive inhibitor of MAO-B, while 3-hydroxyanthranilic acid and xanthrenic acid, other metabolites of tryptophan, inhibited MAO non-competitively with the substrate.	Tryptophan	210-220	monoamine oxidase B	Homo sapiens	129-134
2952905-7	1987	The inhibition of MAO-B by QUIN may be related to the causes of the neurotoxicity of QUIN.	Quinolinic Acid	27-31	monoamine oxidase B	Homo sapiens	18-23
2952905-7	1987	The inhibition of MAO-B by QUIN may be related to the causes of the neurotoxicity of QUIN.	Quinolinic Acid	85-89	monoamine oxidase B	Homo sapiens	18-23
3494215-1	1987	1-Methyl-4-phenylpyridine (MPP+) is now confirmed to be one of the oxidative products of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by type B monoamine oxidase (MAO-B) and is considered to cause a parkinsonism-like syndrome.	mangion-purified polysaccharide (Candida albicans)	27-31	monoamine oxidase B	Homo sapiens	170-175
3099392-3	1987	The anatomical distribution of 11C paralleled the distribution of MAO A and MAO B in human brain in autopsy material.	Carbon-11	31-34	monoamine oxidase B	Homo sapiens	76-81
3494215-1	1987	1-Methyl-4-phenylpyridine (MPP+) is now confirmed to be one of the oxidative products of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by type B monoamine oxidase (MAO-B) and is considered to cause a parkinsonism-like syndrome.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	89-133	monoamine oxidase B	Homo sapiens	170-175
3099392-6	1987	A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl.	Carbon-11	54-57	monoamine oxidase B	Homo sapiens	216-221
3494215-1	1987	1-Methyl-4-phenylpyridine (MPP+) is now confirmed to be one of the oxidative products of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by type B monoamine oxidase (MAO-B) and is considered to cause a parkinsonism-like syndrome.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	135-139	monoamine oxidase B	Homo sapiens	170-175
3099392-6	1987	A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl.	Carbon-11	54-57	monoamine oxidase B	Homo sapiens	294-299
3099392-6	1987	A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl.	Selegiline	111-119	monoamine oxidase B	Homo sapiens	216-221
3494215-1	1987	1-Methyl-4-phenylpyridine (MPP+) is now confirmed to be one of the oxidative products of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by type B monoamine oxidase (MAO-B) and is considered to cause a parkinsonism-like syndrome.	monoamine	151-160	monoamine oxidase B	Homo sapiens	170-175
3099392-6	1987	A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl.	Selegiline	111-119	monoamine oxidase B	Homo sapiens	294-299
3593489-0	1987	Selective inhibition of monoamine oxidase type B by chlormethiazole.	Chlormethiazole	52-67	monoamine oxidase B	Homo sapiens	24-48
3030067-2	1987	L-Deprenyl, a selective inhibitor of MAO-B, was introduced by us into clinical use as an adjunct to L-DOPA some years ago.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	37-42
3030067-4	1987	The mechanism underlying the action of L-deprenyl is thought to be related to its inhibition of MAO-B and thus increased levels of PEA and DA, as measured in the striatal and limbic region of human brain.	Selegiline	39-49	monoamine oxidase B	Homo sapiens	96-101
3030067-0	1987	Localization of MAO-A and MAO-B in human brain: a step in understanding the therapeutic action of L-deprenyl.	Selegiline	98-108	monoamine oxidase B	Homo sapiens	26-31
3556086-2	1987	The offending agent, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has to be converted by monoamine oxidase B perhaps in glia, into the neurotoxin, 1-methyl-4-phenylpyridinium (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	21-65	monoamine oxidase B	Homo sapiens	97-116
3556086-2	1987	The offending agent, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has to be converted by monoamine oxidase B perhaps in glia, into the neurotoxin, 1-methyl-4-phenylpyridinium (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	67-71	monoamine oxidase B	Homo sapiens	97-116
3556086-2	1987	The offending agent, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has to be converted by monoamine oxidase B perhaps in glia, into the neurotoxin, 1-methyl-4-phenylpyridinium (MPP+).	1-Methyl-4-phenylpyridinium	155-182	monoamine oxidase B	Homo sapiens	97-116
3556086-2	1987	The offending agent, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has to be converted by monoamine oxidase B perhaps in glia, into the neurotoxin, 1-methyl-4-phenylpyridinium (MPP+).	mangion-purified polysaccharide (Candida albicans)	184-188	monoamine oxidase B	Homo sapiens	97-116
3498665-7	1987	Our results suggest that excitotoxic mechanisms may participate in the neurotoxic effect of MPTP and they can be abolished by the monoamine-oxidase B (MAO-B) inhibitor.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	92-96	monoamine oxidase B	Homo sapiens	130-149
3498665-7	1987	Our results suggest that excitotoxic mechanisms may participate in the neurotoxic effect of MPTP and they can be abolished by the monoamine-oxidase B (MAO-B) inhibitor.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	92-96	monoamine oxidase B	Homo sapiens	151-156
3108452-4	1987	Moreover, a tetrahydropyridine derivative (MPTP), recently described as an irreversible inhibitor of MAO-B, has been included among the irreversible MAOIs.	Pyrrolidines	12-30	monoamine oxidase B	Homo sapiens	101-106
3108452-4	1987	Moreover, a tetrahydropyridine derivative (MPTP), recently described as an irreversible inhibitor of MAO-B, has been included among the irreversible MAOIs.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	43-47	monoamine oxidase B	Homo sapiens	101-106
3123605-1	1987	L-deprenyl is a potent, well tolerated and safe inhibitor agent of MAO-B.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	67-72
3123595-0	1987	MAO-B-Inhibitor selegiline (R-(-)-deprenyl).	Selegiline	16-26	monoamine oxidase B	Homo sapiens	0-5
3123606-1	1987	The selective monoamine oxidase (MAO) B inhibitor L-deprenyl (Eldepryl, Jumex, Movergan, Selegiline) has gained acceptance as a useful form of adjunctive therapy in the treatment of Parkinson"s disease.	Selegiline	50-60	monoamine oxidase B	Homo sapiens	14-39
3123606-1	1987	The selective monoamine oxidase (MAO) B inhibitor L-deprenyl (Eldepryl, Jumex, Movergan, Selegiline) has gained acceptance as a useful form of adjunctive therapy in the treatment of Parkinson"s disease.	Selegiline	89-99	monoamine oxidase B	Homo sapiens	14-39
3123595-0	1987	MAO-B-Inhibitor selegiline (R-(-)-deprenyl).	r-(-)-deprenyl	28-42	monoamine oxidase B	Homo sapiens	0-5
3295117-1	1987	MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a selective nigrostriatal neurotoxin, is bioactivated by MAO-B (and less effectively by MAO-A) to 2,3-MPDP+ and this intermediate undergoes further oxidation to MPP+, partly through the activity of MAO forms.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	110-115
3480939-1	1987	The absence of initiation of "cheese effect" (potentiation of sympathomimetic action of tyramine) by 1-deprenyl (selective monoamine oxidase, MAO-B inhibitor) was regarded to be an intrinsic property of this inhibitor.	1-deprenyl	101-111	monoamine oxidase B	Homo sapiens	142-147
3794699-0	1987	Binding of [3H]Ro 16-6491, a reversible inhibitor of monoamine oxidase type B, to human brain mitochondria and platelet membranes.	Tritium	12-14	monoamine oxidase B	Homo sapiens	53-77
3480939-2	1987	However, availability of other selective MAO-B inhibitors have clearly shown that this is not the case, since the "cheese effect" is associated with the selective inhibition of MAO-A, the enzyme responsible for intraneuronal oxidation of noradrenaline.	Norepinephrine	238-251	monoamine oxidase B	Homo sapiens	41-46
3295117-1	1987	MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a selective nigrostriatal neurotoxin, is bioactivated by MAO-B (and less effectively by MAO-A) to 2,3-MPDP+ and this intermediate undergoes further oxidation to MPP+, partly through the activity of MAO forms.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	6-50	monoamine oxidase B	Homo sapiens	110-115
3794699-3	1987	Inhibitors and substrates of MAO-B inhibited binding of [3H]Ro 16-6491, whereas MAO-A blockers were much less potent.	Tritium	57-59	monoamine oxidase B	Homo sapiens	29-34
3794699-0	1987	Binding of [3H]Ro 16-6491, a reversible inhibitor of monoamine oxidase type B, to human brain mitochondria and platelet membranes.	Ro 16-6491	15-25	monoamine oxidase B	Homo sapiens	53-77
3794699-4	1987	Ro 16-6491 was also a substrate for MAO-B and a stable unidentified intermediate of the oxidation of Ro 16-6491 possessing high affinity for the enzyme may account for the marked MAO-B inhibitory effect of the drug.	Ro 16-6491	0-10	monoamine oxidase B	Homo sapiens	36-41
3794699-1	1987	The reversible inhibitor of monoamine oxidase type B (MAO-B) [3H]Ro 16-6491 binds specifically and with high affinity to a single population of binding sites in human frontal cortex crude mitochondria and platelet membranes.	Tritium	62-64	monoamine oxidase B	Homo sapiens	28-52
3794699-4	1987	Ro 16-6491 was also a substrate for MAO-B and a stable unidentified intermediate of the oxidation of Ro 16-6491 possessing high affinity for the enzyme may account for the marked MAO-B inhibitory effect of the drug.	Ro 16-6491	0-10	monoamine oxidase B	Homo sapiens	179-184
3794699-4	1987	Ro 16-6491 was also a substrate for MAO-B and a stable unidentified intermediate of the oxidation of Ro 16-6491 possessing high affinity for the enzyme may account for the marked MAO-B inhibitory effect of the drug.	Ro 16-6491	101-111	monoamine oxidase B	Homo sapiens	179-184
3794699-1	1987	The reversible inhibitor of monoamine oxidase type B (MAO-B) [3H]Ro 16-6491 binds specifically and with high affinity to a single population of binding sites in human frontal cortex crude mitochondria and platelet membranes.	Tritium	62-64	monoamine oxidase B	Homo sapiens	54-59
3794699-6	1987	In conclusion, [3H]Ro 16-6491 binds selectively to MAO-B and represents an excellent new radioligand probe for studying the regional tissue distribution of this enzyme in normal and pathological conditions.	Tritium	16-18	monoamine oxidase B	Homo sapiens	51-56
3794699-1	1987	The reversible inhibitor of monoamine oxidase type B (MAO-B) [3H]Ro 16-6491 binds specifically and with high affinity to a single population of binding sites in human frontal cortex crude mitochondria and platelet membranes.	Ro 16-6491	65-75	monoamine oxidase B	Homo sapiens	28-52
3794699-1	1987	The reversible inhibitor of monoamine oxidase type B (MAO-B) [3H]Ro 16-6491 binds specifically and with high affinity to a single population of binding sites in human frontal cortex crude mitochondria and platelet membranes.	Ro 16-6491	65-75	monoamine oxidase B	Homo sapiens	54-59
20501066-6	1987	They could be protected by the presence of the substrate (phenylethylamine) or inhibitors (pargyline and trans-phenylcyclopropylamine) of MAO-B during photolysis.	Pargyline	91-100	monoamine oxidase B	Homo sapiens	138-143
20501066-6	1987	They could be protected by the presence of the substrate (phenylethylamine) or inhibitors (pargyline and trans-phenylcyclopropylamine) of MAO-B during photolysis.	Tranylcypromine	105-133	monoamine oxidase B	Homo sapiens	138-143
20501066-0	1987	4-Fluoro-3-nitrophenyl azide binding sites on purified beef liver monoamine oxidase B.	4-fluoro-3-nitrophenyl azide	0-28	monoamine oxidase B	Homo sapiens	66-85
20501066-1	1987	Previous work from this laboratory has shown that 4-fluoro-3-nitrophenyl azide (FNPA) is an effective photoaffinity labeling probe for MAO-B (Chen et al., Biochem.	4-fluoro-3-nitrophenyl azide	50-78	monoamine oxidase B	Homo sapiens	135-140
20501066-1	1987	Previous work from this laboratory has shown that 4-fluoro-3-nitrophenyl azide (FNPA) is an effective photoaffinity labeling probe for MAO-B (Chen et al., Biochem.	4-fluoro-3-nitrophenyl azide	80-84	monoamine oxidase B	Homo sapiens	135-140
2436247-5	1987	These dose-dependent reductions are consistent with in vitro biochemical and anatomical data from primate brain suggesting that at low doses of deprenyl, MAO-B inhibition might be expected to selectively affect dopamine and serotonin-containing neurons, while at higher doses (which lead to MAO-A as well as MAO-B inhibition), noradrenergic neurons may become relatively more affected by the drug.	Serotonin	224-233	monoamine oxidase B	Homo sapiens	154-159
20501066-6	1987	They could be protected by the presence of the substrate (phenylethylamine) or inhibitors (pargyline and trans-phenylcyclopropylamine) of MAO-B during photolysis.	Phenethylamines	58-74	monoamine oxidase B	Homo sapiens	138-143
2436247-1	1987	Deprenyl, a monoamine oxidase (MAO) inhibitor with selective effects on MAO type-B at low doses, was administered to 13 patients with dementia of the Alzheimer type (DAT), a disorder reported to be associated with increased brain MAO-B activity.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	230-235
2878540-7	1986	Modern treatment strategies (combined L-dopa therapy, dopaminergic agonists, MAO-B inhibitors, amantadine) are able to substitute the deficiency especially of the catecholamines.	Catecholamines	163-177	monoamine oxidase B	Homo sapiens	77-82
2436247-5	1987	These dose-dependent reductions are consistent with in vitro biochemical and anatomical data from primate brain suggesting that at low doses of deprenyl, MAO-B inhibition might be expected to selectively affect dopamine and serotonin-containing neurons, while at higher doses (which lead to MAO-A as well as MAO-B inhibition), noradrenergic neurons may become relatively more affected by the drug.	Selegiline	144-152	monoamine oxidase B	Homo sapiens	154-159
2436247-5	1987	These dose-dependent reductions are consistent with in vitro biochemical and anatomical data from primate brain suggesting that at low doses of deprenyl, MAO-B inhibition might be expected to selectively affect dopamine and serotonin-containing neurons, while at higher doses (which lead to MAO-A as well as MAO-B inhibition), noradrenergic neurons may become relatively more affected by the drug.	Selegiline	144-152	monoamine oxidase B	Homo sapiens	308-313
2436247-5	1987	These dose-dependent reductions are consistent with in vitro biochemical and anatomical data from primate brain suggesting that at low doses of deprenyl, MAO-B inhibition might be expected to selectively affect dopamine and serotonin-containing neurons, while at higher doses (which lead to MAO-A as well as MAO-B inhibition), noradrenergic neurons may become relatively more affected by the drug.	Dopamine	211-219	monoamine oxidase B	Homo sapiens	154-159
3108930-3	1987	L-Deprenyl is a monoamine oxidase (MAO) inhibitor which may selectively inhibit MAO-B at low doses, while at high doses it nonselectively inhibits MAO-A as well as MAO-B.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	80-85
3108930-3	1987	L-Deprenyl is a monoamine oxidase (MAO) inhibitor which may selectively inhibit MAO-B at low doses, while at high doses it nonselectively inhibits MAO-A as well as MAO-B.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	164-169
3490614-5	1986	Our findings support previous evidence indicating a correspondence between 3H-MPTP binding sites and MAO-B enzyme.	3h-mptp	75-82	monoamine oxidase B	Homo sapiens	101-106
3097589-2	1986	Further, utilization of specific inhibitors, deprenyl and clorgyline, also provides evidence that serotonergic neurons contain exclusively MAO-B and catecholaminergic ones contain MAO-A.	Selegiline	45-53	monoamine oxidase B	Homo sapiens	139-144
3097589-2	1986	Further, utilization of specific inhibitors, deprenyl and clorgyline, also provides evidence that serotonergic neurons contain exclusively MAO-B and catecholaminergic ones contain MAO-A.	Clorgyline	58-68	monoamine oxidase B	Homo sapiens	139-144
2420928-6	1986	Brains obtained at autopsy from l-deprenyl-treated Parkinsonian patients showed that, whereas MAO-B was fully inhibited by the therapeutic doses of l-deprenyl, substantial MAO-A activity was still evident.	Selegiline	32-42	monoamine oxidase B	Homo sapiens	94-99
3741695-1	1986	Monoamine oxidase B has been purified from human blood platelets 185-fold to a specific activity of 113 nmole/min/mg protein by a combination of Triton X-100 solubilization and ion exchange chromatography.	Octoxynol	145-157	monoamine oxidase B	Homo sapiens	0-19
3013661-2	1986	Although (-)adrenaline is a good substrate for the platelet enzyme MAO-B, enzymatic inhibition was not a prerequisite to quantify the specific binding of the radioligand to platelet membranes.	Epinephrine	12-22	monoamine oxidase B	Homo sapiens	67-72
2420928-5	1986	N-Desmethylpropargylindane hydrochloride (AGN 1135) was also shown to have MAO-B inhibitory selectivity similar to that of l-deprenyl.	n-desmethylpropargylindane hydrochloride	0-40	monoamine oxidase B	Homo sapiens	75-80
3748456-2	1986	We have found the phospholipid, phosphatidylserine (PS) to be a highly specific inhibitor of MAO-B, which has led us to postulate that the PS-MAO interaction might offer a basis for the lower MAO levels observed in platelets from certain schizophrenic populations.	Phospholipids	18-30	monoamine oxidase B	Homo sapiens	93-98
3748456-2	1986	We have found the phospholipid, phosphatidylserine (PS) to be a highly specific inhibitor of MAO-B, which has led us to postulate that the PS-MAO interaction might offer a basis for the lower MAO levels observed in platelets from certain schizophrenic populations.	Phosphatidylserines	32-50	monoamine oxidase B	Homo sapiens	93-98
3748456-2	1986	We have found the phospholipid, phosphatidylserine (PS) to be a highly specific inhibitor of MAO-B, which has led us to postulate that the PS-MAO interaction might offer a basis for the lower MAO levels observed in platelets from certain schizophrenic populations.	Phosphatidylserines	52-54	monoamine oxidase B	Homo sapiens	93-98
3088511-0	1986	[Treatment of extra-puerperal galactorrhea with the MAO-B inhibitor selegiline].	Selegiline	68-78	monoamine oxidase B	Homo sapiens	52-57
2420928-6	1986	Brains obtained at autopsy from l-deprenyl-treated Parkinsonian patients showed that, whereas MAO-B was fully inhibited by the therapeutic doses of l-deprenyl, substantial MAO-A activity was still evident.	Selegiline	148-158	monoamine oxidase B	Homo sapiens	94-99
2420928-5	1986	N-Desmethylpropargylindane hydrochloride (AGN 1135) was also shown to have MAO-B inhibitory selectivity similar to that of l-deprenyl.	rasagiline	42-50	monoamine oxidase B	Homo sapiens	75-80
2420928-8	1986	These data indicate that the therapeutic actions of l-deprenyl may lie in its selective inhibition of MAO-B resulting in increased brain levels of DA formed from L-dihydroxyphenylacetic acid (L-DOPA).	Selegiline	52-62	monoamine oxidase B	Homo sapiens	102-107
2420928-8	1986	These data indicate that the therapeutic actions of l-deprenyl may lie in its selective inhibition of MAO-B resulting in increased brain levels of DA formed from L-dihydroxyphenylacetic acid (L-DOPA).	amsonic acid	147-149	monoamine oxidase B	Homo sapiens	102-107
2420928-8	1986	These data indicate that the therapeutic actions of l-deprenyl may lie in its selective inhibition of MAO-B resulting in increased brain levels of DA formed from L-dihydroxyphenylacetic acid (L-DOPA).	l-dihydroxyphenylacetic acid	162-190	monoamine oxidase B	Homo sapiens	102-107
2420928-8	1986	These data indicate that the therapeutic actions of l-deprenyl may lie in its selective inhibition of MAO-B resulting in increased brain levels of DA formed from L-dihydroxyphenylacetic acid (L-DOPA).	Levodopa	192-198	monoamine oxidase B	Homo sapiens	102-107
3485717-0	1986	Interaction of monoamine oxidase B with analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine derived from prodine-type analgesics.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	53-97	monoamine oxidase B	Homo sapiens	15-34
3485542-0	1986	Studies on the mechanism of MPTP oxidation by human liver monoamine oxidase B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	28-32	monoamine oxidase B	Homo sapiens	58-77
3485542-1	1986	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its deuterated analogues were oxidized to their corresponding dihydropyridinium species (MPDP+) by preparations of pure human liver MAO B:monoclonal antibody complex to investigate the mechanism of MPTP activation.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	15-59	monoamine oxidase B	Homo sapiens	203-208
3485542-1	1986	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its deuterated analogues were oxidized to their corresponding dihydropyridinium species (MPDP+) by preparations of pure human liver MAO B:monoclonal antibody complex to investigate the mechanism of MPTP activation.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	61-65	monoamine oxidase B	Homo sapiens	203-208
3527152-3	1986	The antibody indirectly precipitates [3H]pargyline-labelled human MAO B both from liver and platelet extracts but fails to precipitate MAO A from liver extracts.	Tritium	38-40	monoamine oxidase B	Homo sapiens	66-71
3527152-3	1986	The antibody indirectly precipitates [3H]pargyline-labelled human MAO B both from liver and platelet extracts but fails to precipitate MAO A from liver extracts.	Pargyline	41-50	monoamine oxidase B	Homo sapiens	66-71
3485542-1	1986	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its deuterated analogues were oxidized to their corresponding dihydropyridinium species (MPDP+) by preparations of pure human liver MAO B:monoclonal antibody complex to investigate the mechanism of MPTP activation.	dihydropyridinium	133-150	monoamine oxidase B	Homo sapiens	203-208
3485542-1	1986	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its deuterated analogues were oxidized to their corresponding dihydropyridinium species (MPDP+) by preparations of pure human liver MAO B:monoclonal antibody complex to investigate the mechanism of MPTP activation.	1-methyl-4-phenyl-2,3-dihydropyridinium	160-164	monoamine oxidase B	Homo sapiens	203-208
3485542-5	1986	These studies support the interpretation that oxidation of MPTP at the C-6 position on the tetrahydropyridine ring is a major rate-determining step in its biotransformation by MAO B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	59-63	monoamine oxidase B	Homo sapiens	176-181
3485542-5	1986	These studies support the interpretation that oxidation of MPTP at the C-6 position on the tetrahydropyridine ring is a major rate-determining step in its biotransformation by MAO B.	Pyrrolidines	91-109	monoamine oxidase B	Homo sapiens	176-181
3485717-0	1986	Interaction of monoamine oxidase B with analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine derived from prodine-type analgesics.	Alphaprodine	111-118	monoamine oxidase B	Homo sapiens	15-34
3083305-0	1986	Monoamine oxidase B(MAO-B) is the major catalyst for 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) oxidation in human brain and other tissues.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	53-97	monoamine oxidase B	Homo sapiens	0-19
3954792-0	1986	Stereospecific deuterium substitution at the alpha-carbon position of dopamine and its effect on oxidative deamination catalyzed by MAO-A and MAO-B from different tissues.	Deuterium	15-24	monoamine oxidase B	Homo sapiens	142-147
3954792-0	1986	Stereospecific deuterium substitution at the alpha-carbon position of dopamine and its effect on oxidative deamination catalyzed by MAO-A and MAO-B from different tissues.	alpha-	45-51	monoamine oxidase B	Homo sapiens	142-147
3954792-0	1986	Stereospecific deuterium substitution at the alpha-carbon position of dopamine and its effect on oxidative deamination catalyzed by MAO-A and MAO-B from different tissues.	Carbon	51-57	monoamine oxidase B	Homo sapiens	142-147
3954792-0	1986	Stereospecific deuterium substitution at the alpha-carbon position of dopamine and its effect on oxidative deamination catalyzed by MAO-A and MAO-B from different tissues.	Dopamine	70-78	monoamine oxidase B	Homo sapiens	142-147
3083305-0	1986	Monoamine oxidase B(MAO-B) is the major catalyst for 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) oxidation in human brain and other tissues.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	53-97	monoamine oxidase B	Homo sapiens	20-25
3083305-0	1986	Monoamine oxidase B(MAO-B) is the major catalyst for 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) oxidation in human brain and other tissues.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	99-103	monoamine oxidase B	Homo sapiens	0-19
3083305-0	1986	Monoamine oxidase B(MAO-B) is the major catalyst for 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) oxidation in human brain and other tissues.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	99-103	monoamine oxidase B	Homo sapiens	20-25
3083305-2	1986	This assay has been used to show that the rate of oxidation of MPTP parallels that of phenylethylamine in a range of human and rodent tissues, providing strong evidence that this reaction is predominantly catalysed by monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	63-67	monoamine oxidase B	Homo sapiens	218-237
3083305-2	1986	This assay has been used to show that the rate of oxidation of MPTP parallels that of phenylethylamine in a range of human and rodent tissues, providing strong evidence that this reaction is predominantly catalysed by monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	63-67	monoamine oxidase B	Homo sapiens	239-244
3083305-2	1986	This assay has been used to show that the rate of oxidation of MPTP parallels that of phenylethylamine in a range of human and rodent tissues, providing strong evidence that this reaction is predominantly catalysed by monoamine oxidase B (MAO-B).	Phenethylamines	86-102	monoamine oxidase B	Homo sapiens	218-237
3083305-2	1986	This assay has been used to show that the rate of oxidation of MPTP parallels that of phenylethylamine in a range of human and rodent tissues, providing strong evidence that this reaction is predominantly catalysed by monoamine oxidase B (MAO-B).	Phenethylamines	86-102	monoamine oxidase B	Homo sapiens	239-244
3083305-3	1986	In human brain the reaction was inhibited by selective doses of the MAO-B inhibitor (-)-deprenyl.	Selegiline	84-96	monoamine oxidase B	Homo sapiens	68-73
3082793-1	1986	A multicenter trial was conducted at 9 Neurology Departments to evaluate the action of L-Deprenyl, a specific monoamine oxidase-B inhibitor, combined with L-Dopa in the treatment of Parkinson disease.	Selegiline	87-97	monoamine oxidase B	Homo sapiens	110-129
3486945-2	1986	PD may possibly be caused by one or more unidentified neurotoxins which chemically resemble N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a substance which after conversion to an active neurotoxin by monoamine oxidase B (MAO-B) can extensively damage dopaminergic nigrostriatal neurons in humans, lower primates and mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	92-136	monoamine oxidase B	Homo sapiens	207-226
3486945-2	1986	PD may possibly be caused by one or more unidentified neurotoxins which chemically resemble N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a substance which after conversion to an active neurotoxin by monoamine oxidase B (MAO-B) can extensively damage dopaminergic nigrostriatal neurons in humans, lower primates and mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	92-136	monoamine oxidase B	Homo sapiens	228-233
3486945-2	1986	PD may possibly be caused by one or more unidentified neurotoxins which chemically resemble N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a substance which after conversion to an active neurotoxin by monoamine oxidase B (MAO-B) can extensively damage dopaminergic nigrostriatal neurons in humans, lower primates and mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	138-142	monoamine oxidase B	Homo sapiens	207-226
3486945-2	1986	PD may possibly be caused by one or more unidentified neurotoxins which chemically resemble N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a substance which after conversion to an active neurotoxin by monoamine oxidase B (MAO-B) can extensively damage dopaminergic nigrostriatal neurons in humans, lower primates and mice.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	138-142	monoamine oxidase B	Homo sapiens	228-233
3753647-0	1986	(Z)-2-(2,4-Dichlorophenoxy)methyl-3-fluoroallylamine (MDL 72638): a clorgyline analogue with surprising selectivity for monoamine oxidase type B.	2-(2,4-Dichlorophenoxy)methyl-3-fluoroallylamine	0-52	monoamine oxidase B	Homo sapiens	120-144
3008207-5	1986	This clorgyline dose was selective for MAO type A inhibition, as MAO-B activity measured in platelets from the same blood samples was unaffected by clorgyline.	Clorgyline	5-15	monoamine oxidase B	Homo sapiens	65-70
3008207-6	1986	In contrast, the selective MAO-B inhibitor deprenyl (10-30 mg/day for 3 weeks) led to a 96 +/- 4% inhibition of platelet MAO-B activity but no significant change in plasma melatonin (5.1 +/- SD 4.2 pg/ml).	Selegiline	43-51	monoamine oxidase B	Homo sapiens	27-32
3008207-6	1986	In contrast, the selective MAO-B inhibitor deprenyl (10-30 mg/day for 3 weeks) led to a 96 +/- 4% inhibition of platelet MAO-B activity but no significant change in plasma melatonin (5.1 +/- SD 4.2 pg/ml).	Selegiline	43-51	monoamine oxidase B	Homo sapiens	121-126
3008207-7	1986	As both serotonin and norepinephrine are preferentially metabolized by MAO-A rather than MAO-B, an increased availability of serotonin (the precursor of melatonin) or enhanced noradrenergic function might mediate the melatonin changes observed to follow MAO-A but not MAO-B inhibition.	Serotonin	8-17	monoamine oxidase B	Homo sapiens	268-273
3008207-7	1986	As both serotonin and norepinephrine are preferentially metabolized by MAO-A rather than MAO-B, an increased availability of serotonin (the precursor of melatonin) or enhanced noradrenergic function might mediate the melatonin changes observed to follow MAO-A but not MAO-B inhibition.	Norepinephrine	22-36	monoamine oxidase B	Homo sapiens	89-94
3008207-7	1986	As both serotonin and norepinephrine are preferentially metabolized by MAO-A rather than MAO-B, an increased availability of serotonin (the precursor of melatonin) or enhanced noradrenergic function might mediate the melatonin changes observed to follow MAO-A but not MAO-B inhibition.	Norepinephrine	22-36	monoamine oxidase B	Homo sapiens	268-273
3008207-7	1986	As both serotonin and norepinephrine are preferentially metabolized by MAO-A rather than MAO-B, an increased availability of serotonin (the precursor of melatonin) or enhanced noradrenergic function might mediate the melatonin changes observed to follow MAO-A but not MAO-B inhibition.	Serotonin	125-134	monoamine oxidase B	Homo sapiens	268-273
3008207-7	1986	As both serotonin and norepinephrine are preferentially metabolized by MAO-A rather than MAO-B, an increased availability of serotonin (the precursor of melatonin) or enhanced noradrenergic function might mediate the melatonin changes observed to follow MAO-A but not MAO-B inhibition.	Melatonin	217-226	monoamine oxidase B	Homo sapiens	268-273
3753647-0	1986	(Z)-2-(2,4-Dichlorophenoxy)methyl-3-fluoroallylamine (MDL 72638): a clorgyline analogue with surprising selectivity for monoamine oxidase type B.	Clorgyline	68-78	monoamine oxidase B	Homo sapiens	120-144
3091760-8	1986	The ability of monoamine oxidase inhibitors to prevent MPTP toxicity is related to the metabolism of MPTP by monoamine oxidase B, probably extraneuronally in glia, to produce MPDP+ and subsequently MPP+.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	55-59	monoamine oxidase B	Homo sapiens	109-128
3942801-1	1986	Phosphatidylserine (PS) has recently been reported to be a specific inhibitor of B-type monoamine oxidase (MAO-B).	Phosphatidylserines	0-18	monoamine oxidase B	Homo sapiens	107-112
3942801-1	1986	Phosphatidylserine (PS) has recently been reported to be a specific inhibitor of B-type monoamine oxidase (MAO-B).	Phosphatidylserines	20-22	monoamine oxidase B	Homo sapiens	107-112
3942801-8	1986	The results were consistent with an in vivo role for PS as an allosteric regulator of platelet MAO-B.	Phosphatidylserines	53-55	monoamine oxidase B	Homo sapiens	95-100
2875125-3	1986	In humans treated with the MAO-A selective inhibitor, clorgyline, or the nonselective inhibitor, tranylcypromine, increased plasma melatonin also occurs; in contrast, the MAO-B selective inhibitor, 1-deprenyl, does not affect plasma melatonin.	Clorgyline	54-64	monoamine oxidase B	Homo sapiens	171-176
2875125-3	1986	In humans treated with the MAO-A selective inhibitor, clorgyline, or the nonselective inhibitor, tranylcypromine, increased plasma melatonin also occurs; in contrast, the MAO-B selective inhibitor, 1-deprenyl, does not affect plasma melatonin.	Tranylcypromine	97-112	monoamine oxidase B	Homo sapiens	171-176
3097254-2	1986	Monoamine oxidase (MAO) B converts MPTP to an actual neurotoxin, 1-methyl-4-phenylpyridinium (MPP+) whilst prior administration of an MAO B inhibitor, (-)deprenyl, prevents the conversion.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	35-39	monoamine oxidase B	Homo sapiens	0-25
3097254-2	1986	Monoamine oxidase (MAO) B converts MPTP to an actual neurotoxin, 1-methyl-4-phenylpyridinium (MPP+) whilst prior administration of an MAO B inhibitor, (-)deprenyl, prevents the conversion.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	35-39	monoamine oxidase B	Homo sapiens	134-139
3097254-2	1986	Monoamine oxidase (MAO) B converts MPTP to an actual neurotoxin, 1-methyl-4-phenylpyridinium (MPP+) whilst prior administration of an MAO B inhibitor, (-)deprenyl, prevents the conversion.	1-Methyl-4-phenylpyridinium	65-92	monoamine oxidase B	Homo sapiens	0-25
3097254-2	1986	Monoamine oxidase (MAO) B converts MPTP to an actual neurotoxin, 1-methyl-4-phenylpyridinium (MPP+) whilst prior administration of an MAO B inhibitor, (-)deprenyl, prevents the conversion.	mangion-purified polysaccharide (Candida albicans)	94-98	monoamine oxidase B	Homo sapiens	0-25
3097254-2	1986	Monoamine oxidase (MAO) B converts MPTP to an actual neurotoxin, 1-methyl-4-phenylpyridinium (MPP+) whilst prior administration of an MAO B inhibitor, (-)deprenyl, prevents the conversion.	mangion-purified polysaccharide (Candida albicans)	94-98	monoamine oxidase B	Homo sapiens	134-139
2875125-3	1986	In humans treated with the MAO-A selective inhibitor, clorgyline, or the nonselective inhibitor, tranylcypromine, increased plasma melatonin also occurs; in contrast, the MAO-B selective inhibitor, 1-deprenyl, does not affect plasma melatonin.	Melatonin	131-140	monoamine oxidase B	Homo sapiens	171-176
2875125-3	1986	In humans treated with the MAO-A selective inhibitor, clorgyline, or the nonselective inhibitor, tranylcypromine, increased plasma melatonin also occurs; in contrast, the MAO-B selective inhibitor, 1-deprenyl, does not affect plasma melatonin.	1-deprenyl	198-208	monoamine oxidase B	Homo sapiens	171-176
3091760-8	1986	The ability of monoamine oxidase inhibitors to prevent MPTP toxicity is related to the metabolism of MPTP by monoamine oxidase B, probably extraneuronally in glia, to produce MPDP+ and subsequently MPP+.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	101-105	monoamine oxidase B	Homo sapiens	109-128
3097254-5	1986	Possibly approaches are by monitoring putative overactivity of the dopamine degrading enzymes, phenolsulphotransferase and MAO B, narrowing the field down further by PET-scan after administering a positron-emitting dopa analogue, 6-18F-labelled dopa.	Dihydroxyphenylalanine	215-219	monoamine oxidase B	Homo sapiens	123-128
3091760-8	1986	The ability of monoamine oxidase inhibitors to prevent MPTP toxicity is related to the metabolism of MPTP by monoamine oxidase B, probably extraneuronally in glia, to produce MPDP+ and subsequently MPP+.	1-methyl-4-phenyl-2,3-dihydropyridinium	175-180	monoamine oxidase B	Homo sapiens	109-128
3097257-2	1986	LTS could depend on the chronic overload of L-dopa + ID and could be due to a consequent "receptor disease" and derangement of the neuronal functionality mainly in regard to the enzymatic chains, storage mechanisms and hyperactivity of the monoamine oxidase type B (MAO B).	Levodopa	44-50	monoamine oxidase B	Homo sapiens	240-264
3097257-3	1986	Deprenyl is a selective MAO-B inhibitor thought to be able to slow down the catabolism of dopamine and therefore to allow a decrease of the therapeutic regimen of L-dopa while in the meantime to obtain a more stable plasma and tissue levels and a constant therapeutic response.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	24-29
3097257-3	1986	Deprenyl is a selective MAO-B inhibitor thought to be able to slow down the catabolism of dopamine and therefore to allow a decrease of the therapeutic regimen of L-dopa while in the meantime to obtain a more stable plasma and tissue levels and a constant therapeutic response.	Dopamine	90-98	monoamine oxidase B	Homo sapiens	24-29
3097257-3	1986	Deprenyl is a selective MAO-B inhibitor thought to be able to slow down the catabolism of dopamine and therefore to allow a decrease of the therapeutic regimen of L-dopa while in the meantime to obtain a more stable plasma and tissue levels and a constant therapeutic response.	Levodopa	163-169	monoamine oxidase B	Homo sapiens	24-29
3097257-7	1986	The association with (-)deprenyl was able to reverse this trend and when the inhibition of MAOB was really effective patients showed an improvement of symptoms even when compared to baseline values.	Selegiline	24-32	monoamine oxidase B	Homo sapiens	91-95
3097261-0	1986	Hydrogen peroxide enhances the activity of monoamine oxidase type-B but not of type-A: a pilot study.	Hydrogen Peroxide	0-17	monoamine oxidase B	Homo sapiens	43-67
3011983-7	1986	Monoamine oxidase inhibitors such as deprenyl, pargyline and harmaline have affinities to the MPTP receptors which parallel their affinity for the B type of monoamine oxidase (MAO B).	Selegiline	37-45	monoamine oxidase B	Homo sapiens	176-181
3011983-7	1986	Monoamine oxidase inhibitors such as deprenyl, pargyline and harmaline have affinities to the MPTP receptors which parallel their affinity for the B type of monoamine oxidase (MAO B).	Pargyline	47-56	monoamine oxidase B	Homo sapiens	176-181
3011983-7	1986	Monoamine oxidase inhibitors such as deprenyl, pargyline and harmaline have affinities to the MPTP receptors which parallel their affinity for the B type of monoamine oxidase (MAO B).	Harmaline	61-70	monoamine oxidase B	Homo sapiens	176-181
3091760-8	1986	The ability of monoamine oxidase inhibitors to prevent MPTP toxicity is related to the metabolism of MPTP by monoamine oxidase B, probably extraneuronally in glia, to produce MPDP+ and subsequently MPP+.	mangion-purified polysaccharide (Candida albicans)	198-202	monoamine oxidase B	Homo sapiens	109-128
3097263-0	1986	Pharmacology of MAO B inhibitors: mode of action of (-)deprenyl in Parkinson"s disease.	Selegiline	55-63	monoamine oxidase B	Homo sapiens	16-21
3097261-2	1986	It could be shown that hydrogen peroxide enhances significantly the activity of MAO-B after short-term incubation (2 min), while no changes have been noted after long-term preincubation (60 min) indicating reversibility of this effect.	Hydrogen Peroxide	23-40	monoamine oxidase B	Homo sapiens	80-85
3091762-1	1986	MPTP is oxidized to its toxic metabolite MPP+ by MAO B in both primate and rodent brains and this reaction can be inhibited by (-)-deprenyl.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	49-54
3097261-5	1986	Inhibition of hydrogen peroxide stimulated MAO-B activity in human cortex by (-)deprenyl was found to be of similar potency compared to hydrogen peroxide free estimations.	Hydrogen Peroxide	14-31	monoamine oxidase B	Homo sapiens	43-48
3097263-1	1986	The selective monoamine oxidase (MAO) type B inhibitor has proven to be a useful adjunct to L-dopa therapy of Parkinson"s disease.	Levodopa	92-98	monoamine oxidase B	Homo sapiens	14-44
3091762-1	1986	MPTP is oxidized to its toxic metabolite MPP+ by MAO B in both primate and rodent brains and this reaction can be inhibited by (-)-deprenyl.	mangion-purified polysaccharide (Candida albicans)	41-45	monoamine oxidase B	Homo sapiens	49-54
3097263-2	1986	Although not all features of its anti-Parkinson action is known, studies on brains obtained at autopsy from patients on (-)deprenyl show that the selective inhibition of MAO B with a concomitant increase of dopamine, but not of serotonin, in the basal ganglia may be responsible for its mode of action.	Selegiline	123-131	monoamine oxidase B	Homo sapiens	170-175
3097263-2	1986	Although not all features of its anti-Parkinson action is known, studies on brains obtained at autopsy from patients on (-)deprenyl show that the selective inhibition of MAO B with a concomitant increase of dopamine, but not of serotonin, in the basal ganglia may be responsible for its mode of action.	Dopamine	207-215	monoamine oxidase B	Homo sapiens	170-175
3097261-5	1986	Inhibition of hydrogen peroxide stimulated MAO-B activity in human cortex by (-)deprenyl was found to be of similar potency compared to hydrogen peroxide free estimations.	Selegiline	77-88	monoamine oxidase B	Homo sapiens	43-48
3097261-8	1986	As a conclusion these data indicate a possible role of hydrogen peroxide in the age-dependent increase of MAO-B in platelets and brain.	Hydrogen Peroxide	55-72	monoamine oxidase B	Homo sapiens	106-111
3091762-1	1986	MPTP is oxidized to its toxic metabolite MPP+ by MAO B in both primate and rodent brains and this reaction can be inhibited by (-)-deprenyl.	Selegiline	127-139	monoamine oxidase B	Homo sapiens	49-54
3091762-3	1986	There is some evidence that MAO B is localized predominantly in glia, and this would explain why dopamine uptake blockers also can prevent MPTP toxicity.	Dopamine	97-105	monoamine oxidase B	Homo sapiens	28-33
3091762-3	1986	There is some evidence that MAO B is localized predominantly in glia, and this would explain why dopamine uptake blockers also can prevent MPTP toxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	139-143	monoamine oxidase B	Homo sapiens	28-33
3872126-5	1985	(1984) 120, 574) that the neurotoxic effects of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which causes Parkinsonian symptoms in humans and other primates, are due to compounds resulting from the oxidation of MPTP by monoamine oxidase B in the brain.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	48-52	monoamine oxidase B	Homo sapiens	227-246
3874094-3	1985	MPDP+, MPTP, and MPP+, but not PTP, were found to be irreversible inhibitors of MAO B.	1-methyl-4-phenyl-2,3-dihydropyridinium	0-5	monoamine oxidase B	Homo sapiens	80-85
3874094-3	1985	MPDP+, MPTP, and MPP+, but not PTP, were found to be irreversible inhibitors of MAO B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	7-11	monoamine oxidase B	Homo sapiens	80-85
3874094-4	1985	Our studies support the hypothesis that MPTP is oxidized in primate brain by MAO B to MPDP+, which is then converted to MPP+, a major metabolite found in the substantia nigra.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	40-44	monoamine oxidase B	Homo sapiens	77-82
3874094-4	1985	Our studies support the hypothesis that MPTP is oxidized in primate brain by MAO B to MPDP+, which is then converted to MPP+, a major metabolite found in the substantia nigra.	1-methyl-4-phenyl-2,3-dihydropyridinium	86-91	monoamine oxidase B	Homo sapiens	77-82
3874094-4	1985	Our studies support the hypothesis that MPTP is oxidized in primate brain by MAO B to MPDP+, which is then converted to MPP+, a major metabolite found in the substantia nigra.	mangion-purified polysaccharide (Candida albicans)	120-124	monoamine oxidase B	Homo sapiens	77-82
3874094-4	1985	Our studies support the hypothesis that MPTP is oxidized in primate brain by MAO B to MPDP+, which is then converted to MPP+, a major metabolite found in the substantia nigra.	nigra	169-174	monoamine oxidase B	Homo sapiens	77-82
3875815-0	1985	Conversion of the neurotoxic precursor 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine into its pyridinium metabolite by human platelet monoamine oxidase type B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	39-83	monoamine oxidase B	Homo sapiens	133-157
3875815-0	1985	Conversion of the neurotoxic precursor 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine into its pyridinium metabolite by human platelet monoamine oxidase type B.	pyridine	93-103	monoamine oxidase B	Homo sapiens	133-157
3875815-2	1985	In the central nervous system, the oxidative metabolism of MPTP to 1-methyl-4-phenyl-pyridinium (MPP+) by monoamine oxidase type B (MAO-B) seems to be a critical feature in the neurotoxic process.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	59-63	monoamine oxidase B	Homo sapiens	106-130
3875815-2	1985	In the central nervous system, the oxidative metabolism of MPTP to 1-methyl-4-phenyl-pyridinium (MPP+) by monoamine oxidase type B (MAO-B) seems to be a critical feature in the neurotoxic process.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	59-63	monoamine oxidase B	Homo sapiens	132-137
3875815-2	1985	In the central nervous system, the oxidative metabolism of MPTP to 1-methyl-4-phenyl-pyridinium (MPP+) by monoamine oxidase type B (MAO-B) seems to be a critical feature in the neurotoxic process.	1-Methyl-4-phenylpyridinium	67-95	monoamine oxidase B	Homo sapiens	106-130
3875815-2	1985	In the central nervous system, the oxidative metabolism of MPTP to 1-methyl-4-phenyl-pyridinium (MPP+) by monoamine oxidase type B (MAO-B) seems to be a critical feature in the neurotoxic process.	1-Methyl-4-phenylpyridinium	67-95	monoamine oxidase B	Homo sapiens	132-137
3875815-3	1985	We now report that [3H]MPTP is rapidly converted in vitro into [3H]MPP+ by human platelet MAO-B.	3h]mptp	20-27	monoamine oxidase B	Homo sapiens	90-95
3875815-3	1985	We now report that [3H]MPTP is rapidly converted in vitro into [3H]MPP+ by human platelet MAO-B.	3-hydroxy-1-methyl-3-phenyl-2-piperidinone	63-70	monoamine oxidase B	Homo sapiens	90-95
3921065-3	1985	With L-deprenyl 10-30 mg/day, the expected MAO B inhibition occurred, as indicated by significant increase in urinary PEA excretion and virtual disappearance of platelet MAO activity.	Selegiline	5-15	monoamine oxidase B	Homo sapiens	43-48
3985989-4	1985	Both molecular forms of MAO, MAO A and MAO B, are present in single nerve cell as shown by clorgyline, a selective inhibitor of MAO A molecular form.	Clorgyline	91-101	monoamine oxidase B	Homo sapiens	39-44
3932340-13	1985	Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis indicated a subunit molecular mass of 60-64 kDa, about 1.5-2.5 kDa higher than human liver monoamine oxidase B.	Sodium Dodecyl Sulfate	12-34	monoamine oxidase B	Homo sapiens	161-180
3874094-0	1985	Metabolism of the neurotoxin in MPTP by human liver monoamine oxidase B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	32-36	monoamine oxidase B	Homo sapiens	52-71
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	15-59	monoamine oxidase B	Homo sapiens	142-161
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	15-59	monoamine oxidase B	Homo sapiens	163-168
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	15-59	monoamine oxidase B	Homo sapiens	198-203
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	15-59	monoamine oxidase B	Homo sapiens	198-203
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	61-65	monoamine oxidase B	Homo sapiens	142-161
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	61-65	monoamine oxidase B	Homo sapiens	163-168
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	61-65	monoamine oxidase B	Homo sapiens	198-203
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	61-65	monoamine oxidase B	Homo sapiens	198-203
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1,4-dihydropyridine	83-98	monoamine oxidase B	Homo sapiens	142-161
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1,4-dihydropyridine	83-98	monoamine oxidase B	Homo sapiens	163-168
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1,4-dihydropyridine	83-98	monoamine oxidase B	Homo sapiens	198-203
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1,4-dihydropyridine	83-98	monoamine oxidase B	Homo sapiens	198-203
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	pyridine mpp+	109-122	monoamine oxidase B	Homo sapiens	142-161
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	pyridine mpp+	109-122	monoamine oxidase B	Homo sapiens	163-168
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	pyridine mpp+	109-122	monoamine oxidase B	Homo sapiens	198-203
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	pyridine mpp+	109-122	monoamine oxidase B	Homo sapiens	198-203
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	251-255	monoamine oxidase B	Homo sapiens	142-161
3874094-1	1985	The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was oxidized to dihydropyridine MPDP+ and pyridine MPP+ by preparations of monoamine oxidase B (MAO B), including pure human liver MAO B:monoclonal antibody complex, Km,app values for MPTP and benzylamine, a preferred MAO B substrate, were 316 and 64 microM, respectively.	benzylamine	260-271	monoamine oxidase B	Homo sapiens	142-161
3875815-4	1985	The formation of [3H]MPP+ in human platelets is prevented by specific MAO-B but not by MAO-A or by 5-hydroxytryptamine uptake inhibitors.	3-hydroxy-1-methyl-3-phenyl-2-piperidinone	17-25	monoamine oxidase B	Homo sapiens	70-75
3928010-2	1985	Both selective MAO-A and MAO-B inhibitors markedly potentiated nictitating membrane contractions in response to beta-phenylethylamine (PEA).	phenethylamine	112-133	monoamine oxidase B	Homo sapiens	25-30
3928010-2	1985	Both selective MAO-A and MAO-B inhibitors markedly potentiated nictitating membrane contractions in response to beta-phenylethylamine (PEA).	phenethylamine	135-138	monoamine oxidase B	Homo sapiens	25-30
3928010-4	1985	The pressor responses to tyramine were potentiated by the selective MAO-A inhibitor clorgyline (2 mg kg-1) but not by selegiline (1.0 mg kg-1) and AGN 1135 (1.5 mg kg-1), selective MAO-B inhibitors.	Tyramine	25-33	monoamine oxidase B	Homo sapiens	181-186
3928010-5	1985	At the doses used selegiline and AGN 1135 caused a near total selective inhibition of liver and brain MAO-B, while clorgyline inhibited MAO-A only in the brain.	Selegiline	18-28	monoamine oxidase B	Homo sapiens	102-107
3928010-5	1985	At the doses used selegiline and AGN 1135 caused a near total selective inhibition of liver and brain MAO-B, while clorgyline inhibited MAO-A only in the brain.	Silver	33-36	monoamine oxidase B	Homo sapiens	102-107
3872126-5	1985	(1984) 120, 574) that the neurotoxic effects of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which causes Parkinsonian symptoms in humans and other primates, are due to compounds resulting from the oxidation of MPTP by monoamine oxidase B in the brain.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	54-98	monoamine oxidase B	Homo sapiens	227-246
6335034-2	1984	MPTP is oxidized by brain mitochondrial preparations in a process which is blocked by deprenyl and pargyline, implying catalysis by monoamine oxidase B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	132-151
3929314-1	1985	Deprenyl has previously been reported to be a selective monoamine oxidase (MAO) type B inhibitor, which is associated with little or no enhancement of the pressor effects of tyramine.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	56-86
3833630-3	1985	On the other hand, beta-phenylethylamine, a specific substrate for MAO B used as a substrate, showed no significant difference between the alcoholic and control groups in the activities.	phenethylamine	19-40	monoamine oxidase B	Homo sapiens	67-72
6508845-6	1984	The MAO-B modulators increased the Km for tryptamine without changing the Vmax.	tryptamine	42-52	monoamine oxidase B	Homo sapiens	4-9
6335034-2	1984	MPTP is oxidized by brain mitochondrial preparations in a process which is blocked by deprenyl and pargyline, implying catalysis by monoamine oxidase B.	Selegiline	86-94	monoamine oxidase B	Homo sapiens	132-151
6517923-3	1984	Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the complex revealed the presence of four polypeptide bands (monoamine oxidase B, 57,900 dalton; antibody heavy chain, 52,200 dalton; and two light chains, 29,400 and 27,700 dalton), and indicated a 1:1 stoichiometric ratio of enzyme to antibody.	sodium dodecyl sulfate-polyacrylamide	0-37	monoamine oxidase B	Homo sapiens	122-141
6335034-2	1984	MPTP is oxidized by brain mitochondrial preparations in a process which is blocked by deprenyl and pargyline, implying catalysis by monoamine oxidase B.	Pargyline	99-108	monoamine oxidase B	Homo sapiens	132-151
6335034-3	1984	The present paper demonstrates that pure MAO B isolated from beef liver oxidizes MPTP 38% as fast as benzylamine with a comparable Km value.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	81-85	monoamine oxidase B	Homo sapiens	41-46
6335034-3	1984	The present paper demonstrates that pure MAO B isolated from beef liver oxidizes MPTP 38% as fast as benzylamine with a comparable Km value.	benzylamine	101-112	monoamine oxidase B	Homo sapiens	41-46
6430257-1	1984	We investigated the antidepressant efficacy of l-deprenyl (selegiline), a selective monoamine oxidase B inhibitor (MAOI), in a six-week open trial of 17 patients with atypical depression.	Selegiline	47-57	monoamine oxidase B	Homo sapiens	84-103
6437857-5	1984	In parkinsonian patients under long-term L-DOPA therapy monoamine oxidase inhibitors type B (MAO-B) e.g. (-)deprenyl and direct dopamine receptor agonists (bromocriptine, lisuride, pergolide etc.	Levodopa	41-47	monoamine oxidase B	Homo sapiens	93-98
6437857-5	1984	In parkinsonian patients under long-term L-DOPA therapy monoamine oxidase inhibitors type B (MAO-B) e.g. (-)deprenyl and direct dopamine receptor agonists (bromocriptine, lisuride, pergolide etc.	Selegiline	108-116	monoamine oxidase B	Homo sapiens	93-98
6437857-5	1984	In parkinsonian patients under long-term L-DOPA therapy monoamine oxidase inhibitors type B (MAO-B) e.g. (-)deprenyl and direct dopamine receptor agonists (bromocriptine, lisuride, pergolide etc.	Bromocriptine	156-169	monoamine oxidase B	Homo sapiens	93-98
6437857-5	1984	In parkinsonian patients under long-term L-DOPA therapy monoamine oxidase inhibitors type B (MAO-B) e.g. (-)deprenyl and direct dopamine receptor agonists (bromocriptine, lisuride, pergolide etc.	Pergolide	181-190	monoamine oxidase B	Homo sapiens	93-98
6437857-7	1984	However, since (-)deprenyl, due to its metabolism to (-)methamphetamine and (-)amphetamine, seem to have indirect sympathomimetic activity, new selective MAO-B inhibitors devoid of indirect sympathomimetic effects should be tested clinically to assess the functional role of pure MAO-B inhibition in the therapy of PD.	Selegiline	18-26	monoamine oxidase B	Homo sapiens	154-159
6437857-7	1984	However, since (-)deprenyl, due to its metabolism to (-)methamphetamine and (-)amphetamine, seem to have indirect sympathomimetic activity, new selective MAO-B inhibitors devoid of indirect sympathomimetic effects should be tested clinically to assess the functional role of pure MAO-B inhibition in the therapy of PD.	Selegiline	18-26	monoamine oxidase B	Homo sapiens	280-285
6863305-2	1983	A strong inhibition of monoamine oxidase B was observed with phosphatidylserine and a moderate activation of monoamine oxidase A with phosphatidylinositol, while cardiolipin had no significant effect on either form.	Phosphatidylinositols	134-154	monoamine oxidase B	Homo sapiens	23-42
6429130-3	1984	Pilot studies with 1-deprenyl, a selective MAO-B inhibitor, indicate that it may be most effective for patients with nonendogenous depression and for those (endogenous or nonendogenous) who present with certain reverse vegetative signs.	1-deprenyl	19-29	monoamine oxidase B	Homo sapiens	43-48
6627826-9	1983	This may reflect the dose of cimoxatone used, the activity of monoamine oxidase form B (MAO-B) in the gut and liver or displacement of the predominantly reversible and predominantly competitive inhibitor, cimoxatone, from the enzyme by a high local tyramine concentration.	Tyramine	249-257	monoamine oxidase B	Homo sapiens	88-93
6359210-4	1983	Pargyline inhibits monoamine oxidase, type B, and its therapeutic efficacy is compatible with the hypothesis that decreased phenethylaminergic function, dopaminergic function, or both play a role in the etiology of the disorder.	Pargyline	0-9	monoamine oxidase B	Homo sapiens	19-44
6408492-5	1983	Enzyme titration studies and comparisons of the substrate specificities of MAO-A and MAO-B across the brain indicated that dopamine was metabolised by the same MAO active centres as other monoamines.	Dopamine	123-131	monoamine oxidase B	Homo sapiens	85-90
6191193-3	1983	All MAO B-containing extracts, regardless of tissue source, inhibited immunoprecipitation of [3H]pargyline-labeled human platelet MAO, and the shapes of the inhibition curves were identical.	3h]pargyline	94-106	monoamine oxidase B	Homo sapiens	4-9
6191193-4	1983	The concentration of immunologically detectable MAO B protein in the extracts was estimated from immunoprecipitation competition data by reference to a standard curve relating observed inhibition of immunoprecipitation to the concentration of catalytically active platelet MAO added (estimated from [3H]pargyline binding data).	Tritium	300-302	monoamine oxidase B	Homo sapiens	48-53
6191193-4	1983	The concentration of immunologically detectable MAO B protein in the extracts was estimated from immunoprecipitation competition data by reference to a standard curve relating observed inhibition of immunoprecipitation to the concentration of catalytically active platelet MAO added (estimated from [3H]pargyline binding data).	Pargyline	303-312	monoamine oxidase B	Homo sapiens	48-53
6871302-0	1983	Tranylcypromine lowers human platelet MAO B activity but not concentration.	Tranylcypromine	0-15	monoamine oxidase B	Homo sapiens	38-43
6871302-4	1983	Since recovery of MAO B activity approximated the reported half-life of blood platelets, these results suggest that recovery of platelet MAO activity after tranylcypromine treatment is due to the replacement of old platelets by new ones which contain catalytically active MAO B.	Tranylcypromine	156-171	monoamine oxidase B	Homo sapiens	272-277
6428144-3	1983	Deprenyl, a selective MAO-B inhibitor, has produced good therapeutic effects in combination either with levodopa alone or with levodopa plus decarboxylase inhibitor in the treatment of end-of-dose akinesia and on-off phenomena.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	22-27
6145282-6	1983	Our findings indicate that MAO-B inhibitors like deprenyl act by blocking neuronal and extra-neuronal MAO-B.	Selegiline	49-57	monoamine oxidase B	Homo sapiens	27-32
6428146-8	1983	It is probable that although enhanced availability of dopamine by MAO-B inhibition partly explains the present neuropsychological findings, also other brain mechanisms are involved.	Dopamine	54-62	monoamine oxidase B	Homo sapiens	66-71
6145282-6	1983	Our findings indicate that MAO-B inhibitors like deprenyl act by blocking neuronal and extra-neuronal MAO-B.	Selegiline	49-57	monoamine oxidase B	Homo sapiens	102-107
6428147-1	1983	The role of deprenyl, a selective monoamine oxidase B inhibitor, in the treatment of Parkinson"s disease has been evaluated with special reference to the multiple pharmacological actions of the monoamine oxidase-inhibitory group of drugs.	Selegiline	12-20	monoamine oxidase B	Homo sapiens	34-53
6428148-14	1983	The possibility of countering these biochemical lesions of ageing by long-term administration of deprenyl, a selective inhibitor of MAO-B which facilitates dopaminergic and "trace-aminergic" activity in the brain, and is a safe drug in man, is considered in detail.	Selegiline	97-105	monoamine oxidase B	Homo sapiens	132-137
24875606-5	1983	Two types of MAO activity similar to adult avian and mammalian MAO-A and MAO-B have been demonstrated by differential clorgyline sensitivity of tryptamine deamination.	Clorgyline	118-128	monoamine oxidase B	Homo sapiens	73-78
24875606-8	1983	Clorgyline injection selectively and completely inhibited MAO-A activity, while injection of clorgyline and deprenyl inhibited both MAO-A and MAO-B activities when embryos were assayed after either 2 or 7 days of embryonic development.	Clorgyline	93-103	monoamine oxidase B	Homo sapiens	142-147
24875606-5	1983	Two types of MAO activity similar to adult avian and mammalian MAO-A and MAO-B have been demonstrated by differential clorgyline sensitivity of tryptamine deamination.	tryptamine	144-154	monoamine oxidase B	Homo sapiens	73-78
24875606-8	1983	Clorgyline injection selectively and completely inhibited MAO-A activity, while injection of clorgyline and deprenyl inhibited both MAO-A and MAO-B activities when embryos were assayed after either 2 or 7 days of embryonic development.	Selegiline	108-116	monoamine oxidase B	Homo sapiens	142-147
24875606-6	1983	In addition, SDS-PAGE of embryonic quail [(3)H]pargyiine-labeled MAO demonstrates that the quail MAO-A and MAO-B flavin-containing subunits have apparent molecular weights of 63,000 and 62,000 respectively.	Sodium Dodecyl Sulfate	13-16	monoamine oxidase B	Homo sapiens	107-112
24875606-6	1983	In addition, SDS-PAGE of embryonic quail [(3)H]pargyiine-labeled MAO demonstrates that the quail MAO-A and MAO-B flavin-containing subunits have apparent molecular weights of 63,000 and 62,000 respectively.	(3)h]pargyiine	42-56	monoamine oxidase B	Homo sapiens	107-112
24875606-6	1983	In addition, SDS-PAGE of embryonic quail [(3)H]pargyiine-labeled MAO demonstrates that the quail MAO-A and MAO-B flavin-containing subunits have apparent molecular weights of 63,000 and 62,000 respectively.	4,6-dinitro-o-cresol	113-119	monoamine oxidase B	Homo sapiens	107-112
6822482-2	1983	The pharmacologic actions of pargyline are discussed with regard to its partial selectivity for MAO-B and presumed action in dopamine systems, and clinicians are alerted to this uncommon drug reaction.	Pargyline	29-38	monoamine oxidase B	Homo sapiens	96-101
6420516-2	1983	The influence of a specific monoamine oxidase B inhibitor (deprenyl) on changes in DA and DOPAC levels was studied in untreated patients or after L-dopa administration.	Dopamine	83-85	monoamine oxidase B	Homo sapiens	28-47
6420516-2	1983	The influence of a specific monoamine oxidase B inhibitor (deprenyl) on changes in DA and DOPAC levels was studied in untreated patients or after L-dopa administration.	3,4-Dihydroxyphenylacetic Acid	90-95	monoamine oxidase B	Homo sapiens	28-47
6314420-0	1983	Clinical efficacy of deprenyl, a specific inhibitor of MAOB.	Selegiline	21-29	monoamine oxidase B	Homo sapiens	55-59
7142171-0	1982	An evaluation of phospholipids as regulators of monoamine oxidase A and monoamine oxidase B activities.	Phospholipids	17-30	monoamine oxidase B	Homo sapiens	72-91
7159481-6	1982	In contrast, the MAO-B in human platelets deaminated l-norepinephrine more readily than serotonin.	Norepinephrine	53-69	monoamine oxidase B	Homo sapiens	17-22
7159481-7	1982	Thus, l-norepinephrine, like dopamine, should be regarded as a substrate for both MAO-A and MAO-B in vitro.	Norepinephrine	6-22	monoamine oxidase B	Homo sapiens	92-97
7159481-7	1982	Thus, l-norepinephrine, like dopamine, should be regarded as a substrate for both MAO-A and MAO-B in vitro.	Dopamine	29-37	monoamine oxidase B	Homo sapiens	92-97
7159481-8	1982	The prominent role of MAO-B in norepinephrine degradation in primates may need to be considered in interpreting laboratory and clinical studies of clorgyline and other selective MAO-inhibiting drugs.	Norepinephrine	31-45	monoamine oxidase B	Homo sapiens	22-27
7159481-8	1982	The prominent role of MAO-B in norepinephrine degradation in primates may need to be considered in interpreting laboratory and clinical studies of clorgyline and other selective MAO-inhibiting drugs.	Clorgyline	147-157	monoamine oxidase B	Homo sapiens	22-27
6802883-0	1982	The relative efficacy of l-deprenyl, a selective monoamine oxidase type B inhibitor, in endogenous and nonendogenous depression.	Selegiline	25-35	monoamine oxidase B	Homo sapiens	49-73
7126245-2	1982	Loosely based upon the structure of clorgyline, it is an irreversible inhibitor of MAO A but is apparently indifferent towards MAO B.	Clorgyline	36-46	monoamine oxidase B	Homo sapiens	127-132
7063850-2	1982	The only discrete polypeptide component that eluted from affinity columns with potassium thiocyanate migrated in sodium dodecyl sulfate-polyacrylamide gels with an apparent molecular weight of 59,000, as expected for human monoamine oxidase B.	potassium thiocyanate	79-100	monoamine oxidase B	Homo sapiens	223-242
7063850-2	1982	The only discrete polypeptide component that eluted from affinity columns with potassium thiocyanate migrated in sodium dodecyl sulfate-polyacrylamide gels with an apparent molecular weight of 59,000, as expected for human monoamine oxidase B.	Sodium Dodecyl Sulfate	113-135	monoamine oxidase B	Homo sapiens	223-242
7063850-2	1982	The only discrete polypeptide component that eluted from affinity columns with potassium thiocyanate migrated in sodium dodecyl sulfate-polyacrylamide gels with an apparent molecular weight of 59,000, as expected for human monoamine oxidase B.	polyacrylamide	136-150	monoamine oxidase B	Homo sapiens	223-242
7327272-2	1981	Three--day cold exposure leaves the monoamine oxidase type B activity unchanged and decreases the monoamine oxidase type A activity by 29--32%; the enzyme of the latter type acquires the ability for deamination of glucosamine, putrescine and GABA.	Glucosamine	214-225	monoamine oxidase B	Homo sapiens	36-60
7130973-5	1982	Harmane, with an I50 of 5 X 10(-6) M, might also play a role as an inhibitor of MAO B.	harman	0-7	monoamine oxidase B	Homo sapiens	80-85
7264664-2	1981	[3H]Pargyline was bound to MAO A in a crude mitochondrial fraction from the placental trophoblast of a male newborn and to MAO B in blood platelets from the umbilical vein of the same newborn.	Tritium	1-3	monoamine oxidase B	Homo sapiens	123-128
7264664-2	1981	[3H]Pargyline was bound to MAO A in a crude mitochondrial fraction from the placental trophoblast of a male newborn and to MAO B in blood platelets from the umbilical vein of the same newborn.	Pargyline	4-13	monoamine oxidase B	Homo sapiens	123-128
7264664-3	1981	[3H]Pargyline was also bound to MAO A and B in a crude mitochondrial fraction from cultured skin fibroblasts of a male adult and to MAO B in blood platelets from the same individual.	Tritium	1-3	monoamine oxidase B	Homo sapiens	132-137
7264664-5	1981	For all tissues, SDS-PAGE of [3H]pargyline-bound samples revealed a labeled protein band of apparent molecular weight 63,000 for MAO A and 60,000 for MAO B.	Tritium	30-32	monoamine oxidase B	Homo sapiens	150-155
6791202-4	1981	The effects of treatment with the selective MAO-A inhibitor clorgyline and the partially selective MAO-B inhibitors pargyline and deprenyl on tyramine"s pressor effects were studied in depressed patients using an IV steady-state tyramine infusion technique.	Tyramine	142-150	monoamine oxidase B	Homo sapiens	99-104
6409196-0	1983	L-Deprenil, a selective monoamine oxidase type B inhibitor, in the treatment of depression: a double blind evaluation.	l-deprenil	0-10	monoamine oxidase B	Homo sapiens	24-48
6785797-0	1981	Is the failure of (-)deprenyl, a selective monoamine oxidase B inhibitor, to alleviate depression related to freedom from the cheese effect?	Selegiline	18-29	monoamine oxidase B	Homo sapiens	43-62
6791210-5	1981	Chronic treatment with the MAO-A inhibitor clorgyline and the MAO-B inhibitor pargyline showed significant inhibition of the alternate MAO enzyme as well, although this crossover effect was greater for pargyline than clorgyline.	Pargyline	78-87	monoamine oxidase B	Homo sapiens	62-67
6791210-5	1981	Chronic treatment with the MAO-A inhibitor clorgyline and the MAO-B inhibitor pargyline showed significant inhibition of the alternate MAO enzyme as well, although this crossover effect was greater for pargyline than clorgyline.	Pargyline	202-211	monoamine oxidase B	Homo sapiens	62-67
6791210-5	1981	Chronic treatment with the MAO-A inhibitor clorgyline and the MAO-B inhibitor pargyline showed significant inhibition of the alternate MAO enzyme as well, although this crossover effect was greater for pargyline than clorgyline.	Clorgyline	217-227	monoamine oxidase B	Homo sapiens	62-67
6791210-6	1981	The MAO-B inhibitor deprenyl appeared to maintain the greatest degree of MAO inhibition selectivity in vivo.	Selegiline	20-28	monoamine oxidase B	Homo sapiens	4-9
6791210-7	1981	Tyramine pressor sensitivity changes accompanying administration of the MAO inhibitors were highly correlated with decreases in plasma MHPG (r = 0.92), supporting our previous data indicating the rank order of clorgyline greater than pargyline greater than deprenyl for enhancement of tyramine pressor sensitivity and, thus, suggesting that tyramine potentiation is primarily a function of MAO-A rather than MAO-B inhibition.	Tyramine	0-8	monoamine oxidase B	Homo sapiens	408-413
6791210-7	1981	Tyramine pressor sensitivity changes accompanying administration of the MAO inhibitors were highly correlated with decreases in plasma MHPG (r = 0.92), supporting our previous data indicating the rank order of clorgyline greater than pargyline greater than deprenyl for enhancement of tyramine pressor sensitivity and, thus, suggesting that tyramine potentiation is primarily a function of MAO-A rather than MAO-B inhibition.	Methoxyhydroxyphenylglycol	135-139	monoamine oxidase B	Homo sapiens	408-413
6791210-7	1981	Tyramine pressor sensitivity changes accompanying administration of the MAO inhibitors were highly correlated with decreases in plasma MHPG (r = 0.92), supporting our previous data indicating the rank order of clorgyline greater than pargyline greater than deprenyl for enhancement of tyramine pressor sensitivity and, thus, suggesting that tyramine potentiation is primarily a function of MAO-A rather than MAO-B inhibition.	Clorgyline	210-220	monoamine oxidase B	Homo sapiens	408-413
6791210-7	1981	Tyramine pressor sensitivity changes accompanying administration of the MAO inhibitors were highly correlated with decreases in plasma MHPG (r = 0.92), supporting our previous data indicating the rank order of clorgyline greater than pargyline greater than deprenyl for enhancement of tyramine pressor sensitivity and, thus, suggesting that tyramine potentiation is primarily a function of MAO-A rather than MAO-B inhibition.	Selegiline	257-265	monoamine oxidase B	Homo sapiens	408-413
6766730-0	1980	Deprenyl is a selective inhibitor of brain MAO-B in the long-term treatment of Parkinsons"s disease.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	43-48
6777463-3	1980	The selective monoamine oxidase type B inhibitor deprenyl, which is extensively metabolised to amphetamine and methamphetamine, has this effect as well as possible actions on dopamine release and re-uptake.	Selegiline	49-57	monoamine oxidase B	Homo sapiens	14-38
7207637-1	1980	The monoamine oxidase B (MAO-B) selective inhibitor J-508 (N-methyl-N-propargyl-(1-indanyl)-ammonium chloride) appears to interact with MAO-B in a manner consistent with a "suicide" reaction.	N-methyl-N-propargyl-(1-indanyl)-ammonium hydrochloride	52-57	monoamine oxidase B	Homo sapiens	4-23
7207637-1	1980	The monoamine oxidase B (MAO-B) selective inhibitor J-508 (N-methyl-N-propargyl-(1-indanyl)-ammonium chloride) appears to interact with MAO-B in a manner consistent with a "suicide" reaction.	N-methyl-N-propargyl-(1-indanyl)-ammonium hydrochloride	52-57	monoamine oxidase B	Homo sapiens	25-30
7207637-1	1980	The monoamine oxidase B (MAO-B) selective inhibitor J-508 (N-methyl-N-propargyl-(1-indanyl)-ammonium chloride) appears to interact with MAO-B in a manner consistent with a "suicide" reaction.	N-methyl-N-propargyl-(1-indanyl)-ammonium hydrochloride	52-57	monoamine oxidase B	Homo sapiens	136-141
7207637-1	1980	The monoamine oxidase B (MAO-B) selective inhibitor J-508 (N-methyl-N-propargyl-(1-indanyl)-ammonium chloride) appears to interact with MAO-B in a manner consistent with a "suicide" reaction.	N-methyl-N-propargyl-(1-indanyl)-ammonium chloride	59-109	monoamine oxidase B	Homo sapiens	4-23
7207637-1	1980	The monoamine oxidase B (MAO-B) selective inhibitor J-508 (N-methyl-N-propargyl-(1-indanyl)-ammonium chloride) appears to interact with MAO-B in a manner consistent with a "suicide" reaction.	N-methyl-N-propargyl-(1-indanyl)-ammonium chloride	59-109	monoamine oxidase B	Homo sapiens	25-30
7207637-1	1980	The monoamine oxidase B (MAO-B) selective inhibitor J-508 (N-methyl-N-propargyl-(1-indanyl)-ammonium chloride) appears to interact with MAO-B in a manner consistent with a "suicide" reaction.	N-methyl-N-propargyl-(1-indanyl)-ammonium chloride	59-109	monoamine oxidase B	Homo sapiens	136-141
7207637-2	1980	Because of this property, J-508 could be used, under the appropriate conditions, to "titrate" the concentration of MAO-B active centres in the human platelet, although some non-specific binding of this compound to sites other than the active centre of this enzyme form was found, thus limiting the accuracy of the titration method.	N-methyl-N-propargyl-(1-indanyl)-ammonium hydrochloride	26-31	monoamine oxidase B	Homo sapiens	115-120
7207637-3	1980	The molecular characteristics of human platelet MAO-B (Km, Vmax, approximate enzyme concentrations and molecular turnover members) towards three of its monoamine substrates have been estimated.	monoamine	152-161	monoamine oxidase B	Homo sapiens	48-53
7207637-4	1980	The natural variation of platelet MAO-B activity from individual to individual is due to a variation in the Vmax without a variation in the Km towards benzylamine is substrate, and is based, at least in part, upon a variation in the concentration of this enzyme form.	benzylamine	151-162	monoamine oxidase B	Homo sapiens	34-39
7422056-2	1980	It was found that the concentration of monoamine oxidase-B determined in this way was the same when either benzylamine or beta-phenethylamine was used to assay for activity, which would indicate that this enzyme form is not heterogeneous.	benzylamine	107-118	monoamine oxidase B	Homo sapiens	39-58
7422056-2	1980	It was found that the concentration of monoamine oxidase-B determined in this way was the same when either benzylamine or beta-phenethylamine was used to assay for activity, which would indicate that this enzyme form is not heterogeneous.	phenethylamine	122-141	monoamine oxidase B	Homo sapiens	39-58
6448885-1	1980	In an open trial study, L-Deprenil, an irreversible selective MAO-B inhibitor without "chesse effect" was given to 14 patients with unipolar and bipolar depression receiving L-5-Hydroxytryptophan (L-5-HTP) and benzerazide.	l-deprenil	24-34	monoamine oxidase B	Homo sapiens	62-67
6777463-3	1980	The selective monoamine oxidase type B inhibitor deprenyl, which is extensively metabolised to amphetamine and methamphetamine, has this effect as well as possible actions on dopamine release and re-uptake.	Amphetamine	95-106	monoamine oxidase B	Homo sapiens	14-38
6777463-3	1980	The selective monoamine oxidase type B inhibitor deprenyl, which is extensively metabolised to amphetamine and methamphetamine, has this effect as well as possible actions on dopamine release and re-uptake.	Methamphetamine	111-126	monoamine oxidase B	Homo sapiens	14-38
6777463-3	1980	The selective monoamine oxidase type B inhibitor deprenyl, which is extensively metabolised to amphetamine and methamphetamine, has this effect as well as possible actions on dopamine release and re-uptake.	Dopamine	175-183	monoamine oxidase B	Homo sapiens	14-38
6768943-0	1980	L-deprenyl, a selective monoamine oxidase type-B inhibitor in endogenous depression.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	24-48
20227955-4	1980	At commonly used substrate concentrations, deamination of Bz (sensitive to 10(-7) M deprenyl) was a better indicator of MAO B activity than deamination of PEA.	benzylamine	58-60	monoamine oxidase B	Homo sapiens	120-125
20227955-4	1980	At commonly used substrate concentrations, deamination of Bz (sensitive to 10(-7) M deprenyl) was a better indicator of MAO B activity than deamination of PEA.	Selegiline	84-92	monoamine oxidase B	Homo sapiens	120-125
20227955-6	1980	However, Bz reacts with benzylamine oxidase (BzAO) as well as MAO B.	benzylamine	9-11	monoamine oxidase B	Homo sapiens	62-67
6776576-0	1980	The effect of deprenyl, a selective monoamine oxidase B inhibitor, on sleep and mood in man.	Selegiline	14-22	monoamine oxidase B	Homo sapiens	36-55
111275-2	1979	During a similar 4-week crossover treatment period with pargyline, a selective MAO-B inhibitor, platelet MAO activity was essentially completely inhibited in the same individuals.	Pargyline	56-65	monoamine oxidase B	Homo sapiens	79-84
6774369-0	1980	Tele-Methylhistamine is a specific MAO B substrate in man.	tele-methylhistamine	0-20	monoamine oxidase B	Homo sapiens	35-40
6774369-1	1980	Tele-methylhistamine, the first metabolite of histamine in tissues which lack diamine oxidase, is shown to be a substrate for human MAO B.	tele-methylhistamine	0-20	monoamine oxidase B	Homo sapiens	132-137
6774369-1	1980	Tele-methylhistamine, the first metabolite of histamine in tissues which lack diamine oxidase, is shown to be a substrate for human MAO B.	Histamine	11-20	monoamine oxidase B	Homo sapiens	132-137
6774369-4	1980	The reaction was inhibited by low concentrations of (-)deprenyl, the specific MAO B inhibitor.	Selegiline	52-63	monoamine oxidase B	Homo sapiens	78-83
6774369-5	1980	Tele-methylhistamine was also found to inhibit competitively the oxidation of phenylethlamine, but not that of 5-hydroxytryptamine, providing further evidence that it is oxidized by MAO B itself and not a related enzyme.	tele-methylhistamine	0-20	monoamine oxidase B	Homo sapiens	182-187
6774369-5	1980	Tele-methylhistamine was also found to inhibit competitively the oxidation of phenylethlamine, but not that of 5-hydroxytryptamine, providing further evidence that it is oxidized by MAO B itself and not a related enzyme.	phenylethlamine	78-93	monoamine oxidase B	Homo sapiens	182-187
111275-3	1979	The differential effects of the two drugs on platelet MAO, which consists exclusively of the MAO-B form, suggests that the in vitro selectivity of clorgyline, and possibly of pargyline, on MAO-A and MAO-B may be maintained in vivo during long-term administration in man.	Clorgyline	147-157	monoamine oxidase B	Homo sapiens	93-98
111275-3	1979	The differential effects of the two drugs on platelet MAO, which consists exclusively of the MAO-B form, suggests that the in vitro selectivity of clorgyline, and possibly of pargyline, on MAO-A and MAO-B may be maintained in vivo during long-term administration in man.	Clorgyline	147-157	monoamine oxidase B	Homo sapiens	199-204
745015-5	1978	Of those tried Deprenyl, an MAO-B inhibitor, given with levodopa and carbidopa has shown the most promise.	Selegiline	15-23	monoamine oxidase B	Homo sapiens	28-33
219389-6	1979	In the present experiments, the administration of the monoamine oxidase type B inhibitor, deprenyl (1 mg per kilogram, IV), did not effect significant changes in cerebral blood flow or cerebral oxygen consumption.	Selegiline	90-98	monoamine oxidase B	Homo sapiens	54-78
96466-0	1978	Deprenyl administration in man: a selective monoamine oxidase B inhibitor without the "cheese effect".	Selegiline	0-8	monoamine oxidase B	Homo sapiens	44-63
745015-5	1978	Of those tried Deprenyl, an MAO-B inhibitor, given with levodopa and carbidopa has shown the most promise.	Levodopa	56-64	monoamine oxidase B	Homo sapiens	28-33
745015-5	1978	Of those tried Deprenyl, an MAO-B inhibitor, given with levodopa and carbidopa has shown the most promise.	Carbidopa	69-78	monoamine oxidase B	Homo sapiens	28-33
745019-1	1978	Deprenyl is an inhibitor of monoamine oxidase type B, the enzyme responsible for 2-phenylethylamine oxidation, and is used in conjunction with L-Dopa therapy in Parkinson"s disease.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	28-52
745019-1	1978	Deprenyl is an inhibitor of monoamine oxidase type B, the enzyme responsible for 2-phenylethylamine oxidation, and is used in conjunction with L-Dopa therapy in Parkinson"s disease.	phenethylamine	81-99	monoamine oxidase B	Homo sapiens	28-52
139953-2	1977	This decrease was prevented by pretreatment of the vesicles with deprenyl, a specific monoamine oxidase type B inhibitor.	Selegiline	65-73	monoamine oxidase B	Homo sapiens	86-110
71602-1	1977	In a double-blind crossover trial, (-)-deprenyl, a fast-acting selective monoamine-oxidase-B inhibitor without a "cheese effect", was given to 41 patients with idiopathic Parkinson"s disease who were receiving maximum tolerated doses of levodopa either alone or combined with carbidopa ("Sinemet").	Selegiline	35-47	monoamine oxidase B	Homo sapiens	73-92
834248-0	1977	Dopamine is a monoamine oxidase B substrate in man.	Dopamine	0-8	monoamine oxidase B	Homo sapiens	14-33
33992221-2	2021	Colorimetric test strips containing tyramine oxidase (TAO), peroxidase and 3,3",5,5"-tetramethylbenzidine (Q-TAO), allow tyramine determination through the RGB chromatic coordinates of the observed blue colour (LOD = 2.6 10-6 M, LOQ = 8.7 10-6 M, RSD% (n = 5; 1.8 10-4 M) = 3.2%).	3,3',5,5'-tetramethylbenzidine	75-105	monoamine oxidase B	Homo sapiens	109-112
1172524-0	1975	The potentiation of the anti akinetic effect after L-dopa treatment by an inhibitor of MAO-B, Deprenil.	Levodopa	51-57	monoamine oxidase B	Homo sapiens	87-92
1172524-0	1975	The potentiation of the anti akinetic effect after L-dopa treatment by an inhibitor of MAO-B, Deprenil.	Selegiline	94-102	monoamine oxidase B	Homo sapiens	87-92
1172524-6	1975	Deprenil is an inhibitor of MAO-B and is characterized by less frequent side effects.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	28-33
4469590-0	1974	[Study of tyramine oxidase by means of structural analogs of flavine adenine dinucleotide].	Flavin-Adenine Dinucleotide	61-89	monoamine oxidase B	Homo sapiens	10-26
33992221-4	2021	Previously, these Q-TAO strips have been also optimized for tyramine determination in cheese extract.	Tyramine	60-68	monoamine oxidase B	Homo sapiens	20-23
34047146-0	2021	New indane derivatives containing 2-hydrazinothiazole as potential acetylcholinesterase and monoamine oxidase-B inhibitors.	indan	4-10	monoamine oxidase B	Homo sapiens	92-111
34047061-3	2021	With few exceptions, the newly synthesized compounds exhibited selectivity toward MAO B over either MAO A and AChE, with the secondary aldimine 9 and phenylhydrazone 20 attaining IC50 values of 0.68 and 0.81 muM, respectively.	phenylhydrazone	150-165	monoamine oxidase B	Homo sapiens	82-87
34047146-0	2021	New indane derivatives containing 2-hydrazinothiazole as potential acetylcholinesterase and monoamine oxidase-B inhibitors.	2-Hydrazinylthiazole	34-53	monoamine oxidase B	Homo sapiens	92-111
34047146-3	2021	In this study, indane ring which are in the structure of anticholinesterase effective molecules and 2-hydrazinothiazole structure whose inhibitory activities reported on monoamine oxidase-B (MAO-B) were combined; 4-(substituted phenyl)-2-[2-(3-phenyl-2,3-dihydro-1H-inden-1-ylidene) hydrazinyl]thiazole derivatives (3a-3i) were synthesized as dual inhibitors.	indan	15-21	monoamine oxidase B	Homo sapiens	170-189
34047146-3	2021	In this study, indane ring which are in the structure of anticholinesterase effective molecules and 2-hydrazinothiazole structure whose inhibitory activities reported on monoamine oxidase-B (MAO-B) were combined; 4-(substituted phenyl)-2-[2-(3-phenyl-2,3-dihydro-1H-inden-1-ylidene) hydrazinyl]thiazole derivatives (3a-3i) were synthesized as dual inhibitors.	indan	15-21	monoamine oxidase B	Homo sapiens	191-196
34047146-3	2021	In this study, indane ring which are in the structure of anticholinesterase effective molecules and 2-hydrazinothiazole structure whose inhibitory activities reported on monoamine oxidase-B (MAO-B) were combined; 4-(substituted phenyl)-2-[2-(3-phenyl-2,3-dihydro-1H-inden-1-ylidene) hydrazinyl]thiazole derivatives (3a-3i) were synthesized as dual inhibitors.	2-Hydrazinylthiazole	100-119	monoamine oxidase B	Homo sapiens	170-189
34047146-3	2021	In this study, indane ring which are in the structure of anticholinesterase effective molecules and 2-hydrazinothiazole structure whose inhibitory activities reported on monoamine oxidase-B (MAO-B) were combined; 4-(substituted phenyl)-2-[2-(3-phenyl-2,3-dihydro-1H-inden-1-ylidene) hydrazinyl]thiazole derivatives (3a-3i) were synthesized as dual inhibitors.	2-Hydrazinylthiazole	100-119	monoamine oxidase B	Homo sapiens	191-196
34047146-3	2021	In this study, indane ring which are in the structure of anticholinesterase effective molecules and 2-hydrazinothiazole structure whose inhibitory activities reported on monoamine oxidase-B (MAO-B) were combined; 4-(substituted phenyl)-2-[2-(3-phenyl-2,3-dihydro-1H-inden-1-ylidene) hydrazinyl]thiazole derivatives (3a-3i) were synthesized as dual inhibitors.	4-(substituted phenyl)-2-[2-(3-phenyl-2,3-dihydro-1h-inden-1-ylidene) hydrazinyl]thiazole	213-302	monoamine oxidase B	Homo sapiens	170-189
34047146-5	2021	When enzyme inhibition activities were evaluated, it was determined that the compounds 3a (42.33%) and 3d (42.39%) on acetylcholinesterase (AChE) enzyme; compounds 3g (75.42%) and 3h (60.33%) showed inhibition on MAO-B enzyme at most, at 10-3 M concentration.	Tritium	180-182	monoamine oxidase B	Homo sapiens	213-218
33913699-4	2021	Contezolid exhibited 2- and 148-fold reduction over linezolid reversible inhibition of MAO-A and MAO-B human enzyme isoforms.	Contezolid	0-10	monoamine oxidase B	Homo sapiens	97-102
34011531-0	2021	Investigation into MAO B-mediated formation of CC112273, a major circulating metabolite of ozanimod, in humans and preclinical species: Stereospecific oxidative deamination of (S)-enantiomer of indaneamine (RP101075) by MAO B.	UNII-F2PE1J7HH9	47-55	monoamine oxidase B	Homo sapiens	19-24
34011531-0	2021	Investigation into MAO B-mediated formation of CC112273, a major circulating metabolite of ozanimod, in humans and preclinical species: Stereospecific oxidative deamination of (S)-enantiomer of indaneamine (RP101075) by MAO B.	ozanimod	91-99	monoamine oxidase B	Homo sapiens	19-24
34011531-0	2021	Investigation into MAO B-mediated formation of CC112273, a major circulating metabolite of ozanimod, in humans and preclinical species: Stereospecific oxidative deamination of (S)-enantiomer of indaneamine (RP101075) by MAO B.	indaneamine	194-205	monoamine oxidase B	Homo sapiens	19-24
34011531-0	2021	Investigation into MAO B-mediated formation of CC112273, a major circulating metabolite of ozanimod, in humans and preclinical species: Stereospecific oxidative deamination of (S)-enantiomer of indaneamine (RP101075) by MAO B.	UNII-EK8WS2OJX0	207-215	monoamine oxidase B	Homo sapiens	19-24
34011531-1	2021	Ozanimod, recently approved for treating relapsing MS, produced a disproportionate, active, MAO B-catalyzed metabolite (CC112273) that showed remarkable interspecies differences and led to challenges in safety testing.	ozanimod	0-8	monoamine oxidase B	Homo sapiens	92-97
34011531-1	2021	Ozanimod, recently approved for treating relapsing MS, produced a disproportionate, active, MAO B-catalyzed metabolite (CC112273) that showed remarkable interspecies differences and led to challenges in safety testing.	UNII-F2PE1J7HH9	120-128	monoamine oxidase B	Homo sapiens	92-97
34011531-7	2021	Docking into MAO B crystal structure suggested that even though both the isomers occupied its active site, only the orientation of RP-101075 presented the C-H on the a-carbon that was ideal for the C-H bond cleavage, which is a requisite for oxidative deamination.	Carbon	168-174	monoamine oxidase B	Homo sapiens	13-18
34011531-11	2021	The study is of significance to the DMD readers given that this oxidation is catalyzed by a non-CYP enzyme and that marked species difference and notable stereospecificity was observed in MAO B catalyzed biotransformation when the indaneamine enantiomers were used as a substrates.	indaneamine	231-242	monoamine oxidase B	Homo sapiens	188-193
34031800-2	2022	Safinamide is a new monoamine oxidase B inhibitor, also exerting a non-dopaminergic effect, recently approved as add-on therapy in fluctuating PD patients.	safinamide	0-10	monoamine oxidase B	Homo sapiens	20-39
34017039-5	2021	We found significant concentration differences in several amino acids, acylcarnitines and polyamines linking delirium-prone patients to known factors in Alzheimer"s disease such as monoamine oxidase B (MAOB) protein.	Polyamines	90-100	monoamine oxidase B	Homo sapiens	181-200
34017039-5	2021	We found significant concentration differences in several amino acids, acylcarnitines and polyamines linking delirium-prone patients to known factors in Alzheimer"s disease such as monoamine oxidase B (MAOB) protein.	Polyamines	90-100	monoamine oxidase B	Homo sapiens	202-206
33913699-4	2021	Contezolid exhibited 2- and 148-fold reduction over linezolid reversible inhibition of MAO-A and MAO-B human enzyme isoforms.	Linezolid	52-61	monoamine oxidase B	Homo sapiens	97-102
33511649-3	2021	Compounds THU-4 and THU-8 were found to be the most potent inhibitors for the cholinesterases and MAO-B, respectively.	thu-4	10-15	monoamine oxidase B	Homo sapiens	98-103
33960511-11	2021	Monoamine oxidase type B inhibitors, as initial levodopa-sparing therapy was more cost-effective, with similar quality-adjusted life-years but lower costs than dopamine agonists.	Levodopa	48-56	monoamine oxidase B	Homo sapiens	0-24
33960511-11	2021	Monoamine oxidase type B inhibitors, as initial levodopa-sparing therapy was more cost-effective, with similar quality-adjusted life-years but lower costs than dopamine agonists.	Dopamine	160-168	monoamine oxidase B	Homo sapiens	0-24
33986613-0	2021	MAOB rs3027452 Modifies Mood Improvement After Tryptophan Supplementation.	Tryptophan	47-57	monoamine oxidase B	Homo sapiens	0-4
33986613-7	2021	Results: MAOB rs3027452 was equally associated with tryptophan supplementation efficacy in the depression subscales of both questionnaires (DeltaT-Score.D; DeltaT-Score.TMD and DeltaPOMS.D p-values <0.01).	Tryptophan	52-62	monoamine oxidase B	Homo sapiens	9-13
33960511-2	2021	OBJECTIVES: The objective was to estimate the cost-effectiveness of levodopa-sparing therapy (dopamine agonists or monoamine oxidase type B inhibitors compared with levodopa alone.	Levodopa	68-76	monoamine oxidase B	Homo sapiens	115-139
33511649-3	2021	Compounds THU-4 and THU-8 were found to be the most potent inhibitors for the cholinesterases and MAO-B, respectively.	thu-8	20-25	monoamine oxidase B	Homo sapiens	98-103
33674268-8	2021	The primary metabolite RP101075 is further metabolized to form major active metabolite CC112273 by monoamine oxidase B which further undergoes reduction by carbonyl reductases (CBR) to form CC1084037 or CYP2C8 mediated oxidation to form RP101509.	UNII-EK8WS2OJX0	23-31	monoamine oxidase B	Homo sapiens	99-118
33759401-3	2021	Our aim was to check the clinical impression that some patients who were given selegiline, a selective inhibitor of monoamine oxidase B, experienced an improvement in their daytime somnolence.	Selegiline	79-89	monoamine oxidase B	Homo sapiens	116-135
33674268-8	2021	The primary metabolite RP101075 is further metabolized to form major active metabolite CC112273 by monoamine oxidase B which further undergoes reduction by carbonyl reductases (CBR) to form CC1084037 or CYP2C8 mediated oxidation to form RP101509.	UNII-F2PE1J7HH9	87-95	monoamine oxidase B	Homo sapiens	99-118
33674268-8	2021	The primary metabolite RP101075 is further metabolized to form major active metabolite CC112273 by monoamine oxidase B which further undergoes reduction by carbonyl reductases (CBR) to form CC1084037 or CYP2C8 mediated oxidation to form RP101509.	UNII-KYS7WW026H	190-199	monoamine oxidase B	Homo sapiens	99-118
33674268-8	2021	The primary metabolite RP101075 is further metabolized to form major active metabolite CC112273 by monoamine oxidase B which further undergoes reduction by carbonyl reductases (CBR) to form CC1084037 or CYP2C8 mediated oxidation to form RP101509.	rp101509	237-245	monoamine oxidase B	Homo sapiens	99-118
33915673-6	2021	The subjects who used catechol-O-methyltransferase (COMT) inhibitors, dopamine agonists, amantadine, and monoamine oxidase-B (MAO-B) inhibitors had significantly higher necessity scores than those who did not use them.	Dopamine	70-78	monoamine oxidase B	Homo sapiens	126-131
33898820-0	2021	Binding mechanism of naringenin with monoamine oxidase - B enzyme: QM/MM and molecular dynamics perspective.	naringenin	21-31	monoamine oxidase B	Homo sapiens	37-58
33887441-0	2021	Novel 1-(prop-2-yn-1-ylamino)-2,3-dihydro-1H-indene-4-thiol derivatives as potent selective human monoamine oxidase B inhibitors: design, SAR development, and biological evaluation.	1-(prop-2-yn-1-ylamino)-2,3-dihydro-1h-indene-4-thiol	6-59	monoamine oxidase B	Homo sapiens	98-117
33887441-3	2021	Herein we report 1-(prop-2-yn-1-ylamino)-2,3-dihydro-1H-indene-4-thiol derivatives as hMAO-B inhibitors, which were designed by employing a fragment-based drug design strategy to link rasagiline to hydrophobic fragments.	1-(prop-2-yn-1-ylamino)-2,3-dihydro-1h-indene-4-thiol	17-70	monoamine oxidase B	Homo sapiens	86-92
33887441-3	2021	Herein we report 1-(prop-2-yn-1-ylamino)-2,3-dihydro-1H-indene-4-thiol derivatives as hMAO-B inhibitors, which were designed by employing a fragment-based drug design strategy to link rasagiline to hydrophobic fragments.	rasagiline	184-194	monoamine oxidase B	Homo sapiens	86-92
33921982-0	2021	Coumarin-Chalcone Hybrids as Inhibitors of MAO-B: Biological Activity and In Silico Studies.	coumarin	0-8	monoamine oxidase B	Homo sapiens	43-48
33921982-0	2021	Coumarin-Chalcone Hybrids as Inhibitors of MAO-B: Biological Activity and In Silico Studies.	Chalcone	9-17	monoamine oxidase B	Homo sapiens	43-48
33921982-5	2021	Of the fourteen chalcocumarins evaluated here against MAO-B, ChC4 showed the strongest activity in vitro, with IC50 = 0.76 +- 0.08 microM.	chalcocumarins	16-30	monoamine oxidase B	Homo sapiens	54-59
33921982-5	2021	Of the fourteen chalcocumarins evaluated here against MAO-B, ChC4 showed the strongest activity in vitro, with IC50 = 0.76 +- 0.08 microM.	chc4	61-65	monoamine oxidase B	Homo sapiens	54-59
33932769-0	2021	Novel 2,5-disubstituted-1,3,4-oxadiazole derivatives as MAO-B inhibitors: Synthesis, biological evaluation and molecular modeling studies.	2,5-disubstituted-1,3,4-oxadiazole	6-40	monoamine oxidase B	Homo sapiens	56-61
33932769-5	2021	Among them, the compounds H8, H9 and H12 bearing chloro substituent at the fourth position of phenylurea were found to show potent monoamine oxidase B inhibitory activity with IC50 values 0.039-0.066 microM.	Hydrochloric Acid	49-55	monoamine oxidase B	Homo sapiens	131-150
33898820-1	2021	The reduced level of dopamine at midbrain (substantia nigra) leads to Parkinson disease by the influence of monoamine oxidation process of monoamine oxidase B (MAO-B) enzyme.	Dopamine	21-29	monoamine oxidase B	Homo sapiens	139-158
33898820-1	2021	The reduced level of dopamine at midbrain (substantia nigra) leads to Parkinson disease by the influence of monoamine oxidation process of monoamine oxidase B (MAO-B) enzyme.	Dopamine	21-29	monoamine oxidase B	Homo sapiens	160-165
33898820-3	2021	Reports outline that the naringenin molecule acts as an inhibitor of MAO-B enzyme and it potentially prevents the development of PD.	naringenin	25-35	monoamine oxidase B	Homo sapiens	69-74
33898820-4	2021	To elucidate the binding mechanism of naringenin with MAO-B, we performed the molecular docking, QM/MM and molecular dynamics (MD) simulations.	naringenin	38-48	monoamine oxidase B	Homo sapiens	54-59
33898820-5	2021	The molecular docking results confirm that the naringenin strongly binds with the substrate binding site of MAO-B enzyme (-12.0 kcal/mol).	naringenin	47-57	monoamine oxidase B	Homo sapiens	108-113
33898820-6	2021	The low values of RMSD, RMSF and Rg indicate that the naringenin - MAO-B complex is stable over the entire period of MD simulation.	naringenin	54-64	monoamine oxidase B	Homo sapiens	67-72
33898820-9	2021	The QM/MM study coupled with the charge density analysis reveals the charge density distribution and the strength of intermolecular interactions of naringenin-MAO-B complex.	naringenin	148-158	monoamine oxidase B	Homo sapiens	159-164
33743158-0	2021	Piperazine-substituted chalcones: a new class of MAO-B, AChE, and BACE-1 inhibitors for the treatment of neurological disorders.	Piperazine	0-10	monoamine oxidase B	Homo sapiens	49-54
33855088-4	2021	Results: The norepinephrine levels were markedly high in gastric cancer tissue, while the norepinephrine-degrading enzymes MAOA and MAOB showed low expression.	Norepinephrine	90-104	monoamine oxidase B	Homo sapiens	132-136
33855088-8	2021	The norepinephrine-degrading enzymes MAOA and MAOB have significant expression differences in cancer and normal tissue, and their missing or low expression may predict immune therapy outcomes for gastric cancer patients.	Norepinephrine	4-18	monoamine oxidase B	Homo sapiens	46-50
33640631-2	2021	To develop new hMAO-B inhibitors with neuroprotection, a novel series of 3,4-dihydrocoumarins was designed as selective and reversible hMAO-B inhibitors to treat PD.	3,4-dihydrocoumarin	73-93	monoamine oxidase B	Homo sapiens	15-21
33640631-2	2021	To develop new hMAO-B inhibitors with neuroprotection, a novel series of 3,4-dihydrocoumarins was designed as selective and reversible hMAO-B inhibitors to treat PD.	3,4-dihydrocoumarin	73-93	monoamine oxidase B	Homo sapiens	135-141
33640631-4	2021	Among them, compound 4d was the most potent hMAO-B inhibitor (IC50 = 0.37 nM) being about 20783-fold more active than iproniazid, and exhibited the highest selectivity for hMAO-B (SI > 270,270).	Iproniazid	118-128	monoamine oxidase B	Homo sapiens	44-50
33743158-0	2021	Piperazine-substituted chalcones: a new class of MAO-B, AChE, and BACE-1 inhibitors for the treatment of neurological disorders.	Chalcones	23-32	monoamine oxidase B	Homo sapiens	49-54
33743158-2	2021	Compounds PC10 and PC11 remarkably inhibited MAO-B with IC50 values of 0.65 and 0.71 muM, respectively.	pc11	19-23	monoamine oxidase B	Homo sapiens	45-50
33743158-5	2021	Reversibility and kinetic studies showed that PC10 and PC11 were reversible and competitive inhibitors of MAO-B with Ki values of 0.63 +- 0.13 and 0.53 +- 0.068 muM, respectively.	pc11	55-59	monoamine oxidase B	Homo sapiens	106-111
33743158-7	2021	Molecular docking simulations showed that fluorine atom and trifluoromethyl group on PC10 and PC11, respectively, interacted with the substrate cavity of the MAO-B active site.	Fluorine	42-50	monoamine oxidase B	Homo sapiens	158-163
33376014-3	2021	Based on these considerations, the present study synthesizes a series of 22 pyrazolo[1,5-a]quinoxalin-4-one derivatives and evaluated them as potential inhibitors of human MAO-A and MAO-B.	Pyrazolo[1,5-a]quinoxalin-4(5H)-one	76-107	monoamine oxidase B	Homo sapiens	182-187
33493825-3	2021	The data showed the N-(3,4-dichlorophenyl)-1-methyl-4-oxo-1,4-dihydroquinoline-3-carboxamide 10 was the most potent and selective MAO-B inhibitor (IC50 = 5.30 +- 0.74 nM and SI: >=1887).	n-(3,4-dichlorophenyl)-1-methyl-4-oxo-1,4-dihydroquinoline-3-carboxamide	20-92	monoamine oxidase B	Homo sapiens	130-135
32093545-2	2021	MD-simulation studies of dopamine (DOP) and benzylamine (BZA) complexed hMAO B structures have revealed the conformational dynamics of the gating residues Ile199 and Phe103.	benzylamine	57-60	monoamine oxidase B	Homo sapiens	72-78
33387637-6	2021	Nevertheless, evidence from multiple preclinical studies suggested a potent, selective and reversible inhibitory activity of safinamide against monoamine oxidase (MAO)-B enzyme which is responsible for degrading dopamine, a neurotransmitter primarily implicated in the pathophysiology of PD.	safinamide	125-135	monoamine oxidase B	Homo sapiens	144-169
33387637-6	2021	Nevertheless, evidence from multiple preclinical studies suggested a potent, selective and reversible inhibitory activity of safinamide against monoamine oxidase (MAO)-B enzyme which is responsible for degrading dopamine, a neurotransmitter primarily implicated in the pathophysiology of PD.	Dopamine	212-220	monoamine oxidase B	Homo sapiens	144-169
33571810-0	2021	Combined 3D-QSAR and docking analysis for the design and synthesis of chalcones as potent and selective monoamine oxidase B inhibitors.	Chalcones	70-79	monoamine oxidase B	Homo sapiens	104-123
33571810-3	2021	In the current work, we focused our attention on the understanding of theoretical models that may predict the MAO-B activity and selectivity of new chalcones.	Chalcones	148-157	monoamine oxidase B	Homo sapiens	110-115
33571810-5	2021	All the synthetized molecules proved to inhibit MAO-B, being ten out of them MAO-B potent and selective inhibitors, with IC50 against this isoform in the nanomolar range, being (E)-3-(4-hydroxyphenyl)-1-(2,2-dimethylchroman-6-yl)prop-2-en-1-one (152) the best MAO-B inhibitor (IC50 of 170 nM).	(e)-3-(4-hydroxyphenyl)-1-(2,2-dimethylchroman-6-yl)prop-2-en-1-one	177-244	monoamine oxidase B	Homo sapiens	48-53
33571810-5	2021	All the synthetized molecules proved to inhibit MAO-B, being ten out of them MAO-B potent and selective inhibitors, with IC50 against this isoform in the nanomolar range, being (E)-3-(4-hydroxyphenyl)-1-(2,2-dimethylchroman-6-yl)prop-2-en-1-one (152) the best MAO-B inhibitor (IC50 of 170 nM).	(e)-3-(4-hydroxyphenyl)-1-(2,2-dimethylchroman-6-yl)prop-2-en-1-one	177-244	monoamine oxidase B	Homo sapiens	77-82
33571810-5	2021	All the synthetized molecules proved to inhibit MAO-B, being ten out of them MAO-B potent and selective inhibitors, with IC50 against this isoform in the nanomolar range, being (E)-3-(4-hydroxyphenyl)-1-(2,2-dimethylchroman-6-yl)prop-2-en-1-one (152) the best MAO-B inhibitor (IC50 of 170 nM).	(e)-3-(4-hydroxyphenyl)-1-(2,2-dimethylchroman-6-yl)prop-2-en-1-one	177-244	monoamine oxidase B	Homo sapiens	77-82
32093545-0	2021	The conformational dynamics of wing gates Ile199 and Phe103 on the binding of dopamine and benzylamine substrates in human Monoamine oxidase B.	Dopamine	78-86	monoamine oxidase B	Homo sapiens	123-142
32093545-0	2021	The conformational dynamics of wing gates Ile199 and Phe103 on the binding of dopamine and benzylamine substrates in human Monoamine oxidase B.	benzylamine	91-102	monoamine oxidase B	Homo sapiens	123-142
32093545-1	2021	The human Monoamine oxidase B (hMAO B) is an important flavoenzyme that metabolizes several biogenic amine neurotransmitters, regulates their concentration in the living cells and is involved in different neurological disorders and diseases.	Amines	14-19	monoamine oxidase B	Homo sapiens	31-37
32093545-2	2021	MD-simulation studies of dopamine (DOP) and benzylamine (BZA) complexed hMAO B structures have revealed the conformational dynamics of the gating residues Ile199 and Phe103.	Dopamine	25-33	monoamine oxidase B	Homo sapiens	72-78
32093545-3	2021	In the presence of large or small size substrate (DOP or BZA) molecules the inner Ile199 gate is observed to adopt an open conformation which forces the outer Phe103 gate to adopt a close conformation and it will possibly restrict the entry of any other ligand into the protein which could be the probable reason for low affinity binding of imidazole (2BFI) inhibitors in catalytically active hMAO B enzyme.	Dopamine	50-53	monoamine oxidase B	Homo sapiens	393-399
32093545-2	2021	MD-simulation studies of dopamine (DOP) and benzylamine (BZA) complexed hMAO B structures have revealed the conformational dynamics of the gating residues Ile199 and Phe103.	Dopamine	35-38	monoamine oxidase B	Homo sapiens	72-78
32093545-2	2021	MD-simulation studies of dopamine (DOP) and benzylamine (BZA) complexed hMAO B structures have revealed the conformational dynamics of the gating residues Ile199 and Phe103.	benzylamine	44-55	monoamine oxidase B	Homo sapiens	72-78
32093545-3	2021	In the presence of large or small size substrate (DOP or BZA) molecules the inner Ile199 gate is observed to adopt an open conformation which forces the outer Phe103 gate to adopt a close conformation and it will possibly restrict the entry of any other ligand into the protein which could be the probable reason for low affinity binding of imidazole (2BFI) inhibitors in catalytically active hMAO B enzyme.	imidazole	341-350	monoamine oxidase B	Homo sapiens	393-399
32093545-3	2021	In the presence of large or small size substrate (DOP or BZA) molecules the inner Ile199 gate is observed to adopt an open conformation which forces the outer Phe103 gate to adopt a close conformation and it will possibly restrict the entry of any other ligand into the protein which could be the probable reason for low affinity binding of imidazole (2BFI) inhibitors in catalytically active hMAO B enzyme.	2-(2-benzofuranyl)-2-imidazoline	352-356	monoamine oxidase B	Homo sapiens	393-399
33085988-1	2021	We herein report the biological evaluation of 3-arylcoumarin derivatives (3a-l) as potential human monoamine oxidase-A and -B (hMAO-A and hMAO-B) inhibitors.	3-arylcoumarin	46-60	monoamine oxidase B	Homo sapiens	138-144
33444985-3	2021	Substitution patterns on both the phenyl ring and the benzofuran moiety determine the affinity for MAO-A or MAO-B.	benzofuran	54-64	monoamine oxidase B	Homo sapiens	108-113
33444985-4	2021	The 2-(3-methoxyphenyl)-5-nitrobenzofuran 9 was the most potent MAO-B inhibitor (IC50 = 0.024 microM) identified in this series, whereas 7-nitro-2-phenylbenzofuran 7 was the most potent MAO-A inhibitor (IC50 = 0.168 microM), both acting as reversible inhibitors.	2-(3-methoxyphenyl)-5-nitrobenzofuran	4-41	monoamine oxidase B	Homo sapiens	64-69
33444985-4	2021	The 2-(3-methoxyphenyl)-5-nitrobenzofuran 9 was the most potent MAO-B inhibitor (IC50 = 0.024 microM) identified in this series, whereas 7-nitro-2-phenylbenzofuran 7 was the most potent MAO-A inhibitor (IC50 = 0.168 microM), both acting as reversible inhibitors.	7-nitro-2-phenylbenzofuran	137-163	monoamine oxidase B	Homo sapiens	64-69
32476010-1	2021	Selegiline is a selective, irreversible monoamine oxidase-B inhibitor, used for reducing symptoms in early-stage Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	40-59
33085988-2	2021	The result indicated that 7,8-dihydroxy-3-(4-nitrophenyl)coumarin (3j) was most effective against MAO-A (inhibition concentration [IC50 ] = 6.46 +- 0.02 microM) and MAO-B (IC50  = 3.8 +- 0.3 microM) enzymes than other synthesized compounds and reference compounds (pargyline and moclobemide).	7,8-dihydroxy-3-(4-nitrophenyl)coumarin	26-65	monoamine oxidase B	Homo sapiens	165-170
33068177-1	2021	Safinamide is a monoamine-oxidase-B inhibitor with peculiar features.	safinamide	0-10	monoamine oxidase B	Homo sapiens	16-35
32086435-2	2021	MAOB, a crucial monoamine oxidase for dopamine metabolism, triggers oxidative stress in dopaminergic neurons and alpha-Syn aggregation.	Dopamine	38-46	monoamine oxidase B	Homo sapiens	0-4
33279529-1	2021	Monoamine oxidases (MAO-A and MAO-B) are the two flavin adenine dinucleotide (FAD) enzymes that play an important role in neurotransmitter homeostasis and in protection against biogenic amines.	Flavin-Adenine Dinucleotide	49-76	monoamine oxidase B	Homo sapiens	30-35
33279529-1	2021	Monoamine oxidases (MAO-A and MAO-B) are the two flavin adenine dinucleotide (FAD) enzymes that play an important role in neurotransmitter homeostasis and in protection against biogenic amines.	Flavin-Adenine Dinucleotide	78-81	monoamine oxidase B	Homo sapiens	30-35
33279529-1	2021	Monoamine oxidases (MAO-A and MAO-B) are the two flavin adenine dinucleotide (FAD) enzymes that play an important role in neurotransmitter homeostasis and in protection against biogenic amines.	Amines	186-192	monoamine oxidase B	Homo sapiens	30-35
32646880-3	2021	A novel selective and reversible MAO-B tracer, (S)-(2-methylpyrid-5-yl)-6-[(3-[18F]fluoro-2-hydroxy)propoxy]quinoline, (18F-SMBT-1), was successfully developed via lead optimization from first-generation tau positron-emission tomography (PET) tracer 18F-THK-5351.	(s)-(2-methylpyrid-5-yl)-6-[(3-[18f]fluoro-2-hydroxy)propoxy]quinoline	47-117	monoamine oxidase B	Homo sapiens	33-38
32646880-3	2021	A novel selective and reversible MAO-B tracer, (S)-(2-methylpyrid-5-yl)-6-[(3-[18F]fluoro-2-hydroxy)propoxy]quinoline, (18F-SMBT-1), was successfully developed via lead optimization from first-generation tau positron-emission tomography (PET) tracer 18F-THK-5351.	(18f-smbt-1	119-130	monoamine oxidase B	Homo sapiens	33-38
32646880-3	2021	A novel selective and reversible MAO-B tracer, (S)-(2-methylpyrid-5-yl)-6-[(3-[18F]fluoro-2-hydroxy)propoxy]quinoline, (18F-SMBT-1), was successfully developed via lead optimization from first-generation tau positron-emission tomography (PET) tracer 18F-THK-5351.	uridine triacetate	204-207	monoamine oxidase B	Homo sapiens	33-38
32646880-3	2021	A novel selective and reversible MAO-B tracer, (S)-(2-methylpyrid-5-yl)-6-[(3-[18F]fluoro-2-hydroxy)propoxy]quinoline, (18F-SMBT-1), was successfully developed via lead optimization from first-generation tau positron-emission tomography (PET) tracer 18F-THK-5351.	thk	254-257	monoamine oxidase B	Homo sapiens	33-38
32646880-6	2021	The binding selectivity of 18F-SMBT-1 to MAO-B was evaluated by autoradiography of frozen human brain tissues.	18f-smbt-1	27-37	monoamine oxidase B	Homo sapiens	41-46
32970293-4	2021	The most potent inhibitor was a 1-tetralone derivative (1h) with IC50 values of 0.036 and 0.0011 microM for MAO-A and MAO-B, respectively.	Tetralones	32-43	monoamine oxidase B	Homo sapiens	118-123
32970293-4	2021	The most potent inhibitor was a 1-tetralone derivative (1h) with IC50 values of 0.036 and 0.0011 microM for MAO-A and MAO-B, respectively.	Hydrogen	56-58	monoamine oxidase B	Homo sapiens	118-123
32970293-6	2021	Among these 1-tetralol derivatives, 1p (IC50 = 0.785 muM) and 1o (IC50 = 0.0075 muM) were identified as particularly potent inhibitors of MAO-A and MAO-B, respectively.	1,2,3,4-Tetrahydro-1-naphthol	12-22	monoamine oxidase B	Homo sapiens	148-153
33360082-0	2021	Synthetic approaches to unsymmetrical 2,5-disubstituted 1,3,4-oxadiazoles and their MAO-B inhibitory activity.	2,5-disubstituted	38-55	monoamine oxidase B	Homo sapiens	84-89
33530616-0	2021	Selective Inhibition of Human Monoamine Oxidase B by 5-hydroxy-2-methyl-chroman-4-one Isolated from an Endogenous Lichen Fungus Daldinia fissa.	5-hydroxy-2-methylchroman-4-one	53-85	monoamine oxidase B	Homo sapiens	30-49
32700464-4	2021	MAO-B reversibility profile of 7-(4"-chlorobenzamido)-4-methylcoumarin ( 10 ) was investigated, being this compound a reversible inhibitor.	7-(4"-chlorobenzamido)-4-methylcoumarin	31-70	monoamine oxidase B	Homo sapiens	0-5
33360082-0	2021	Synthetic approaches to unsymmetrical 2,5-disubstituted 1,3,4-oxadiazoles and their MAO-B inhibitory activity.	1,3,4-oxadiazole	56-73	monoamine oxidase B	Homo sapiens	84-89
33360082-3	2021	Aiming at the elucidation of MAO-B inhibitors with 1,3,4-oxadiazole scaffolds, we make a comprehensive update on the new and old chemical methods employed for the synthesis of the unsymmetrical oxadiazole derivatives that lead to high yield compounds.	1,3,4-oxadiazole	51-67	monoamine oxidase B	Homo sapiens	29-34
33036760-0	2021	Effects of sevoflurane anaesthesia on radioligand binding to monoamine oxidase-B in vivo.	Sevoflurane	11-22	monoamine oxidase B	Homo sapiens	61-80
33360082-3	2021	Aiming at the elucidation of MAO-B inhibitors with 1,3,4-oxadiazole scaffolds, we make a comprehensive update on the new and old chemical methods employed for the synthesis of the unsymmetrical oxadiazole derivatives that lead to high yield compounds.	Oxadiazoles	57-67	monoamine oxidase B	Homo sapiens	29-34
33036760-2	2021	Unexpected observations in positron emission tomography (PET) studies with [11C]AZD9272, a metabotropic glutamate receptor 5 (mGluR5) radioligand with possible affinity for monoamine oxidase-B (MAO-B), suggest that its binding is sensitive to anaesthesia with sevoflurane.	AZD9272	80-87	monoamine oxidase B	Homo sapiens	173-192
33036760-2	2021	Unexpected observations in positron emission tomography (PET) studies with [11C]AZD9272, a metabotropic glutamate receptor 5 (mGluR5) radioligand with possible affinity for monoamine oxidase-B (MAO-B), suggest that its binding is sensitive to anaesthesia with sevoflurane.	AZD9272	80-87	monoamine oxidase B	Homo sapiens	194-199
33360082-4	2021	We summarize a state of the selective MAO-B inhibitors with oxadiazole scaffold, describing the results, structures, structure-activity relationships (SARs) and medicinal chemistry strategies over the years.	Oxadiazoles	60-70	monoamine oxidase B	Homo sapiens	38-43
33036760-2	2021	Unexpected observations in positron emission tomography (PET) studies with [11C]AZD9272, a metabotropic glutamate receptor 5 (mGluR5) radioligand with possible affinity for monoamine oxidase-B (MAO-B), suggest that its binding is sensitive to anaesthesia with sevoflurane.	Sevoflurane	260-271	monoamine oxidase B	Homo sapiens	173-192
33360082-5	2021	The analysis of the recent papers would facilitate tracking the increasing number of oxadiazole derivatives as new chemical spaces with MAO-B inhibitory potential designed to ensure the safe use of the compounds and elimination of the unwanted drug-drug interactions.	Oxadiazoles	85-95	monoamine oxidase B	Homo sapiens	136-141
32924264-2	2020	The present work describes the syntheses of selected 1,3-benzodioxine-containing chalcones (CD3, CD8 and CD10), and their inhibitory activities against MAO-A, MAO-B, acetylcholinesterase (AChE), and butyrylcholinesterase (BChE).	1,3-benzodioxine	53-69	monoamine oxidase B	Homo sapiens	159-164
33071056-0	2021	Pyrimido[1,2-b]indazole derivatives: Selective inhibitors of human monoamine oxidase B with neuroprotective activity.	pyrimido[1,2-b]indazole	0-23	monoamine oxidase B	Homo sapiens	67-86
33071056-4	2021	Derivatives 4a-t selectively inhibited human MAO-B isoform in a reversible and competitive manner as confirmed by kinetic experiments and docking studies.	4a-t	12-16	monoamine oxidase B	Homo sapiens	45-50
33097301-6	2021	Enzymatic studies confirmed that pOBz competitively inhibited the activity of purified human MAO-B (Ki = 0.041 muM versus Ki = 0.92 muM for salidroside), and pOBz was highly selective for MAO-B over MAO-A.	pobz	33-37	monoamine oxidase B	Homo sapiens	93-98
33097301-6	2021	Enzymatic studies confirmed that pOBz competitively inhibited the activity of purified human MAO-B (Ki = 0.041 muM versus Ki = 0.92 muM for salidroside), and pOBz was highly selective for MAO-B over MAO-A.	pobz	33-37	monoamine oxidase B	Homo sapiens	188-193
33097301-6	2021	Enzymatic studies confirmed that pOBz competitively inhibited the activity of purified human MAO-B (Ki = 0.041 muM versus Ki = 0.92 muM for salidroside), and pOBz was highly selective for MAO-B over MAO-A.	rhodioloside	140-151	monoamine oxidase B	Homo sapiens	93-98
33097301-6	2021	Enzymatic studies confirmed that pOBz competitively inhibited the activity of purified human MAO-B (Ki = 0.041 muM versus Ki = 0.92 muM for salidroside), and pOBz was highly selective for MAO-B over MAO-A.	pobz	158-162	monoamine oxidase B	Homo sapiens	188-193
33249607-4	2021	Eugenol showed inhibitory activity against MAO-B enzyme, free radical scavenging activity, and anti-aggregation activity against Abeta peptides than other phytoconstituents.	Eugenol	0-7	monoamine oxidase B	Homo sapiens	43-48
33249607-9	2021	Eugenol can bind to different Alzheimer"s targets such as beta-secretase (BACE1), Monoamine oxidase B (MAO-B), Cholinesterase"s, and amyloid beta1-42 fibrils and might have a disease-modifying potential.	Eugenol	0-7	monoamine oxidase B	Homo sapiens	82-101
33249607-9	2021	Eugenol can bind to different Alzheimer"s targets such as beta-secretase (BACE1), Monoamine oxidase B (MAO-B), Cholinesterase"s, and amyloid beta1-42 fibrils and might have a disease-modifying potential.	Eugenol	0-7	monoamine oxidase B	Homo sapiens	103-108
33008589-8	2020	In vitro experiment using the brain slice culture demonstrated that extracellular perfusion of D-arginine significantly elevated the mRNA expression level of monoamine oxidase B, the major enzyme involved in DA metabolism, in the locus coeruleus region of the brainstem.	D-Arginine	95-105	monoamine oxidase B	Homo sapiens	158-177
33008589-8	2020	In vitro experiment using the brain slice culture demonstrated that extracellular perfusion of D-arginine significantly elevated the mRNA expression level of monoamine oxidase B, the major enzyme involved in DA metabolism, in the locus coeruleus region of the brainstem.	Dopamine	208-210	monoamine oxidase B	Homo sapiens	158-177
33284012-0	2020	Synthesis and Autoradiography of Novel F-18 Labeled Reversible Radioligands for Detection of Monoamine Oxidase B.	Fluorine-18	39-43	monoamine oxidase B	Homo sapiens	93-112
33284012-2	2020	Selective MAO-B inhibitors have been labeled with carbon-11 or fluorine-18 to visualize the localization of MAO-B in vivo by positron emission tomography (PET) and thereby have been useful for studying neurodegenerative diseases.	Carbon-11	50-59	monoamine oxidase B	Homo sapiens	10-15
33284012-2	2020	Selective MAO-B inhibitors have been labeled with carbon-11 or fluorine-18 to visualize the localization of MAO-B in vivo by positron emission tomography (PET) and thereby have been useful for studying neurodegenerative diseases.	Fluorine-18	63-74	monoamine oxidase B	Homo sapiens	10-15
33284012-2	2020	Selective MAO-B inhibitors have been labeled with carbon-11 or fluorine-18 to visualize the localization of MAO-B in vivo by positron emission tomography (PET) and thereby have been useful for studying neurodegenerative diseases.	Fluorine-18	63-74	monoamine oxidase B	Homo sapiens	108-113
33284012-3	2020	The aim of this study was to develop promising fluorine-18 labeled reversible MAO-B PET radioligands and their biological evaluation in vitro by autoradiography.	Fluorine	47-55	monoamine oxidase B	Homo sapiens	78-83
33284012-10	2020	The ARG binding density of only 18F-GEH200449 was consistent with known MAO-B expression in the human brain.	Arginine	4-7	monoamine oxidase B	Homo sapiens	72-77
33284012-11	2020	Radiolabeling of five new fluorine-18 MAO-B reversible inhibitors was successfully accomplished.	Fluorine	26-34	monoamine oxidase B	Homo sapiens	38-43
33284012-12	2020	Compound 18F-GEH200449 binds specifically to MAO-B in vitro postmortem brain and could be a potential candidate for in vivo PET investigation.	18f-geh200449	9-22	monoamine oxidase B	Homo sapiens	45-50
33375412-0	2020	First Synthesis of Racemic Trans Propargylamino-Donepezil, a Pleiotrope Agent Able to Both Inhibit AChE and MAO-B, with Potential Interest against Alzheimer"s Disease.	trans propargylamino-donepezil	27-57	monoamine oxidase B	Homo sapiens	108-113
33375412-2	2020	Among the numerous targets which are today validated against AD, acetylcholinesterase (ACh) and Monoamine Oxidase-B (MAO-B) appear as particularly convincing, especially if displayed by a sole agent such as ladostigil, currently in clinical trial in AD.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	207-217	monoamine oxidase B	Homo sapiens	96-115
33375412-2	2020	Among the numerous targets which are today validated against AD, acetylcholinesterase (ACh) and Monoamine Oxidase-B (MAO-B) appear as particularly convincing, especially if displayed by a sole agent such as ladostigil, currently in clinical trial in AD.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	207-217	monoamine oxidase B	Homo sapiens	117-122
33375412-3	2020	Considering these results, we wanted to take benefit of the structural analogy lying in donepezil (DPZ) and rasagiline, two indane derivatives marketed as AChE and MAO-B inhibitors, respectively, and to propose the synthesis and the preliminary in vitro biological characterization of a structural compromise between these two compounds, we called propargylaminodonepezil (PADPZ).	Donepezil	88-97	monoamine oxidase B	Homo sapiens	164-169
33375412-3	2020	Considering these results, we wanted to take benefit of the structural analogy lying in donepezil (DPZ) and rasagiline, two indane derivatives marketed as AChE and MAO-B inhibitors, respectively, and to propose the synthesis and the preliminary in vitro biological characterization of a structural compromise between these two compounds, we called propargylaminodonepezil (PADPZ).	Donepezil	99-102	monoamine oxidase B	Homo sapiens	164-169
33375412-3	2020	Considering these results, we wanted to take benefit of the structural analogy lying in donepezil (DPZ) and rasagiline, two indane derivatives marketed as AChE and MAO-B inhibitors, respectively, and to propose the synthesis and the preliminary in vitro biological characterization of a structural compromise between these two compounds, we called propargylaminodonepezil (PADPZ).	rasagiline	108-118	monoamine oxidase B	Homo sapiens	164-169
33375412-4	2020	The synthesis of racemic trans PADPZ was achieved and its biological evaluation established its inhibitory activities towards both (h)AChE (IC50 = 0.4 microM) and (h)MAO-B (IC50 = 6.4 microM).	trans padpz	25-36	monoamine oxidase B	Homo sapiens	166-171
33210537-2	2020	Inhibition of monoamine oxidase-B (MAO-B), which is mainly found in the glial cells of the brain, may lead to an elevated level of dopamine (DA) in patients.	Dopamine	131-139	monoamine oxidase B	Homo sapiens	14-33
33210537-2	2020	Inhibition of monoamine oxidase-B (MAO-B), which is mainly found in the glial cells of the brain, may lead to an elevated level of dopamine (DA) in patients.	Dopamine	131-139	monoamine oxidase B	Homo sapiens	35-40
33210537-2	2020	Inhibition of monoamine oxidase-B (MAO-B), which is mainly found in the glial cells of the brain, may lead to an elevated level of dopamine (DA) in patients.	Dopamine	141-143	monoamine oxidase B	Homo sapiens	14-33
33210537-2	2020	Inhibition of monoamine oxidase-B (MAO-B), which is mainly found in the glial cells of the brain, may lead to an elevated level of dopamine (DA) in patients.	Dopamine	141-143	monoamine oxidase B	Homo sapiens	35-40
33210537-7	2020	In vitro biological evaluations revealed that (S)-1-(4-((3-fluorobenzyl)oxy)benzyl)azetidine-2-carboxamide (C3) was more potent and selective than safinamide, a promising drug for regulating MAO-B.	(s)-1-(4-((3-fluorobenzyl)oxy)benzyl)azetidine-2-carboxamide	46-106	monoamine oxidase B	Homo sapiens	191-196
32924264-2	2020	The present work describes the syntheses of selected 1,3-benzodioxine-containing chalcones (CD3, CD8 and CD10), and their inhibitory activities against MAO-A, MAO-B, acetylcholinesterase (AChE), and butyrylcholinesterase (BChE).	Chalcones	81-90	monoamine oxidase B	Homo sapiens	159-164
33025342-12	2020	While CC112273 and CC1084037 selectively inhibited monoamine oxidase (MAO)-B in vitro, both active metabolites do not inhibit platelet MAO-B activity in vivo.	UNII-F2PE1J7HH9	6-14	monoamine oxidase B	Homo sapiens	51-76
33025342-12	2020	While CC112273 and CC1084037 selectively inhibited monoamine oxidase (MAO)-B in vitro, both active metabolites do not inhibit platelet MAO-B activity in vivo.	UNII-KYS7WW026H	19-28	monoamine oxidase B	Homo sapiens	51-76
33199896-3	2020	Mechanistically, excessive hydrogen peroxide (H2O2) originated from monoamine oxidase B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and eventual death, which are significantly prevented by AAD-2004, a potent H2O2 scavenger.	Hydrogen Peroxide	27-44	monoamine oxidase B	Homo sapiens	68-87
32705910-0	2020	Design, synthesis, and evaluation of 1, 4-benzodioxan-substituted chalcones as selective and reversible inhibitors of human monoamine oxidase B.	1, 4-benzodioxan-substituted	37-65	monoamine oxidase B	Homo sapiens	124-143
32705910-0	2020	Design, synthesis, and evaluation of 1, 4-benzodioxan-substituted chalcones as selective and reversible inhibitors of human monoamine oxidase B.	Chalcones	66-75	monoamine oxidase B	Homo sapiens	124-143
32705910-2	2020	In this study, a series of 1, 4-benzodioxan-substituted chalcone derivatives were designed, synthesised and evaluated for their inhibitory activity against human MAO-B (hMAO-B).	1,4-benzodioxan	27-43	monoamine oxidase B	Homo sapiens	162-167
32705910-2	2020	In this study, a series of 1, 4-benzodioxan-substituted chalcone derivatives were designed, synthesised and evaluated for their inhibitory activity against human MAO-B (hMAO-B).	1,4-benzodioxan	27-43	monoamine oxidase B	Homo sapiens	169-175
32705910-2	2020	In this study, a series of 1, 4-benzodioxan-substituted chalcone derivatives were designed, synthesised and evaluated for their inhibitory activity against human MAO-B (hMAO-B).	Chalcone	56-64	monoamine oxidase B	Homo sapiens	162-167
32705910-2	2020	In this study, a series of 1, 4-benzodioxan-substituted chalcone derivatives were designed, synthesised and evaluated for their inhibitory activity against human MAO-B (hMAO-B).	Chalcone	56-64	monoamine oxidase B	Homo sapiens	169-175
32752896-0	2020	Discovery of N-(1-(3-fluorobenzoyl)-1H-indol-5-yl)pyrazine-2-carboxamide: a novel, selective, and competitive indole-based lead inhibitor for human monoamine oxidase B.	n-(1-(3-fluorobenzoyl)-1h-indol-5-yl)pyrazine-2-carboxamide	13-72	monoamine oxidase B	Homo sapiens	148-167
32752896-0	2020	Discovery of N-(1-(3-fluorobenzoyl)-1H-indol-5-yl)pyrazine-2-carboxamide: a novel, selective, and competitive indole-based lead inhibitor for human monoamine oxidase B.	indole	110-116	monoamine oxidase B	Homo sapiens	148-167
32752896-1	2020	Herein, two new series of N-substituted indole-based analogues were rationally designed, synthesized via microwave heating technology, and evaluated as noteworthy MAO-B potential inhibitors.	n-substituted indole	26-46	monoamine oxidase B	Homo sapiens	163-168
32752896-2	2020	Compared to the reported indazole-based hits VI and VII, compounds 4b and 4e exhibited higher inhibitory activities over MAO-B with IC50 values of 1.65 and 0.78 microM, respectively.	Indazoles	25-33	monoamine oxidase B	Homo sapiens	121-126
32752896-3	2020	When compared to the modest selectivity index of rasagiline (II, a well-known MAO-B inhibitor, SI > 50), both 4b and 4e also showed better selectivity indices (SI > 60 and 120, respectively).	rasagiline	49-59	monoamine oxidase B	Homo sapiens	78-83
32752896-6	2020	Accordingly, the remarkable MAO-B inhibitory activity of 4e (N-(1-(3-fluorobenzoyl)-1H-indol-5-yl)pyrazine-2-carboxamide), with its selectivity and competitive inhibition, advocates its potential role as a promising lead worthy of further optimization.	4e (n-(1-(3-fluorobenzoyl)-1h-indol-5-yl)pyrazine-2-carboxamide	57-120	monoamine oxidase B	Homo sapiens	28-33
32602377-0	2020	Synthesis, in vitro enzyme activity and molecular docking studies of new benzylamine-sulfonamide derivatives as selective MAO-B inhibitors.	benzylamine-sulfonamide	73-96	monoamine oxidase B	Homo sapiens	122-127
32602377-1	2020	Many studies have been conducted on the selective inhibition of human monoamine oxidase B (hMAO-B) enzyme using benzylamine-sulphonamide derivatives.	benzylamine	112-123	monoamine oxidase B	Homo sapiens	70-89
32602377-1	2020	Many studies have been conducted on the selective inhibition of human monoamine oxidase B (hMAO-B) enzyme using benzylamine-sulphonamide derivatives.	benzylamine	112-123	monoamine oxidase B	Homo sapiens	91-97
32602377-1	2020	Many studies have been conducted on the selective inhibition of human monoamine oxidase B (hMAO-B) enzyme using benzylamine-sulphonamide derivatives.	Sulfonamides	124-136	monoamine oxidase B	Homo sapiens	70-89
32602377-1	2020	Many studies have been conducted on the selective inhibition of human monoamine oxidase B (hMAO-B) enzyme using benzylamine-sulphonamide derivatives.	Sulfonamides	124-136	monoamine oxidase B	Homo sapiens	91-97
32602377-2	2020	Using various chemical modifications on BB-4h, which was reported previously by our team and showed a significant level of MAO-B inhibition, novel benzylamine-sulphonamide derivatives were designed, synthesised, and their MAO inhibition potentials were evaluated.	bb-4h	40-45	monoamine oxidase B	Homo sapiens	123-128
33199896-3	2020	Mechanistically, excessive hydrogen peroxide (H2O2) originated from monoamine oxidase B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and eventual death, which are significantly prevented by AAD-2004, a potent H2O2 scavenger.	Hydrogen Peroxide	46-50	monoamine oxidase B	Homo sapiens	68-87
33199896-3	2020	Mechanistically, excessive hydrogen peroxide (H2O2) originated from monoamine oxidase B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and eventual death, which are significantly prevented by AAD-2004, a potent H2O2 scavenger.	Hydrogen Peroxide	282-286	monoamine oxidase B	Homo sapiens	68-87
33212830-10	2020	The natural O-methylated flavonoid (1) with highly potent inhibition (IC50 33 nM; Ki 37.9 nM) and >292 fold selectivity against human MAO-A (vs. MAO-B) provides a new drug lead for the treatment of neurological disorders.	Flavonoids	25-34	monoamine oxidase B	Homo sapiens	145-150
33103897-0	2020	Click-Reaction-Triggered SERS Signals for Specific Detection of Monoamine Oxidase B Activity.	sers	25-29	monoamine oxidase B	Homo sapiens	64-83
33103897-3	2020	In this work, a novel surface-enhanced Raman scattering (SERS) sensor was fabricated and the MAOB activity was specifically determined by detecting the SERS signals of an enzyme-catalyzed reaction product via an amine-aldehyde click reaction.	sers	57-61	monoamine oxidase B	Homo sapiens	93-97
33103897-3	2020	In this work, a novel surface-enhanced Raman scattering (SERS) sensor was fabricated and the MAOB activity was specifically determined by detecting the SERS signals of an enzyme-catalyzed reaction product via an amine-aldehyde click reaction.	sers	152-156	monoamine oxidase B	Homo sapiens	93-97
33103897-3	2020	In this work, a novel surface-enhanced Raman scattering (SERS) sensor was fabricated and the MAOB activity was specifically determined by detecting the SERS signals of an enzyme-catalyzed reaction product via an amine-aldehyde click reaction.	amine-aldehyde	212-226	monoamine oxidase B	Homo sapiens	93-97
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenethylamine	6-20	monoamine oxidase B	Homo sapiens	53-57
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenethylamine	6-20	monoamine oxidase B	Homo sapiens	220-224
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenethylamine	22-24	monoamine oxidase B	Homo sapiens	53-57
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenethylamine	22-24	monoamine oxidase B	Homo sapiens	220-224
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenylacetaldehyde	78-96	monoamine oxidase B	Homo sapiens	53-57
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenylacetaldehyde	78-96	monoamine oxidase B	Homo sapiens	220-224
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenylacetaldehyde	98-101	monoamine oxidase B	Homo sapiens	53-57
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenylacetaldehyde	98-101	monoamine oxidase B	Homo sapiens	220-224
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	amine-aldehyde	150-164	monoamine oxidase B	Homo sapiens	53-57
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	amine-aldehyde	150-164	monoamine oxidase B	Homo sapiens	220-224
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenethylamine	98-100	monoamine oxidase B	Homo sapiens	53-57
33103897-5	2020	Using phenethylamine (PA) as a specific substrate of MAOB, the enzyme product phenylacetaldehyde (PAA) will produce significant Raman signals via the amine-aldehyde click reaction with CA, while other molecules, such as MAOB and PA, have no signal output because they cannot form close interaction with nanoparticles due to the existence of a CA layer.	phenethylamine	98-100	monoamine oxidase B	Homo sapiens	220-224
33212876-0	2020	Design, Synthesis, and Biological Evaluation of Pyridazinones Containing the (2-Fluorophenyl) Piperazine Moiety as Selective MAO-B Inhibitors.	pyridazinones	48-61	monoamine oxidase B	Homo sapiens	125-130
33212876-0	2020	Design, Synthesis, and Biological Evaluation of Pyridazinones Containing the (2-Fluorophenyl) Piperazine Moiety as Selective MAO-B Inhibitors.	(2-fluorophenyl) piperazine	77-104	monoamine oxidase B	Homo sapiens	125-130
33212876-2	2020	T6 was found to be the most potent MAO-B inhibitor with an IC50 value of 0.013 microM, followed by T3 (IC50 = 0.039 microM).	t6	0-2	monoamine oxidase B	Homo sapiens	35-40
33212876-4	2020	For para substitution, inhibitory potencies for MAO-B were as follows: -Cl (T3) > -N(CH3)2 (T12) > -OCH3 (T9) > Br (T7) > F (T5) > -CH3 (T11) > -H (T1).	Triiodothyronine	76-79	monoamine oxidase B	Homo sapiens	48-53
33212876-5	2020	T6 and T3 efficiently inhibited MAO-A with IC50 values of 1.57 and 4.19 microM and had the highest selectivity indices (SIs) for MAO-B (120.8 and 107.4, respectively).	t6	0-2	monoamine oxidase B	Homo sapiens	129-134
33212876-5	2020	T6 and T3 efficiently inhibited MAO-A with IC50 values of 1.57 and 4.19 microM and had the highest selectivity indices (SIs) for MAO-B (120.8 and 107.4, respectively).	Triiodothyronine	7-9	monoamine oxidase B	Homo sapiens	129-134
32830978-8	2020	Illudinine was found to inhibit monoamine oxidase B (MAO-B) with an IC50 of 18 +- 7.1 microM in preliminary assays.	illudinine	0-10	monoamine oxidase B	Homo sapiens	32-51
32942081-1	2020	Monoamine oxidases (MAO-A and MAO-B) are mammalian flavoenzyme, which catalyze the oxidative deamination of several neurotransmitters like norepinephrine, dopamine, tyramine, serotonin, and some other amines.	Norepinephrine	139-153	monoamine oxidase B	Homo sapiens	30-35
32942081-1	2020	Monoamine oxidases (MAO-A and MAO-B) are mammalian flavoenzyme, which catalyze the oxidative deamination of several neurotransmitters like norepinephrine, dopamine, tyramine, serotonin, and some other amines.	Dopamine	155-163	monoamine oxidase B	Homo sapiens	30-35
32942081-1	2020	Monoamine oxidases (MAO-A and MAO-B) are mammalian flavoenzyme, which catalyze the oxidative deamination of several neurotransmitters like norepinephrine, dopamine, tyramine, serotonin, and some other amines.	Tyramine	165-173	monoamine oxidase B	Homo sapiens	30-35
32942081-1	2020	Monoamine oxidases (MAO-A and MAO-B) are mammalian flavoenzyme, which catalyze the oxidative deamination of several neurotransmitters like norepinephrine, dopamine, tyramine, serotonin, and some other amines.	Serotonin	175-184	monoamine oxidase B	Homo sapiens	30-35
32942081-1	2020	Monoamine oxidases (MAO-A and MAO-B) are mammalian flavoenzyme, which catalyze the oxidative deamination of several neurotransmitters like norepinephrine, dopamine, tyramine, serotonin, and some other amines.	Amines	201-207	monoamine oxidase B	Homo sapiens	30-35
32830978-8	2020	Illudinine was found to inhibit monoamine oxidase B (MAO-B) with an IC50 of 18 +- 7.1 microM in preliminary assays.	illudinine	0-10	monoamine oxidase B	Homo sapiens	53-58
33114548-0	2020	Newly Synthesized Fluorinated Cinnamylpiperazines Possessing Low In Vitro MAO-B Binding.	cinnamylpiperazines	30-49	monoamine oxidase B	Homo sapiens	74-79
33146735-18	2020	Neighborhood deprivation was found to be associated with 3 cytosine-phosphate-guanine sites, with 1 of these annotated to a known gene MAOB (P = 9.71 x 10-08).	cytosine-phosphate-guanine	59-85	monoamine oxidase B	Homo sapiens	135-139
32657863-4	2020	F-THK5351 reportedly binds to monoamine oxidase B highly expressed in astrocytes.	THK5351	2-9	monoamine oxidase B	Homo sapiens	30-49
32621059-1	2020	Whereas monoamine oxidase (MAO) type B inhibitors are used as adjunct to L-3,4-dihydroxyphenylalanine (L-DOPA) in the treatment of Parkinson"s disease (PD), the enzyme MAO type A (MAO-A) also participates in the metabolism of dopamine in the human and primate striatum.	Dopamine	226-234	monoamine oxidase B	Homo sapiens	8-38
33114548-1	2020	Herein, we report on the synthesis and pharmacological evaluation of ten novel fluorinated cinnamylpiperazines as potential monoamine oxidase B (MAO-B) ligands.	cinnamylpiperazines	91-110	monoamine oxidase B	Homo sapiens	124-143
33114548-1	2020	Herein, we report on the synthesis and pharmacological evaluation of ten novel fluorinated cinnamylpiperazines as potential monoamine oxidase B (MAO-B) ligands.	cinnamylpiperazines	91-110	monoamine oxidase B	Homo sapiens	145-150
33114548-5	2020	Docking studies revealed that the compounds 8-17 were stabilized in both MAO-B entrance and substrate cavities, thus resembling the binding pose of l-Deprenyl.	Selegiline	148-158	monoamine oxidase B	Homo sapiens	73-78
32583952-0	2020	1-[4-(morpholin-4-yl)phenyl]-5-phenylpenta-2,4-dien-1-one as a new potent and selective monoamine oxidase-B inhibitor with extended conjugation in chalcone framework.	1-[4-(morpholin-4-yl)phenyl]-5-phenylpenta-2,4-dien-1-one	0-57	monoamine oxidase B	Homo sapiens	88-107
32682215-2	2020	Safinamide is a novel inhibitor of monoamine oxidase B (MAOB) with neuroprotective properties.	safinamide	0-10	monoamine oxidase B	Homo sapiens	35-54
32682215-2	2020	Safinamide is a novel inhibitor of monoamine oxidase B (MAOB) with neuroprotective properties.	safinamide	0-10	monoamine oxidase B	Homo sapiens	56-60
32682215-6	2020	Previous studies have shown that safinamide, a monoamine oxidase-B (MAOB) inhibitor, can function as a neuroprotective agent and inhibit the neurodegenerative process especially in Parkinson"s disease but its impact on other neurodegenerative processes and drug-induced neurotoxicity remain unclear.	safinamide	33-43	monoamine oxidase B	Homo sapiens	47-66
32682215-6	2020	Previous studies have shown that safinamide, a monoamine oxidase-B (MAOB) inhibitor, can function as a neuroprotective agent and inhibit the neurodegenerative process especially in Parkinson"s disease but its impact on other neurodegenerative processes and drug-induced neurotoxicity remain unclear.	safinamide	33-43	monoamine oxidase B	Homo sapiens	68-72
32869630-3	2020	Here, luteolin exhibited selective inhibition of hMAO-A (IC50 = 8.57 +- 0.47 microM) over hMAO-B (IC50 > 100 microM).	Luteolin	6-14	monoamine oxidase B	Homo sapiens	90-96
32652406-0	2020	Design, synthesis and biological evaluation of rasagiline-clorgyline hybrids as novel dual inhibitors of monoamine oxidase-B and amyloid-beta aggregation against Alzheimer"s disease.	rasagiline	47-57	monoamine oxidase B	Homo sapiens	105-124
32652406-0	2020	Design, synthesis and biological evaluation of rasagiline-clorgyline hybrids as novel dual inhibitors of monoamine oxidase-B and amyloid-beta aggregation against Alzheimer"s disease.	Clorgyline	58-68	monoamine oxidase B	Homo sapiens	105-124
32652406-3	2020	7-((5-(methyl(prop-2-yn-1-yl)amino) pentyl)oxy)chroman-4-one (6j) was the most interesting compound identified in this research, endowed with higher hMAO-B potency (IC50 = 4 nM) and selectivity (SI > 25000) compared to the reference selective inhibitor rasagiline (IC50 = 141 nM, SI > 355), and exhibited good inhibitory activity against Abeta1-42 aggregation (40.78%, 25 muM).	7-((5-(methyl(prop-2-yn-1-yl)amino) pentyl)oxy)chroman-4-one	0-60	monoamine oxidase B	Homo sapiens	149-155
32673884-1	2020	INTRODUCTION: Safinamide, a selective, reversible monoamine oxidase B inhibitor with a sodium channel inhibitory effect, improves symptoms in advanced Parkinson"s disease (PD).	safinamide	14-24	monoamine oxidase B	Homo sapiens	50-69
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	Amines	132-138	monoamine oxidase B	Homo sapiens	0-19
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	Amines	132-138	monoamine oxidase B	Homo sapiens	21-25
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	benzylamine	147-158	monoamine oxidase B	Homo sapiens	0-19
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	benzylamine	147-158	monoamine oxidase B	Homo sapiens	21-25
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	phenethylamine	160-174	monoamine oxidase B	Homo sapiens	0-19
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	phenethylamine	160-174	monoamine oxidase B	Homo sapiens	21-25
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	Dopamine	179-187	monoamine oxidase B	Homo sapiens	0-19
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	Dopamine	179-187	monoamine oxidase B	Homo sapiens	21-25
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	Flavin-Adenine Dinucleotide	205-232	monoamine oxidase B	Homo sapiens	0-19
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	Flavin-Adenine Dinucleotide	205-232	monoamine oxidase B	Homo sapiens	21-25
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	Flavin-Adenine Dinucleotide	234-237	monoamine oxidase B	Homo sapiens	0-19
33081086-1	2020	Monoamine oxidase B (MAOB) is expressed in the mitochondrial membrane and has a key role in degrading various neurologically active amines such as benzylamine, phenethylamine and dopamine with the help of Flavin adenine dinucleotide (FAD) cofactor.	Flavin-Adenine Dinucleotide	234-237	monoamine oxidase B	Homo sapiens	21-25
33081086-2	2020	The Parkinson"s disease associated symptoms can be treated using inhibitors of MAO-B as the dopamine degradation can be reduced.	Dopamine	92-100	monoamine oxidase B	Homo sapiens	79-84
32711021-0	2020	Highly efficient synthesis and monoamine oxidase B inhibitory profile of demethyleneberberine, columbamine and palmatine.	demethyleneberberine	73-93	monoamine oxidase B	Homo sapiens	31-50
32711021-0	2020	Highly efficient synthesis and monoamine oxidase B inhibitory profile of demethyleneberberine, columbamine and palmatine.	columbamine	95-106	monoamine oxidase B	Homo sapiens	31-50
32711021-0	2020	Highly efficient synthesis and monoamine oxidase B inhibitory profile of demethyleneberberine, columbamine and palmatine.	palmatine	111-120	monoamine oxidase B	Homo sapiens	31-50
32711021-4	2020	Furthermore, we found that DMB (IC50, 9.06 muM) inhibited the activity of monoamine oxidase B (MAO-B), an enzyme that deaminates dopamine and is particularly involved in the pathology of Parkinson"s disease.	demethyleneberberine	27-30	monoamine oxidase B	Homo sapiens	74-93
32711021-4	2020	Furthermore, we found that DMB (IC50, 9.06 muM) inhibited the activity of monoamine oxidase B (MAO-B), an enzyme that deaminates dopamine and is particularly involved in the pathology of Parkinson"s disease.	demethyleneberberine	27-30	monoamine oxidase B	Homo sapiens	95-100
32711021-4	2020	Furthermore, we found that DMB (IC50, 9.06 muM) inhibited the activity of monoamine oxidase B (MAO-B), an enzyme that deaminates dopamine and is particularly involved in the pathology of Parkinson"s disease.	Dopamine	129-137	monoamine oxidase B	Homo sapiens	74-93
32711021-4	2020	Furthermore, we found that DMB (IC50, 9.06 muM) inhibited the activity of monoamine oxidase B (MAO-B), an enzyme that deaminates dopamine and is particularly involved in the pathology of Parkinson"s disease.	Dopamine	129-137	monoamine oxidase B	Homo sapiens	95-100
32711021-5	2020	Besides, columbamine was able to decrease MAO-B activity by approximately 40%.	columbamine	9-20	monoamine oxidase B	Homo sapiens	42-47
32583952-0	2020	1-[4-(morpholin-4-yl)phenyl]-5-phenylpenta-2,4-dien-1-one as a new potent and selective monoamine oxidase-B inhibitor with extended conjugation in chalcone framework.	Chalcone	147-155	monoamine oxidase B	Homo sapiens	88-107
32583952-3	2020	The title compound MO10 was assessed for inhibitory activities against two human MAO isoforms, i.e., MAO-A and MAO-B.	mo10	19-23	monoamine oxidase B	Homo sapiens	111-116
32583952-4	2020	Interestingly, MO10 showed a remarkable inhibition against MAO-B with an IC 50 value of 0.044 microM along with a selectivity index of 366.13.	mo10	15-19	monoamine oxidase B	Homo sapiens	59-64
32583952-6	2020	Kinetics studies revealed that MO10 acted as a competitive inhibitor for MAO-B, with a K i value of 0.0080 microM.	mo10	31-35	monoamine oxidase B	Homo sapiens	73-78
32583952-7	2020	In reversibility experiments, MO10 was found to be a reversible inhibitor by observations of inhibition recoveries of MAO-B, comparing to the reference levels.	mo10	30-34	monoamine oxidase B	Homo sapiens	118-123
32588409-2	2020	MAO-B inhibitors are used as monotherapy as well as in combination with levodopa, whereas COMT inhibitors exert their effects only in conjungtion with levodopa.	Levodopa	72-80	monoamine oxidase B	Homo sapiens	0-5
33109837-5	2020	Gold fish brain has the "nucleus pars medialis," similar to the substanitia nigra of the human brain can be destructed by chemicals like MPTP, 6-hydroxydopamine and has selective protection by L-Dopa (Levodopa) and MAO-B (Monoamine oxidase B) inhibitors.	Levodopa	201-209	monoamine oxidase B	Homo sapiens	222-241
32859055-0	2020	Inhibition of Butyrylcholinesterase and Human Monoamine Oxidase-B by the Coumarin Glycyrol and Liquiritigenin Isolated from Glycyrrhiza uralensis.	coumarin glycyrol	73-90	monoamine oxidase B	Homo sapiens	46-65
33109837-5	2020	Gold fish brain has the "nucleus pars medialis," similar to the substanitia nigra of the human brain can be destructed by chemicals like MPTP, 6-hydroxydopamine and has selective protection by L-Dopa (Levodopa) and MAO-B (Monoamine oxidase B) inhibitors.	Levodopa	201-209	monoamine oxidase B	Homo sapiens	215-220
32859055-0	2020	Inhibition of Butyrylcholinesterase and Human Monoamine Oxidase-B by the Coumarin Glycyrol and Liquiritigenin Isolated from Glycyrrhiza uralensis.	liquiritigenin	95-109	monoamine oxidase B	Homo sapiens	46-65
32786232-2	2020	The disease state is associated with dopamine deprival, and so the inhibitors of MAO-B can serve as therapeutic drugs for PD.	Dopamine	37-45	monoamine oxidase B	Homo sapiens	81-86
32474182-0	2020	3-Arylcoumarins as highly potent and selective monoamine oxidase B inhibitors: Which chemical features matter?	3-arylcoumarins	0-15	monoamine oxidase B	Homo sapiens	47-66
32459875-3	2020	UV-visible spectrophotometry and steady-state kinetics experiments demonstrate that DPI acts as a competitive MAO inhibitor with Ki values of 1.7 microM and 0.3 microM for MAO A and MAO B, respectively.	diphenyleneiodonium	84-87	monoamine oxidase B	Homo sapiens	182-187
32459875-4	2020	Elucidation of the crystal structure of human MAO B bound to the inhibitor revealed that DPI binds deeply in the active-site cavity to establish multiple hydrophobic interactions with the surrounding side chains and the flavin.	diphenyleneiodonium	89-92	monoamine oxidase B	Homo sapiens	46-51
32459875-4	2020	Elucidation of the crystal structure of human MAO B bound to the inhibitor revealed that DPI binds deeply in the active-site cavity to establish multiple hydrophobic interactions with the surrounding side chains and the flavin.	4,6-dinitro-o-cresol	220-226	monoamine oxidase B	Homo sapiens	46-51
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	diosmetin	76-85	monoamine oxidase B	Homo sapiens	49-53
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	diosmetin	76-85	monoamine oxidase B	Homo sapiens	176-180
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	acacetin	87-95	monoamine oxidase B	Homo sapiens	49-53
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	acacetin	87-95	monoamine oxidase B	Homo sapiens	176-180
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	Catechin	97-108	monoamine oxidase B	Homo sapiens	176-180
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	eriodictyol	110-121	monoamine oxidase B	Homo sapiens	176-180
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	capillin	126-134	monoamine oxidase B	Homo sapiens	49-53
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	capillin	126-134	monoamine oxidase B	Homo sapiens	176-180
32746771-7	2021	This study mainly represents that Galuteolin and Linarin in the Akt pathway can be perceived for OSCC treatment and other five CYP inhibitors - Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin for the treatment of other diseases and cancers caused by overexpression of MAOB.	luteolin-7-glucoside	34-44	monoamine oxidase B	Homo sapiens	279-283
32746771-7	2021	This study mainly represents that Galuteolin and Linarin in the Akt pathway can be perceived for OSCC treatment and other five CYP inhibitors - Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin for the treatment of other diseases and cancers caused by overexpression of MAOB.	linarin	49-56	monoamine oxidase B	Homo sapiens	279-283
32858935-0	2020	Hydride Abstraction as the Rate-Limiting Step of the Irreversible Inhibition of Monoamine Oxidase B by Rasagiline and Selegiline: A Computational Empirical Valence Bond Study.	rasagiline	103-113	monoamine oxidase B	Homo sapiens	80-99
32858935-0	2020	Hydride Abstraction as the Rate-Limiting Step of the Irreversible Inhibition of Monoamine Oxidase B by Rasagiline and Selegiline: A Computational Empirical Valence Bond Study.	Selegiline	118-128	monoamine oxidase B	Homo sapiens	80-99
32753686-4	2021	Ethanol treatment resulted in decreased 5-HT concentrations in human induced pluripotent stem cell (iPSC)-derived neuron culture media, and the downregulation of gene expression of TSPAN5, DDC, MAOA, MAOB, TPH1, and TPH2 in those cells.	Ethanol	0-7	monoamine oxidase B	Homo sapiens	200-204
32474182-4	2020	Monoamine oxidase B inhibition is essential to maintain the balance of dopamine, and one of its major functions is to combat dopamine degradation, a phenomenon linked to Parkinson"s disease.	Dopamine	71-79	monoamine oxidase B	Homo sapiens	0-19
32474182-4	2020	Monoamine oxidase B inhibition is essential to maintain the balance of dopamine, and one of its major functions is to combat dopamine degradation, a phenomenon linked to Parkinson"s disease.	Dopamine	125-133	monoamine oxidase B	Homo sapiens	0-19
32474182-5	2020	In this work, we study small-molecule inhibitors based on the 3-arylcoumarin scaffold and their monoamine oxidase B selective inhibition.	3-arylcoumarin	62-76	monoamine oxidase B	Homo sapiens	96-115
30289026-8	2020	These data provide a clear time course of the reversible inhibition of MAO-B after the single consumption of a of New Zealand "Blackadder" blackcurrant juice standardised at 500 mg of polyphenols and, therefore, provide a therapeutic window on which to base future nutritional interventions.	Polyphenols	184-195	monoamine oxidase B	Homo sapiens	71-76
32648512-4	2020	The pharmacological profile of safinamide includes reversible monoamine oxidase B inhibition and modulation of voltage-dependent sodium- and calcium channels with consecutive decline of glutamate release.	safinamide	31-41	monoamine oxidase B	Homo sapiens	62-81
32681474-1	2021	Safinamide (SF) is a third-generation monoamine-oxidase-B inhibitor that proved efficacy as add-on to levodopa in fluctuating Parkinson"s disease (PD) patients.	safinamide	0-10	monoamine oxidase B	Homo sapiens	38-57
32681474-1	2021	Safinamide (SF) is a third-generation monoamine-oxidase-B inhibitor that proved efficacy as add-on to levodopa in fluctuating Parkinson"s disease (PD) patients.	safinamide	12-14	monoamine oxidase B	Homo sapiens	38-57
32705963-0	2021	Revealing the role of fluorine pharmacophore in chalcone scaffold for shifting the MAO-B selectivity: investigation of a detailed molecular dynamics and quantum chemical study.	Fluorine	22-30	monoamine oxidase B	Homo sapiens	83-88
32705963-0	2021	Revealing the role of fluorine pharmacophore in chalcone scaffold for shifting the MAO-B selectivity: investigation of a detailed molecular dynamics and quantum chemical study.	Chalcone	48-56	monoamine oxidase B	Homo sapiens	83-88
32705963-2	2021	Recent study documented that shifting of fluorine atom from para to ortho position on the phenyl B ring of heteroaryl chalcones shown a remarkable shift in the selectivity and potency between MAO-A and MAO-B isoforms.	Fluorine	41-49	monoamine oxidase B	Homo sapiens	202-207
32705963-2	2021	Recent study documented that shifting of fluorine atom from para to ortho position on the phenyl B ring of heteroaryl chalcones shown a remarkable shift in the selectivity and potency between MAO-A and MAO-B isoforms.	heteroaryl chalcones	107-127	monoamine oxidase B	Homo sapiens	202-207
32705963-3	2021	Despite the large plethora of the design of new selective MAO-B inhibitors, the current paper illustrates the role and orientation of fluorine atom with remarkable MAO-B selectivity of three compounds (O23, O24 and O25), which differ from all other substituents encountered in the chalcone scaffolds is recently reported by our group.	Fluorine	134-142	monoamine oxidase B	Homo sapiens	58-63
32705963-3	2021	Despite the large plethora of the design of new selective MAO-B inhibitors, the current paper illustrates the role and orientation of fluorine atom with remarkable MAO-B selectivity of three compounds (O23, O24 and O25), which differ from all other substituents encountered in the chalcone scaffolds is recently reported by our group.	Fluorine	134-142	monoamine oxidase B	Homo sapiens	164-169
32705963-3	2021	Despite the large plethora of the design of new selective MAO-B inhibitors, the current paper illustrates the role and orientation of fluorine atom with remarkable MAO-B selectivity of three compounds (O23, O24 and O25), which differ from all other substituents encountered in the chalcone scaffolds is recently reported by our group.	Chalcone	281-289	monoamine oxidase B	Homo sapiens	58-63
32705963-3	2021	Despite the large plethora of the design of new selective MAO-B inhibitors, the current paper illustrates the role and orientation of fluorine atom with remarkable MAO-B selectivity of three compounds (O23, O24 and O25), which differ from all other substituents encountered in the chalcone scaffolds is recently reported by our group.	Chalcone	281-289	monoamine oxidase B	Homo sapiens	164-169
32380361-6	2020	Additionally, N-propargylpiperidine 16 is an irreversible and time-dependent inhibitor of MAO-B, while N-benzylpiperidine 10 is reversible.	1-(prop-2-yn-1-yl)piperidine	14-35	monoamine oxidase B	Homo sapiens	90-95
32299731-2	2020	Based on this, nitrocatechol derivatives of chalcone have been proposed to represent dual-target-directed compounds that may inhibit both MAO-B and COMT.	nitrocatechol	15-28	monoamine oxidase B	Homo sapiens	138-143
32299731-2	2020	Based on this, nitrocatechol derivatives of chalcone have been proposed to represent dual-target-directed compounds that may inhibit both MAO-B and COMT.	Chalcone	44-52	monoamine oxidase B	Homo sapiens	138-143
32299731-1	2020	Literature reports that chalcones inhibit the monoamine oxidase (MAO) enzymes, mostly with specificity for the MAO-B isoform, while nitrocatechol compounds are established inhibitors of catechol-O-methyltransferase (COMT).	Chalcones	24-33	monoamine oxidase B	Homo sapiens	111-116
32299731-4	2020	The present study expands on the discovery of dual MAO-B/COMT inhibitors by synthesising additional nitrocatechol derivatives of chalcones which include heterocyclic derivatives, and converting them to the corresponding pyrazoline derivatives.	nitrocatechol	100-113	monoamine oxidase B	Homo sapiens	51-56
32299731-4	2020	The present study expands on the discovery of dual MAO-B/COMT inhibitors by synthesising additional nitrocatechol derivatives of chalcones which include heterocyclic derivatives, and converting them to the corresponding pyrazoline derivatives.	Chalcones	129-138	monoamine oxidase B	Homo sapiens	51-56
32299731-4	2020	The present study expands on the discovery of dual MAO-B/COMT inhibitors by synthesising additional nitrocatechol derivatives of chalcones which include heterocyclic derivatives, and converting them to the corresponding pyrazoline derivatives.	heterocyclic	153-165	monoamine oxidase B	Homo sapiens	51-56
32299731-4	2020	The present study expands on the discovery of dual MAO-B/COMT inhibitors by synthesising additional nitrocatechol derivatives of chalcones which include heterocyclic derivatives, and converting them to the corresponding pyrazoline derivatives.	pyrazoline	220-230	monoamine oxidase B	Homo sapiens	51-56
32527030-0	2020	Rutamarin: Efficient Liquid-Liquid Chromatographic Isolation from Ruta graveolens L. and Evaluation of Its In Vitro and In Silico MAO-B Inhibitory Activity.	rutamarin	0-9	monoamine oxidase B	Homo sapiens	130-135
32527030-4	2020	The crude DCM (9.78 mg/mL) and rutamarin (6.17 M) were found to be effective inhibitors of human monoamine oxidase B (hMAO-B) with inhibition percentages of 89.98% and 95.26%, respectively.	dcm	10-13	monoamine oxidase B	Homo sapiens	97-116
32527030-4	2020	The crude DCM (9.78 mg/mL) and rutamarin (6.17 M) were found to be effective inhibitors of human monoamine oxidase B (hMAO-B) with inhibition percentages of 89.98% and 95.26%, respectively.	dcm	10-13	monoamine oxidase B	Homo sapiens	118-124
32527030-4	2020	The crude DCM (9.78 mg/mL) and rutamarin (6.17 M) were found to be effective inhibitors of human monoamine oxidase B (hMAO-B) with inhibition percentages of 89.98% and 95.26%, respectively.	rutamarin	31-40	monoamine oxidase B	Homo sapiens	97-116
32527030-4	2020	The crude DCM (9.78 mg/mL) and rutamarin (6.17 M) were found to be effective inhibitors of human monoamine oxidase B (hMAO-B) with inhibition percentages of 89.98% and 95.26%, respectively.	rutamarin	31-40	monoamine oxidase B	Homo sapiens	118-124
32527030-7	2020	To examine the molecular interaction of rutamarin with hMAO- B, an in silico evaluation was implemented.	rutamarin	40-49	monoamine oxidase B	Homo sapiens	55-62
32527030-9	2020	The (S)-rutamarin was found to bind stronger to the hMAO-B binging cavity.	rutamarin	4-17	monoamine oxidase B	Homo sapiens	52-58
32446176-1	2020	INTRODUCTION: Safinamide is a reversible and selective monoamine oxidase-B (MAO-B) and sodium channel inhibitor with demonstrated efficacy in mid-to late-stage Parkinson"s disease (PD) as an adjunct to l-DOPA.	safinamide	14-24	monoamine oxidase B	Homo sapiens	55-74
32446176-1	2020	INTRODUCTION: Safinamide is a reversible and selective monoamine oxidase-B (MAO-B) and sodium channel inhibitor with demonstrated efficacy in mid-to late-stage Parkinson"s disease (PD) as an adjunct to l-DOPA.	safinamide	14-24	monoamine oxidase B	Homo sapiens	76-81
32087226-0	2020	Calycosin and 8-O-methylretusin isolated from Maackia amurensis as potent and selective reversible inhibitors of human monoamine oxidase-B.	7,3'-dihydroxy-4'-methoxyisoflavone	0-9	monoamine oxidase B	Homo sapiens	119-138
32144745-0	2020	Synthesis, molecular modelling and biological activity of some pyridazinone derivatives as selective human monoamine oxidase-B inhibitors.	2-phenyl-3(2H)-pyridazinone	63-75	monoamine oxidase B	Homo sapiens	107-126
32144745-9	2020	Compound 4b was found as the most potent (ki = 0.022 +- 0.001 microM) and selective (SI (Ki hMAO-A/hMAO-B) = 206.82) hMAO-B inhibitor in this series.	Silicon	85-87	monoamine oxidase B	Homo sapiens	99-105
32443652-0	2020	Novel Class of Chalcone Oxime Ethers as Potent Monoamine Oxidase-B and Acetylcholinesterase Inhibitors.	chalcone oxime ethers	15-36	monoamine oxidase B	Homo sapiens	47-66
32443652-4	2020	COE-7, and COE-22 were also active against MAO-B, both had an IC50 value of 0.028 microM, which was 67 and 1.5 times lower than those of clorgyline and lazabemide, respectively.	lazabemide	152-162	monoamine oxidase B	Homo sapiens	43-48
32443652-6	2020	COE-13 most potently inhibited MAO-A (IC50 = 0.88 microM) and also significantly inhibited MAO-B (IC50 = 0.13 microM), and it could be considered as a potential nonselective MAO inhibitor.	coe-13	0-6	monoamine oxidase B	Homo sapiens	91-96
32087226-0	2020	Calycosin and 8-O-methylretusin isolated from Maackia amurensis as potent and selective reversible inhibitors of human monoamine oxidase-B.	8-O-methylretusin	14-31	monoamine oxidase B	Homo sapiens	119-138
32087226-2	2020	Among the compounds isolated, flavonoids calycosin (5) and 8-O-methylretusin (6) were found to potently and selectively inhibit hMAO-B (IC50 = 0.24 and 0.23 muM, respectively) but not hMAO-A with high selectivity index (SI) values (SI = 293.8 and 81.3, respectively).	Flavonoids	30-40	monoamine oxidase B	Homo sapiens	128-134
32087226-2	2020	Among the compounds isolated, flavonoids calycosin (5) and 8-O-methylretusin (6) were found to potently and selectively inhibit hMAO-B (IC50 = 0.24 and 0.23 muM, respectively) but not hMAO-A with high selectivity index (SI) values (SI = 293.8 and 81.3, respectively).	7,3'-dihydroxy-4'-methoxyisoflavone	41-50	monoamine oxidase B	Homo sapiens	128-134
32087226-2	2020	Among the compounds isolated, flavonoids calycosin (5) and 8-O-methylretusin (6) were found to potently and selectively inhibit hMAO-B (IC50 = 0.24 and 0.23 muM, respectively) but not hMAO-A with high selectivity index (SI) values (SI = 293.8 and 81.3, respectively).	8-O-methylretusin	59-76	monoamine oxidase B	Homo sapiens	128-134
32087226-4	2020	A pterocarpan (-)-medicarpin (18) was also observed to strongly inhibit hMAO-B (IC50 = 0.30 muM).	Pterocarpans	2-13	monoamine oxidase B	Homo sapiens	72-78
32087226-4	2020	A pterocarpan (-)-medicarpin (18) was also observed to strongly inhibit hMAO-B (IC50 = 0.30 muM).	medicarpin	14-28	monoamine oxidase B	Homo sapiens	72-78
32087226-7	2020	Compound 5 was found to interact by hydrogen bonding with hMAO-B at Cys172 residue (distance: 3.250 A); no hydrogen bonding was predicted between 5 and hMAO-A.	Hydrogen	36-44	monoamine oxidase B	Homo sapiens	58-64
32408504-2	2020	A combination of monoamine oxidase B (MAO B) inhibition with histamine H3 receptor (H3R) antagonism could have positive effects on dopamine regulation.	Dopamine	131-139	monoamine oxidase B	Homo sapiens	17-36
32408504-2	2020	A combination of monoamine oxidase B (MAO B) inhibition with histamine H3 receptor (H3R) antagonism could have positive effects on dopamine regulation.	Dopamine	131-139	monoamine oxidase B	Homo sapiens	38-43
32408504-7	2020	However, the most balanced activity against both biological targets showed DL76 (hH3R: Ki = 38 nM and hMAO B: IC50 = 48 nM).	dl76	75-79	monoamine oxidase B	Homo sapiens	102-108
32094232-0	2020	Hepatic monoamine oxidase B is involved in endogenous geranylgeranoic acid synthesis in mammalian liver cells.	geranylgeranic acid	54-74	monoamine oxidase B	Homo sapiens	8-27
32403270-4	2020	In this investigation, twenty synthesized flavonoid derivatives, defined as KKR compounds were screened for their inhibitory potentials against human MAO-A and MAO-B isozymes.	Flavonoids	42-51	monoamine oxidase B	Homo sapiens	160-165
32162782-0	2020	Novel, dual target-directed annelated xanthine derivatives acting on adenosine receptors and monoamine oxidase B.	Xanthine	38-46	monoamine oxidase B	Homo sapiens	93-112
32162782-6	2020	Such dual acting ligands, by selectively blocking A 2A AR, accompanied by the inhibition of dopamine metabolizing enzyme MAO-B might provide symptomatic and neuroprotective effects in e.g. Parkinson disease treatment.	Dopamine	92-100	monoamine oxidase B	Homo sapiens	121-126
32357811-3	2020	In thecase of MAO-B the rhamnetin, quercetin, piperine, eugenol,and umbelliferone exhibited highest dock score -10.57, -9.938, -9.445, - 8.757and 7.821respectively.	rhamnetin	24-33	monoamine oxidase B	Homo sapiens	14-19
32357811-3	2020	In thecase of MAO-B the rhamnetin, quercetin, piperine, eugenol,and umbelliferone exhibited highest dock score -10.57, -9.938, -9.445, - 8.757and 7.821respectively.	Quercetin	35-44	monoamine oxidase B	Homo sapiens	14-19
32357811-3	2020	In thecase of MAO-B the rhamnetin, quercetin, piperine, eugenol,and umbelliferone exhibited highest dock score -10.57, -9.938, -9.445, - 8.757and 7.821respectively.	piperine	46-54	monoamine oxidase B	Homo sapiens	14-19
32357811-3	2020	In thecase of MAO-B the rhamnetin, quercetin, piperine, eugenol,and umbelliferone exhibited highest dock score -10.57, -9.938, -9.445, - 8.757and 7.821respectively.	Eugenol	56-63	monoamine oxidase B	Homo sapiens	14-19
32357811-3	2020	In thecase of MAO-B the rhamnetin, quercetin, piperine, eugenol,and umbelliferone exhibited highest dock score -10.57, -9.938, -9.445, - 8.757and 7.821respectively.	7-hydroxycoumarin	68-81	monoamine oxidase B	Homo sapiens	14-19
32357811-7	2020	In case of hMAO-B activity lead compound rhamnetin has shown the value of 10.32+-0.044 microM (SI value of 3.096) as compared with pargyline (reference compound) with IC50 value of 20.04+-0.095 microM.	rhamnetin	41-50	monoamine oxidase B	Homo sapiens	11-17
32094232-7	2020	Using either HuH-7 cell lysates or recombinant human MAOB, we found (i) that the MAO inhibitor tranylcypromine dose-dependently down-regulates endogenous GGA levels in HuH-7 cells, and (ii) that siRNA-mediated MAOB silencing reduces intracellular GGA levels in HuH-7 and Hep3B cells.	Tranylcypromine	95-110	monoamine oxidase B	Homo sapiens	53-57
32094232-7	2020	Using either HuH-7 cell lysates or recombinant human MAOB, we found (i) that the MAO inhibitor tranylcypromine dose-dependently down-regulates endogenous GGA levels in HuH-7 cells, and (ii) that siRNA-mediated MAOB silencing reduces intracellular GGA levels in HuH-7 and Hep3B cells.	Tranylcypromine	95-110	monoamine oxidase B	Homo sapiens	210-214
32346620-0	2020	Monoamine oxidase B rs1799836 G allele polymorphism is a risk factor for early development of levodopa-induced dyskinesia in Parkinson"s disease.	Levodopa	94-102	monoamine oxidase B	Homo sapiens	0-19
31836905-1	2020	Monoamine oxidase type B inhibitors act in Parkinson"s disease (PD) via potentiation of dopamine, but may also have neuroprotective effects by reducing oxidative damage.	Dopamine	88-96	monoamine oxidase B	Homo sapiens	0-24
31836905-1	2020	Monoamine oxidase type B inhibitors act in Parkinson"s disease (PD) via potentiation of dopamine, but may also have neuroprotective effects by reducing oxidative damage.	BUTONATE	98-101	monoamine oxidase B	Homo sapiens	0-24
32279709-6	2020	Adjunct MAO-B and COMT inhibitors as well as dopamine agonists and continuous infusions of levodopa intestinal gel or subcutaneous apomorphine are efficacious in reducing motor fluctuations and amantadine is the only drug with established efficacy in reducing dyskinesias.	Amantadine	194-204	monoamine oxidase B	Homo sapiens	8-13
32316576-1	2020	Monoamine oxidases (MAOs) including MAOA and MAOB are enzymes located on the outer membranes of mitochondria, which are responsible for catalyzing monoamine oxidation.	monoamine	147-156	monoamine oxidase B	Homo sapiens	45-49
31562557-1	2020	Monoamine oxidase B (MAO-B) inhibitors have an established role in the treatment of Parkinson"s disease as monotherapy or adjuvant to levodopa.	Levodopa	134-142	monoamine oxidase B	Homo sapiens	0-19
31562557-1	2020	Monoamine oxidase B (MAO-B) inhibitors have an established role in the treatment of Parkinson"s disease as monotherapy or adjuvant to levodopa.	Levodopa	134-142	monoamine oxidase B	Homo sapiens	21-26
31562557-3	2020	The first was the elucidation of the novel pharmacological properties of selegiline as a selective MAO-B inhibitor by Knoll and Magyar and the original idea of Riederer and Youdim, supported by Birkmayer, to explore its effect in parkinsonian patients with on-off phases.	Selegiline	73-83	monoamine oxidase B	Homo sapiens	99-104
31562557-6	2020	Later studies demonstrated that MAO-B, mainly located in glial cells, is important for dopamine metabolism in the brain.	Dopamine	87-95	monoamine oxidase B	Homo sapiens	32-37
31562557-7	2020	Recently, cell and molecular studies revealed interesting properties of selegiline opening new possibilities for neuroprotective mechanisms and a disease-modifying effect of MAO-B inhibitors.	Selegiline	72-82	monoamine oxidase B	Homo sapiens	174-179
31115748-7	2020	MAO-B-specific inhibitors such as some of the quinazolinone compounds investigated here may act as leads for the design of therapies for neurodegenerative disorders such as Parkinson"s disease.	Quinazolinones	46-59	monoamine oxidase B	Homo sapiens	0-5
31471933-4	2020	Computational analysis revealed that the malononitrile group can find an advantageous position with the aromatic cleft and FAD of MAO A or MAO B.	dicyanmethane	41-54	monoamine oxidase B	Homo sapiens	139-144
30127471-3	2020	Such control of DA homeostasis occurs through the coordinated activity of astroglial vesicular monoamine transporter 2 (VMAT2) together with organic cation transporter 3 and monoamine oxidase type B, two key proteins for DA uptake and metabolism.	Dopamine	16-18	monoamine oxidase B	Homo sapiens	174-198
31954292-10	2020	While all the phytochemicals showed potential in inhibiting the enzymes, Rutin, Demethoxycurcumin and Acteoside were found to be most effective inhibitors of MAO-B, COMT and AChE respectively.	Rutin	73-78	monoamine oxidase B	Homo sapiens	158-163
31954292-10	2020	While all the phytochemicals showed potential in inhibiting the enzymes, Rutin, Demethoxycurcumin and Acteoside were found to be most effective inhibitors of MAO-B, COMT and AChE respectively.	demethoxycurcumin	80-97	monoamine oxidase B	Homo sapiens	158-163
31954292-10	2020	While all the phytochemicals showed potential in inhibiting the enzymes, Rutin, Demethoxycurcumin and Acteoside were found to be most effective inhibitors of MAO-B, COMT and AChE respectively.	acteoside	102-111	monoamine oxidase B	Homo sapiens	158-163
30127471-3	2020	Such control of DA homeostasis occurs through the coordinated activity of astroglial vesicular monoamine transporter 2 (VMAT2) together with organic cation transporter 3 and monoamine oxidase type B, two key proteins for DA uptake and metabolism.	Dopamine	221-223	monoamine oxidase B	Homo sapiens	174-198
31834986-3	2020	Based on this, the present study evaluated 22 dyes, many of which are structurally related to methylene blue, as potential inhibitors of human MAO-A and MAO-B.	Methylene Blue	94-108	monoamine oxidase B	Homo sapiens	153-158
32189109-0	2020	Retraction Note to: Meniere"s disease: combined pharmacotherapy with betahistine and the MAO-B inhibitor selegiline-an observational study.	Selegiline	105-115	monoamine oxidase B	Homo sapiens	89-94
32037726-0	2020	Coumarin-rasagiline hybrids as potent and selective hMAO-B inhibitors, antioxidants and neuroprotective agents.	rasagiline	0-19	monoamine oxidase B	Homo sapiens	52-58
32037726-5	2020	Half of the studied hybrids turned out to be selective monoamine oxidase B (hMAO-B) inhibitors in the low micro/nanomolar range, demonstrating that positions 3 (compounds 1-3) and 7 (compounds 8 and 10) of the coumarin scaffold are the most suitable for the incorporation of the alkynylamine chain.	coumarin	210-218	monoamine oxidase B	Homo sapiens	76-82
31834986-5	2020	Acridine orange was found to be a MAO-A specific inhibitor (IC50 = 0.017 muM), whereas oxazine 170 is a MAO-B specific inhibitor (IC50 = 0.0065 muM).	Oxazines	87-94	monoamine oxidase B	Homo sapiens	104-109
31818478-4	2020	In particular, compound 6c bearing a pyrrolidine group showed the highest activities against self- and Cu2+-induced Abeta1-42 aggregation (70.65% and 54.89% at 25.0 microM, respectively), highly selective inhibition towards AChE and MAO-B (IC50 = 7.15 muM and 0.43 muM respectively), good antioxidant ability and metal-chelating property.	Copper	103-107	monoamine oxidase B	Homo sapiens	233-238
32072299-3	2020	Tyramine has been determined using its enzymatic reaction with tyramine oxidase (TAO).	Tyramine	0-8	monoamine oxidase B	Homo sapiens	63-79
32072299-3	2020	Tyramine has been determined using its enzymatic reaction with tyramine oxidase (TAO).	Tyramine	0-8	monoamine oxidase B	Homo sapiens	81-84
32072299-6	2020	Working at room temperature, under optimal conditions (phosphate buffer pH 7.0, TAO 0.5 U.mL-1 Au(III) 1 mM), the linear response ranges from 2.5 x 10-5 M to 3.3 x 10-4 M Tyramine (5.6% RSD) and the LOD is 2.9 x 10-6 M. Under these conditions, the signal is measured after 30 min reaction (to obtain the highest sensitivity), but this time can be significantly reduced by increasing the temperature (the reaction is finished after 4 min when working at 50  C).	Gold	95-102	monoamine oxidase B	Homo sapiens	80-83
32072299-9	2020	Graphical abstractTyramine is determined by measuring the plasmon band of the gold nanoparticles formed during its enzymatic reaction with Tyramine oxidase.	Tyramine	18-26	monoamine oxidase B	Homo sapiens	139-155
31639490-0	2020	New role for crinamine as a potent, safe and selective inhibitor of human monoamine oxidase B: In vitro and in silico pharmacology and modeling.	crinamine	13-22	monoamine oxidase B	Homo sapiens	74-93
32099324-0	2020	Reversible Small Molecule Inhibitors of MAO A and MAO B with Anilide Motifs.	Anilides	61-68	monoamine oxidase B	Homo sapiens	50-55
32099324-7	2020	Results: N-(2,4-Dinitrophenyl)benzo[d][1,3]dioxole-5-carboxamide (55, ST-2043) was found to be a reversible competitive moderately selective MAO B inhibitor (IC50 = 56 nM, Ki = 6.3 nM), while N-(2,4-dinitrophenyl)benzamide (7, ST-2023) showed higher preference for MAO A (IC50 = 126 nM).	n-(2,4-dinitrophenyl)benzo[d][1,3]dioxole-5-carboxamide	9-64	monoamine oxidase B	Homo sapiens	141-146
32099324-7	2020	Results: N-(2,4-Dinitrophenyl)benzo[d][1,3]dioxole-5-carboxamide (55, ST-2043) was found to be a reversible competitive moderately selective MAO B inhibitor (IC50 = 56 nM, Ki = 6.3 nM), while N-(2,4-dinitrophenyl)benzamide (7, ST-2023) showed higher preference for MAO A (IC50 = 126 nM).	st-2043	70-77	monoamine oxidase B	Homo sapiens	141-146
31740200-4	2020	Three derivatives (3c, 8c and 16c) exhibited both MAO-B inhibitory and neuroprotective activity.	3c, 8c and 16c	19-33	monoamine oxidase B	Homo sapiens	50-55
30470136-0	2020	A new tetracyclic saponin from Astragalus glycyphyllos L. and its neuroprotective and hMAO-B inhibiting activity.	Saponins	18-25	monoamine oxidase B	Homo sapiens	86-92
33132375-5	2020	Considering the IC50 values and selectivity indices of the other synthetic compounds, the presence of the methoxy group on the chromone ring (R2) of 7c seemed to increase MAO-B inhibition.	Chromones	127-135	monoamine oxidase B	Homo sapiens	171-176
33132375-7	2020	Our results suggest that 3-(N-cyclicamino)chromones are useful lead compounds for the development of MAO-B inhibitors.	3-(n-cyclicamino)chromones	25-51	monoamine oxidase B	Homo sapiens	101-106
32723232-5	2020	CONCLUSION: The current perspective described the recent updates of chalcone moiety linked with the pharmacophores of flurbiprofen and rivastigmine hybrids as selective ChE/MAO-B inhibitors for the prophylactic agents for AD.	Chalcone	68-76	monoamine oxidase B	Homo sapiens	173-178
32238135-10	2020	Clinical evidence illustrated that MAO-B inhibitors are recommended as monotherapy and added on therapy to levodopa.	Levodopa	107-115	monoamine oxidase B	Homo sapiens	35-40
32703142-7	2020	We furthermore review current evidence of the L-dopa-induced side effects and perspectives of L-dopa treatment in PD compared to other established treatments such as DA-agonists and the inhibitors of catechol-o-methyltransferase and monoamine oxidase B.	Levodopa	46-52	monoamine oxidase B	Homo sapiens	233-252
32703142-7	2020	We furthermore review current evidence of the L-dopa-induced side effects and perspectives of L-dopa treatment in PD compared to other established treatments such as DA-agonists and the inhibitors of catechol-o-methyltransferase and monoamine oxidase B.	Levodopa	94-100	monoamine oxidase B	Homo sapiens	233-252
32723232-5	2020	CONCLUSION: The current perspective described the recent updates of chalcone moiety linked with the pharmacophores of flurbiprofen and rivastigmine hybrids as selective ChE/MAO-B inhibitors for the prophylactic agents for AD.	Flurbiprofen	118-130	monoamine oxidase B	Homo sapiens	173-178
32723232-5	2020	CONCLUSION: The current perspective described the recent updates of chalcone moiety linked with the pharmacophores of flurbiprofen and rivastigmine hybrids as selective ChE/MAO-B inhibitors for the prophylactic agents for AD.	Rivastigmine	135-147	monoamine oxidase B	Homo sapiens	173-178
30129404-9	2020	The administration of the xanthines has been proposed as a non-dopaminergic strategy for neuroprotection in PD and the mechanisms of protection have been associated with antagonism of adenosine A2A receptors and Monoamine Oxidase type B (MAO-B) inhibition.	Xanthines	26-35	monoamine oxidase B	Homo sapiens	212-236
30129404-9	2020	The administration of the xanthines has been proposed as a non-dopaminergic strategy for neuroprotection in PD and the mechanisms of protection have been associated with antagonism of adenosine A2A receptors and Monoamine Oxidase type B (MAO-B) inhibition.	Xanthines	26-35	monoamine oxidase B	Homo sapiens	238-243
30129404-9	2020	The administration of the xanthines has been proposed as a non-dopaminergic strategy for neuroprotection in PD and the mechanisms of protection have been associated with antagonism of adenosine A2A receptors and Monoamine Oxidase type B (MAO-B) inhibition.	Adenosine	184-193	monoamine oxidase B	Homo sapiens	238-243
32493193-2	2020	The two isoforms of the MAO enzymes, MAO-A and MAO-B are responsible of the degradation of monoamine neurotransmitters and due to this, relevant efforts have been devoted to find new compounds with more selectivity and less side effects.	monoamine	91-100	monoamine oxidase B	Homo sapiens	47-52
32250219-5	2020	TV-3326 combines the neurorestorative/neuroprotective actions of the cholinesterase (ChE) inhibitory activity of rivastigmine with rasagiline (a selective monoamine oxidase-B inhibitor and novel antiparkinsonian agent) in a single molecule.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	0-7	monoamine oxidase B	Homo sapiens	155-174
32250219-5	2020	TV-3326 combines the neurorestorative/neuroprotective actions of the cholinesterase (ChE) inhibitory activity of rivastigmine with rasagiline (a selective monoamine oxidase-B inhibitor and novel antiparkinsonian agent) in a single molecule.	rasagiline	131-141	monoamine oxidase B	Homo sapiens	155-174
31146671-0	2020	Design, Synthesis and Evaluation of 8-Thiosubstituted 1,3,7- Trimethylxanthine Hydrazones with In-vitro Neuroprotective and MAO-B Inhibitory Activities.	1,3,7- trimethylxanthine hydrazones	54-89	monoamine oxidase B	Homo sapiens	124-129
31711793-0	2020	Design of novel monoamine oxidase-B inhibitors based on piperine scaffold: Structure-activity-toxicity, drug-likeness and efflux transport studies.	piperine	56-64	monoamine oxidase B	Homo sapiens	16-35
31711793-2	2020	Accordingly, we prepared a small library of piperine derivatives and screened the inhibitory activities towards human MAO isoforms (hMAO-A and hMAO-B).	piperine	44-52	monoamine oxidase B	Homo sapiens	143-149
31711793-3	2020	Structure-activity relationship (SAR) studies pointed out that the combination of alpha-cyano and benzyl ester groups increased both potency and selectivity towards hMAO-B.	5-cyano-2'-deoxyuridine	82-93	monoamine oxidase B	Homo sapiens	165-171
31711793-3	2020	Structure-activity relationship (SAR) studies pointed out that the combination of alpha-cyano and benzyl ester groups increased both potency and selectivity towards hMAO-B.	benzyl acetate	98-110	monoamine oxidase B	Homo sapiens	165-171
31711793-6	2020	Compound 15 stands out as the most potent piperine-based hMAO-B inhibitor (IC50 = 47.4 nM), displaying favourable drug-like properties and a broad safety window.	piperine	42-50	monoamine oxidase B	Homo sapiens	57-63
31771069-3	2020	Catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAOB) are the enzymes that regulate degradation of dopamine, while dopamine beta-hydroxylase (DBH) is involved in synthesis of noradrenaline.	Dopamine	112-120	monoamine oxidase B	Homo sapiens	40-59
31771069-3	2020	Catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAOB) are the enzymes that regulate degradation of dopamine, while dopamine beta-hydroxylase (DBH) is involved in synthesis of noradrenaline.	Dopamine	112-120	monoamine oxidase B	Homo sapiens	61-65
31771069-3	2020	Catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAOB) are the enzymes that regulate degradation of dopamine, while dopamine beta-hydroxylase (DBH) is involved in synthesis of noradrenaline.	Norepinephrine	188-201	monoamine oxidase B	Homo sapiens	40-59
31771069-3	2020	Catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAOB) are the enzymes that regulate degradation of dopamine, while dopamine beta-hydroxylase (DBH) is involved in synthesis of noradrenaline.	Norepinephrine	188-201	monoamine oxidase B	Homo sapiens	61-65
31146671-4	2020	The performed monoamine oxidase B (MAO-B) inhibition study in vitro show that compounds 6g and 6i possess a significant MAO-B inhibition activity close to L-deprenyl.	Selegiline	155-165	monoamine oxidase B	Homo sapiens	35-40
31146671-4	2020	The performed monoamine oxidase B (MAO-B) inhibition study in vitro show that compounds 6g and 6i possess a significant MAO-B inhibition activity close to L-deprenyl.	Selegiline	155-165	monoamine oxidase B	Homo sapiens	120-125
31686637-3	2020	The monoamine oxidase B (MAO-B) degrades dopamine, promoting the glutamate accumulation and oxidative stress with the release of free radicals, causing excitotoxicity.	Dopamine	41-49	monoamine oxidase B	Homo sapiens	4-23
31686637-3	2020	The monoamine oxidase B (MAO-B) degrades dopamine, promoting the glutamate accumulation and oxidative stress with the release of free radicals, causing excitotoxicity.	Dopamine	41-49	monoamine oxidase B	Homo sapiens	25-30
31686637-3	2020	The monoamine oxidase B (MAO-B) degrades dopamine, promoting the glutamate accumulation and oxidative stress with the release of free radicals, causing excitotoxicity.	Glutamic Acid	65-74	monoamine oxidase B	Homo sapiens	4-23
31686637-3	2020	The monoamine oxidase B (MAO-B) degrades dopamine, promoting the glutamate accumulation and oxidative stress with the release of free radicals, causing excitotoxicity.	Glutamic Acid	65-74	monoamine oxidase B	Homo sapiens	25-30
31589885-0	2020	The pro-psychotic metabotropic glutamate receptor compounds fenobam and AZD9272 share binding sites with monoamine oxidase-B inhibitors in humans.	fenobam	60-67	monoamine oxidase B	Homo sapiens	105-124
31785348-8	2020	Along with anti-inflammatory properties, chrysin has also been shown to increase dopamine levels in the striatum via monoamino-oxidase B (MAO-B) inhibition while it restores the behavioral deficits in PD animal models.	chrysin	41-48	monoamine oxidase B	Homo sapiens	117-136
31785348-8	2020	Along with anti-inflammatory properties, chrysin has also been shown to increase dopamine levels in the striatum via monoamino-oxidase B (MAO-B) inhibition while it restores the behavioral deficits in PD animal models.	chrysin	41-48	monoamine oxidase B	Homo sapiens	138-143
31589885-0	2020	The pro-psychotic metabotropic glutamate receptor compounds fenobam and AZD9272 share binding sites with monoamine oxidase-B inhibitors in humans.	AZD9272	72-79	monoamine oxidase B	Homo sapiens	105-124
31589885-6	2020	In PET studies of NHP brain administration of the MAO-B ligand L-deprenyl inhibited binding of radiolabeled AZD9272 and administration of fenobam inhibited binding of [11C]L-deprenyl-D2.	Selegiline	63-73	monoamine oxidase B	Homo sapiens	50-55
31589885-6	2020	In PET studies of NHP brain administration of the MAO-B ligand L-deprenyl inhibited binding of radiolabeled AZD9272 and administration of fenobam inhibited binding of [11C]L-deprenyl-D2.	AZD9272	108-115	monoamine oxidase B	Homo sapiens	50-55
31589885-7	2020	Binding of radiolabeled AZD9272 in vitro was potently inhibited by fenobam or MAO-B compounds, and [11C]L-deprenyl-D2 binding was inhibited by fenobam or AZD9272.	AZD9272	24-31	monoamine oxidase B	Homo sapiens	78-83
31589885-8	2020	The findings are consistent with the hypothesis that both fenobam and AZD9272 bind to the MAO-B, which may be of relevance for understanding the mechanism of the psychosis-like adverse events reported for these compounds.	fenobam	58-65	monoamine oxidase B	Homo sapiens	90-95
31589885-8	2020	The findings are consistent with the hypothesis that both fenobam and AZD9272 bind to the MAO-B, which may be of relevance for understanding the mechanism of the psychosis-like adverse events reported for these compounds.	AZD9272	70-77	monoamine oxidase B	Homo sapiens	90-95
31891098-6	2019	A concomitant inhibition of human acetylcholinesterase and human monoamine oxidase B, with IC50 values of 5.58 and 7.20 muM, respectively, was achieved with the dual-target 6-(4-(piperidin-1-yl)butoxy)-4H-chromen-4-one (7).	7-(4-(4-(6-fluorobenzo(d)isoxazol-3-yl)-piperidin-1-yl)butoxy)-4-methyl-8-chloro-2H-chromen-2-one	173-218	monoamine oxidase B	Homo sapiens	65-84
32378642-4	2020	Treatment with monoamine oxidase B (MAO-B) inhibitors also improves Parkinson"s disease symptoms by inhibiting the striatal dopamine metabolism and increasing the intracerebral dopamine concentration.	Dopamine	177-185	monoamine oxidase B	Homo sapiens	36-41
32378642-5	2020	Rasagiline is a potent and specific MAO-B inhibitor and is currently approved as an antiparkinsonian drug in more than 50 countries, including the United States and European countries.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	36-41
32612042-4	2020	Safinamide is a novel, selective, and reversible inhibitor of monoamine oxidase B expected to increase dopamine levels in the brain and improve the symptoms of Parkinson"s disease.	safinamide	0-10	monoamine oxidase B	Homo sapiens	62-81
32612042-4	2020	Safinamide is a novel, selective, and reversible inhibitor of monoamine oxidase B expected to increase dopamine levels in the brain and improve the symptoms of Parkinson"s disease.	Dopamine	103-111	monoamine oxidase B	Homo sapiens	62-81
31322459-7	2020	Glucocorticoids and glucocorticoid-metabolizing enzymes interact closely with other biomolecules such as inflammatory cytokines, monoamines, and some monoamine-metabolizing enzymes, namely the monoamine oxidase type A (MAO-A) and B (MAO-B).	monoamines	129-139	monoamine oxidase B	Homo sapiens	233-238
31322459-7	2020	Glucocorticoids and glucocorticoid-metabolizing enzymes interact closely with other biomolecules such as inflammatory cytokines, monoamines, and some monoamine-metabolizing enzymes, namely the monoamine oxidase type A (MAO-A) and B (MAO-B).	monoamine	129-138	monoamine oxidase B	Homo sapiens	233-238
32378642-4	2020	Treatment with monoamine oxidase B (MAO-B) inhibitors also improves Parkinson"s disease symptoms by inhibiting the striatal dopamine metabolism and increasing the intracerebral dopamine concentration.	Dopamine	124-132	monoamine oxidase B	Homo sapiens	15-34
32378642-4	2020	Treatment with monoamine oxidase B (MAO-B) inhibitors also improves Parkinson"s disease symptoms by inhibiting the striatal dopamine metabolism and increasing the intracerebral dopamine concentration.	Dopamine	124-132	monoamine oxidase B	Homo sapiens	36-41
32378642-4	2020	Treatment with monoamine oxidase B (MAO-B) inhibitors also improves Parkinson"s disease symptoms by inhibiting the striatal dopamine metabolism and increasing the intracerebral dopamine concentration.	Dopamine	177-185	monoamine oxidase B	Homo sapiens	15-34
31835376-0	2019	Chasing ChEs-MAO B Multi-Targeting 4-Aminomethyl-7-Benzyloxy-2H-Chromen-2-ones.	4-aminomethyl-7-benzyloxy-2h-chromen-2-ones	35-78	monoamine oxidase B	Homo sapiens	13-18
31835376-1	2019	A series of 4-aminomethyl-7-benzyloxy-2H-chromen-2-ones was investigated with the aim of identifying multiple inhibitors of cholinesterases (acetyl- and butyryl-, AChE and BChE) and monoamine oxidase B (MAO B) as potential anti-Alzheimer molecules.	4-aminomethyl-7-benzyloxy-2h-chromen-2-ones	12-55	monoamine oxidase B	Homo sapiens	182-201
31835376-1	2019	A series of 4-aminomethyl-7-benzyloxy-2H-chromen-2-ones was investigated with the aim of identifying multiple inhibitors of cholinesterases (acetyl- and butyryl-, AChE and BChE) and monoamine oxidase B (MAO B) as potential anti-Alzheimer molecules.	4-aminomethyl-7-benzyloxy-2h-chromen-2-ones	12-55	monoamine oxidase B	Homo sapiens	203-208
31291696-1	2019	The two human monoamine oxidase isoforms (namely MAO A and MAO B) are enzymes involved in the catabolism of monoamines, including neurotransmitters, and for this reason are well-known and attractive pharmacological targets in neuropsychiatric and neurodegenerative diseases, for which novel pharmacological approaches are necessary.	monoamines	108-118	monoamine oxidase B	Homo sapiens	59-64
30712420-2	2019	We have identified compound 14n as promising multitarget small molecule showing strong BuChE inhibition (IC50 = 11.90 +- 0.05 nM), moderate hAChE (IC50 = 1.73 +- 0.34 muM), hMAO A (IC50 = 2.78 +- 0.12 muM), and MAO B (IC50 = 21.29 +- 3.85 muM) inhibition, while keeping a strong antioxidant power (3.04 TE, ORAC test).	4-(4-methylpiperazin-1-yl)benzoic acid	28-31	monoamine oxidase B	Homo sapiens	211-216
31416364-1	2019	MAO-B leads to an increase in the levels of hydrogen peroxide and oxidative free radicals, which contribute to the aetiology of the AD.	Hydrogen Peroxide	44-61	monoamine oxidase B	Homo sapiens	0-5
31416364-1	2019	MAO-B leads to an increase in the levels of hydrogen peroxide and oxidative free radicals, which contribute to the aetiology of the AD.	Free Radicals	76-89	monoamine oxidase B	Homo sapiens	0-5
31781365-10	2019	In conclusion, L-dopa is now the most commonly prescribed medication for cases of PD but there is large variation in the prescribing rates of catechol-O-methyltransferase (COMT) inhibitors, monoamine oxidase B (MAO-B) inhibitors, amantadine, and anticholinergics between countries.	Levodopa	15-21	monoamine oxidase B	Homo sapiens	211-216
30727777-3	2019	The results of the biological testing demonstrated that the presence of the hydrazothiazole nucleus bearing at C4 a phenyl ring functionalised at the meta position with a nitro group represents an important pharmacophoric feature to obtain selective and reversible human MAO-B inhibition for the treatment of neurodegenerative disorders.	hydrazothiazole	76-91	monoamine oxidase B	Homo sapiens	271-276
30727777-3	2019	The results of the biological testing demonstrated that the presence of the hydrazothiazole nucleus bearing at C4 a phenyl ring functionalised at the meta position with a nitro group represents an important pharmacophoric feature to obtain selective and reversible human MAO-B inhibition for the treatment of neurodegenerative disorders.	nitro	171-176	monoamine oxidase B	Homo sapiens	271-276
31557622-5	2019	Among the compounds, 2 exhibited the highest hMAO inhibitory activity with an IC50 value of 3.23 microM for hMAO-A and 15.31 microM for hMAO-B.	hmao	45-49	monoamine oxidase B	Homo sapiens	136-142
31537422-0	2019	1,3,4-Oxadiazol-2-ylbenzenesulfonamides as privileged structures for the inhibition of monoamine oxidase B.	1,3,4-oxadiazol-2-ylbenzenesulfonamides	0-39	monoamine oxidase B	Homo sapiens	87-106
31537422-5	2019	An analysis of the structure-activity relationships shows that the 4-benzenesulfonamides are significantly more potent MAO-B inhibitors than the corresponding 3-benzenesulfonamides, and that the corresponding N,N"-diacylhydrazine synthetic precursors are weak MAO inhibitors.	4-benzenesulfonamides	67-88	monoamine oxidase B	Homo sapiens	119-124
31561103-0	2019	2-Styrylchromone derivatives as potent and selective monoamine oxidase B inhibitors.	2-styrylchromone	0-16	monoamine oxidase B	Homo sapiens	53-72
31561103-3	2019	Of the eighteen derivatives, compound 9 having methoxy group at R1 and chlorine at R4 showed both the best MAO-B inhibitory activity (IC50 = 17 +- 2.4 nM) and the best MAO-B selectivity (IC50 for MAO-A/IC50 for MAO-B = 1500).	Chlorine	71-79	monoamine oxidase B	Homo sapiens	107-112
31561103-3	2019	Of the eighteen derivatives, compound 9 having methoxy group at R1 and chlorine at R4 showed both the best MAO-B inhibitory activity (IC50 = 17 +- 2.4 nM) and the best MAO-B selectivity (IC50 for MAO-A/IC50 for MAO-B = 1500).	Chlorine	71-79	monoamine oxidase B	Homo sapiens	168-173
31561103-3	2019	Of the eighteen derivatives, compound 9 having methoxy group at R1 and chlorine at R4 showed both the best MAO-B inhibitory activity (IC50 = 17 +- 2.4 nM) and the best MAO-B selectivity (IC50 for MAO-A/IC50 for MAO-B = 1500).	Chlorine	71-79	monoamine oxidase B	Homo sapiens	168-173
31561103-5	2019	Quantitative structure-activity relationship (QSAR) analyses of the 2-styrylchromone derivatives were conducted using their pIC50 values with the use of Molecular Operating Environment (MOE) and Dragon, demonstrating that the descriptors of MAO-B inhibitory activity and MAO-B selectivity were 1734 and 121, respectively, that showed significant correlations (P < 0.05).	2-styrylchromone	68-84	monoamine oxidase B	Homo sapiens	241-246
31561103-5	2019	Quantitative structure-activity relationship (QSAR) analyses of the 2-styrylchromone derivatives were conducted using their pIC50 values with the use of Molecular Operating Environment (MOE) and Dragon, demonstrating that the descriptors of MAO-B inhibitory activity and MAO-B selectivity were 1734 and 121, respectively, that showed significant correlations (P < 0.05).	2-styrylchromone	68-84	monoamine oxidase B	Homo sapiens	271-276
31561103-8	2019	These data suggested that the 2-styrylchromone structure might be a useful scaffold for the design and development of novel MAO-B inhibitors.	2-styrylchromone	30-46	monoamine oxidase B	Homo sapiens	124-129
31556440-2	2019	This work measures a reduction in selectivity for the MAOB isoform of 3 to 9.5 kJ mol-1 upon the addition of hydroxy functional groups to a phenethylamine scaffold.	phenethylamine	140-154	monoamine oxidase B	Homo sapiens	54-58
31348537-3	2019	The results show that, with the exception of one compound, all indole-5,6-dicarbonitrile derivatives (10) exhibit submicromolar IC50 values for the inhibition of MAO, with the most potent MAO-A inhibitor exhibiting an IC50 value of 0.006 muM while the most potent MAO-B inhibitor exhibits an IC50 value of 0.058 muM.	1H-indole-5,6-dicarbonitrile	63-88	monoamine oxidase B	Homo sapiens	264-269
31872661-0	2019	[Synthesis and monoamine oxidase B inhibitory activities of isoquiritigenin derivatives].	isoquiritigenin	60-75	monoamine oxidase B	Homo sapiens	15-34
30666491-4	2019	Generally, the esters exhibited weak MAO inhibition, while the chromane-2,4-dione derivatives showed promise as selective MAO-B inhibitors with IC50 values in the micromolar range.	chromane-2,4-dione	63-81	monoamine oxidase B	Homo sapiens	122-127
30666491-8	2019	Good potency MAO-B inhibitors may act as leads for the design and development of therapy for Parkinson"s disease where these agents reduce the central metabolism of dopamine.	Dopamine	165-173	monoamine oxidase B	Homo sapiens	13-18
31556440-3	2019	Replacement of hydroxy functional groups on the phenethylamine scaffold by hydrophobic substituents measures an increase in selectivity for MAOB of -1.1 to -6.9 kJ mol-1.	phenethylamine	48-62	monoamine oxidase B	Homo sapiens	140-144
31745479-10	2019	The odds of using monoamine oxidase B inhibitors was 52% higher in 2017 than in 2010 (P &lt; 0.0001), 38% lower for catechol-O-methyltransferase inhibitors (P &lt; 0.0001), 25% lower for amantadine (P &lt; 0.0001), and 31% lower for anticholinergics (P = 0.0153).	Amantadine	187-197	monoamine oxidase B	Homo sapiens	18-37
31325784-0	2019	Design, synthesis and biological evaluation of hydroxypyridinone-coumarin hybrids as multimodal monoamine oxidase B inhibitors and iron chelates against Alzheimer"s disease.	1-hydroxy-2(1H)-pyridinone	47-64	monoamine oxidase B	Homo sapiens	96-115
31325784-0	2019	Design, synthesis and biological evaluation of hydroxypyridinone-coumarin hybrids as multimodal monoamine oxidase B inhibitors and iron chelates against Alzheimer"s disease.	coumarin	65-73	monoamine oxidase B	Homo sapiens	96-115
31325784-1	2019	A series of hybrids of hydroxypyridinone and coumarin were rationally designed, synthesized and biologically evaluated for their iron ion chelating and MAO-B inhibitory activities.	1-hydroxy-2(1H)-pyridinone	23-40	monoamine oxidase B	Homo sapiens	152-157
31325784-1	2019	A series of hybrids of hydroxypyridinone and coumarin were rationally designed, synthesized and biologically evaluated for their iron ion chelating and MAO-B inhibitory activities.	coumarin	45-53	monoamine oxidase B	Homo sapiens	152-157
31421966-1	2019	The irreversible monoamine oxidase B (MAO B) inhibitor rasagiline has been described with multiple disease modifying effects in vitro on models of Parkinson"s disease.	rasagiline	55-65	monoamine oxidase B	Homo sapiens	17-36
31421966-1	2019	The irreversible monoamine oxidase B (MAO B) inhibitor rasagiline has been described with multiple disease modifying effects in vitro on models of Parkinson"s disease.	rasagiline	55-65	monoamine oxidase B	Homo sapiens	38-43
31421966-4	2019	It showed nanomolar affinities at the desired targets (MAO B IC50 = 256 nM; hH3R Ki = 2.6 nM) with a high preference over monoamine oxidase A (MAO A) and negligible affinity at histamine H1, H4, dopamine D2, D3 receptors or acetyl-/butyrylcholinesterases.	Histamine	177-186	monoamine oxidase B	Homo sapiens	55-60
31444085-5	2019	The structure-active-relationship also indicated that the O-alkylamine fragment remarkably decreased hMAO-B inhibitory activity, compound TM-2 exhibited potent hMAO-B inhibitory activity (IC50 = 6.8 muM), which was supported by the molecular docking study.	o-alkylamine	58-70	monoamine oxidase B	Homo sapiens	101-107
31421966-4	2019	It showed nanomolar affinities at the desired targets (MAO B IC50 = 256 nM; hH3R Ki = 2.6 nM) with a high preference over monoamine oxidase A (MAO A) and negligible affinity at histamine H1, H4, dopamine D2, D3 receptors or acetyl-/butyrylcholinesterases.	Dopamine	195-203	monoamine oxidase B	Homo sapiens	55-60
31271801-0	2019	Potent and selective inhibition of human monoamine oxidase-B by 4-dimethylaminochalcone and selected chalcone derivatives.	4-dimethylaminochalcone	64-87	monoamine oxidase B	Homo sapiens	41-60
31444085-7	2019	Therefore, the structure-active-relationship of 2-acetylphenol-donepezil hybrids could encourage the development of multifunction agents with selective AChE inhibition or selective MAO-B inhibition for the treatment of Alzheimer"s disease.	2'-Hydroxyacetophenone	48-62	monoamine oxidase B	Homo sapiens	181-186
31444085-7	2019	Therefore, the structure-active-relationship of 2-acetylphenol-donepezil hybrids could encourage the development of multifunction agents with selective AChE inhibition or selective MAO-B inhibition for the treatment of Alzheimer"s disease.	Donepezil	63-72	monoamine oxidase B	Homo sapiens	181-186
31265934-0	2019	Carboxamides vs. methanimines: Crystal structures, binding interactions, photophysical studies, and biological evaluation of (indazole-5-yl)methanimines as monoamine oxidase B and acetylcholinesterase inhibitors.	carboxamides	0-12	monoamine oxidase B	Homo sapiens	156-175
31265934-0	2019	Carboxamides vs. methanimines: Crystal structures, binding interactions, photophysical studies, and biological evaluation of (indazole-5-yl)methanimines as monoamine oxidase B and acetylcholinesterase inhibitors.	(indazole-5-yl)methanimines	125-152	monoamine oxidase B	Homo sapiens	156-175
31265934-7	2019	Molecular modeling studies into the human MAO-B enzyme-binding site supported by a HYDE analysis suggested that the imine linker similarly contributes to the total binding energy in methanimines 17-22 as the amide spacer in their carboxamide analogs 11-16.	Imines	116-121	monoamine oxidase B	Homo sapiens	42-47
31265934-7	2019	Molecular modeling studies into the human MAO-B enzyme-binding site supported by a HYDE analysis suggested that the imine linker similarly contributes to the total binding energy in methanimines 17-22 as the amide spacer in their carboxamide analogs 11-16.	methyleneimine	182-194	monoamine oxidase B	Homo sapiens	42-47
31265934-7	2019	Molecular modeling studies into the human MAO-B enzyme-binding site supported by a HYDE analysis suggested that the imine linker similarly contributes to the total binding energy in methanimines 17-22 as the amide spacer in their carboxamide analogs 11-16.	Amides	208-213	monoamine oxidase B	Homo sapiens	42-47
31539917-3	2019	(+-)-Kavain was found to be a good potency in vitro inhibitor of human MAO-B with an IC50 of 5.34 microM.	kavain	5-11	monoamine oxidase B	Homo sapiens	71-76
31539917-5	2019	Under the same experimental conditions, the reference MAO inhibitor, curcumin, displays IC50 values of 5.01 microM and 2.55 microM for the inhibition of MAO-A and MAO-B, respectively.	Curcumin	69-77	monoamine oxidase B	Homo sapiens	163-168
31539917-6	2019	It was further established that (+-)-kavain interacts reversibly and competitively with MAO-A and MAO-B with enzyme-inhibitor dissociation constants (Ki) of 7.72 and 5.10 microM, respectively.	kavain	37-43	monoamine oxidase B	Homo sapiens	98-103
31539917-9	2019	Yangonin proved to be the most potent MAO inhibitor with IC50 values of 1.29 and 0.085 microM for MAO-A and MAO-B, respectively.	yangonin	0-8	monoamine oxidase B	Homo sapiens	108-113
31322823-0	2019	2-Phenyloxazole-4-carboxamide as a Scaffold for Selective Inhibition of Human Monoamine Oxidase B.	2-phenyloxazole-4-carboxamide	0-29	monoamine oxidase B	Homo sapiens	78-97
30877626-1	2019	Rasagiline mesylate is an irreversible MAO-B inhibitor which requires daily oral administration for treatment of Parkinson"s disease due to its short half-life.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	39-44
31265934-7	2019	Molecular modeling studies into the human MAO-B enzyme-binding site supported by a HYDE analysis suggested that the imine linker similarly contributes to the total binding energy in methanimines 17-22 as the amide spacer in their carboxamide analogs 11-16.	carboxamide	230-241	monoamine oxidase B	Homo sapiens	42-47
31271496-6	2019	More importantly, miR-522 could decreased MAOB expression by binding to MAOB with a putative site, thereby promoting cell proliferation, migration, and invasion through in vitro functional analyses, including MTT assay, wound-healing and transwell invasion experiments.	monooxyethylene trimethylolpropane tristearate	209-212	monoamine oxidase B	Homo sapiens	42-46
31271496-6	2019	More importantly, miR-522 could decreased MAOB expression by binding to MAOB with a putative site, thereby promoting cell proliferation, migration, and invasion through in vitro functional analyses, including MTT assay, wound-healing and transwell invasion experiments.	monooxyethylene trimethylolpropane tristearate	209-212	monoamine oxidase B	Homo sapiens	72-76
31271801-0	2019	Potent and selective inhibition of human monoamine oxidase-B by 4-dimethylaminochalcone and selected chalcone derivatives.	Chalcone	79-87	monoamine oxidase B	Homo sapiens	41-60
31271801-2	2019	Compounds 4-dimethylaminochalcone (2), 4"-chloro-4-dimethylaminochalcone (5), and 2,4"-dichloro-4-dimethylaminochalcone (1) potently inhibited hMAO-B with IC50 values of 0.029, 0.061, and 0.075 muM, respectively.	4-dimethylaminochalcone	10-33	monoamine oxidase B	Homo sapiens	143-149
31271801-2	2019	Compounds 4-dimethylaminochalcone (2), 4"-chloro-4-dimethylaminochalcone (5), and 2,4"-dichloro-4-dimethylaminochalcone (1) potently inhibited hMAO-B with IC50 values of 0.029, 0.061, and 0.075 muM, respectively.	4"-chloro-4-dimethylaminochalcone	39-72	monoamine oxidase B	Homo sapiens	143-149
31271801-2	2019	Compounds 4-dimethylaminochalcone (2), 4"-chloro-4-dimethylaminochalcone (5), and 2,4"-dichloro-4-dimethylaminochalcone (1) potently inhibited hMAO-B with IC50 values of 0.029, 0.061, and 0.075 muM, respectively.	2,4"-dichloro-4-dimethylaminochalcone	82-119	monoamine oxidase B	Homo sapiens	143-149
31271801-3	2019	4-Nitrochalcone (4) and 4-chlorochalcone (3) also potently inhibited hMAO-B with IC50 values of 0.066 and 0.082 muM, respectively (2.3- and 2.6-fold less than compound 2).	4-Nitrochalcone	0-15	monoamine oxidase B	Homo sapiens	69-75
31271801-3	2019	4-Nitrochalcone (4) and 4-chlorochalcone (3) also potently inhibited hMAO-B with IC50 values of 0.066 and 0.082 muM, respectively (2.3- and 2.6-fold less than compound 2).	4-Chlorochalcone	24-40	monoamine oxidase B	Homo sapiens	69-75
31271801-8	2019	Docking simulations showed binding affinities of compounds 1 to 5 for hMAO-B were higher than those for hMAO-A or AChE and suggested these five chalcones form hydrogen bonds with MAO-B at Cys172 but that they do not form hydrogen bonds with hMAO-A or AChE.	Hydrogen	159-167	monoamine oxidase B	Homo sapiens	70-76
31271801-8	2019	Docking simulations showed binding affinities of compounds 1 to 5 for hMAO-B were higher than those for hMAO-A or AChE and suggested these five chalcones form hydrogen bonds with MAO-B at Cys172 but that they do not form hydrogen bonds with hMAO-A or AChE.	Hydrogen	159-167	monoamine oxidase B	Homo sapiens	71-76
31271801-8	2019	Docking simulations showed binding affinities of compounds 1 to 5 for hMAO-B were higher than those for hMAO-A or AChE and suggested these five chalcones form hydrogen bonds with MAO-B at Cys172 but that they do not form hydrogen bonds with hMAO-A or AChE.	Hydrogen	221-229	monoamine oxidase B	Homo sapiens	70-76
31271801-8	2019	Docking simulations showed binding affinities of compounds 1 to 5 for hMAO-B were higher than those for hMAO-A or AChE and suggested these five chalcones form hydrogen bonds with MAO-B at Cys172 but that they do not form hydrogen bonds with hMAO-A or AChE.	Hydrogen	221-229	monoamine oxidase B	Homo sapiens	71-76
30604512-5	2019	It also highlights the recent developments in the discovery of potential MAO-B inhibitors (MAO-BIs) belonging to diverse chemical scaffolds, arising from intensive chemical-mechanistic and computational studies documented during past 3 years (2015-2018), with emphases on their potency and selectivity.	mao-bis	91-98	monoamine oxidase B	Homo sapiens	73-78
31323226-5	2019	Fucoxanthin displayed weak inhibition with IC50 values of 197.41 +- 2.20 and 211.12 +- 1.17 muM over two isoenzymes hMAO-A and hMAO-B, respectively.	fucoxanthin	0-11	monoamine oxidase B	Homo sapiens	127-133
31375128-3	2019	This positive affective response correlated with the ability of blackcurrant polyphenols to support monoamine neurotransmission via inhibition of monoamine oxidase-B (MAO-B) activity.	Polyphenols	77-88	monoamine oxidase B	Homo sapiens	146-165
30986504-6	2019	Garcinol serves as a potent natural HAT inhibitor and has unveiled promising results in molecular interaction studies against Monoamine oxidase B (MAO-B) and Catechol-O-Methyltransferase (COMT), as well as in L-DOPA induced dyskinesia.	garcinol	0-8	monoamine oxidase B	Homo sapiens	126-145
30986504-6	2019	Garcinol serves as a potent natural HAT inhibitor and has unveiled promising results in molecular interaction studies against Monoamine oxidase B (MAO-B) and Catechol-O-Methyltransferase (COMT), as well as in L-DOPA induced dyskinesia.	garcinol	0-8	monoamine oxidase B	Homo sapiens	147-152
31464590-2	2019	Recent data support the hypothesis that THK5351 binds to monoamine oxidase B (MAO-B) expressed from reactive astrocytes and that flortaucipir has an affinity toward MAO-A and B; however, pathological evidence is lacking.	THK5351	40-47	monoamine oxidase B	Homo sapiens	57-76
31464590-2	2019	Recent data support the hypothesis that THK5351 binds to monoamine oxidase B (MAO-B) expressed from reactive astrocytes and that flortaucipir has an affinity toward MAO-A and B; however, pathological evidence is lacking.	THK5351	40-47	monoamine oxidase B	Homo sapiens	78-83
31464590-10	2019	CONCLUSIONS: Our findings add pathological evidence that increased THK5351 uptake in sporadic CJD patients might be caused by an off-target binding driven by its high affinity for MAO-B.	THK5351	67-74	monoamine oxidase B	Homo sapiens	180-185
31264403-3	2019	Still, despite this practical importance, the precise chemical mechanisms underlying the irreversible inhibition of the MAO B isoform with clinical drugs rasagiline (RAS) and selegiline (SEL) remained unknown.	rasagiline	154-164	monoamine oxidase B	Homo sapiens	120-125
31264403-3	2019	Still, despite this practical importance, the precise chemical mechanisms underlying the irreversible inhibition of the MAO B isoform with clinical drugs rasagiline (RAS) and selegiline (SEL) remained unknown.	rasagiline	166-169	monoamine oxidase B	Homo sapiens	120-125
31264403-3	2019	Still, despite this practical importance, the precise chemical mechanisms underlying the irreversible inhibition of the MAO B isoform with clinical drugs rasagiline (RAS) and selegiline (SEL) remained unknown.	Selegiline	175-185	monoamine oxidase B	Homo sapiens	120-125
31264403-3	2019	Still, despite this practical importance, the precise chemical mechanisms underlying the irreversible inhibition of the MAO B isoform with clinical drugs rasagiline (RAS) and selegiline (SEL) remained unknown.	Selegiline	187-190	monoamine oxidase B	Homo sapiens	120-125
31375128-3	2019	This positive affective response correlated with the ability of blackcurrant polyphenols to support monoamine neurotransmission via inhibition of monoamine oxidase-B (MAO-B) activity.	Polyphenols	77-88	monoamine oxidase B	Homo sapiens	167-172
31375128-3	2019	This positive affective response correlated with the ability of blackcurrant polyphenols to support monoamine neurotransmission via inhibition of monoamine oxidase-B (MAO-B) activity.	monoamine	100-109	monoamine oxidase B	Homo sapiens	146-165
31375128-3	2019	This positive affective response correlated with the ability of blackcurrant polyphenols to support monoamine neurotransmission via inhibition of monoamine oxidase-B (MAO-B) activity.	monoamine	100-109	monoamine oxidase B	Homo sapiens	167-172
30963543-1	2019	OBJECTIVES: To evaluate whether the prescription of monoamine oxidase B inhibitors (MAOB-I), rasagiline and safinamide, contributes to the reduction of levodopa and/or dopamine agonists (DA) dose in order to minimize adverse effects.	Levodopa	152-160	monoamine oxidase B	Homo sapiens	52-71
31336891-0	2019	Boosting Drug Discovery for Parkinson"s: Enhancement of the Delivery of a Monoamine Oxidase-B Inhibitor by Brain-Targeted PEGylated Polycaprolactone-Based Nanoparticles.	polycaprolactone	132-148	monoamine oxidase B	Homo sapiens	74-93
31336891-1	2019	The current pharmacological treatments for Parkinson"s disease only offer symptomatic relief to the patients and are based on the administration of levodopa and catechol-O-methyltransferase or monoamine oxidase-B inhibitors (IMAO-B).	imao-b	225-231	monoamine oxidase B	Homo sapiens	193-212
30963543-1	2019	OBJECTIVES: To evaluate whether the prescription of monoamine oxidase B inhibitors (MAOB-I), rasagiline and safinamide, contributes to the reduction of levodopa and/or dopamine agonists (DA) dose in order to minimize adverse effects.	Dopamine	168-176	monoamine oxidase B	Homo sapiens	52-71
30919054-6	2019	RESULTS: The computational modelling studies identified a binding site for all the tau tracers on MAO-B; this was the same site as that for safinamide.	safinamide	140-150	monoamine oxidase B	Homo sapiens	98-103
30933784-4	2019	Comparison of the inhibitory activities of 1a vs. 9a vs. 13a and 1b vs. 7b vs. 11b suggested that methoxy substitution at R1 on the A-rings of flavonoids increases MAO-A inhibition whereas methoxy substitution at R2 increased MAO-B inhibition.	Flavonoids	143-153	monoamine oxidase B	Homo sapiens	226-231
30933784-6	2019	Comparison of the MAO-B inhibitory effects of the flavone-indole hybrids and aurone-indole hybrids showed that most of the aurone-indole hybrids were stronger inhibitors than the corresponding flavone-indole hybrids.	flavone	50-57	monoamine oxidase B	Homo sapiens	18-23
30933784-6	2019	Comparison of the MAO-B inhibitory effects of the flavone-indole hybrids and aurone-indole hybrids showed that most of the aurone-indole hybrids were stronger inhibitors than the corresponding flavone-indole hybrids.	indole	58-64	monoamine oxidase B	Homo sapiens	18-23
30933784-6	2019	Comparison of the MAO-B inhibitory effects of the flavone-indole hybrids and aurone-indole hybrids showed that most of the aurone-indole hybrids were stronger inhibitors than the corresponding flavone-indole hybrids.	aurone-indole	77-90	monoamine oxidase B	Homo sapiens	18-23
30933784-6	2019	Comparison of the MAO-B inhibitory effects of the flavone-indole hybrids and aurone-indole hybrids showed that most of the aurone-indole hybrids were stronger inhibitors than the corresponding flavone-indole hybrids.	aurone	77-83	monoamine oxidase B	Homo sapiens	18-23
30933784-6	2019	Comparison of the MAO-B inhibitory effects of the flavone-indole hybrids and aurone-indole hybrids showed that most of the aurone-indole hybrids were stronger inhibitors than the corresponding flavone-indole hybrids.	flavone	193-200	monoamine oxidase B	Homo sapiens	18-23
30933784-8	2019	This is the first report identifying aurone-indole hybrids as potent MAO-B inhibitors.	aurone-indole	37-50	monoamine oxidase B	Homo sapiens	69-74
30933784-9	2019	The results reported here suggest that 2-(1H-indol-1-ylmethylene)-6-methoxy-3(2H)-benzofuranone (9a) might be a useful lead for the design and development of novel MAO-B inhibitors.	2-(1h-indol-1-ylmethylene)-6-methoxy-3(2h)-benzofuranone	39-95	monoamine oxidase B	Homo sapiens	164-169
31060887-1	2019	Carbon-11 labeled SL25.1188 is a promising reversible monoamine oxidase-B (MAO-B) radioligand that was recently translated for human positron emission tomography (PET) imaging.	Carbon-11	0-9	monoamine oxidase B	Homo sapiens	54-73
31060887-1	2019	Carbon-11 labeled SL25.1188 is a promising reversible monoamine oxidase-B (MAO-B) radioligand that was recently translated for human positron emission tomography (PET) imaging.	Carbon-11	0-9	monoamine oxidase B	Homo sapiens	75-80
31060887-2	2019	Herein, we report the development of a novel fluorinated derivative, namely, [18F](S)-3-(6-(3-fluoropropoxy)benzo[d]isoxazol-3-yl)-5-(methoxymethyl)oxazolidin-2-one ([18F]FSL25.1188; [18F]6), as a candidate 18F-labeled MAO-B radioligand, and, its subsequent preclinical evaluation in non-human primates (NHP).	[18f](s)-3-(6-(3-fluoropropoxy)benzo[d]isoxazol-3-yl)-5-(methoxymethyl)oxazolidin-2-one	77-164	monoamine oxidase B	Homo sapiens	219-224
31005056-3	2019	Among the derivatives, 3-(3-(dimethylamino)propanoyl)-7-hydroxy-5-methyl- 2H-chromen-2-one hydrochloride (24) exhibited the most potent and selective hMAO-B inhibitory activity, and anti-inflammatory and neuroprotective effects in the in vitro studies.	3-(3-(dimethylamino)propanoyl)-7-hydroxy-5-methyl- 2h-chromen-2-one hydrochloride	23-104	monoamine oxidase B	Homo sapiens	150-156
31238535-5	2019	Among the tested phlorotannins, PFF-A showed the strongest inhibitory activity against both hMAO isoforms, with higher selectivity toward hMAO-B than hMAO-A.	phlorofucofuroeckol A	32-37	monoamine oxidase B	Homo sapiens	138-144
30897526-7	2019	Further, the molecular docking studies of these compounds demonstrated a good selectivity profile with Monoamine oxidase B with better binding affinity and confirms AMB is a potent antioxidant.	Amlodipine	165-168	monoamine oxidase B	Homo sapiens	103-122
30919054-7	2019	The binding affinity and free energy of binding for the tau tracers to MAO-B was substantial and in a similar range to those for safinamide.	safinamide	129-139	monoamine oxidase B	Homo sapiens	71-76
30919054-8	2019	The most recently developed tau tracers MK-6240, JNJ-311 and PI-2620 appeared, in silico, to have the lowest relative affinity for MAO-B.	MK-6240	40-47	monoamine oxidase B	Homo sapiens	131-136
30919054-10	2019	The binding relationship between [18F]THK5317 and [11C]DED depended on the availability of the MAO-B enzyme.	6-((3-fluoro-2-hydroxy)propoxy)-2-(4-methylaminophenyl)quinoline	38-45	monoamine oxidase B	Homo sapiens	95-100
30840042-1	2019	Importance: Monoamine oxidase B (MAO-B) is an important, high-density enzyme in the brain that generates oxidative stress by hydrogen peroxide production, alters mitochondrial function, and metabolizes nonserotonergic monoamines.	Hydrogen Peroxide	125-142	monoamine oxidase B	Homo sapiens	12-31
30840042-1	2019	Importance: Monoamine oxidase B (MAO-B) is an important, high-density enzyme in the brain that generates oxidative stress by hydrogen peroxide production, alters mitochondrial function, and metabolizes nonserotonergic monoamines.	Hydrogen Peroxide	125-142	monoamine oxidase B	Homo sapiens	33-38
30840042-13	2019	Greater MAO-B VT is an index of MAO-B overexpression, which may contribute to pathologies of mitochondrial dysfunction, elevated synthesis of neurotoxic products, and increased metabolism of nonserotonergic monoamines.	monoamines	207-217	monoamine oxidase B	Homo sapiens	8-13
30840042-13	2019	Greater MAO-B VT is an index of MAO-B overexpression, which may contribute to pathologies of mitochondrial dysfunction, elevated synthesis of neurotoxic products, and increased metabolism of nonserotonergic monoamines.	monoamines	207-217	monoamine oxidase B	Homo sapiens	32-37
30849741-10	2019	Moreover, it is possible for BDT to improve PSHS through the functional targets including GLO1, MAOA and MAOB, which are closely related to monoamine neurotransmitters.	bdt	29-32	monoamine oxidase B	Homo sapiens	105-109
30762003-0	2019	Preliminary in vitro evaluation of neuroprotective and monoamine oxidase type B inhibitory effects of newly synthesized 8-aminocaffeines.	8-aminocaffeines	120-136	monoamine oxidase B	Homo sapiens	55-79
30849741-10	2019	Moreover, it is possible for BDT to improve PSHS through the functional targets including GLO1, MAOA and MAOB, which are closely related to monoamine neurotransmitters.	monoamine	140-149	monoamine oxidase B	Homo sapiens	105-109
30964996-2	2019	Human monoamine oxidase B (MAO-B) catalyzes the oxidation of amines and is inhibited for the treatment of both Parkinson"s disease and depression.	Amines	61-67	monoamine oxidase B	Homo sapiens	6-25
30964996-2	2019	Human monoamine oxidase B (MAO-B) catalyzes the oxidation of amines and is inhibited for the treatment of both Parkinson"s disease and depression.	Amines	61-67	monoamine oxidase B	Homo sapiens	27-32
30964996-4	2019	Evidence of a radical in either the transition state or the resting state of MAO-B is present throughout the literature and is suggested to be a flavin semiquinone, a tyrosyl radical, or both.	flavin semiquinone	145-163	monoamine oxidase B	Homo sapiens	77-82
30964996-4	2019	Evidence of a radical in either the transition state or the resting state of MAO-B is present throughout the literature and is suggested to be a flavin semiquinone, a tyrosyl radical, or both.	Tyrosyl radical	167-182	monoamine oxidase B	Homo sapiens	77-82
30833108-0	2019	Discovery of novel 2,3-dihydro-1H-inden-1-amine derivatives as selective monoamine oxidase B inhibitors.	1-aminoindan	19-47	monoamine oxidase B	Homo sapiens	73-92
30833108-2	2019	To find more potent and selective MAO-B inhibitors with novel chemical scaffold, we designed and synthesized a series of new 2,3-dihydro-1H-inden-1-amine derivatives on basis of our previous study.	1-aminoindan	125-153	monoamine oxidase B	Homo sapiens	34-39
30599413-8	2019	This study identifies suitable substitution patterns for the design of 4(3H)-quinazolinone derivatives as MAO-B inhibitors.	4-hydroxyquinazoline	71-90	monoamine oxidase B	Homo sapiens	106-111
30792039-1	2019	Herein we report our efforts of developing reversible selective hMAO-B inhibitors based on isatin, a fragment in an X-ray crystal structure.	Isatin	91-97	monoamine oxidase B	Homo sapiens	64-70
30792039-4	2019	However, the endeavors to modify the polar 3-one group of isatin, that is in a hydrophobic environment in the binding site of hMAO-B, to small nonpolar hydrophobic groups did not bring about improved hMAO-B inhibitors, which may challenge our understanding of molecular interactions and molecular recognition in biological systems.	Isatin	58-64	monoamine oxidase B	Homo sapiens	126-132
31017021-4	2019	Accordingly, monoamine oxidase-B inhibitors provide a symptomatic effect via dopamine on motor symptoms in patients with Parkinson"s disease.	Dopamine	77-85	monoamine oxidase B	Homo sapiens	13-32
31017021-9	2019	In patients, concomitant inhibition of monoamine oxidase-B caused less increase of levodopa dosages over five years.	Levodopa	83-91	monoamine oxidase B	Homo sapiens	39-58
31303592-2	2019	In this research paper, ligand based virtual screening has been performed in order to predict the inhibitors for monoamine oxidase (MAO-B), an enzyme specifically involved in the metabolism of non-hydroxylated amines such as benzylamine and beta-phenylethylamine (PEA), thus, could be the target to treat various neurodegenerative disorders like Parkinson"s disease.	Amines	210-216	monoamine oxidase B	Homo sapiens	132-137
31303592-2	2019	In this research paper, ligand based virtual screening has been performed in order to predict the inhibitors for monoamine oxidase (MAO-B), an enzyme specifically involved in the metabolism of non-hydroxylated amines such as benzylamine and beta-phenylethylamine (PEA), thus, could be the target to treat various neurodegenerative disorders like Parkinson"s disease.	benzylamine	225-236	monoamine oxidase B	Homo sapiens	132-137
31303592-2	2019	In this research paper, ligand based virtual screening has been performed in order to predict the inhibitors for monoamine oxidase (MAO-B), an enzyme specifically involved in the metabolism of non-hydroxylated amines such as benzylamine and beta-phenylethylamine (PEA), thus, could be the target to treat various neurodegenerative disorders like Parkinson"s disease.	phenethylamine	241-262	monoamine oxidase B	Homo sapiens	132-137
31303592-2	2019	In this research paper, ligand based virtual screening has been performed in order to predict the inhibitors for monoamine oxidase (MAO-B), an enzyme specifically involved in the metabolism of non-hydroxylated amines such as benzylamine and beta-phenylethylamine (PEA), thus, could be the target to treat various neurodegenerative disorders like Parkinson"s disease.	phenethylamine	264-267	monoamine oxidase B	Homo sapiens	132-137
31303592-5	2019	As an outcome of this screening, 31 compounds out of 968 compounds from Afro Database (compounds from African medicinal plants) are predicted to be active as MAO-B inhibitor, Out of the 31 predicted active compounds, Norlichexanthone (ZINC05765089) is predicted to be most active against MAO-B with highest RF score 0.795181, along with the other top hits, could be the putative drug candidates for the prevention/ treatment of Parkinson"s disease.	norlichexanthone	217-233	monoamine oxidase B	Homo sapiens	158-163
31303592-5	2019	As an outcome of this screening, 31 compounds out of 968 compounds from Afro Database (compounds from African medicinal plants) are predicted to be active as MAO-B inhibitor, Out of the 31 predicted active compounds, Norlichexanthone (ZINC05765089) is predicted to be most active against MAO-B with highest RF score 0.795181, along with the other top hits, could be the putative drug candidates for the prevention/ treatment of Parkinson"s disease.	norlichexanthone	217-233	monoamine oxidase B	Homo sapiens	288-293
31303592-5	2019	As an outcome of this screening, 31 compounds out of 968 compounds from Afro Database (compounds from African medicinal plants) are predicted to be active as MAO-B inhibitor, Out of the 31 predicted active compounds, Norlichexanthone (ZINC05765089) is predicted to be most active against MAO-B with highest RF score 0.795181, along with the other top hits, could be the putative drug candidates for the prevention/ treatment of Parkinson"s disease.	zinc05765089	235-247	monoamine oxidase B	Homo sapiens	158-163
31303592-5	2019	As an outcome of this screening, 31 compounds out of 968 compounds from Afro Database (compounds from African medicinal plants) are predicted to be active as MAO-B inhibitor, Out of the 31 predicted active compounds, Norlichexanthone (ZINC05765089) is predicted to be most active against MAO-B with highest RF score 0.795181, along with the other top hits, could be the putative drug candidates for the prevention/ treatment of Parkinson"s disease.	zinc05765089	235-247	monoamine oxidase B	Homo sapiens	288-293
30663112-0	2019	Potent and highly selective dual-targeting monoamine oxidase-B inhibitors: Fluorinated chalcones of morpholine versus imidazole.	fluorinated chalcones	75-96	monoamine oxidase B	Homo sapiens	43-62
30663112-0	2019	Potent and highly selective dual-targeting monoamine oxidase-B inhibitors: Fluorinated chalcones of morpholine versus imidazole.	morpholine	100-110	monoamine oxidase B	Homo sapiens	43-62
30663112-0	2019	Potent and highly selective dual-targeting monoamine oxidase-B inhibitors: Fluorinated chalcones of morpholine versus imidazole.	imidazole	118-127	monoamine oxidase B	Homo sapiens	43-62
30663112-2	2019	Our results indicate that morpholine containing chalcones are highly selective MAO-B inhibitors having reversibility properties.	morpholine	26-36	monoamine oxidase B	Homo sapiens	79-84
30663112-2	2019	Our results indicate that morpholine containing chalcones are highly selective MAO-B inhibitors having reversibility properties.	Chalcones	48-57	monoamine oxidase B	Homo sapiens	79-84
30663112-4	2019	Among the tested compounds, (2E)-3-(3-fluorophenyl)-1-[4-(morpholin-4-yl)phenyl]prop-2-en-1-one (f2) showed potent inhibitory activity for recombinant human MAO-B (IC50  = 0.087 muM) with a high selectivity index (SI) of 517.2.	(2e)-3-(3-fluorophenyl)-1-[4-(morpholin-4-yl)phenyl]prop-2-en-1-one	28-95	monoamine oxidase B	Homo sapiens	157-162
30599413-3	2019	Since monoamine oxidase (MAO) B is a key dopamine metabolising enzyme in the brain, MAO-B inhibitors are often used as adjuvants to l-dopa.	Dopamine	41-49	monoamine oxidase B	Homo sapiens	6-31
30599413-3	2019	Since monoamine oxidase (MAO) B is a key dopamine metabolising enzyme in the brain, MAO-B inhibitors are often used as adjuvants to l-dopa.	Dopamine	41-49	monoamine oxidase B	Homo sapiens	84-89
30808606-0	2019	Novel multi-target directed ligands based on annelated xanthine scaffold with aromatic substituents acting on adenosine receptor and monoamine oxidase B.	Xanthine	55-63	monoamine oxidase B	Homo sapiens	133-152
30386930-0	2019	Inhibitors of MAO-B and COMT: their effects on brain dopamine levels and uses in Parkinson"s disease.	Dopamine	53-61	monoamine oxidase B	Homo sapiens	14-19
30808606-2	2019	N9-Benzyl-substituted imidazo-, pyrimido- and 1,3-diazepino[2,1-f]purinediones were designed as dual-target-directed ligands combining A2A adenosine receptor (AR) antagonistic activity with blockade of monoamine oxidase B (MAO-B).	n9-benzyl-substituted imidazo-, pyrimido- and 1,3-diazepino[2,1-f]purinediones	0-78	monoamine oxidase B	Homo sapiens	202-221
30808606-2	2019	N9-Benzyl-substituted imidazo-, pyrimido- and 1,3-diazepino[2,1-f]purinediones were designed as dual-target-directed ligands combining A2A adenosine receptor (AR) antagonistic activity with blockade of monoamine oxidase B (MAO-B).	n9-benzyl-substituted imidazo-, pyrimido- and 1,3-diazepino[2,1-f]purinediones	0-78	monoamine oxidase B	Homo sapiens	223-228
30808606-5	2019	Moreover, some potent, selective MAO-B inhibitors were identified in the group of pyrimido- and 1,3-diazepino[2,1-f]purinediones.	pyrimido- and 1,3-diazepino[2,1-f]purinediones	82-128	monoamine oxidase B	Homo sapiens	33-38
31140884-1	2019	Aim: Due to the pivotal role in the oxidative deamination of monoamine neurotransmitters, two distinct monoamine oxidase (MAO) subtypes, MAO-A and MAO-B, present a significant pharmacological interest.	monoamine	61-70	monoamine oxidase B	Homo sapiens	147-152
30386930-1	2019	MAO-B and COMT are both enzymes involved in dopamine breakdown and metabolism.	Dopamine	44-52	monoamine oxidase B	Homo sapiens	0-5
30396116-4	2019	Among the compounds isolated, rhamnocitrin (5) was found to potently and selectively inhibit human MAO-A (hMAO-A, IC50 = 0.051 microM) and effectively inhibit hMAO-B (IC50 = 2.97 microM).	kaempferol-7-methyl ether	30-42	monoamine oxidase B	Homo sapiens	159-165
30738894-13	2019	Interestingly, Sp1/Egr1/CREB/miR-1224 levels correlate with MAO-B expression in rodent models of hypertension/MPTP-induced neurodegeneration, indicating their roles in governing MAO-B gene expression in these disease states.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	110-114	monoamine oxidase B	Homo sapiens	60-65
30738894-13	2019	Interestingly, Sp1/Egr1/CREB/miR-1224 levels correlate with MAO-B expression in rodent models of hypertension/MPTP-induced neurodegeneration, indicating their roles in governing MAO-B gene expression in these disease states.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	110-114	monoamine oxidase B	Homo sapiens	178-183
30738894-14	2019	Taken together, this study elucidates the previously unknown roles of the transcription factors Sp1/Egr1/CREB and microRNAs miR-1224/miR-300 in regulating MAO-B gene expression under basal/disease states involving dysregulated catecholamine levels.	Catecholamines	227-240	monoamine oxidase B	Homo sapiens	155-160
30481645-6	2019	Also, compounds 3a (IC50 = 0.114 microM), 3h (IC50 = 0.049 microM), and 3i (IC50 = 0.054 microM) were the most active derivatives against MAO-B enzyme activity.	Tritium	42-44	monoamine oxidase B	Homo sapiens	138-143
30906861-2	2019	Although short-term treatment with irreversible MAO-B inhibitors, such as selegiline, improves cognitive deficits in AD patients, long-term treatments have shown disappointing results.	Selegiline	74-84	monoamine oxidase B	Homo sapiens	48-53
30686752-7	2019	Docking simulations also implied that 6 interacted with hMAO-A at Phe208 and with hMAO-B at Ile199 by carbon hydrogen bondings.	Carbon	102-108	monoamine oxidase B	Homo sapiens	82-88
30686752-7	2019	Docking simulations also implied that 6 interacted with hMAO-A at Phe208 and with hMAO-B at Ile199 by carbon hydrogen bondings.	Hydrogen	109-117	monoamine oxidase B	Homo sapiens	82-88
30738894-1	2019	Monoamine oxidase B (MAO-B), a flavoenzyme located in the outer mitochondrial membrane, is involved in the catabolism of monoamines.	monoamines	121-131	monoamine oxidase B	Homo sapiens	0-19
30738894-1	2019	Monoamine oxidase B (MAO-B), a flavoenzyme located in the outer mitochondrial membrane, is involved in the catabolism of monoamines.	monoamines	121-131	monoamine oxidase B	Homo sapiens	21-26
30738894-11	2019	Dopamine dose-dependently enhanced MAO-B transcript and protein levels via increased binding of CREB to MAO-B promoter and reduced miR-1224/miR-300 levels.	Dopamine	0-8	monoamine oxidase B	Homo sapiens	35-40
30738894-11	2019	Dopamine dose-dependently enhanced MAO-B transcript and protein levels via increased binding of CREB to MAO-B promoter and reduced miR-1224/miR-300 levels.	Dopamine	0-8	monoamine oxidase B	Homo sapiens	104-109
30738894-12	2019	8-Bromo-cAMP and forskolin augmented MAO-B expression, whereas inhibition of PKA diminished the gene expression suggesting involvement of cAMP-PKA axis.	8-Bromo Cyclic Adenosine Monophosphate	0-12	monoamine oxidase B	Homo sapiens	37-42
30738894-12	2019	8-Bromo-cAMP and forskolin augmented MAO-B expression, whereas inhibition of PKA diminished the gene expression suggesting involvement of cAMP-PKA axis.	Colforsin	17-26	monoamine oxidase B	Homo sapiens	37-42
30738894-12	2019	8-Bromo-cAMP and forskolin augmented MAO-B expression, whereas inhibition of PKA diminished the gene expression suggesting involvement of cAMP-PKA axis.	Cyclic AMP	8-12	monoamine oxidase B	Homo sapiens	37-42
30857558-9	2019	Of note, [F-18]-MK-6240 and [F-18]-AV-1451 autoradiographic binding signals were only weakly displaced by competing concentrations of selective MAO-B inhibitor deprenyl but not by MAO-A inhibitor clorgyline, suggesting that MAO enzymes do not appear to be a significant binding target of any of these two tracers.	MK-6240	16-23	monoamine oxidase B	Homo sapiens	144-149
30857558-9	2019	Of note, [F-18]-MK-6240 and [F-18]-AV-1451 autoradiographic binding signals were only weakly displaced by competing concentrations of selective MAO-B inhibitor deprenyl but not by MAO-A inhibitor clorgyline, suggesting that MAO enzymes do not appear to be a significant binding target of any of these two tracers.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	28-42	monoamine oxidase B	Homo sapiens	144-149
30857558-9	2019	Of note, [F-18]-MK-6240 and [F-18]-AV-1451 autoradiographic binding signals were only weakly displaced by competing concentrations of selective MAO-B inhibitor deprenyl but not by MAO-A inhibitor clorgyline, suggesting that MAO enzymes do not appear to be a significant binding target of any of these two tracers.	Selegiline	160-168	monoamine oxidase B	Homo sapiens	144-149
30428433-7	2019	This report is the first to identify pyrano[4,3-b][1]benzopyranone derivatives as potent and selective MAO-B inhibitors.	pyrano[4,3-b][1]benzopyranone	37-66	monoamine oxidase B	Homo sapiens	103-108
30428433-8	2019	3-Butoxy-8-chloro-pyrano[4,3-b][1]benzopyranone (5b) may be useful as a lead compound for the development of MAO-B inhibitors.	3-butoxy-8-chloro-pyrano[4,3-b][1]benzopyranone	0-47	monoamine oxidase B	Homo sapiens	109-114
30396116-7	2019	Genkwanin (4) was also observed to strongly inhibit hMAO-A and hMAO-B (IC50 = 0.14 and 0.35 microM, respectively), and competitively inhibit hMAO-A and hMAO-B (Ki = 0.097 and 0.12 microM, respectively).	genkwanin	0-9	monoamine oxidase B	Homo sapiens	63-69
30396116-7	2019	Genkwanin (4) was also observed to strongly inhibit hMAO-A and hMAO-B (IC50 = 0.14 and 0.35 microM, respectively), and competitively inhibit hMAO-A and hMAO-B (Ki = 0.097 and 0.12 microM, respectively).	genkwanin	0-9	monoamine oxidase B	Homo sapiens	152-158
30396116-9	2019	Compound 5 interacts with hMAO-A at four possible residues (Asn181, Gln215, Thr336, and Tyr444), while hMAO-B forms a single hydrogen bond at Glu84.	Hydrogen	125-133	monoamine oxidase B	Homo sapiens	103-109
30689042-1	2019	Rasagiline is a monoamine oxidase B inhibitor with demonstrated efficacy and safety in patients with Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	16-35
30813423-0	2019	Selective Inhibition of Human Monoamine Oxidase B by Acacetin 7-Methyl Ether Isolated from Turnera diffusa (Damiana).	acacetin 7-methyl ether	53-76	monoamine oxidase B	Homo sapiens	30-49
30205936-1	2019	BACKGROUND: Rasagiline is a monoamine oxidase type-B inhibitor in development in Japan for Parkinson"s disease (PD).	rasagiline	12-22	monoamine oxidase B	Homo sapiens	28-52
30813423-6	2019	The binding of acacetin 7-methyl ether to MAO-B was reversible and time-independent, as revealed by enzyme-inhibitor complex equilibrium dialysis assays.	acacetin 7-methyl ether	15-38	monoamine oxidase B	Homo sapiens	42-47
30813423-1	2019	The investigation of the constituents that were isolated from Turnera diffusa (damiana) for their inhibitory activities against recombinant human monoamine oxidases (MAO-A and MAO-B) in vitro identified acacetin 7-methyl ether as a potent selective inhibitor of MAO-B (IC50 = 198 nM).	acacetin 7-methyl ether	203-226	monoamine oxidase B	Homo sapiens	176-181
30813423-1	2019	The investigation of the constituents that were isolated from Turnera diffusa (damiana) for their inhibitory activities against recombinant human monoamine oxidases (MAO-A and MAO-B) in vitro identified acacetin 7-methyl ether as a potent selective inhibitor of MAO-B (IC50 = 198 nM).	acacetin 7-methyl ether	203-226	monoamine oxidase B	Homo sapiens	262-267
30813423-3	2019	Acacetin 7-methyl ether was four-fold less potent as an inhibitor of MAO-B when compared to acacetin (IC50 = 50 nM).	acacetin 7-methyl ether	0-23	monoamine oxidase B	Homo sapiens	69-74
30813423-4	2019	However, acacetin 7-methyl ether was >500-fold selective against MAO-B over MAO-A as compared to only two-fold selectivity shown by acacetin.	acacetin 7-methyl ether	9-32	monoamine oxidase B	Homo sapiens	65-70
30813423-4	2019	However, acacetin 7-methyl ether was >500-fold selective against MAO-B over MAO-A as compared to only two-fold selectivity shown by acacetin.	acacetin	9-17	monoamine oxidase B	Homo sapiens	65-70
30813423-5	2019	Even though the IC50 for inhibition of MAO-B by acacetin 7-methyl ether was ~four-fold higher than that of the standard drug deprenyl (i.e., SelegilineTM or ZelaparTM, a selective MAO-B inhibitor), acacetin 7-methyl ether"s selectivity for MAO-B over MAO-A inhibition was greater than that of deprenyl (>500- vs. 450-fold).	acacetin 7-methyl ether	48-71	monoamine oxidase B	Homo sapiens	39-44
30813423-5	2019	Even though the IC50 for inhibition of MAO-B by acacetin 7-methyl ether was ~four-fold higher than that of the standard drug deprenyl (i.e., SelegilineTM or ZelaparTM, a selective MAO-B inhibitor), acacetin 7-methyl ether"s selectivity for MAO-B over MAO-A inhibition was greater than that of deprenyl (>500- vs. 450-fold).	acacetin 7-methyl ether	48-71	monoamine oxidase B	Homo sapiens	180-185
30813423-5	2019	Even though the IC50 for inhibition of MAO-B by acacetin 7-methyl ether was ~four-fold higher than that of the standard drug deprenyl (i.e., SelegilineTM or ZelaparTM, a selective MAO-B inhibitor), acacetin 7-methyl ether"s selectivity for MAO-B over MAO-A inhibition was greater than that of deprenyl (>500- vs. 450-fold).	acacetin 7-methyl ether	48-71	monoamine oxidase B	Homo sapiens	180-185
30678358-4	2019	Differently substituted flavonoids have been prepared and investigated as MAO-A and MAO-B inhibitors.	Flavonoids	24-34	monoamine oxidase B	Homo sapiens	84-89
30192007-1	2019	INTRODUCTION: Rasagiline is a monoamine oxidase B (MAO-B) inhibitor with possible neuroprotective effects in patients with amyotrophic lateral sclerosis (ALS).	rasagiline	14-24	monoamine oxidase B	Homo sapiens	30-49
30192007-1	2019	INTRODUCTION: Rasagiline is a monoamine oxidase B (MAO-B) inhibitor with possible neuroprotective effects in patients with amyotrophic lateral sclerosis (ALS).	rasagiline	14-24	monoamine oxidase B	Homo sapiens	51-56
30522087-0	2019	(Pyrrolo-pyridin-5-yl)benzamides: BBB permeable monoamine oxidase B inhibitors with neuroprotective effect on cortical neurons.	(pyrrolo-pyridin-5-yl)benzamides	0-32	monoamine oxidase B	Homo sapiens	48-67
30809547-5	2019	Kynuramine metabolism by human recombinant MAO-A and MAO-B leads to formation of 4-hydroxyquinoline, with Vmax values of 10.2+-0.2 and 7.35+-0.69 nmol/mg/min, respectively, and Km values of 23.1+-0.8 muM and 18.0+-2.3 muM, respectively.	Kynuramine	0-10	monoamine oxidase B	Homo sapiens	53-58
30809547-5	2019	Kynuramine metabolism by human recombinant MAO-A and MAO-B leads to formation of 4-hydroxyquinoline, with Vmax values of 10.2+-0.2 and 7.35+-0.69 nmol/mg/min, respectively, and Km values of 23.1+-0.8 muM and 18.0+-2.3 muM, respectively.	4-hydroxyquinoline	81-99	monoamine oxidase B	Homo sapiens	53-58
30809547-10	2019	Pterostilbene was selective for MAO-B, with IC50 of 0.138+-0.013 muM and selectivity index of 0.0103.	pterostilbene	0-13	monoamine oxidase B	Homo sapiens	32-37
30809547-11	2019	The inhibition of resveratrol (MAO-A) and pterostilbene (MAO-B) was consistent with competitive time-independent mechanisms.	Resveratrol	18-29	monoamine oxidase B	Homo sapiens	57-62
30809547-11	2019	The inhibition of resveratrol (MAO-A) and pterostilbene (MAO-B) was consistent with competitive time-independent mechanisms.	pterostilbene	42-55	monoamine oxidase B	Homo sapiens	57-62
30522087-1	2019	An extensive study was performed to develop a series of (pyrrolo-pyridin-5-yl)benzamides as reversible MAO-B inhibitors.	(pyrrolo-pyridin-5-yl)benzamides	56-88	monoamine oxidase B	Homo sapiens	103-108
30522087-4	2019	The reversible MAO-B inhibitor 14 (NTZ-2020) exhibits a neuroprotective effect on cortical neuron survival and induces neurite network outgrowth.	ntz-2020	35-43	monoamine oxidase B	Homo sapiens	15-20
30366255-0	2019	Investigating alkyl nitrates as nitric oxide releasing precursors of multitarget acetylcholinesterase-monoamine oxidase B inhibitors.	alkyl nitrates	14-28	monoamine oxidase B	Homo sapiens	102-121
31258092-2	2019	To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine.	Levodopa	27-33	monoamine oxidase B	Homo sapiens	128-153
31258092-2	2019	To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine.	Levodopa	180-186	monoamine oxidase B	Homo sapiens	128-153
31258092-2	2019	To enhance the efficacy of L-dopa, it is often combined with inhibitors of the enzymes, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) B, key metabolic enzymes of L-dopa and dopamine.	Dopamine	191-199	monoamine oxidase B	Homo sapiens	128-153
31550216-0	2019	Ethyl Acetohydroxamate Incorporated Chalcones: Unveiling a Novel Class of Chalcones for Multitarget Monoamine Oxidase-B Inhibitors Against Alzheimer"s Disease.	ethyl acetate	0-22	monoamine oxidase B	Homo sapiens	100-119
31550216-0	2019	Ethyl Acetohydroxamate Incorporated Chalcones: Unveiling a Novel Class of Chalcones for Multitarget Monoamine Oxidase-B Inhibitors Against Alzheimer"s Disease.	Chalcones	36-45	monoamine oxidase B	Homo sapiens	100-119
31550216-0	2019	Ethyl Acetohydroxamate Incorporated Chalcones: Unveiling a Novel Class of Chalcones for Multitarget Monoamine Oxidase-B Inhibitors Against Alzheimer"s Disease.	Chalcones	74-83	monoamine oxidase B	Homo sapiens	100-119
31550216-1	2019	BACKGROUND: Chalcones are considered as the selective scaffold for the inhibition of MAO-B.	Chalcones	12-21	monoamine oxidase B	Homo sapiens	85-90
31550216-8	2019	Among the substitutentin ring Aof ethyl acetohydroxamate-chalcones (L1-L9), F atom at pposition (L3) showed highest inhibitory effect against hMAO-B.	Chalcones	34-66	monoamine oxidase B	Homo sapiens	142-148
31550216-11	2019	Inhibitions of hMAO-B by L3 or L4 were recovered to the level of the reversible reference (lazabemide), and were competitive with Ki values of 0.0030 +- 0.0002 and 0.0046 +- 0.0005 muM, respectively.	lazabemide	91-101	monoamine oxidase B	Homo sapiens	15-21
30160213-4	2019	Selegiline and rasagiline are irreversible inhibitors forming a covalent bond within the active site of MAOB.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	104-108
30160213-4	2019	Selegiline and rasagiline are irreversible inhibitors forming a covalent bond within the active site of MAOB.	rasagiline	15-25	monoamine oxidase B	Homo sapiens	104-108
30160213-5	2019	In contrast, safinamide is a reversible MAOB inhibitor, and also inhibits voltage- sensitive sodium channels and glutamate release.	safinamide	13-23	monoamine oxidase B	Homo sapiens	40-44
30160213-6	2019	Safinamide is the prototype of a new generation of multi-active MAOB inhibitors, which includes the antiepileptic drug, zonisamide.	safinamide	0-10	monoamine oxidase B	Homo sapiens	64-68
30160213-6	2019	Safinamide is the prototype of a new generation of multi-active MAOB inhibitors, which includes the antiepileptic drug, zonisamide.	Zonisamide	120-130	monoamine oxidase B	Homo sapiens	64-68
30160213-7	2019	Inhibition of MAOB-mediated dopamine metabolism largely accounts for the antiparkinsonian effect of the three drugs.	Dopamine	28-36	monoamine oxidase B	Homo sapiens	14-18
30160213-8	2019	Dopamine metabolism by MAOB generates reactive oxygen species, which contribute to nigro-striatal degeneration.	Dopamine	0-8	monoamine oxidase B	Homo sapiens	23-27
30160213-8	2019	Dopamine metabolism by MAOB generates reactive oxygen species, which contribute to nigro-striatal degeneration.	Oxygen	47-53	monoamine oxidase B	Homo sapiens	23-27
30160213-9	2019	Among all antiparkinsonian agents, MAOB inhibitors are those with the greatest neuroprotective potential because of inhibition of dopamine metabolism, induction of neurotrophic factors, and, in the case of safinamide, inhibition of glutamate release.	Dopamine	130-138	monoamine oxidase B	Homo sapiens	35-39
30160213-9	2019	Among all antiparkinsonian agents, MAOB inhibitors are those with the greatest neuroprotective potential because of inhibition of dopamine metabolism, induction of neurotrophic factors, and, in the case of safinamide, inhibition of glutamate release.	safinamide	206-216	monoamine oxidase B	Homo sapiens	35-39
30160213-9	2019	Among all antiparkinsonian agents, MAOB inhibitors are those with the greatest neuroprotective potential because of inhibition of dopamine metabolism, induction of neurotrophic factors, and, in the case of safinamide, inhibition of glutamate release.	Glutamic Acid	232-241	monoamine oxidase B	Homo sapiens	35-39
30455149-3	2019	Among the 2-imidazolines, good potency inhibitors were discovered with compound 9p (IC50 = 0.012 microM) being the most potent MAO-B inhibitor, while compound 9d (IC50 = 0.751 microM) was the most potent MAO-A inhibitor of the series.	Imidazolines	11-24	monoamine oxidase B	Homo sapiens	127-132
30451121-2	2019	METHODS: The ChE inhibitory ability of some halogenated thiophene chalcone-based molecules known to be selective hMAO-B inhibitors was evaluated.	thiophene chalcone	56-74	monoamine oxidase B	Homo sapiens	113-119
30366255-4	2019	Nitrate 14 proved to be a brain permeant, potent AChE-MAO B inhibitor by itself.	nitrate 14	0-10	monoamine oxidase B	Homo sapiens	54-59
30366255-0	2019	Investigating alkyl nitrates as nitric oxide releasing precursors of multitarget acetylcholinesterase-monoamine oxidase B inhibitors.	Nitric Oxide	32-44	monoamine oxidase B	Homo sapiens	102-121
30366255-1	2019	Herein we envisaged the possibility of exploiting alkyl nitrates as precursors of alcohol-bearing dual inhibitors targeting acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), key enzymes in neurodegenerative syndromes such as Alzheimer"s disease (AD), through biotransformation unmasking an alcoholic function upon nitric oxide (NO) release.	alkyl nitrates	50-64	monoamine oxidase B	Homo sapiens	156-175
30366255-1	2019	Herein we envisaged the possibility of exploiting alkyl nitrates as precursors of alcohol-bearing dual inhibitors targeting acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), key enzymes in neurodegenerative syndromes such as Alzheimer"s disease (AD), through biotransformation unmasking an alcoholic function upon nitric oxide (NO) release.	alkyl nitrates	50-64	monoamine oxidase B	Homo sapiens	177-182
30366255-1	2019	Herein we envisaged the possibility of exploiting alkyl nitrates as precursors of alcohol-bearing dual inhibitors targeting acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), key enzymes in neurodegenerative syndromes such as Alzheimer"s disease (AD), through biotransformation unmasking an alcoholic function upon nitric oxide (NO) release.	Alcohols	82-89	monoamine oxidase B	Homo sapiens	156-175
30366255-1	2019	Herein we envisaged the possibility of exploiting alkyl nitrates as precursors of alcohol-bearing dual inhibitors targeting acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), key enzymes in neurodegenerative syndromes such as Alzheimer"s disease (AD), through biotransformation unmasking an alcoholic function upon nitric oxide (NO) release.	Alcohols	82-89	monoamine oxidase B	Homo sapiens	177-182
30366255-1	2019	Herein we envisaged the possibility of exploiting alkyl nitrates as precursors of alcohol-bearing dual inhibitors targeting acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), key enzymes in neurodegenerative syndromes such as Alzheimer"s disease (AD), through biotransformation unmasking an alcoholic function upon nitric oxide (NO) release.	Nitric Oxide	325-337	monoamine oxidase B	Homo sapiens	156-175
30366255-1	2019	Herein we envisaged the possibility of exploiting alkyl nitrates as precursors of alcohol-bearing dual inhibitors targeting acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), key enzymes in neurodegenerative syndromes such as Alzheimer"s disease (AD), through biotransformation unmasking an alcoholic function upon nitric oxide (NO) release.	Nitric Oxide	325-337	monoamine oxidase B	Homo sapiens	177-182
31795034-0	2019	Rasagiline, a monoamine oxidase B inhibitor, reduces in vivo [18F]THK5351 uptake in progressive supranuclear palsy.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	14-33
31795034-0	2019	Rasagiline, a monoamine oxidase B inhibitor, reduces in vivo [18F]THK5351 uptake in progressive supranuclear palsy.	THK5351	66-73	monoamine oxidase B	Homo sapiens	14-33
31795034-2	2019	However, the interpretation of [18F]THK5351 uptake has been shown to be confounded by high monoamine oxidase B (MAO-B) availability across the brain in AD.	THK5351	36-43	monoamine oxidase B	Homo sapiens	91-110
31795034-2	2019	However, the interpretation of [18F]THK5351 uptake has been shown to be confounded by high monoamine oxidase B (MAO-B) availability across the brain in AD.	THK5351	36-43	monoamine oxidase B	Homo sapiens	112-117
31795034-3	2019	OBJECTIVES: To test the hypothesis that the MAO-B inhibitor, rasagiline reduces [18F]THK5351 uptake in PSP.	rasagiline	61-71	monoamine oxidase B	Homo sapiens	44-49
31795034-9	2019	CONCLUSIONS: Similar to AD, the interpretation of [18F]THK5351 uptake in PSP is likely confounded by off-target binding to MAO-B binding sites.	THK5351	55-62	monoamine oxidase B	Homo sapiens	123-128
30279044-3	2018	Among the quinazolinone derivatives investigated, seven compounds (IC50 < 1 microM) proved to be potent and specific MAO-B inhibitors, with the most potent inhibitor, 2-[(3-iodobenzyl)thio]quinazolin-4(3H)-one, exhibiting an IC50 value of 0.142 muM.	Quinazolinones	10-23	monoamine oxidase B	Homo sapiens	117-122
30618616-4	2018	With the experimental rate constant of 0.147 s-1, the dopamine autoxidation reaction is comparably as fast as the monoamine oxidase B catalyzed dopamine decomposition with a rate constant of 1 s-1.	Dopamine	54-62	monoamine oxidase B	Homo sapiens	114-133
30618616-4	2018	With the experimental rate constant of 0.147 s-1, the dopamine autoxidation reaction is comparably as fast as the monoamine oxidase B catalyzed dopamine decomposition with a rate constant of 1 s-1.	Dopamine	144-152	monoamine oxidase B	Homo sapiens	114-133
29098902-5	2018	Docking studies revealed that these compounds were well-accommodated within MAO-B and ChE active sites through stable hydrogen bonding and/or hydrophobic interactions.	Hydrogen	118-126	monoamine oxidase B	Homo sapiens	76-81
29098902-6	2018	This study revealed the requirement of small heteroaryl ring at amino terminal of semicarbazone template for preferential inhibition and selectivity towards MAO-B.	Semicarbazones	82-95	monoamine oxidase B	Homo sapiens	157-162
30404719-4	2018	Among them, 1-(3-(4-tert-pPentylphenoxy)propyl)pyrrolidine (5) exhibited hMAO B inhibitory activity with an IC50 value of 4.5 nM.	1-(3-(4-tert-ppentylphenoxy)propyl)pyrrolidine	12-58	monoamine oxidase B	Homo sapiens	73-79
30404719-6	2018	Further, recently described potent histamine H3 receptor ligands - 4-tert-pentylphenoxyalkyl derivatives (with a 4-8 carbon spacer) - were evaluated for hMAO B inhibitory activity, and some of them displayed activity in the submicromolar range.	pentylphenoxyalkyl	74-92	monoamine oxidase B	Homo sapiens	153-159
30534374-1	2018	Background: Rasagiline is a monoamine oxidase-B inhibitor used for Parkinson"s disease (PD) treatment, but its effectiveness on Chinese patients is unclear.	rasagiline	12-22	monoamine oxidase B	Homo sapiens	28-47
29758567-3	2018	These compounds are related to the 2-benzylidene-1-indanone class of compounds which has previously been shown to inhibit the MAOs, with specificity for the MAO-B isoform.	2-benzylidene-1-indanone	35-59	monoamine oxidase B	Homo sapiens	157-162
29758567-7	2018	The effect of the heteroaromatic substituent on MAO-B inhibition activity, in decreasing order was found to be: cyclohexyl, phenyl&gt;thiophene&gt;pyridine, furane, pyrrole, cyclopentyl.	Thiophenes	134-143	monoamine oxidase B	Homo sapiens	48-53
29758567-7	2018	The effect of the heteroaromatic substituent on MAO-B inhibition activity, in decreasing order was found to be: cyclohexyl, phenyl&gt;thiophene&gt;pyridine, furane, pyrrole, cyclopentyl.	pyridine	147-155	monoamine oxidase B	Homo sapiens	48-53
29758567-7	2018	The effect of the heteroaromatic substituent on MAO-B inhibition activity, in decreasing order was found to be: cyclohexyl, phenyl&gt;thiophene&gt;pyridine, furane, pyrrole, cyclopentyl.	furan	157-163	monoamine oxidase B	Homo sapiens	48-53
29758567-7	2018	The effect of the heteroaromatic substituent on MAO-B inhibition activity, in decreasing order was found to be: cyclohexyl, phenyl&gt;thiophene&gt;pyridine, furane, pyrrole, cyclopentyl.	Pyrroles	165-172	monoamine oxidase B	Homo sapiens	48-53
29758567-8	2018	This study concludes that, although some 2-heteroarylidene-1-tetralone derivatives are good potency MAO inhibitors, in general their inhibition potencies, particularly for MAO-B, are lower than structurally related chalcones and 1-indanone derivatives that were previously studied.	2-heteroarylidene-1-tetralone	41-70	monoamine oxidase B	Homo sapiens	172-177
30272370-6	2018	L-deprenyl is known to target monoamine oxidase-B (MAO-B) on the outer membrane of mitochondria, therefore, the activity of MAO-A and -B was measured based on the fluorometric detection of H2O2 produced by the enzyme reaction.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	30-49
30272370-6	2018	L-deprenyl is known to target monoamine oxidase-B (MAO-B) on the outer membrane of mitochondria, therefore, the activity of MAO-A and -B was measured based on the fluorometric detection of H2O2 produced by the enzyme reaction.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	51-56
30279044-3	2018	Among the quinazolinone derivatives investigated, seven compounds (IC50 < 1 microM) proved to be potent and specific MAO-B inhibitors, with the most potent inhibitor, 2-[(3-iodobenzyl)thio]quinazolin-4(3H)-one, exhibiting an IC50 value of 0.142 muM.	2-[(3-iodobenzyl)thio]quinazolin-4(3h)-	167-206	monoamine oxidase B	Homo sapiens	117-122
30279044-6	2018	Analysis of the structure-activity relationships (SARs) for MAO-B inhibition shows that substitution on the C2 position of quinazolinone with a benzylthio moiety bearing a Cl, Br or I on the meta position yields the most potent inhibitors of the series.	Quinazolinones	123-136	monoamine oxidase B	Homo sapiens	60-65
30279044-6	2018	Analysis of the structure-activity relationships (SARs) for MAO-B inhibition shows that substitution on the C2 position of quinazolinone with a benzylthio moiety bearing a Cl, Br or I on the meta position yields the most potent inhibitors of the series.	benzylthio	144-154	monoamine oxidase B	Homo sapiens	60-65
30279044-6	2018	Analysis of the structure-activity relationships (SARs) for MAO-B inhibition shows that substitution on the C2 position of quinazolinone with a benzylthio moiety bearing a Cl, Br or I on the meta position yields the most potent inhibitors of the series.	Bromine	176-178	monoamine oxidase B	Homo sapiens	60-65
30279044-7	2018	In contrast, substitution with the unsubstituted benzylthio moiety (IC50 = 3.03 microM) resulted in significantly weaker inhibition activity towards MAO-B.	benzylthio	49-59	monoamine oxidase B	Homo sapiens	149-154
30279044-8	2018	This study suggests that quinazolinones are promising leads for the development of selective MAO-B inhibitors which may be used for the treatment of neurodegenerative disorders such as Parkinson"s disease.	Quinazolinones	25-39	monoamine oxidase B	Homo sapiens	93-98
30167931-2	2018	Both MAO A and MAO B feature a two-domain topology characterized by the Rossmann fold, interacting with dinucleotide cofactors, which is intimately associated to a substrate-binding domain.	Dinucleoside Phosphates	104-116	monoamine oxidase B	Homo sapiens	15-20
29279995-3	2018	MAO-B produces hydrogen peroxide and plays a vital role in neuronal loss of neurodegenerative disorders, such as Parkinson"s and Alzheimer"s diseases.	Hydrogen Peroxide	15-32	monoamine oxidase B	Homo sapiens	0-5
29279995-7	2018	MAO-B inhibitors selegiline and rasagiline protect neurons via increase expression of anti-apoptotic Bcl-2 and pro-survival neurotrophic factors in human neuroblastoma SH-SY5Y and glioblastoma U118MG cell lines.	Selegiline	17-27	monoamine oxidase B	Homo sapiens	0-5
29279995-7	2018	MAO-B inhibitors selegiline and rasagiline protect neurons via increase expression of anti-apoptotic Bcl-2 and pro-survival neurotrophic factors in human neuroblastoma SH-SY5Y and glioblastoma U118MG cell lines.	rasagiline	32-42	monoamine oxidase B	Homo sapiens	0-5
29279995-8	2018	MAO-A knockdown suppressed the rasagiline-induced gene expression in SH-SY5Y cells, whereas MAO-B silencing enhanced the basal- and selegiline-induced gene expression in U118MG cells.	Selegiline	132-142	monoamine oxidase B	Homo sapiens	92-97
30167931-8	2018	Some structural features are highly conserved in the two isozymes, such as a Tyr-Tyr aromatic sandwich in front of the flavin ring and a Lys residue hydrogen-bonded to the cofactor N5 atom, whereas a pair of gating residues (Phe208/Ile335 in MAO A; Ile199/Tyr326 in MAO B) specifically determines the different substrate and inhibitor properties of the two enzymes.	Hydrogen	149-157	monoamine oxidase B	Homo sapiens	266-271
30242487-2	2018	The monoamine oxidases A and B (MAOA/MAOB) are prime candidates for the investigation into the role of DNA methylation in mental disorders, given their pivotal role in the metabolism of monoamines and as pharmacological targets of potent antidepressant drugs such as tranylcypromine, phenelzine or moclobemide.	monoamines	186-196	monoamine oxidase B	Homo sapiens	37-41
29417334-0	2018	Pharmacological aspects of the neuroprotective effects of irreversible MAO-B inhibitors, selegiline and rasagiline, in Parkinson"s disease.	Selegiline	89-99	monoamine oxidase B	Homo sapiens	71-76
29417334-0	2018	Pharmacological aspects of the neuroprotective effects of irreversible MAO-B inhibitors, selegiline and rasagiline, in Parkinson"s disease.	rasagiline	104-114	monoamine oxidase B	Homo sapiens	71-76
29417334-4	2018	It was revealed early on that selective, even irreversible inhibition of MAO-B is free from the severe side effect of the non-selective MAO inhibitors, the potentiation of tyramine, resulting in the so-called "cheese effect".	Tyramine	172-180	monoamine oxidase B	Homo sapiens	73-78
29417334-5	2018	Since MAO-B is involved mainly in the degradation of dopamine, the inhibitors lack any antidepressant effect; however, they became first-line medications for the therapy of Parkinson"s disease based on their dopamine-sparing activity.	Dopamine	53-61	monoamine oxidase B	Homo sapiens	6-11
29417334-5	2018	Since MAO-B is involved mainly in the degradation of dopamine, the inhibitors lack any antidepressant effect; however, they became first-line medications for the therapy of Parkinson"s disease based on their dopamine-sparing activity.	Dopamine	208-216	monoamine oxidase B	Homo sapiens	6-11
29417334-6	2018	Extensive studies with selegiline indicated its complex pharmacological activity profile with MAO-B-independent mechanisms involved.	Selegiline	23-33	monoamine oxidase B	Homo sapiens	94-99
30242487-2	2018	The monoamine oxidases A and B (MAOA/MAOB) are prime candidates for the investigation into the role of DNA methylation in mental disorders, given their pivotal role in the metabolism of monoamines and as pharmacological targets of potent antidepressant drugs such as tranylcypromine, phenelzine or moclobemide.	Tranylcypromine	267-282	monoamine oxidase B	Homo sapiens	37-41
30242487-2	2018	The monoamine oxidases A and B (MAOA/MAOB) are prime candidates for the investigation into the role of DNA methylation in mental disorders, given their pivotal role in the metabolism of monoamines and as pharmacological targets of potent antidepressant drugs such as tranylcypromine, phenelzine or moclobemide.	Phenelzine	284-294	monoamine oxidase B	Homo sapiens	37-41
30242487-2	2018	The monoamine oxidases A and B (MAOA/MAOB) are prime candidates for the investigation into the role of DNA methylation in mental disorders, given their pivotal role in the metabolism of monoamines and as pharmacological targets of potent antidepressant drugs such as tranylcypromine, phenelzine or moclobemide.	Moclobemide	298-309	monoamine oxidase B	Homo sapiens	37-41
30341696-1	2018	In early 1920s, tyramine oxidase was discovered that metabolized tyramine and in 1933 Blaschko demonstrated that this enzyme also metabolized adrenaline, noradrenaline and dopamine.	Epinephrine	142-152	monoamine oxidase B	Homo sapiens	16-32
30341696-1	2018	In early 1920s, tyramine oxidase was discovered that metabolized tyramine and in 1933 Blaschko demonstrated that this enzyme also metabolized adrenaline, noradrenaline and dopamine.	Norepinephrine	154-167	monoamine oxidase B	Homo sapiens	16-32
30341696-1	2018	In early 1920s, tyramine oxidase was discovered that metabolized tyramine and in 1933 Blaschko demonstrated that this enzyme also metabolized adrenaline, noradrenaline and dopamine.	Dopamine	172-180	monoamine oxidase B	Homo sapiens	16-32
30341696-6	2018	Selective inhibitors of MAO-B (selegiline, rasagiline and safinamide) have found a therapeutic role in the treatment of Parkinson"s disease and reversible inhibitors of MAO-A offered antidepressant activity without the serious side effects of the earlier nonselective MAO inhibitors.	Selegiline	31-41	monoamine oxidase B	Homo sapiens	24-29
30341696-6	2018	Selective inhibitors of MAO-B (selegiline, rasagiline and safinamide) have found a therapeutic role in the treatment of Parkinson"s disease and reversible inhibitors of MAO-A offered antidepressant activity without the serious side effects of the earlier nonselective MAO inhibitors.	rasagiline	43-53	monoamine oxidase B	Homo sapiens	24-29
30341696-6	2018	Selective inhibitors of MAO-B (selegiline, rasagiline and safinamide) have found a therapeutic role in the treatment of Parkinson"s disease and reversible inhibitors of MAO-A offered antidepressant activity without the serious side effects of the earlier nonselective MAO inhibitors.	safinamide	58-68	monoamine oxidase B	Homo sapiens	24-29
29956417-11	2018	Long-term administration of rasagiline can increase colonic DA thereby inhibiting colonic motility, suggesting that colonic MAO-B could be a potential drug target for colonic dysmotility.	rasagiline	28-38	monoamine oxidase B	Homo sapiens	124-129
29417334-8	2018	The second MAO-B inhibitor approved for the treatment of Parkinson"s disease, rasagiline also possesses this structural element and shows similar pharmacological characteristics.	rasagiline	78-88	monoamine oxidase B	Homo sapiens	11-16
29569037-1	2018	This invited narrative review emphasizes the role of MAO-B inhibition in the drug portfolio for dopamine substitution in patients with Parkinson"s disease.	Dopamine	96-104	monoamine oxidase B	Homo sapiens	53-58
29569037-2	2018	Neuronal and glial MAO-B inhibition contributes to more stable levels of dopamine and other biogenic amines in the synaptic cleft.	Dopamine	73-81	monoamine oxidase B	Homo sapiens	19-24
29569037-2	2018	Neuronal and glial MAO-B inhibition contributes to more stable levels of dopamine and other biogenic amines in the synaptic cleft.	Amines	101-107	monoamine oxidase B	Homo sapiens	19-24
29569037-3	2018	Accordingly, symptomatic effects of MAO-B inhibition for a limited amelioration of impaired motor behaviour and wearing-off phenomena in patients with Parkinson"s disease are well proven, even when MAO-B inhibitors are only applied together with dopamine agonists.	Dopamine	246-254	monoamine oxidase B	Homo sapiens	36-41
29569037-9	2018	Treatment with MAO-B inhibitors is advantageous as it enables sparing of dopamine agonist and levodopa dosing.	Dopamine	73-81	monoamine oxidase B	Homo sapiens	15-20
29569037-9	2018	Treatment with MAO-B inhibitors is advantageous as it enables sparing of dopamine agonist and levodopa dosing.	Levodopa	94-102	monoamine oxidase B	Homo sapiens	15-20
29956417-11	2018	Long-term administration of rasagiline can increase colonic DA thereby inhibiting colonic motility, suggesting that colonic MAO-B could be a potential drug target for colonic dysmotility.	Dopamine	60-62	monoamine oxidase B	Homo sapiens	124-129
30142650-1	2018	AIM: Safinamide (Xadago ) is a newly approved selective MAO-B inhibitor for the treatment of Parkinson"s Disease (PD).	safinamide	5-15	monoamine oxidase B	Homo sapiens	56-61
30142650-1	2018	AIM: Safinamide (Xadago ) is a newly approved selective MAO-B inhibitor for the treatment of Parkinson"s Disease (PD).	safinamide	17-23	monoamine oxidase B	Homo sapiens	56-61
29532287-0	2018	Meniere"s disease: combined pharmacotherapy with betahistine and the MAO-B inhibitor selegiline-an observational study.	Selegiline	85-95	monoamine oxidase B	Homo sapiens	69-74
29532287-11	2018	CONCLUSIONS: The achievement of the same clinical effect with a significantly lower (about 1/5) dosage of betahistine can be explained by the inhibition of the MAO-B by selegiline leading to higher serum concentrations of betahistine.	Betahistine	106-117	monoamine oxidase B	Homo sapiens	160-165
30004136-4	2018	In our study, we first observed that the SP1 protein level and SP1 binding activity in the MAO B promoter were increased in 1-methyl-4-phenylpyridinium (MPP+ ) neurotoxin-induced SH-SY5Y cells.	1-Methyl-4-phenylpyridinium	124-151	monoamine oxidase B	Homo sapiens	91-96
30004136-4	2018	In our study, we first observed that the SP1 protein level and SP1 binding activity in the MAO B promoter were increased in 1-methyl-4-phenylpyridinium (MPP+ ) neurotoxin-induced SH-SY5Y cells.	mangion-purified polysaccharide (Candida albicans)	153-157	monoamine oxidase B	Homo sapiens	91-96
29532287-11	2018	CONCLUSIONS: The achievement of the same clinical effect with a significantly lower (about 1/5) dosage of betahistine can be explained by the inhibition of the MAO-B by selegiline leading to higher serum concentrations of betahistine.	Selegiline	169-179	monoamine oxidase B	Homo sapiens	160-165
30004136-5	2018	Inhibition of SP1 by pretreatment with SP1 inhibitor mithramycin A (MMA) attenuated the abnormal increase in SP1 binding activity and the MAO B protein level to basal levels.	mithramycin A	53-66	monoamine oxidase B	Homo sapiens	138-143
30004136-5	2018	Inhibition of SP1 by pretreatment with SP1 inhibitor mithramycin A (MMA) attenuated the abnormal increase in SP1 binding activity and the MAO B protein level to basal levels.	mithramycin A	68-71	monoamine oxidase B	Homo sapiens	138-143
30216543-0	2018	Functional monoamine oxidase B gene intron 13 polymorphism predicts putaminal dopamine turnover in de novo Parkinson"s disease.	Dopamine	78-86	monoamine oxidase B	Homo sapiens	11-30
29958841-3	2018	Virodhamine inhibited both MAO-A and -B (IC50 values of 38.70 and 0.71 muM, respectively) with ~55-fold greater inhibition of MAO-B.	virodhamine	0-11	monoamine oxidase B	Homo sapiens	126-131
29958841-4	2018	Two other endocannabinoids (noladin ether and anandamide) also showed good inhibition of MAO-B with IC50 values of 18.18 and 39.98 muM, respectively.	noladin ether	28-41	monoamine oxidase B	Homo sapiens	89-94
29958841-4	2018	Two other endocannabinoids (noladin ether and anandamide) also showed good inhibition of MAO-B with IC50 values of 18.18 and 39.98 muM, respectively.	anandamide	46-56	monoamine oxidase B	Homo sapiens	89-94
29958841-5	2018	Virodhamine was further evaluated for kinetic characteristics and mechanism of inhibition of human MAO-B.	virodhamine	0-11	monoamine oxidase B	Homo sapiens	99-104
29958841-6	2018	Virodhamine inhibited MAO-B (Ki value of 0.258 +- 0.037 muM) through a mixed mechanism/irreversible binding and showed a time-dependent irreversible mechanism.	virodhamine	0-11	monoamine oxidase B	Homo sapiens	22-27
29958841-9	2018	A molecular modeling study of virodhamine with MAO-B and its cofactor flavin adenine dinucleotide (FAD) predicted virodhamine"s terminal -NH2 group to be positioned near the N5 position of FAD, but for docking to MAO-A, virodhamine"s terminal -NH2 group was far away (~6.52 A) from the N5 position of FAD, and encountered bad contacts with nearby water molecules.	virodhamine	30-41	monoamine oxidase B	Homo sapiens	47-52
29958841-9	2018	A molecular modeling study of virodhamine with MAO-B and its cofactor flavin adenine dinucleotide (FAD) predicted virodhamine"s terminal -NH2 group to be positioned near the N5 position of FAD, but for docking to MAO-A, virodhamine"s terminal -NH2 group was far away (~6.52 A) from the N5 position of FAD, and encountered bad contacts with nearby water molecules.	virodhamine	114-125	monoamine oxidase B	Homo sapiens	47-52
29958841-9	2018	A molecular modeling study of virodhamine with MAO-B and its cofactor flavin adenine dinucleotide (FAD) predicted virodhamine"s terminal -NH2 group to be positioned near the N5 position of FAD, but for docking to MAO-A, virodhamine"s terminal -NH2 group was far away (~6.52 A) from the N5 position of FAD, and encountered bad contacts with nearby water molecules.	Flavin-Adenine Dinucleotide	189-192	monoamine oxidase B	Homo sapiens	47-52
29958841-9	2018	A molecular modeling study of virodhamine with MAO-B and its cofactor flavin adenine dinucleotide (FAD) predicted virodhamine"s terminal -NH2 group to be positioned near the N5 position of FAD, but for docking to MAO-A, virodhamine"s terminal -NH2 group was far away (~6.52 A) from the N5 position of FAD, and encountered bad contacts with nearby water molecules.	virodhamine	114-125	monoamine oxidase B	Homo sapiens	47-52
29958841-9	2018	A molecular modeling study of virodhamine with MAO-B and its cofactor flavin adenine dinucleotide (FAD) predicted virodhamine"s terminal -NH2 group to be positioned near the N5 position of FAD, but for docking to MAO-A, virodhamine"s terminal -NH2 group was far away (~6.52 A) from the N5 position of FAD, and encountered bad contacts with nearby water molecules.	Flavin-Adenine Dinucleotide	189-192	monoamine oxidase B	Homo sapiens	47-52
29958841-9	2018	A molecular modeling study of virodhamine with MAO-B and its cofactor flavin adenine dinucleotide (FAD) predicted virodhamine"s terminal -NH2 group to be positioned near the N5 position of FAD, but for docking to MAO-A, virodhamine"s terminal -NH2 group was far away (~6.52 A) from the N5 position of FAD, and encountered bad contacts with nearby water molecules.	Water	347-352	monoamine oxidase B	Homo sapiens	47-52
29958841-10	2018	This difference could explain virodhamine"s higher potency and preference for MAO-B.	virodhamine	30-41	monoamine oxidase B	Homo sapiens	78-83
29958841-11	2018	The binding free energies for the computationally-predicted poses also showed that virodhamine was selective for MAO-B.	virodhamine	83-94	monoamine oxidase B	Homo sapiens	113-118
29847694-10	2018	We also found all MAO-B inhibitors to be efficient when given together with levodopa.	Levodopa	76-84	monoamine oxidase B	Homo sapiens	18-23
29847694-11	2018	When ranking the MAO-B inhibitors given in combination with levodopa, selegiline was the most effective and rasagiline was the second best.	Selegiline	70-80	monoamine oxidase B	Homo sapiens	17-22
29847694-11	2018	When ranking the MAO-B inhibitors given in combination with levodopa, selegiline was the most effective and rasagiline was the second best.	rasagiline	108-118	monoamine oxidase B	Homo sapiens	17-22
29847694-13	2018	Combination therapy with MAO-B inhibitors and levodopa showed that all three MAO-B inhibitors were effective compared to placebo, but selegiline was the most effective drug.	Levodopa	46-54	monoamine oxidase B	Homo sapiens	77-82
29847694-13	2018	Combination therapy with MAO-B inhibitors and levodopa showed that all three MAO-B inhibitors were effective compared to placebo, but selegiline was the most effective drug.	Selegiline	134-144	monoamine oxidase B	Homo sapiens	25-30
29847694-13	2018	Combination therapy with MAO-B inhibitors and levodopa showed that all three MAO-B inhibitors were effective compared to placebo, but selegiline was the most effective drug.	Selegiline	134-144	monoamine oxidase B	Homo sapiens	77-82
29498006-9	2018	However, (-) deprenyl, a monoamine oxidase B (MAO B) inhibitor, attenuated MPTP-induced autophagic response and protected cell death.	Selegiline	13-21	monoamine oxidase B	Homo sapiens	25-44
29498006-9	2018	However, (-) deprenyl, a monoamine oxidase B (MAO B) inhibitor, attenuated MPTP-induced autophagic response and protected cell death.	Selegiline	13-21	monoamine oxidase B	Homo sapiens	46-51
29498006-9	2018	However, (-) deprenyl, a monoamine oxidase B (MAO B) inhibitor, attenuated MPTP-induced autophagic response and protected cell death.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	75-79	monoamine oxidase B	Homo sapiens	25-44
29498006-9	2018	However, (-) deprenyl, a monoamine oxidase B (MAO B) inhibitor, attenuated MPTP-induced autophagic response and protected cell death.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	75-79	monoamine oxidase B	Homo sapiens	46-51
30568755-4	2018	Furthermore, SB11 showed a high selectivity index (SI &gt; 37.0) for MAO-B.	sb11	13-17	monoamine oxidase B	Homo sapiens	69-74
30568755-5	2018	The effects of fluorine orientation revealed that SB11 (m-fluorine) showed 28.2 times higher inhibitory activity than SB12 (o-fluorine) against MAO-B.	sb11	50-54	monoamine oxidase B	Homo sapiens	144-149
30568755-5	2018	The effects of fluorine orientation revealed that SB11 (m-fluorine) showed 28.2 times higher inhibitory activity than SB12 (o-fluorine) against MAO-B.	Fluorine	58-66	monoamine oxidase B	Homo sapiens	144-149
30568755-5	2018	The effects of fluorine orientation revealed that SB11 (m-fluorine) showed 28.2 times higher inhibitory activity than SB12 (o-fluorine) against MAO-B.	zwittergent 3-12	118-122	monoamine oxidase B	Homo sapiens	144-149
30568755-6	2018	Furthermore, inhibitions by SB5 and SB11 against MAO-A and MAO-B, respectively, were recovered to near reference levels in reversibility experiments.	sb11	36-40	monoamine oxidase B	Homo sapiens	59-64
30568755-8	2018	These results indicate that SB5 and SB11 are selective, reversible and competitive inhibitors of MAO-A and MAO-B, respectively.	sb11	36-40	monoamine oxidase B	Homo sapiens	107-112
30143367-1	2018	In the studied a series novel of lazabemide derivatives were designed, synthesized and evaluated as inhibitors of monoamine oxidase (MAO-A or MAO-B).	lazabemide	33-43	monoamine oxidase B	Homo sapiens	142-147
30153955-3	2018	Among the synthesized derivatives, 12a exhibited reversible and potent inhibition (IC50 = 0.41 muM) and high selectivity over the MAO-A and MAO-B.	12a	35-38	monoamine oxidase B	Homo sapiens	140-145
30216543-5	2018	CONCLUSIONS: The MAOB (rs1799836) polymorphism predicts putaminal dopamine turnover in early PD with the MAOBTT allele linked to high enzyme activity leading to higher intrinsic dopamine turnover, which has been demonstrated to constitute a risk factor for motor complications.	Dopamine	66-74	monoamine oxidase B	Homo sapiens	17-21
30216543-5	2018	CONCLUSIONS: The MAOB (rs1799836) polymorphism predicts putaminal dopamine turnover in early PD with the MAOBTT allele linked to high enzyme activity leading to higher intrinsic dopamine turnover, which has been demonstrated to constitute a risk factor for motor complications.	Dopamine	178-186	monoamine oxidase B	Homo sapiens	17-21
30016860-2	2018	To target peripheral tissues using MAO-B inhibitors that do not permeate the blood-brain barrier (BBB) the MAO-B-selective inhibitor deprenyl was remodeled by replacing the terminal acetylene with a CO2H function, and incorporating a para-OCH2Ar motif (compounds 10a-s).	Selegiline	133-141	monoamine oxidase B	Homo sapiens	35-40
30076899-0	2018	Uranium exposure of human dopaminergic cells results in low cytotoxicity, accumulation within sub-cytoplasmic regions, and down regulation of MAO-B.	Uranium	0-7	monoamine oxidase B	Homo sapiens	142-147
30076899-12	2018	The expression of monoamine oxidase B (MAO-B) gene was statistically significantly decreased after exposure to uranium while other dopamine-related genes were not modified.	Uranium	111-118	monoamine oxidase B	Homo sapiens	18-37
30076899-12	2018	The expression of monoamine oxidase B (MAO-B) gene was statistically significantly decreased after exposure to uranium while other dopamine-related genes were not modified.	Uranium	111-118	monoamine oxidase B	Homo sapiens	39-44
30076899-14	2018	This original result suggests that the inhibition of dopamine catabolism, but also of other MAO-B substrates, could constitute selective effects of uranium neurotoxicity.	Uranium	148-155	monoamine oxidase B	Homo sapiens	92-97
30016860-2	2018	To target peripheral tissues using MAO-B inhibitors that do not permeate the blood-brain barrier (BBB) the MAO-B-selective inhibitor deprenyl was remodeled by replacing the terminal acetylene with a CO2H function, and incorporating a para-OCH2Ar motif (compounds 10a-s).	Selegiline	133-141	monoamine oxidase B	Homo sapiens	107-112
30016860-2	2018	To target peripheral tissues using MAO-B inhibitors that do not permeate the blood-brain barrier (BBB) the MAO-B-selective inhibitor deprenyl was remodeled by replacing the terminal acetylene with a CO2H function, and incorporating a para-OCH2Ar motif (compounds 10a-s).	Acetylene	182-191	monoamine oxidase B	Homo sapiens	107-112
30016860-2	2018	To target peripheral tissues using MAO-B inhibitors that do not permeate the blood-brain barrier (BBB) the MAO-B-selective inhibitor deprenyl was remodeled by replacing the terminal acetylene with a CO2H function, and incorporating a para-OCH2Ar motif (compounds 10a-s).	co2h	199-203	monoamine oxidase B	Homo sapiens	107-112
29925480-5	2018	Molecular docking simulations revealed that the binding affinity of chelerythrine for MAO-A (-9.7 kcal/mol) was greater than that for MAO-B (-4.6 kcal/mol).	chelerythrine	68-81	monoamine oxidase B	Homo sapiens	134-139
30018949-5	2018	Surprisingly, the p-nitrophenyl-substituted (1,3-selenazol-2-yl)hydrazone 4 showed MAO B inhibition in a nanomolar concentration range (IC50 = 73 nM).	p-nitrophenyl-substituted (1,3-selenazol-2-yl)hydrazone	18-73	monoamine oxidase B	Homo sapiens	83-88
29671581-1	2018	Monoamine oxidase (MAO) enzymes MAO-A and MAO-B play a critical role in the metabolism of monoamine neurotransmitters.	monoamine	90-99	monoamine oxidase B	Homo sapiens	42-47
29671581-9	2018	The evaluation of docking results and pharmacokinetic profile predictions together with the MD simulations enabled us to identify one hit molecule (ligand 1, Otava ID: 3463218) which displayed higher selectivity toward MAO-B than a positive control selegiline which is a commercially used drug for PD therapeutic purposes.	Selegiline	249-259	monoamine oxidase B	Homo sapiens	219-224
30077198-0	2018	Garcinol, an effective monoamine oxidase-B inhibitor for the treatment of Parkinson"s disease.	garcinol	0-8	monoamine oxidase B	Homo sapiens	23-42
30077198-3	2018	To reduce the daily dosing of L-DOPA in patients, inhibitors of dopamine catabolizing enzymes, particularly monoamine oxidase-B (MAO-B), are prescribed.	Levodopa	30-36	monoamine oxidase B	Homo sapiens	108-127
30077198-3	2018	To reduce the daily dosing of L-DOPA in patients, inhibitors of dopamine catabolizing enzymes, particularly monoamine oxidase-B (MAO-B), are prescribed.	Levodopa	30-36	monoamine oxidase B	Homo sapiens	129-134
30077198-3	2018	To reduce the daily dosing of L-DOPA in patients, inhibitors of dopamine catabolizing enzymes, particularly monoamine oxidase-B (MAO-B), are prescribed.	Dopamine	64-72	monoamine oxidase B	Homo sapiens	108-127
30077198-3	2018	To reduce the daily dosing of L-DOPA in patients, inhibitors of dopamine catabolizing enzymes, particularly monoamine oxidase-B (MAO-B), are prescribed.	Dopamine	64-72	monoamine oxidase B	Homo sapiens	129-134
30077198-4	2018	The most widely used MAO-B inhibitor to maintain the bioavailability of dopamine in the brain of PD patients is L-deprenyl, despite of its potential side-effects.	Dopamine	72-80	monoamine oxidase B	Homo sapiens	21-26
30077198-4	2018	The most widely used MAO-B inhibitor to maintain the bioavailability of dopamine in the brain of PD patients is L-deprenyl, despite of its potential side-effects.	Selegiline	112-122	monoamine oxidase B	Homo sapiens	21-26
30077198-5	2018	The present study identified Garcinol as a potential candidate in the treatment paradigm of PD by virtue of its exorbitant MAO-B inhibitory potential.	garcinol	29-37	monoamine oxidase B	Homo sapiens	123-128
29748109-1	2018	INTRODUCTION: Rasagiline, a selective, irreversible monoamine oxidase-B inhibitor, is in development in Japan as adjunctive therapy to levodopa.	rasagiline	14-24	monoamine oxidase B	Homo sapiens	52-71
29526790-3	2018	A clinical study in PD patients with motor complications has demonstrated that selegiline, a monoamine oxidase type B inhibitor, is effective in reducing off time without worsening dyskinesia, although another study has shown worsening dyskinesia.	Selegiline	79-89	monoamine oxidase B	Homo sapiens	93-117
29578580-0	2018	MAO-B and COMT Genetic Variations Associated With Levodopa Treatment Response in Patients With Parkinson"s Disease.	Levodopa	50-58	monoamine oxidase B	Homo sapiens	0-5
29578580-2	2018	Monoamine oxidase-B (MAO-B) and catechol-o-methyl transferase (COMT) are enzymes involved in the metabolism and regulation of dopamine availability.	Dopamine	126-134	monoamine oxidase B	Homo sapiens	0-19
29578580-2	2018	Monoamine oxidase-B (MAO-B) and catechol-o-methyl transferase (COMT) are enzymes involved in the metabolism and regulation of dopamine availability.	Dopamine	126-134	monoamine oxidase B	Homo sapiens	21-26
29578580-3	2018	In our study we investigated the possible relation among selected single-nucleotide polymorphisms (SNPs) in the MAO-B (rs1799836) and COMT (rs4680) genes and the therapeutic response to levodopa (l-dopa).	Levodopa	186-194	monoamine oxidase B	Homo sapiens	112-117
29578580-3	2018	In our study we investigated the possible relation among selected single-nucleotide polymorphisms (SNPs) in the MAO-B (rs1799836) and COMT (rs4680) genes and the therapeutic response to levodopa (l-dopa).	Levodopa	196-202	monoamine oxidase B	Homo sapiens	112-117
29578580-8	2018	We observed that patients carrying MAO-B (rs1799836) A and AA genotypes and COMT (rs4680) LL genotype suffered more frequently from levodopa-induced-dyskinesia.	Levodopa	132-140	monoamine oxidase B	Homo sapiens	35-40
29578580-9	2018	In addition, we found an increased risk of 2.84-fold for male individuals carrying the MAO-B G allele to be treated with higher doses of levodopa (P = .04).	Levodopa	137-145	monoamine oxidase B	Homo sapiens	87-92
29578580-10	2018	We concluded that before beginning PD pharmacological treatment, it is important to consider the genetic variants of the MAO-B and COMT genes and the sex, reinforcing the evidence that sexual dimorphism in the genes related to dopamine metabolism might affect PD treatment.	Dopamine	227-235	monoamine oxidase B	Homo sapiens	121-126
29998095-3	2018	Substituted benzyl or phenethyl residues were attached to the N8 of the resulting 1,3-dialkyl-tetrahydropyrazino[2,1-f ]purinediones with the aim to obtain multi-target drugs that block human A1 and A2A adenosine receptors (ARs) and monoaminoxidase B (MAO-B).	2-phenylethyl acetate	22-31	monoamine oxidase B	Homo sapiens	233-250
29958546-6	2018	Regional [18F]THK5351 standardized uptake value ratio (SUVR) in antemortem PET was significantly correlated with monoamine oxidase-B (MAO-B) level, reactive astrocytes density, and tau pathology at postmortem examination.	THK5351	14-21	monoamine oxidase B	Homo sapiens	113-132
29958546-6	2018	Regional [18F]THK5351 standardized uptake value ratio (SUVR) in antemortem PET was significantly correlated with monoamine oxidase-B (MAO-B) level, reactive astrocytes density, and tau pathology at postmortem examination.	THK5351	14-21	monoamine oxidase B	Homo sapiens	134-139
29958546-7	2018	In in vitro autoradiography, specific THK5351 binding was detected in the area of antemortem [18F]THK5351 retention, and binding was blocked completely by a reversible selective MAO-B inhibitor, lazabemide, in brain samples from these patients.	THK5351	38-45	monoamine oxidase B	Homo sapiens	178-183
29958546-7	2018	In in vitro autoradiography, specific THK5351 binding was detected in the area of antemortem [18F]THK5351 retention, and binding was blocked completely by a reversible selective MAO-B inhibitor, lazabemide, in brain samples from these patients.	lazabemide	195-205	monoamine oxidase B	Homo sapiens	178-183
29958546-8	2018	In conclusion, [18F]THK5351 PET signals reflect MAO-B expressing reactive astrocytes, which may be associated with tau accumulation in PSP.	THK5351	20-27	monoamine oxidase B	Homo sapiens	48-53
29998095-3	2018	Substituted benzyl or phenethyl residues were attached to the N8 of the resulting 1,3-dialkyl-tetrahydropyrazino[2,1-f ]purinediones with the aim to obtain multi-target drugs that block human A1 and A2A adenosine receptors (ARs) and monoaminoxidase B (MAO-B).	2-phenylethyl acetate	22-31	monoamine oxidase B	Homo sapiens	252-257
29998095-3	2018	Substituted benzyl or phenethyl residues were attached to the N8 of the resulting 1,3-dialkyl-tetrahydropyrazino[2,1-f ]purinediones with the aim to obtain multi-target drugs that block human A1 and A2A adenosine receptors (ARs) and monoaminoxidase B (MAO-B).	1,3-dialkyl-tetrahydropyrazino[2,1-f ]purinediones	82-132	monoamine oxidase B	Homo sapiens	233-250
29998095-3	2018	Substituted benzyl or phenethyl residues were attached to the N8 of the resulting 1,3-dialkyl-tetrahydropyrazino[2,1-f ]purinediones with the aim to obtain multi-target drugs that block human A1 and A2A adenosine receptors (ARs) and monoaminoxidase B (MAO-B).	1,3-dialkyl-tetrahydropyrazino[2,1-f ]purinediones	82-132	monoamine oxidase B	Homo sapiens	252-257
30109004-6	2018	Removal of the chlorine from 2 disrupted the favorable intermolecular interactions and resulted in a selectivity change towards hMAO-B.	Chlorine	15-23	monoamine oxidase B	Homo sapiens	128-134
29844863-0	2018	PAM-OBG: A monoamine oxidase B specific prodrug that inhibits MGMT and generates DNA interstrand crosslinks, potentiating temozolomide and chemoradiation therapy in intracranial glioblastoma.	Temozolomide	122-134	monoamine oxidase B	Homo sapiens	11-30
29888263-9	2018	Tonic inhibition mediated by GABA could also be a promising target and drugs that block the GABA synthesizing enzyme, MAO-B, have shown efficacy.	gamma-Aminobutyric Acid	29-33	monoamine oxidase B	Homo sapiens	118-123
29888263-9	2018	Tonic inhibition mediated by GABA could also be a promising target and drugs that block the GABA synthesizing enzyme, MAO-B, have shown efficacy.	gamma-Aminobutyric Acid	92-96	monoamine oxidase B	Homo sapiens	118-123
29691318-3	2018	We have previously reported that astrocytic GABA, synthesized by monoamine oxidase B (MAOB), mediates tonic inhibition via GABA-permeable bestrophin 1 (Best1) channel in the cerebellum.	gamma-Aminobutyric Acid	44-48	monoamine oxidase B	Homo sapiens	65-84
29691318-3	2018	We have previously reported that astrocytic GABA, synthesized by monoamine oxidase B (MAOB), mediates tonic inhibition via GABA-permeable bestrophin 1 (Best1) channel in the cerebellum.	gamma-Aminobutyric Acid	44-48	monoamine oxidase B	Homo sapiens	86-90
29691318-3	2018	We have previously reported that astrocytic GABA, synthesized by monoamine oxidase B (MAOB), mediates tonic inhibition via GABA-permeable bestrophin 1 (Best1) channel in the cerebellum.	gamma-Aminobutyric Acid	123-127	monoamine oxidase B	Homo sapiens	65-84
29691318-3	2018	We have previously reported that astrocytic GABA, synthesized by monoamine oxidase B (MAOB), mediates tonic inhibition via GABA-permeable bestrophin 1 (Best1) channel in the cerebellum.	gamma-Aminobutyric Acid	123-127	monoamine oxidase B	Homo sapiens	86-90
29691318-5	2018	Here, we report that a reduction of tonic GABA release by genetic removal or pharmacological inhibition of Best1 or MAOB caused an enhanced neuronal excitability in cerebellar granule cells (GCs), synaptic transmission at the parallel fiber-Purkinje cell (PF-PC) synapses, and motor performance on the rotarod test, whereas an augmentation of tonic GABA release by astrocyte-specific overexpression of MAOB resulted in a reduced neuronal excitability, synaptic transmission, and motor performance.	gamma-Aminobutyric Acid	42-46	monoamine oxidase B	Homo sapiens	116-120
29691318-5	2018	Here, we report that a reduction of tonic GABA release by genetic removal or pharmacological inhibition of Best1 or MAOB caused an enhanced neuronal excitability in cerebellar granule cells (GCs), synaptic transmission at the parallel fiber-Purkinje cell (PF-PC) synapses, and motor performance on the rotarod test, whereas an augmentation of tonic GABA release by astrocyte-specific overexpression of MAOB resulted in a reduced neuronal excitability, synaptic transmission, and motor performance.	gamma-Aminobutyric Acid	42-46	monoamine oxidase B	Homo sapiens	402-406
29691318-5	2018	Here, we report that a reduction of tonic GABA release by genetic removal or pharmacological inhibition of Best1 or MAOB caused an enhanced neuronal excitability in cerebellar granule cells (GCs), synaptic transmission at the parallel fiber-Purkinje cell (PF-PC) synapses, and motor performance on the rotarod test, whereas an augmentation of tonic GABA release by astrocyte-specific overexpression of MAOB resulted in a reduced neuronal excitability, synaptic transmission, and motor performance.	gamma-Aminobutyric Acid	349-353	monoamine oxidase B	Homo sapiens	116-120
29691318-6	2018	The bidirectional modulation of astrocytic GABA by genetic alteration of Best1 or MAOB was confirmed by immunostaining and in vivo microdialysis.	gamma-Aminobutyric Acid	43-47	monoamine oxidase B	Homo sapiens	82-86
29477356-2	2018	The objective of this study was to investigate anodal co-iontophoresis of pramipexole (PRAM; dopamine agonist) and rasagiline (RAS; MAO-B inhibitor) in vitro and in vivo.	rasagiline	127-130	monoamine oxidase B	Homo sapiens	132-137
29127552-4	2018	Here, we retrospectively investigated if MAO-B inhibitors in clinical doses affect flortaucipir binding.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	83-95	monoamine oxidase B	Homo sapiens	41-46
29648817-0	2018	Tight-Binding Inhibition of Human Monoamine Oxidase B by Chromone Analogs: A Kinetic, Crystallographic, and Biological Analysis.	Chromones	57-65	monoamine oxidase B	Homo sapiens	34-53
29648817-2	2018	Chromone derivatives were identified as novel potent and reversible MAO-B inhibitors, and herewith we report on a crystallographic and biochemical analysis to investigate their inhibition mechanism.	Chromones	0-8	monoamine oxidase B	Homo sapiens	68-73
29648817-3	2018	The crystal structures of human MAO-B in complex with three chromone analogs bearing different substituents on the exocyclic aromatic ring (determined at 1.6-1.8 A resolution) showed that they all bind in the active site cavity of the protein with the chromone moiety located in front of the FAD cofactor.	Chromones	60-68	monoamine oxidase B	Homo sapiens	32-37
29648817-3	2018	The crystal structures of human MAO-B in complex with three chromone analogs bearing different substituents on the exocyclic aromatic ring (determined at 1.6-1.8 A resolution) showed that they all bind in the active site cavity of the protein with the chromone moiety located in front of the FAD cofactor.	Chromones	252-260	monoamine oxidase B	Homo sapiens	32-37
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	Acrolein	223-231	monoamine oxidase B	Homo sapiens	78-82
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	Acrolein	223-231	monoamine oxidase B	Homo sapiens	139-143
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	O(6)-benzylguanine	168-184	monoamine oxidase B	Homo sapiens	57-76
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	O(6)-benzylguanine	168-184	monoamine oxidase B	Homo sapiens	78-82
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	O(6)-benzylguanine	168-184	monoamine oxidase B	Homo sapiens	139-143
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	O(6)-benzylguanine	186-190	monoamine oxidase B	Homo sapiens	57-76
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	O(6)-benzylguanine	186-190	monoamine oxidase B	Homo sapiens	78-82
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	O(6)-benzylguanine	186-190	monoamine oxidase B	Homo sapiens	139-143
29844863-3	2018	We have designed and tested both in vitro and in vivo, a monoamine oxidase B (MAOB) specific prodrug, PAM-OBG, that is converted by glioma MAOB into the MGMT inhibitor O6-benzylguanine (O6BG) and the DNA crosslinking agent acrolein.	Acrolein	223-231	monoamine oxidase B	Homo sapiens	57-76
29760163-1	2018	Safinamide (Xadago - Zambon S.p.A) is a monoamine-oxidase B (MAO-B) inhibitor licensed as add-on therapy for people with idiopathic Parkinson"s disease who are experiencing motor fluctuations with levodopa.1 Currently there is no cure for Parkinson"s disease and drugs are used to reduce motor symptoms and improve daily activities.2,3 Here, we review the evidence for this MAO-B inhibitor.	safinamide	0-10	monoamine oxidase B	Homo sapiens	40-59
29955193-7	2018	Data Synthesis: The search identified 8 studies evaluating the potential interaction between SSRIs and the MAO-B inhibitors selegiline and rasagiline.	Selegiline	124-134	monoamine oxidase B	Homo sapiens	107-112
29955193-7	2018	Data Synthesis: The search identified 8 studies evaluating the potential interaction between SSRIs and the MAO-B inhibitors selegiline and rasagiline.	rasagiline	139-149	monoamine oxidase B	Homo sapiens	107-112
29760163-1	2018	Safinamide (Xadago - Zambon S.p.A) is a monoamine-oxidase B (MAO-B) inhibitor licensed as add-on therapy for people with idiopathic Parkinson"s disease who are experiencing motor fluctuations with levodopa.1 Currently there is no cure for Parkinson"s disease and drugs are used to reduce motor symptoms and improve daily activities.2,3 Here, we review the evidence for this MAO-B inhibitor.	safinamide	0-10	monoamine oxidase B	Homo sapiens	61-66
29760163-1	2018	Safinamide (Xadago - Zambon S.p.A) is a monoamine-oxidase B (MAO-B) inhibitor licensed as add-on therapy for people with idiopathic Parkinson"s disease who are experiencing motor fluctuations with levodopa.1 Currently there is no cure for Parkinson"s disease and drugs are used to reduce motor symptoms and improve daily activities.2,3 Here, we review the evidence for this MAO-B inhibitor.	safinamide	0-10	monoamine oxidase B	Homo sapiens	374-379
29760163-1	2018	Safinamide (Xadago - Zambon S.p.A) is a monoamine-oxidase B (MAO-B) inhibitor licensed as add-on therapy for people with idiopathic Parkinson"s disease who are experiencing motor fluctuations with levodopa.1 Currently there is no cure for Parkinson"s disease and drugs are used to reduce motor symptoms and improve daily activities.2,3 Here, we review the evidence for this MAO-B inhibitor.	xadago - zambon s	12-29	monoamine oxidase B	Homo sapiens	40-59
29760163-1	2018	Safinamide (Xadago - Zambon S.p.A) is a monoamine-oxidase B (MAO-B) inhibitor licensed as add-on therapy for people with idiopathic Parkinson"s disease who are experiencing motor fluctuations with levodopa.1 Currently there is no cure for Parkinson"s disease and drugs are used to reduce motor symptoms and improve daily activities.2,3 Here, we review the evidence for this MAO-B inhibitor.	xadago - zambon s	12-29	monoamine oxidase B	Homo sapiens	61-66
28460566-0	2018	Recognition dynamics of dopamine to human Monoamine oxidase B: role of Leu171/Gln206 and conserved water molecules in the active site cavity.	Dopamine	24-32	monoamine oxidase B	Homo sapiens	42-61
28460566-0	2018	Recognition dynamics of dopamine to human Monoamine oxidase B: role of Leu171/Gln206 and conserved water molecules in the active site cavity.	Water	99-104	monoamine oxidase B	Homo sapiens	42-61
28460566-2	2018	Extensive MD simulation studies of dopamine-docked hMAO B structures have revealed the stabilization of amino-terminal of the substrate by a direct and water-mediated interaction of catalytic tyrosines, Gln206, and Leu171 residues.	Dopamine	35-43	monoamine oxidase B	Homo sapiens	51-57
28460566-2	2018	Extensive MD simulation studies of dopamine-docked hMAO B structures have revealed the stabilization of amino-terminal of the substrate by a direct and water-mediated interaction of catalytic tyrosines, Gln206, and Leu171 residues.	Water	152-157	monoamine oxidase B	Homo sapiens	51-57
28460566-2	2018	Extensive MD simulation studies of dopamine-docked hMAO B structures have revealed the stabilization of amino-terminal of the substrate by a direct and water-mediated interaction of catalytic tyrosines, Gln206, and Leu171 residues.	Tyrosine	192-201	monoamine oxidase B	Homo sapiens	51-57
28460566-8	2018	The topology of conserved water molecular sites along with the hydration dynamics of catalytic residues, FAD, and dopamine has added a new feature on the substrate binding chemistry in hMAO B which may be useful for substrate analog inhibitor design.	Water	26-31	monoamine oxidase B	Homo sapiens	185-191
28460566-8	2018	The topology of conserved water molecular sites along with the hydration dynamics of catalytic residues, FAD, and dopamine has added a new feature on the substrate binding chemistry in hMAO B which may be useful for substrate analog inhibitor design.	Flavin-Adenine Dinucleotide	105-108	monoamine oxidase B	Homo sapiens	185-191
28460566-8	2018	The topology of conserved water molecular sites along with the hydration dynamics of catalytic residues, FAD, and dopamine has added a new feature on the substrate binding chemistry in hMAO B which may be useful for substrate analog inhibitor design.	Dopamine	114-122	monoamine oxidase B	Homo sapiens	185-191
29534334-9	2018	Thus, propargyl-substituted pyrimidine derivatives can be promising leads in the development of potent, selective and reversible MAO-B inhibitors for the treatment of Parkinson"s disease.	propargyl-substituted pyrimidine	6-38	monoamine oxidase B	Homo sapiens	129-134
28864633-4	2018	Results: Regional in vivo 18F-THK5351 retention was significantly correlated with the density of tau aggregates in the neocortex and monoamine oxidase-B in the whole brain, but not correlated with that of insoluble amyloid-beta.	THK5351	30-37	monoamine oxidase B	Homo sapiens	133-152
29421700-2	2018	In the present study, two series of 4-substituted phenylpiperazine and 1-benzhydrylpiperazine (1-21) derivatives were synthesized and screened for their MAO-A and MAO-B inhibitory activity using Amplex Red assay.	4-substituted phenylpiperazine	36-66	monoamine oxidase B	Homo sapiens	163-168
29421700-2	2018	In the present study, two series of 4-substituted phenylpiperazine and 1-benzhydrylpiperazine (1-21) derivatives were synthesized and screened for their MAO-A and MAO-B inhibitory activity using Amplex Red assay.	norcyclizine	71-93	monoamine oxidase B	Homo sapiens	163-168
29542008-2	2018	Safinamide has a multimodal mechanism of action, dopaminergic (reversible MAO-B inhibition) and non-dopaminergic (modulation of the abnormal glutamate release), that might be beneficial for both motor and non-motor symptoms.	safinamide	0-10	monoamine oxidase B	Homo sapiens	74-79
29448189-0	2018	3-(E)-Styryl-2H-chromene derivatives as potent and selective monoamine oxidase B inhibitors.	3-(e)-styryl-2h-chromene	0-24	monoamine oxidase B	Homo sapiens	61-80
29448189-5	2018	QSAR analyses of 3-(E)-styryl-2H-chromene derivatives with pIC50 values for MAO-B demonstrated that 140 descriptors showed significant correlations.	3-(e)-styryl-2h-chromene	17-41	monoamine oxidase B	Homo sapiens	76-81
29448189-7	2018	This is the first report identifying 3-(E)-styryl-2H-chromene derivatives as potent and selective MAO-B inhibitors.	3-(e)-styryl-2h-chromene	37-61	monoamine oxidase B	Homo sapiens	98-103
29477889-0	2018	Novel indanone derivatives as MAO B/H3R dual-targeting ligands for treatment of Parkinson"s disease.	indacrinone	6-14	monoamine oxidase B	Homo sapiens	30-35
29365357-9	2018	The largest DSA variation in median allocation MELD score was seen in NYRT-OP1 LiveOnNY (MELD score variation 11), AZOB-OP1 Donor Network of Arizona (MELD score variation 11), MAOB-OP1 New England Organ Bank (MELD score variation 9), and TXGC-OP1 LifeGift Organ Donation Ctr (MELD score variation 9).	dsa	12-15	monoamine oxidase B	Homo sapiens	176-180
29477889-3	2018	Three series of compounds were developed by attaching the H3R pharmacophore to indanone-related MAO B motifs, leading to development of MAO B/H3R DTLs.	indacrinone	79-87	monoamine oxidase B	Homo sapiens	96-101
29477889-3	2018	Three series of compounds were developed by attaching the H3R pharmacophore to indanone-related MAO B motifs, leading to development of MAO B/H3R DTLs.	indacrinone	79-87	monoamine oxidase B	Homo sapiens	136-141
29477889-4	2018	Among synthesized indanone DTLs, compounds bearing the 2-benzylidene-1-indanone core structure showed MAO B preferring inhibition capabilities along with nanomolar hH3R affinity.	indacrinone	18-26	monoamine oxidase B	Homo sapiens	102-107
29477889-4	2018	Among synthesized indanone DTLs, compounds bearing the 2-benzylidene-1-indanone core structure showed MAO B preferring inhibition capabilities along with nanomolar hH3R affinity.	dtls	27-31	monoamine oxidase B	Homo sapiens	102-107
29477889-4	2018	Among synthesized indanone DTLs, compounds bearing the 2-benzylidene-1-indanone core structure showed MAO B preferring inhibition capabilities along with nanomolar hH3R affinity.	2-benzylidene-1-indanone	55-79	monoamine oxidase B	Homo sapiens	102-107
29477889-5	2018	Substitution of C5 and C6 position of the 2-benzylidene-1-indanones with lipophilic substituents revealed three promising candidates exhibiting inhibitory potencies for MAO B with IC50 values ranging from 1931 nM to 276 nM and high affinities at hH3R (Ki < 50 nM).	2-benzylidene-1-indanone	42-67	monoamine oxidase B	Homo sapiens	169-174
29477889-6	2018	Compound 3f ((E)-5-((4-bromobenzyl)oxy)-2-(4-(3-(piperidin-1-yl)propoxy)benzylidene)-2,3-dihydro-1H-inden-1-one, MAO B IC50 = 276 nM, hH3R Ki = 6.5 nM) showed highest preference for MAO B over MAO A (SI > 36).	3f (	9-13	monoamine oxidase B	Homo sapiens	113-118
29477889-6	2018	Compound 3f ((E)-5-((4-bromobenzyl)oxy)-2-(4-(3-(piperidin-1-yl)propoxy)benzylidene)-2,3-dihydro-1H-inden-1-one, MAO B IC50 = 276 nM, hH3R Ki = 6.5 nM) showed highest preference for MAO B over MAO A (SI > 36).	3f (	9-13	monoamine oxidase B	Homo sapiens	182-187
29477889-6	2018	Compound 3f ((E)-5-((4-bromobenzyl)oxy)-2-(4-(3-(piperidin-1-yl)propoxy)benzylidene)-2,3-dihydro-1H-inden-1-one, MAO B IC50 = 276 nM, hH3R Ki = 6.5 nM) showed highest preference for MAO B over MAO A (SI > 36).	(e)-5-((4-bromobenzyl)oxy)-2-(4-(3-(piperidin-1-yl)propoxy)benzylidene)-2,3-dihydro-1h-inden-1-one	13-111	monoamine oxidase B	Homo sapiens	182-187
29477889-9	2018	Thus, indanone-substituted derivatives are promising lead structures for the design of MAO B/hH3R DTLs as novel therapeutic approach of PD therapy.	indacrinone	6-14	monoamine oxidase B	Homo sapiens	87-92
29195801-0	2018	Discovery of potent and reversible MAO-B inhibitors as furanochalcones.	furanochalcones	55-70	monoamine oxidase B	Homo sapiens	35-40
29561824-4	2018	"Brava" oil exhibited the best inhibitory activity against all enzymes, when they are compared to "Mansa" oil: BuChE (IC50 = 245 +- 5 and 591 +- 23 mg mL-1), 5-LOX (IC50 = 45 +- 7 and 106 +- 14 mg mL-1), hMAO-A (IC50 = 30 +- 1 and 72 +- 10 mg mL-1) and hMAO-B (IC50 = 191 +- 8 and 208 +- 14 mg mL-1), respectively.	brava" oil	1-11	monoamine oxidase B	Homo sapiens	253-259
29552556-1	2018	Monoamine oxidase B (MAO-B) catalyzes deamination of monoamines such as neurotransmitters dopamine and norepinephrine.	monoamines	53-63	monoamine oxidase B	Homo sapiens	0-19
29552556-1	2018	Monoamine oxidase B (MAO-B) catalyzes deamination of monoamines such as neurotransmitters dopamine and norepinephrine.	monoamines	53-63	monoamine oxidase B	Homo sapiens	21-26
29552556-1	2018	Monoamine oxidase B (MAO-B) catalyzes deamination of monoamines such as neurotransmitters dopamine and norepinephrine.	Dopamine	90-98	monoamine oxidase B	Homo sapiens	0-19
29552556-1	2018	Monoamine oxidase B (MAO-B) catalyzes deamination of monoamines such as neurotransmitters dopamine and norepinephrine.	Dopamine	90-98	monoamine oxidase B	Homo sapiens	21-26
29552556-1	2018	Monoamine oxidase B (MAO-B) catalyzes deamination of monoamines such as neurotransmitters dopamine and norepinephrine.	Norepinephrine	103-117	monoamine oxidase B	Homo sapiens	0-19
29552556-1	2018	Monoamine oxidase B (MAO-B) catalyzes deamination of monoamines such as neurotransmitters dopamine and norepinephrine.	Norepinephrine	103-117	monoamine oxidase B	Homo sapiens	21-26
29552556-2	2018	Accordingly, small-molecule MAO-B inhibitors potentially alleviate the symptoms of dopamine-linked neuropathologies such as depression or Parkinson"s disease.	Dopamine	83-91	monoamine oxidase B	Homo sapiens	28-33
29552556-3	2018	Coumarin with a functionalized 3-phenyl ring system is a promising scaffold for building potent MAO-B inhibitors.	coumarin	0-8	monoamine oxidase B	Homo sapiens	96-101
29339106-2	2018	Recently licensed by the European Medicine Agency (EMA) and US Food and Drug Administration (FDA), safinamide [a monoamine oxidase B (MOA-B) inhibitor] is an alternative to L-DOPA; as we discuss here, it enhances dopaminergic transmission with decreased secondary effects compared with L-DOPA.	safinamide	99-109	monoamine oxidase B	Homo sapiens	113-132
29339106-2	2018	Recently licensed by the European Medicine Agency (EMA) and US Food and Drug Administration (FDA), safinamide [a monoamine oxidase B (MOA-B) inhibitor] is an alternative to L-DOPA; as we discuss here, it enhances dopaminergic transmission with decreased secondary effects compared with L-DOPA.	safinamide	99-109	monoamine oxidase B	Homo sapiens	134-139
29451686-1	2018	We previously reported that KW-2449, (E)-1-{4-[2-(1H-Indazol-3-yl)vinyl]benzoyl}piperazine, a novel multikinase inhibitor developed for the treatment of leukemia patients, was oxidized to an iminium ion intermediate by monoamine oxidase B (MAO-B) and then converted to its oxo-piperazine form (M1) by aldehyde oxidase (AO).	KW 2449	28-35	monoamine oxidase B	Homo sapiens	219-238
29451686-1	2018	We previously reported that KW-2449, (E)-1-{4-[2-(1H-Indazol-3-yl)vinyl]benzoyl}piperazine, a novel multikinase inhibitor developed for the treatment of leukemia patients, was oxidized to an iminium ion intermediate by monoamine oxidase B (MAO-B) and then converted to its oxo-piperazine form (M1) by aldehyde oxidase (AO).	KW 2449	28-35	monoamine oxidase B	Homo sapiens	240-245
29451686-1	2018	We previously reported that KW-2449, (E)-1-{4-[2-(1H-Indazol-3-yl)vinyl]benzoyl}piperazine, a novel multikinase inhibitor developed for the treatment of leukemia patients, was oxidized to an iminium ion intermediate by monoamine oxidase B (MAO-B) and then converted to its oxo-piperazine form (M1) by aldehyde oxidase (AO).	KW 2449	37-90	monoamine oxidase B	Homo sapiens	219-238
29451686-1	2018	We previously reported that KW-2449, (E)-1-{4-[2-(1H-Indazol-3-yl)vinyl]benzoyl}piperazine, a novel multikinase inhibitor developed for the treatment of leukemia patients, was oxidized to an iminium ion intermediate by monoamine oxidase B (MAO-B) and then converted to its oxo-piperazine form (M1) by aldehyde oxidase (AO).	KW 2449	37-90	monoamine oxidase B	Homo sapiens	240-245
29451686-4	2018	These results clearly suggest that MAO-B catalysed iminium ion metabolite inhibited AO, prompting us to investigate whether or not the iminium ion metabolite covalently binds to endogenous proteins, as has been reported with other reactive metabolites as a cause for idiosyncratic toxicity.	iminium	51-58	monoamine oxidase B	Homo sapiens	35-40
29451686-5	2018	The association of the radioactivity derived from 14 C-KW-2449 with endogenous proteins both in vivo and in vitro was confirmed and it was verified that this covalent binding was inhibited by the addition of sodium cyanide, an iminium ion-trapping reagent, and pargyline, a MAO-B inhibitor.	Sodium Cyanide	208-222	monoamine oxidase B	Homo sapiens	274-279
29570223-3	2018	Analyzes of the MAO inhibition properties of the synthesized compounds show that among the pyrrolo[3,4-f]indole-5,7-dione derivatives good potency MAO inhibitors exist as exemplified by 10, which possesses IC50 values for the inhibition of MAO-A and MAO-B of 0.023 and 0.178 microM, respectively.	pyrrolo[3,4-f]indole-5,7-dione	91-121	monoamine oxidase B	Homo sapiens	250-255
29195801-2	2018	Among the series, compound (2E, 4E)-1-(furan-2-yl)-5-phenylpenta-2, 4-dien-1-one (F1), which was analyzed by single-crystal X-ray diffraction, showed potent and selective MAO-B inhibitory activity with an inhibition constant (Ki) value of 0.0041 muM and selectivity index of (SI) 172.4, and exhibited competitive inhibition.	(2e, 4e)-1-(furan-2-yl)-5-phenylpenta-2, 4-dien-1-one	27-80	monoamine oxidase B	Homo sapiens	171-176
29195801-5	2018	The Ki value of F1 is the lowest among the values of chalcone derivatives and furthermore lower than that (0.0079 muM) of the reversible MAO-B inhibitor, lazabemide, a marketed drug.	Chalcone	53-61	monoamine oxidase B	Homo sapiens	137-142
29195801-5	2018	The Ki value of F1 is the lowest among the values of chalcone derivatives and furthermore lower than that (0.0079 muM) of the reversible MAO-B inhibitor, lazabemide, a marketed drug.	lazabemide	154-164	monoamine oxidase B	Homo sapiens	137-142
29309800-0	2018	Partial reversal of the effort-related motivational effects of tetrabenazine with the MAO-B inhibitor deprenyl (selegiline): Implications for treating motivational dysfunctions.	Tetrabenazine	63-76	monoamine oxidase B	Homo sapiens	86-91
29309800-0	2018	Partial reversal of the effort-related motivational effects of tetrabenazine with the MAO-B inhibitor deprenyl (selegiline): Implications for treating motivational dysfunctions.	Selegiline	102-110	monoamine oxidase B	Homo sapiens	86-91
29309800-0	2018	Partial reversal of the effort-related motivational effects of tetrabenazine with the MAO-B inhibitor deprenyl (selegiline): Implications for treating motivational dysfunctions.	Selegiline	112-122	monoamine oxidase B	Homo sapiens	86-91
29309800-7	2018	These effects of 0.75mg/kg tetrabenazine were attenuated by co-administration of the MAO-B inhibitor deprenyl (selegiline).	Tetrabenazine	27-40	monoamine oxidase B	Homo sapiens	85-90
29309800-7	2018	These effects of 0.75mg/kg tetrabenazine were attenuated by co-administration of the MAO-B inhibitor deprenyl (selegiline).	Selegiline	101-109	monoamine oxidase B	Homo sapiens	85-90
29309800-7	2018	These effects of 0.75mg/kg tetrabenazine were attenuated by co-administration of the MAO-B inhibitor deprenyl (selegiline).	Selegiline	111-121	monoamine oxidase B	Homo sapiens	85-90
29395970-1	2018	Hispidol, an aurone, isolated from Glycine max Merrill, was found to potently and selectively inhibit an isoform of recombinant human monoamine oxidase-A (MAO-A), with an IC50 value of 0.26 microM, and to inhibit MAO-B, but with lower potency (IC50 = 2.45 microM).	Hispidol	0-8	monoamine oxidase B	Homo sapiens	213-218
29390885-3	2018	The aim of the current study was to design multi-targeted directed lead structures based on the coumarin scaffold with inhibitory properties at two key enzymes in disease relevant systems, i.e. acetylcholinesterase (AChE) and monoamine oxidase B (MAO-B).	coumarin	96-104	monoamine oxidase B	Homo sapiens	226-245
29390885-3	2018	The aim of the current study was to design multi-targeted directed lead structures based on the coumarin scaffold with inhibitory properties at two key enzymes in disease relevant systems, i.e. acetylcholinesterase (AChE) and monoamine oxidase B (MAO-B).	coumarin	96-104	monoamine oxidase B	Homo sapiens	247-252
29395970-5	2018	A comparison of their chemical structures showed that the 3"-hydroxyl group of sulfuretin might reduce its inhibitory activities against MAO-A and MAO-B.	sulfuretin	79-89	monoamine oxidase B	Homo sapiens	147-152
29395970-6	2018	Flexible docking simulation revealed that the binding affinity of hispidol for MAO-A (-9.1 kcal/mol) was greater than its affinity for MAO-B (-8.7 kcal/mol).	Hispidol	66-74	monoamine oxidase B	Homo sapiens	135-140
29395970-7	2018	The docking simulation showed hispidol binds to the major pocket of MAO-A or MAO-B.	Hispidol	30-38	monoamine oxidase B	Homo sapiens	77-82
29221756-7	2018	Selective monoamine oxidase B inhibitor, selegiline competed for the same site as [3H]d-deprenyl, but failed to differentiate the samples with regard to their inflammation grade.	Selegiline	41-51	monoamine oxidase B	Homo sapiens	10-29
29339253-0	2018	Design, synthesis and bioevalucation of novel 2,3-dihydro-1H-inden-1-amine derivatives as potent and selective human monoamine oxidase B inhibitors based on rasagiline.	1-aminoindan	46-74	monoamine oxidase B	Homo sapiens	117-136
29339253-0	2018	Design, synthesis and bioevalucation of novel 2,3-dihydro-1H-inden-1-amine derivatives as potent and selective human monoamine oxidase B inhibitors based on rasagiline.	rasagiline	157-167	monoamine oxidase B	Homo sapiens	117-136
29339253-2	2018	Herein we report rasagiline derivatives as novel potent and selective hMAO-B inhibitors.	rasagiline	17-27	monoamine oxidase B	Homo sapiens	70-76
29339253-3	2018	They were designed by employing fragment-based drug design strategy to link rasagiline and hydrophobic fragments, which may target a hydrophobic pocket in the entrance cavity of hMAO-B.	rasagiline	76-86	monoamine oxidase B	Homo sapiens	178-184
29339253-5	2018	A promising selective hMAO-B inhibitor D14 with similar inhibitory activity as rasagiline and improved isoform selectivity was yielded.	rasagiline	79-89	monoamine oxidase B	Homo sapiens	22-28
29360121-0	2018	Why does the Y326I mutant of monoamine oxidase B decompose an endogenous amphetamine at a slower rate than the wild type enzyme?	Amphetamine	73-84	monoamine oxidase B	Homo sapiens	29-48
29360121-2	2018	This work investigates the Y326I point mutation effect on the kinetics of oxidative deamination of phenylethylamine (PEA) catalyzed by the monoamine oxidase B (MAO B) enzyme.	Phenethylamines	99-115	monoamine oxidase B	Homo sapiens	139-158
29360121-2	2018	This work investigates the Y326I point mutation effect on the kinetics of oxidative deamination of phenylethylamine (PEA) catalyzed by the monoamine oxidase B (MAO B) enzyme.	Phenethylamines	99-115	monoamine oxidase B	Homo sapiens	160-165
29360121-2	2018	This work investigates the Y326I point mutation effect on the kinetics of oxidative deamination of phenylethylamine (PEA) catalyzed by the monoamine oxidase B (MAO B) enzyme.	Phenethylamines	117-120	monoamine oxidase B	Homo sapiens	139-158
29360121-2	2018	This work investigates the Y326I point mutation effect on the kinetics of oxidative deamination of phenylethylamine (PEA) catalyzed by the monoamine oxidase B (MAO B) enzyme.	Phenethylamines	117-120	monoamine oxidase B	Homo sapiens	160-165
29159774-1	2018	BACKGROUND AND OBJECTIVES: Rasagiline tablet is an oral MAO-B inhibitor applied in early or advanced Parkinson"s disease (PD).	rasagiline	27-37	monoamine oxidase B	Homo sapiens	56-61
29202379-5	2018	Platelet MAO-B activity was measured with 2-phenylethylamine (b-PEA) as substrate.	phenethylamine	42-60	monoamine oxidase B	Homo sapiens	9-14
29202379-5	2018	Platelet MAO-B activity was measured with 2-phenylethylamine (b-PEA) as substrate.	9,10-bis(phenylethynyl)anthracene	62-67	monoamine oxidase B	Homo sapiens	9-14
30108930-5	2018	The compounds possessing the propargylamine moiety showed good MAO-B inhibitory activity with 6 and 8 portraying IC50 values between 14-20 fold better than ladostigil.	propargylamine	29-43	monoamine oxidase B	Homo sapiens	63-68
29268246-7	2018	As determined by HPLC-DAD, beta-carbolines, methylene blue, kaempferol and clorgyline inhibited MAO-A and methylene blue, 5-nitroindazole, norharman and deprenyl inhibited MAO-B, and all of them inhibited the oxidation of TMB in the same extent.	Clorgyline	75-85	monoamine oxidase B	Homo sapiens	172-177
29268246-7	2018	As determined by HPLC-DAD, beta-carbolines, methylene blue, kaempferol and clorgyline inhibited MAO-A and methylene blue, 5-nitroindazole, norharman and deprenyl inhibited MAO-B, and all of them inhibited the oxidation of TMB in the same extent.	Carbolines	27-42	monoamine oxidase B	Homo sapiens	172-177
29268246-7	2018	As determined by HPLC-DAD, beta-carbolines, methylene blue, kaempferol and clorgyline inhibited MAO-A and methylene blue, 5-nitroindazole, norharman and deprenyl inhibited MAO-B, and all of them inhibited the oxidation of TMB in the same extent.	Methylene Blue	44-58	monoamine oxidase B	Homo sapiens	172-177
29268246-7	2018	As determined by HPLC-DAD, beta-carbolines, methylene blue, kaempferol and clorgyline inhibited MAO-A and methylene blue, 5-nitroindazole, norharman and deprenyl inhibited MAO-B, and all of them inhibited the oxidation of TMB in the same extent.	kaempferol	60-70	monoamine oxidase B	Homo sapiens	172-177
30108930-5	2018	The compounds possessing the propargylamine moiety showed good MAO-B inhibitory activity with 6 and 8 portraying IC50 values between 14-20 fold better than ladostigil.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	156-166	monoamine oxidase B	Homo sapiens	63-68
30108930-7	2018	MAO-A and MAO-B docking results showed that the propargylamine moiety was positioned in close proximity to the FAD cofactor suggesting that the good inhibitory activity may be attributed to the propargylamine moiety and irreversible inhibition as confirmed in the reversibility studies.	propargylamine	48-62	monoamine oxidase B	Homo sapiens	10-15
30108930-7	2018	MAO-A and MAO-B docking results showed that the propargylamine moiety was positioned in close proximity to the FAD cofactor suggesting that the good inhibitory activity may be attributed to the propargylamine moiety and irreversible inhibition as confirmed in the reversibility studies.	propargylamine	194-208	monoamine oxidase B	Homo sapiens	10-15
29126721-1	2018	Three series of 4-hydroxy-N"-[benzylidene/1-phenylethylidene]-2-H/methyl/benzyl-1,2-benzothiazine-3-carbohydrazide 1,1-dioxides (9-11)a-l were synthesized and unraveled to be highly potent dual inhibitors of monoamine oxidases (MAO-A and MAO-B).	benzyl-1,2-benzothiazine-3-carbohydrazide 1,1-dioxides	73-127	monoamine oxidase B	Homo sapiens	238-243
29697034-4	2018	Monoamine Oxidase (MAO), in turn, metabolises dopamine in the brain, and MAO-B inhibitors may exert a dopamine sparing effect in the brain.	Dopamine	102-110	monoamine oxidase B	Homo sapiens	73-78
29697034-7	2018	The chalcone class of compounds is well known to potently inhibit MAO-B, while nitrocatechol derivatives (e.g. tolcapone and entacapone) are clinically used COMT inhibitors.	Chalcone	4-12	monoamine oxidase B	Homo sapiens	66-71
29697034-10	2018	The chalcones are less potent as inhibitors of MAO with the most potent inhibitor possessing a Ki of 4.6 microM for the in vitro inhibition of human MAO-B.	Chalcones	4-13	monoamine oxidase B	Homo sapiens	149-154
29697034-11	2018	CONCLUSION: This study shows that nitrocatechol derivatives of chalcone may act as COMT and MAO-B inhibitors, and proposes a general strategy for further enhancing MAO-B inhibition while retaining the potent COMT inhibition activity of this class.	nitrocatechol	34-47	monoamine oxidase B	Homo sapiens	92-97
29697034-11	2018	CONCLUSION: This study shows that nitrocatechol derivatives of chalcone may act as COMT and MAO-B inhibitors, and proposes a general strategy for further enhancing MAO-B inhibition while retaining the potent COMT inhibition activity of this class.	nitrocatechol	34-47	monoamine oxidase B	Homo sapiens	164-169
29697034-11	2018	CONCLUSION: This study shows that nitrocatechol derivatives of chalcone may act as COMT and MAO-B inhibitors, and proposes a general strategy for further enhancing MAO-B inhibition while retaining the potent COMT inhibition activity of this class.	Chalcone	63-71	monoamine oxidase B	Homo sapiens	92-97
29697034-11	2018	CONCLUSION: This study shows that nitrocatechol derivatives of chalcone may act as COMT and MAO-B inhibitors, and proposes a general strategy for further enhancing MAO-B inhibition while retaining the potent COMT inhibition activity of this class.	Chalcone	63-71	monoamine oxidase B	Homo sapiens	164-169
29126721-1	2018	Three series of 4-hydroxy-N"-[benzylidene/1-phenylethylidene]-2-H/methyl/benzyl-1,2-benzothiazine-3-carbohydrazide 1,1-dioxides (9-11)a-l were synthesized and unraveled to be highly potent dual inhibitors of monoamine oxidases (MAO-A and MAO-B).	4-hydroxy-n"-[benzylidene	16-41	monoamine oxidase B	Homo sapiens	238-243
29714148-5	2018	The MAO inhibitory properties of the chalcone derivatives were evaluated with the recombinant human MAO-A and MAO-B enzymes and the potencies were expressed as the IC50 values.	Chalcone	37-45	monoamine oxidase B	Homo sapiens	110-115
29714148-7	2018	RESULTS: The results showed that the cyclic chalcones are in general good potency, and in most instances specific inhibitors of the MAO-B isoform.	cyclic chalcones	37-53	monoamine oxidase B	Homo sapiens	132-137
29714148-8	2018	Among these compounds, the 4-chromanone derivative was the most potent MAO-B inhibitor with an IC50 value of 0.156 microM.	4-chromanone	27-39	monoamine oxidase B	Homo sapiens	71-76
29714148-10	2018	Most 2-benzylidene-1-tetralones possess good inhibitory activity and specificity for MAO-B with the most potent inhibitor displaying an IC50 value of 0.0064 microM, while the most potent MAO-A inhibitor possessed an IC50 value of 0.754 microM.	2-benzylidene-1-tetralones	5-31	monoamine oxidase B	Homo sapiens	85-90
29714148-11	2018	CONCLUSION: This study thus shows that certain cyclic chalcones are human MAO-B inhibitors, compounds that could be suitable for the treatment of neurodegenerative disorders such as Parkinson"s disease.	cyclic chalcones	47-63	monoamine oxidase B	Homo sapiens	74-79
29126727-1	2018	New 4-(3-nitrophenyl)thiazol-2-ylhydrazone derivatives are proposed as dual-target-directed monoamine oxidase B (MAO-B) and acetylcholinesterase (AChE) inhibitors, as well as antioxidant agents, for the treatment of neurodegenerative disorders such as Parkinson"s disease.	4-(3-nitrophenyl)thiazol-2-ylhydrazone	4-42	monoamine oxidase B	Homo sapiens	92-111
29126727-1	2018	New 4-(3-nitrophenyl)thiazol-2-ylhydrazone derivatives are proposed as dual-target-directed monoamine oxidase B (MAO-B) and acetylcholinesterase (AChE) inhibitors, as well as antioxidant agents, for the treatment of neurodegenerative disorders such as Parkinson"s disease.	4-(3-nitrophenyl)thiazol-2-ylhydrazone	4-42	monoamine oxidase B	Homo sapiens	113-118
29154867-5	2018	Compound 1 demonstrated preferential inhibition against hMAO-A isoenzyme (IC50 0.62muM, SIA/B 0.02) while S-naringenin (13) and isoliquiritigein (15) demonstrated preferential hMAO-B inhibition (IC50 0.27 and 0.51muM, SIA/B 31.77 and 44.69, respectively).	naringenin	106-118	monoamine oxidase B	Homo sapiens	176-182
29154867-5	2018	Compound 1 demonstrated preferential inhibition against hMAO-A isoenzyme (IC50 0.62muM, SIA/B 0.02) while S-naringenin (13) and isoliquiritigein (15) demonstrated preferential hMAO-B inhibition (IC50 0.27 and 0.51muM, SIA/B 31.77 and 44.69, respectively).	isoliquiritigein	128-144	monoamine oxidase B	Homo sapiens	176-182
29154867-8	2018	It suggested that 1 interacts with Gln215, Ala111, Phe352, and Phe208 amino acid residues which have a role in the orientation and stabilization of the inhibitor binding to hMAO-A, while S-naringenin (13) occupies both entrance and substrate cavities and interacts with Tyr326, a critical residue in inhibitor recognition in hMAO-B.	naringenin	189-199	monoamine oxidase B	Homo sapiens	325-331
29464559-3	2018	Currently, the treatment of Parkinson"s disease involves the use of selective MAO B inhibitors such as rasagiline and safinamide.	rasagiline	103-113	monoamine oxidase B	Homo sapiens	78-83
29464559-3	2018	Currently, the treatment of Parkinson"s disease involves the use of selective MAO B inhibitors such as rasagiline and safinamide.	safinamide	118-128	monoamine oxidase B	Homo sapiens	78-83
29031059-2	2017	Tranylcypromine (TCP) is an antidepressant originally known to target the monoamine oxidases A and B (MAO-A and MAO-B), which are structurally related to LSD1.	Tranylcypromine	0-15	monoamine oxidase B	Homo sapiens	112-117
29229003-9	2017	Competition with the MAO-B inhibitor 3H-L-deprenyl was observed for THK5117 and T807 in the hippocampus (THK5117 K i = 286 nM; T807 K i = 227 nM) and the putamen (THK5117 K i = 148 nM; T807 K i = 135 nM).	3h-l-deprenyl	37-50	monoamine oxidase B	Homo sapiens	21-26
29229003-9	2017	Competition with the MAO-B inhibitor 3H-L-deprenyl was observed for THK5117 and T807 in the hippocampus (THK5117 K i = 286 nM; T807 K i = 227 nM) and the putamen (THK5117 K i = 148 nM; T807 K i = 135 nM).	6-((3-fluoro-2-hydroxy)propoxy)-2-(4-methylaminophenyl)quinoline	68-75	monoamine oxidase B	Homo sapiens	21-26
29229003-12	2017	Both THK5117 and T807 demonstrated off-target binding in the hippocampus and putamen with a ten times lower binding affinity to the MAO-B inhibitor deprenyl compared with 3H-THK5351.	6-((3-fluoro-2-hydroxy)propoxy)-2-(4-methylaminophenyl)quinoline	5-12	monoamine oxidase B	Homo sapiens	132-137
29229003-12	2017	Both THK5117 and T807 demonstrated off-target binding in the hippocampus and putamen with a ten times lower binding affinity to the MAO-B inhibitor deprenyl compared with 3H-THK5351.	Selegiline	148-156	monoamine oxidase B	Homo sapiens	132-137
29318309-0	2017	Synthesis, Crystal Structures, Molecular Docking and MAO-B Inhibitory Activity of Transition Metal Complexes Derived from 2-(4-(Pyridin-2-yl)piperazin-1-yl)acetic Acid.	Metals	93-98	monoamine oxidase B	Homo sapiens	53-58
29318309-0	2017	Synthesis, Crystal Structures, Molecular Docking and MAO-B Inhibitory Activity of Transition Metal Complexes Derived from 2-(4-(Pyridin-2-yl)piperazin-1-yl)acetic Acid.	1-Piperazineacetic acid, 4-(2-pyridinyl)-	122-167	monoamine oxidase B	Homo sapiens	53-58
29065322-0	2017	Sulfonyl hydrazones derived from 3-formylchromone as non-selective inhibitors of MAO-A and MAO-B: Synthesis, molecular modelling and in-silico ADME evaluation.	sulfonyl hydrazones	0-19	monoamine oxidase B	Homo sapiens	91-96
29065322-0	2017	Sulfonyl hydrazones derived from 3-formylchromone as non-selective inhibitors of MAO-A and MAO-B: Synthesis, molecular modelling and in-silico ADME evaluation.	Chromone-3-carboxaldehyde	33-49	monoamine oxidase B	Homo sapiens	91-96
29065322-1	2017	A series of sulfonyl hydrazones derived from 3-formylchromone was synthesized and discovered to be effective, non-selective inhibitors of monoamine oxidases (MAO-A and MAO-B).	sulfonyl hydrazones	12-31	monoamine oxidase B	Homo sapiens	168-173
29065322-1	2017	A series of sulfonyl hydrazones derived from 3-formylchromone was synthesized and discovered to be effective, non-selective inhibitors of monoamine oxidases (MAO-A and MAO-B).	Chromone-3-carboxaldehyde	45-61	monoamine oxidase B	Homo sapiens	168-173
28857544-0	2017	Identification of 5-(1-Methyl-5-(trifluoromethyl)-1H-pyrazol-3-yl)thiophene-2-Carboxamides as Novel and Selective Monoamine Oxidase B Inhibitors Used to Improve Memory and Cognition.	5-(1-methyl-5-(trifluoromethyl)-1h-pyrazol-3-yl)thiophene-2-carboxamides	18-90	monoamine oxidase B	Homo sapiens	114-133
28583428-5	2017	By using multiscale simulation on the Empirical Valence Bond (EVB) level, we studied the chemical reactivity of the monoamine oxidase B catalyzed decomposition of PEA and its two derivatives: p-chloro-beta-methylphenylamine (p-CMP) and p-methoxy-beta-methylphenethylamine (p-MMP).	4-Sulfocalix[8]arene	62-65	monoamine oxidase B	Homo sapiens	116-135
28583428-5	2017	By using multiscale simulation on the Empirical Valence Bond (EVB) level, we studied the chemical reactivity of the monoamine oxidase B catalyzed decomposition of PEA and its two derivatives: p-chloro-beta-methylphenylamine (p-CMP) and p-methoxy-beta-methylphenethylamine (p-MMP).	4-chloro-beta-methylphenethylamine	192-223	monoamine oxidase B	Homo sapiens	116-135
28583428-5	2017	By using multiscale simulation on the Empirical Valence Bond (EVB) level, we studied the chemical reactivity of the monoamine oxidase B catalyzed decomposition of PEA and its two derivatives: p-chloro-beta-methylphenylamine (p-CMP) and p-methoxy-beta-methylphenethylamine (p-MMP).	4-chloro-beta-methylphenethylamine	225-230	monoamine oxidase B	Homo sapiens	116-135
28583428-5	2017	By using multiscale simulation on the Empirical Valence Bond (EVB) level, we studied the chemical reactivity of the monoamine oxidase B catalyzed decomposition of PEA and its two derivatives: p-chloro-beta-methylphenylamine (p-CMP) and p-methoxy-beta-methylphenethylamine (p-MMP).	p-methoxy-beta-methylphenethylamine	236-271	monoamine oxidase B	Homo sapiens	116-135
28583428-5	2017	By using multiscale simulation on the Empirical Valence Bond (EVB) level, we studied the chemical reactivity of the monoamine oxidase B catalyzed decomposition of PEA and its two derivatives: p-chloro-beta-methylphenylamine (p-CMP) and p-methoxy-beta-methylphenethylamine (p-MMP).	p-mmp	273-278	monoamine oxidase B	Homo sapiens	116-135
29232838-0	2017	Design and Synthesis of New Benzothiazole Compounds as Selective hMAO-B Inhibitors.	benzothiazole compounds	28-51	monoamine oxidase B	Homo sapiens	65-71
29232838-1	2017	In the current work a new class of novel benzothiazole-hydrazone derivatives was designed and synthesized as hMAO-B inhibitors.	benzothiazole-hydrazone	41-64	monoamine oxidase B	Homo sapiens	109-115
28634836-0	2017	Test-retest reproducibility of [11C]-L-deprenyl-D2 binding to MAO-B in the human brain.	Carbon-11	32-35	monoamine oxidase B	Homo sapiens	62-67
28634836-0	2017	Test-retest reproducibility of [11C]-L-deprenyl-D2 binding to MAO-B in the human brain.	l-deprenyl-d2	37-50	monoamine oxidase B	Homo sapiens	62-67
28634836-1	2017	BACKGROUND: [11C]-L-deprenyl-D2 is a positron emission tomography (PET) radioligand for measurement of the monoamine oxidase B (MAO-B) activity in vivo brain.	11c]-l-deprenyl-d2	13-31	monoamine oxidase B	Homo sapiens	107-126
28634836-1	2017	BACKGROUND: [11C]-L-deprenyl-D2 is a positron emission tomography (PET) radioligand for measurement of the monoamine oxidase B (MAO-B) activity in vivo brain.	11c]-l-deprenyl-d2	13-31	monoamine oxidase B	Homo sapiens	128-133
29031059-2	2017	Tranylcypromine (TCP) is an antidepressant originally known to target the monoamine oxidases A and B (MAO-A and MAO-B), which are structurally related to LSD1.	Tranylcypromine	17-20	monoamine oxidase B	Homo sapiens	112-117
28097874-0	2017	Through scaffold modification to 3,5-diaryl-4,5-dihydroisoxazoles: new potent and selective inhibitors of monoamine oxidase B.	3,5-diaryl-4,5-dihydroisoxazoles	33-65	monoamine oxidase B	Homo sapiens	106-125
29130466-2	2017	Safinamide, a new drug that has MAO-B inhibition and antiglutamatergic effects through inhibition of sodium channels, has shown efficacy for the treatment of fluctuations at doses of 50-100 mg/day.	safinamide	0-10	monoamine oxidase B	Homo sapiens	32-37
28726524-0	2017	Subnanomolar indazole-5-carboxamide inhibitors of monoamine oxidase B (MAO-B) continued: indications of iron binding, experimental evidence for optimised solubility and brain penetration.	1H-indazole-5-carboxamide	13-35	monoamine oxidase B	Homo sapiens	50-69
28726524-0	2017	Subnanomolar indazole-5-carboxamide inhibitors of monoamine oxidase B (MAO-B) continued: indications of iron binding, experimental evidence for optimised solubility and brain penetration.	1H-indazole-5-carboxamide	13-35	monoamine oxidase B	Homo sapiens	71-76
28726524-0	2017	Subnanomolar indazole-5-carboxamide inhibitors of monoamine oxidase B (MAO-B) continued: indications of iron binding, experimental evidence for optimised solubility and brain penetration.	Iron	104-108	monoamine oxidase B	Homo sapiens	71-76
28726524-2	2017	The compounds are highly brain permeable, selective, reversible, and competitive monoamine oxidase B (MAO-B) inhibitors with improved water-solubility and subnanomolar potency (pIC50 &gt;8.8).	Water	134-139	monoamine oxidase B	Homo sapiens	81-100
28726524-2	2017	The compounds are highly brain permeable, selective, reversible, and competitive monoamine oxidase B (MAO-B) inhibitors with improved water-solubility and subnanomolar potency (pIC50 &gt;8.8).	Water	134-139	monoamine oxidase B	Homo sapiens	102-107
28034283-3	2017	METHODS: Ursolic acid has been docked with monoamine oxidase isoforms: MAO-A and MAO-B, LeuT (homologue of SERT, NET, DAT) and Human C-terminal CAP1 using GRIP docking methodology.	ursolic acid	9-21	monoamine oxidase B	Homo sapiens	81-86
29033232-0	2017	Design, synthesis and biological evaluation of phthalimide-alkylamine derivatives as balanced multifunctional cholinesterase and monoamine oxidase-B inhibitors for the treatment of Alzheimer"s disease.	phthalimide-alkylamine	47-69	monoamine oxidase B	Homo sapiens	129-148
28634060-6	2017	AMG was predicted to bind to MAO-B with an energy of -23.1kcal/mol by possible hydrogen-bond formation between an oxygen atom of Ile477 residue and a hydrogen atom (H17) of AMG.	Hydrogen	79-87	monoamine oxidase B	Homo sapiens	29-34
28577983-1	2017	The MAO-B inhibitory activity of chalcone (1, 3- diphenyl-2-propen-1-one) based compounds arise from its structural similarity with 1, 4-diphenyl-2-butene, a known MAO-B inhibitor.	Chalcone	33-41	monoamine oxidase B	Homo sapiens	4-9
28577983-1	2017	The MAO-B inhibitory activity of chalcone (1, 3- diphenyl-2-propen-1-one) based compounds arise from its structural similarity with 1, 4-diphenyl-2-butene, a known MAO-B inhibitor.	Chalcone	33-41	monoamine oxidase B	Homo sapiens	164-169
28577983-1	2017	The MAO-B inhibitory activity of chalcone (1, 3- diphenyl-2-propen-1-one) based compounds arise from its structural similarity with 1, 4-diphenyl-2-butene, a known MAO-B inhibitor.	Chalcone	43-72	monoamine oxidase B	Homo sapiens	4-9
28577983-1	2017	The MAO-B inhibitory activity of chalcone (1, 3- diphenyl-2-propen-1-one) based compounds arise from its structural similarity with 1, 4-diphenyl-2-butene, a known MAO-B inhibitor.	Chalcone	43-72	monoamine oxidase B	Homo sapiens	164-169
29140741-9	2017	CONCLUSIONS: The expression of MAO B measured by 11C-DED uptake or immunocytochemistry was not significantly different in grade III or IV cells.	Carbon-11	49-52	monoamine oxidase B	Homo sapiens	31-36
28634060-2	2017	Acacetin, a flavonoid, potently inhibited recombinant human MAO-A and MAO-B (IC50=0.19 and 0.17muM, respectively), and reversibly and competitively inhibited MAO-A and MAO-B (Ki=0.045 and 0.037muM, respectively).	acacetin	0-8	monoamine oxidase B	Homo sapiens	70-75
28634060-2	2017	Acacetin, a flavonoid, potently inhibited recombinant human MAO-A and MAO-B (IC50=0.19 and 0.17muM, respectively), and reversibly and competitively inhibited MAO-A and MAO-B (Ki=0.045 and 0.037muM, respectively).	acacetin	0-8	monoamine oxidase B	Homo sapiens	168-173
28634060-6	2017	AMG was predicted to bind to MAO-B with an energy of -23.1kcal/mol by possible hydrogen-bond formation between an oxygen atom of Ile477 residue and a hydrogen atom (H17) of AMG.	Oxygen	114-120	monoamine oxidase B	Homo sapiens	29-34
28577983-1	2017	The MAO-B inhibitory activity of chalcone (1, 3- diphenyl-2-propen-1-one) based compounds arise from its structural similarity with 1, 4-diphenyl-2-butene, a known MAO-B inhibitor.	1, 4-diphenyl-2-butene	132-154	monoamine oxidase B	Homo sapiens	4-9
28634060-6	2017	AMG was predicted to bind to MAO-B with an energy of -23.1kcal/mol by possible hydrogen-bond formation between an oxygen atom of Ile477 residue and a hydrogen atom (H17) of AMG.	Hydrogen	150-158	monoamine oxidase B	Homo sapiens	29-34
28577983-1	2017	The MAO-B inhibitory activity of chalcone (1, 3- diphenyl-2-propen-1-one) based compounds arise from its structural similarity with 1, 4-diphenyl-2-butene, a known MAO-B inhibitor.	1, 4-diphenyl-2-butene	132-154	monoamine oxidase B	Homo sapiens	164-169
28634060-3	2017	Acacetin 7-O-(6-O-malonylglucoside) (AMG) was also found to effectively inhibit MAO-A and MAO-B (IC50=2.34 and 1.87muM, respectively), and to reversibly and competitively inhibit MAO-A and MAO-B (Ki=1.06 and 0.38muM, respectively).	acacetin 7-o-(6-o-malonylglucoside)	0-35	monoamine oxidase B	Homo sapiens	90-95
28634060-3	2017	Acacetin 7-O-(6-O-malonylglucoside) (AMG) was also found to effectively inhibit MAO-A and MAO-B (IC50=2.34 and 1.87muM, respectively), and to reversibly and competitively inhibit MAO-A and MAO-B (Ki=1.06 and 0.38muM, respectively).	acacetin 7-o-(6-o-malonylglucoside)	0-35	monoamine oxidase B	Homo sapiens	189-194
28577983-2	2017	Based on our previous report, the methoxy-substituted with fluorine containing chalcones are promising reversible MAO-B inhibitors, while in the present study, a series of methoxylated chalcones (C1-C9) bearing substitution on the para position of ring B was synthesized and evaluated for their human monoamine oxidase inhibitory activity.	Fluorine	59-67	monoamine oxidase B	Homo sapiens	114-119
28185143-3	2017	METHODS: Inhibition potential of 1-aminobenzotriazole and ketoconazole was studied in mice, rat and human liver microsomes, S9 fractions, MAO-A and MAO-B expressed enzymes by monitoring the formation of 4-hydroxyquinoline (4-HQ) from kynuramine, a specific substrate of MAO by liquid chromatography-tandem mass spectrometry (LC-MS/MS).	1-aminobenzotriazole	33-53	monoamine oxidase B	Homo sapiens	148-153
28577983-2	2017	Based on our previous report, the methoxy-substituted with fluorine containing chalcones are promising reversible MAO-B inhibitors, while in the present study, a series of methoxylated chalcones (C1-C9) bearing substitution on the para position of ring B was synthesized and evaluated for their human monoamine oxidase inhibitory activity.	Chalcones	79-88	monoamine oxidase B	Homo sapiens	114-119
28577983-2	2017	Based on our previous report, the methoxy-substituted with fluorine containing chalcones are promising reversible MAO-B inhibitors, while in the present study, a series of methoxylated chalcones (C1-C9) bearing substitution on the para position of ring B was synthesized and evaluated for their human monoamine oxidase inhibitory activity.	Chalcones	185-194	monoamine oxidase B	Homo sapiens	114-119
28923922-8	2017	Accordingly, MAO-B inhibitor rasagiline disrupts alpha-Syn/TrkB complex and rescues TrkB neurotrophic signaling, preventing alpha-Syn-induced dopaminergic neuronal death and restoring motor functions.	rasagiline	29-39	monoamine oxidase B	Homo sapiens	13-18
28634060-3	2017	Acacetin 7-O-(6-O-malonylglucoside) (AMG) was also found to effectively inhibit MAO-A and MAO-B (IC50=2.34 and 1.87muM, respectively), and to reversibly and competitively inhibit MAO-A and MAO-B (Ki=1.06 and 0.38muM, respectively).	methyl-galactopyranoside	37-40	monoamine oxidase B	Homo sapiens	90-95
28634060-3	2017	Acacetin 7-O-(6-O-malonylglucoside) (AMG) was also found to effectively inhibit MAO-A and MAO-B (IC50=2.34 and 1.87muM, respectively), and to reversibly and competitively inhibit MAO-A and MAO-B (Ki=1.06 and 0.38muM, respectively).	methyl-galactopyranoside	37-40	monoamine oxidase B	Homo sapiens	189-194
28634060-5	2017	Molecular docking simulation revealed the binding energy of acacetin for MAO-B (-44.2kcal/mol) was greater than its energy for MAO-A (-27.0kcal/mol), and that the Cys172 residue of MAO-B was important for hydrogen bonding with acacetin.	acacetin	60-68	monoamine oxidase B	Homo sapiens	73-78
28634060-5	2017	Molecular docking simulation revealed the binding energy of acacetin for MAO-B (-44.2kcal/mol) was greater than its energy for MAO-A (-27.0kcal/mol), and that the Cys172 residue of MAO-B was important for hydrogen bonding with acacetin.	acacetin	60-68	monoamine oxidase B	Homo sapiens	181-186
28634060-5	2017	Molecular docking simulation revealed the binding energy of acacetin for MAO-B (-44.2kcal/mol) was greater than its energy for MAO-A (-27.0kcal/mol), and that the Cys172 residue of MAO-B was important for hydrogen bonding with acacetin.	Hydrogen	205-213	monoamine oxidase B	Homo sapiens	73-78
28634060-5	2017	Molecular docking simulation revealed the binding energy of acacetin for MAO-B (-44.2kcal/mol) was greater than its energy for MAO-A (-27.0kcal/mol), and that the Cys172 residue of MAO-B was important for hydrogen bonding with acacetin.	acacetin	227-235	monoamine oxidase B	Homo sapiens	73-78
28738644-3	2017	The sensor consists of a screen printed carbon working electrode modified with 20% manganese dioxide (MnO2) and the enzyme hMAO B, which was immobilised on the electrode via a dialysis membrane (regenerated cellulose, molecular weight cut-off 14000).	Cellulose	207-216	monoamine oxidase B	Homo sapiens	123-129
28738644-4	2017	Inhibition of hMAO B is evaluated by adding different concentrations of the inhibitor selegiline hydrochloride to the enzyme and applying a defined amount of the hMAO B substrate phenylethylamine (PEA).	Selegiline	86-110	monoamine oxidase B	Homo sapiens	14-20
28738644-4	2017	Inhibition of hMAO B is evaluated by adding different concentrations of the inhibitor selegiline hydrochloride to the enzyme and applying a defined amount of the hMAO B substrate phenylethylamine (PEA).	Phenethylamines	179-195	monoamine oxidase B	Homo sapiens	14-20
28738644-4	2017	Inhibition of hMAO B is evaluated by adding different concentrations of the inhibitor selegiline hydrochloride to the enzyme and applying a defined amount of the hMAO B substrate phenylethylamine (PEA).	Phenethylamines	179-195	monoamine oxidase B	Homo sapiens	162-168
28738644-4	2017	Inhibition of hMAO B is evaluated by adding different concentrations of the inhibitor selegiline hydrochloride to the enzyme and applying a defined amount of the hMAO B substrate phenylethylamine (PEA).	Phenethylamines	197-200	monoamine oxidase B	Homo sapiens	14-20
28738644-4	2017	Inhibition of hMAO B is evaluated by adding different concentrations of the inhibitor selegiline hydrochloride to the enzyme and applying a defined amount of the hMAO B substrate phenylethylamine (PEA).	Phenethylamines	197-200	monoamine oxidase B	Homo sapiens	162-168
29114238-2	2017	Methods: Using the PGR, we recorded the daily walking profiles of 14 PD patients before and after the addition or increase in dose of an MAO-B inhibitor (selegiline, average dose: 4.0 mg/day) as part of their medicine regimen, and evaluated their gait using the unified Parkinson"s disease rating scale (UPDRS) and scores from a freezing of gait (FOG) questionnaire.	Selegiline	154-164	monoamine oxidase B	Homo sapiens	137-142
28797881-0	2017	Synthesis and structure-activity relationship study of novel 3-heteroarylcoumarins based on pyridazine scaffold as selective MAO-B inhibitors.	3-heteroarylcoumarins	61-82	monoamine oxidase B	Homo sapiens	125-130
28797881-0	2017	Synthesis and structure-activity relationship study of novel 3-heteroarylcoumarins based on pyridazine scaffold as selective MAO-B inhibitors.	pyridazine	92-102	monoamine oxidase B	Homo sapiens	125-130
28797881-1	2017	Compounds of hybrid structure pyridazine-coumarin were discovered as potent, selective and reversible inhibitors of monoamine oxidase B (MAO-B).	pyridazine	30-40	monoamine oxidase B	Homo sapiens	116-135
28797881-1	2017	Compounds of hybrid structure pyridazine-coumarin were discovered as potent, selective and reversible inhibitors of monoamine oxidase B (MAO-B).	pyridazine	30-40	monoamine oxidase B	Homo sapiens	137-142
28797881-1	2017	Compounds of hybrid structure pyridazine-coumarin were discovered as potent, selective and reversible inhibitors of monoamine oxidase B (MAO-B).	coumarin	41-49	monoamine oxidase B	Homo sapiens	116-135
28797881-1	2017	Compounds of hybrid structure pyridazine-coumarin were discovered as potent, selective and reversible inhibitors of monoamine oxidase B (MAO-B).	coumarin	41-49	monoamine oxidase B	Homo sapiens	137-142
29044437-1	2017	Coumarins are natural and synthetic active ingredients widely applied in diverse types of medicinal treatments, such as cancer, inflammation, infection, and enzyme inhibition (monoamine oxidase B).	Coumarins	0-9	monoamine oxidase B	Homo sapiens	176-195
28751116-0	2017	Monoamine oxidase B oxidizes a novel multikinase inhibitor KW-2449 to its iminium ion and aldehyde oxidase further converts it to the oxo-piperazine form in human.	KW 2449	59-66	monoamine oxidase B	Homo sapiens	0-19
28751116-0	2017	Monoamine oxidase B oxidizes a novel multikinase inhibitor KW-2449 to its iminium ion and aldehyde oxidase further converts it to the oxo-piperazine form in human.	oxo-piperazine	134-148	monoamine oxidase B	Homo sapiens	0-19
28751116-3	2017	An inhibition study suggested that monoamine oxidase-B (MAO-B) oxidizes KW-2449 to an iminium (intermediate) and aldehyde oxidase (AO) then metabolizes the intermediate to M1.	KW 2449	72-79	monoamine oxidase B	Homo sapiens	35-54
28751116-3	2017	An inhibition study suggested that monoamine oxidase-B (MAO-B) oxidizes KW-2449 to an iminium (intermediate) and aldehyde oxidase (AO) then metabolizes the intermediate to M1.	KW 2449	72-79	monoamine oxidase B	Homo sapiens	56-61
28751116-3	2017	An inhibition study suggested that monoamine oxidase-B (MAO-B) oxidizes KW-2449 to an iminium (intermediate) and aldehyde oxidase (AO) then metabolizes the intermediate to M1.	iminium	86-93	monoamine oxidase B	Homo sapiens	35-54
28751116-3	2017	An inhibition study suggested that monoamine oxidase-B (MAO-B) oxidizes KW-2449 to an iminium (intermediate) and aldehyde oxidase (AO) then metabolizes the intermediate to M1.	iminium	86-93	monoamine oxidase B	Homo sapiens	56-61
28751116-4	2017	The conversion of KW-2449 to the iminium (intermediate) by MAO-B was confirmed by the formation of its cyanide adduct.	KW 2449	18-25	monoamine oxidase B	Homo sapiens	59-64
28751116-4	2017	The conversion of KW-2449 to the iminium (intermediate) by MAO-B was confirmed by the formation of its cyanide adduct.	iminium	33-40	monoamine oxidase B	Homo sapiens	59-64
28751116-4	2017	The conversion of KW-2449 to the iminium (intermediate) by MAO-B was confirmed by the formation of its cyanide adduct.	Cyanides	103-110	monoamine oxidase B	Homo sapiens	59-64
28751116-5	2017	This cooperative metabolic pathway by MAO-B and AO was newly identified in the metabolism of piperazine.	Piperazine	93-103	monoamine oxidase B	Homo sapiens	38-43
28751116-8	2017	Finally, we found that (E)-3-amino-1-{4-[2-(1H-Indazol-3-yl)vinyl]benzoyl}-pyrrolidine (Compound A) as a stable compound against MAO-B and AO.	(e)-3-amino-1-{4-[2-(1h-indazol-3-yl)vinyl]benzoyl}-pyrrolidine	23-86	monoamine oxidase B	Homo sapiens	129-134
28185143-3	2017	METHODS: Inhibition potential of 1-aminobenzotriazole and ketoconazole was studied in mice, rat and human liver microsomes, S9 fractions, MAO-A and MAO-B expressed enzymes by monitoring the formation of 4-hydroxyquinoline (4-HQ) from kynuramine, a specific substrate of MAO by liquid chromatography-tandem mass spectrometry (LC-MS/MS).	Ketoconazole	58-70	monoamine oxidase B	Homo sapiens	148-153
28185143-5	2017	RESULTS: 1-aminobenzotriazole and ketoconazole inhibited both MAO isozymes (MAO-A and MAO-B) with more specificity towards MAO-B.	1-aminobenzotriazole	9-29	monoamine oxidase B	Homo sapiens	86-91
28185143-5	2017	RESULTS: 1-aminobenzotriazole and ketoconazole inhibited both MAO isozymes (MAO-A and MAO-B) with more specificity towards MAO-B.	1-aminobenzotriazole	9-29	monoamine oxidase B	Homo sapiens	123-128
28185143-5	2017	RESULTS: 1-aminobenzotriazole and ketoconazole inhibited both MAO isozymes (MAO-A and MAO-B) with more specificity towards MAO-B.	Ketoconazole	34-46	monoamine oxidase B	Homo sapiens	86-91
28185143-5	2017	RESULTS: 1-aminobenzotriazole and ketoconazole inhibited both MAO isozymes (MAO-A and MAO-B) with more specificity towards MAO-B.	Ketoconazole	34-46	monoamine oxidase B	Homo sapiens	123-128
29018297-0	2017	Xadago (Safinamide): A Monoamine Oxidase B Inhibitor for the Adjunct Treatment of Motor Symptoms in Parkinson"s Disease.	safinamide	0-6	monoamine oxidase B	Homo sapiens	23-42
29018297-0	2017	Xadago (Safinamide): A Monoamine Oxidase B Inhibitor for the Adjunct Treatment of Motor Symptoms in Parkinson"s Disease.	safinamide	8-18	monoamine oxidase B	Homo sapiens	23-42
29018297-1	2017	Xadago (safinamide), a monoamine oxidase B inhibitor for the adjunct treatment of motor symptoms in Parkinson"s disease.	safinamide	0-6	monoamine oxidase B	Homo sapiens	23-42
29018297-1	2017	Xadago (safinamide), a monoamine oxidase B inhibitor for the adjunct treatment of motor symptoms in Parkinson"s disease.	safinamide	8-18	monoamine oxidase B	Homo sapiens	23-42
29050386-0	2017	Brain monoamine oxidase B and A in human parkinsonian dopamine deficiency disorders.	Dopamine	54-62	monoamine oxidase B	Homo sapiens	6-25
28682929-6	2017	Patients on rasagiline or safinamide showed lower monoamine oxidase-B enzyme activity compared with patients without monoamine oxidase B inhibitor intake.	safinamide	26-36	monoamine oxidase B	Homo sapiens	117-136
28293967-1	2017	OBJECTIVE: Rasagiline is a second-generation potent selective inhibitor of monoamine oxidase-B.	rasagiline	11-21	monoamine oxidase B	Homo sapiens	75-94
28682929-2	2017	Rasagiline is an irreversible inhibitor of monoamine oxidase B.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	43-62
28682929-6	2017	Patients on rasagiline or safinamide showed lower monoamine oxidase-B enzyme activity compared with patients without monoamine oxidase B inhibitor intake.	rasagiline	12-22	monoamine oxidase B	Homo sapiens	50-69
28682929-6	2017	Patients on rasagiline or safinamide showed lower monoamine oxidase-B enzyme activity compared with patients without monoamine oxidase B inhibitor intake.	rasagiline	12-22	monoamine oxidase B	Homo sapiens	117-136
28682929-6	2017	Patients on rasagiline or safinamide showed lower monoamine oxidase-B enzyme activity compared with patients without monoamine oxidase B inhibitor intake.	safinamide	26-36	monoamine oxidase B	Homo sapiens	50-69
28577058-2	2017	MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neurons in animal and cellular models of neurodegeneration.	rasagiline	18-28	monoamine oxidase B	Homo sapiens	0-5
28577058-2	2017	MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neurons in animal and cellular models of neurodegeneration.	Selegiline	45-56	monoamine oxidase B	Homo sapiens	0-5
28577058-5	2017	Selegiline significantly increased Mao-B, which was suppressed by Mao-A knockdown with short interfering (si)RNA, whereas rasagiline less markedly increased Mao-B, which was not affected by Mao-A knockdown.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	35-40
28577058-5	2017	Selegiline significantly increased Mao-B, which was suppressed by Mao-A knockdown with short interfering (si)RNA, whereas rasagiline less markedly increased Mao-B, which was not affected by Mao-A knockdown.	rasagiline	122-132	monoamine oxidase B	Homo sapiens	157-162
28577058-6	2017	Mao-A mRNA was also markedly increased by rasagiline and selegiline, and Mao-B knockdown significantly enhanced the induction by selegiline, but not by rasagiline.	Selegiline	129-139	monoamine oxidase B	Homo sapiens	73-78
28577058-8	2017	Selegiline synergistically enhanced the expression of these genes in Mao-B knockdown cells, but Mao-A knockdown suppressed the increase.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	69-74
28577058-9	2017	Rasagiline increased BDNF and GDNF, which Mao-B and Mao-A knockdown inhibited.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	42-47
28577058-10	2017	These results show that MAO-B might function as a repressor and MAO-A as a mediator in the constitutional expression of pro-survival genes, and that MAO-B and MAO-A might regulate different signal pathways for rasagiline and selegiline to induce neuroprotective genes.	rasagiline	210-220	monoamine oxidase B	Homo sapiens	24-29
28577058-10	2017	These results show that MAO-B might function as a repressor and MAO-A as a mediator in the constitutional expression of pro-survival genes, and that MAO-B and MAO-A might regulate different signal pathways for rasagiline and selegiline to induce neuroprotective genes.	rasagiline	210-220	monoamine oxidase B	Homo sapiens	149-154
28577058-10	2017	These results show that MAO-B might function as a repressor and MAO-A as a mediator in the constitutional expression of pro-survival genes, and that MAO-B and MAO-A might regulate different signal pathways for rasagiline and selegiline to induce neuroprotective genes.	Selegiline	225-235	monoamine oxidase B	Homo sapiens	149-154
28642233-0	2017	Sembragiline: A Novel, Selective Monoamine Oxidase Type B Inhibitor for the Treatment of Alzheimer"s Disease.	sembragiline	0-12	monoamine oxidase B	Homo sapiens	33-57
28642233-4	2017	Therefore, reduction of ROS-induced oxidative stress via inhibition of MAO-B activity may delay the progression of the disease.	Reactive Oxygen Species	24-27	monoamine oxidase B	Homo sapiens	71-76
28642233-5	2017	In the present study we report the pharmacological properties of sembragiline, a novel selective MAO-B inhibitor specifically developed for the treatment of AD, and on its effect on ROS-mediated neuronal injury and astrogliosis in MAO-B transgenic animals.	sembragiline	65-77	monoamine oxidase B	Homo sapiens	97-102
28642233-5	2017	In the present study we report the pharmacological properties of sembragiline, a novel selective MAO-B inhibitor specifically developed for the treatment of AD, and on its effect on ROS-mediated neuronal injury and astrogliosis in MAO-B transgenic animals.	sembragiline	65-77	monoamine oxidase B	Homo sapiens	231-236
28642233-6	2017	Sembragiline showed potent and long-lasting MAO-B-selective inhibition and did not inhibit MAO-A at doses where full inhibition of MAO-B was observed.	sembragiline	0-12	monoamine oxidase B	Homo sapiens	44-49
28642233-9	2017	Additionally, in experiments using a transgenic animal model conditionally overexpressing MAO-B in astroglia, sembragiline protected against neuronal loss and reduced both ROS formation and reactive astrogliosis.	sembragiline	110-122	monoamine oxidase B	Homo sapiens	90-95
28685208-0	2017	Iron modulates the activity of monoamine oxidase B in SH-SY5Y cells.	Iron	0-4	monoamine oxidase B	Homo sapiens	31-50
28685208-2	2017	However, the association of iron with MAO-B activity was poorly understood.	Iron	28-32	monoamine oxidase B	Homo sapiens	38-43
28685208-3	2017	Here we took advantage of highly sensitive and specific fluorescence probes to examine the change in MAO-B activity in human dopaminergic neuroblastoma (SH-SY5Y) cells upon iron exposure.	Iron	173-177	monoamine oxidase B	Homo sapiens	101-106
28685208-4	2017	Both ferric and ferrous ions could significantly enhance the activity of MAO-B, instead of MAO-A, in SH-SY5Y cells.	Ferric enterobactin ion	5-11	monoamine oxidase B	Homo sapiens	73-78
28685208-4	2017	Both ferric and ferrous ions could significantly enhance the activity of MAO-B, instead of MAO-A, in SH-SY5Y cells.	ammonium ferrous sulfate	16-23	monoamine oxidase B	Homo sapiens	73-78
28685208-5	2017	In addition, iron-induced increase in MAO-B probe fluorescence could be prevented by pargyline and other newly developed MAO-B inhibitors, suggesting that it was MAO-B activity-dependent.	Iron	13-17	monoamine oxidase B	Homo sapiens	38-43
28685208-5	2017	In addition, iron-induced increase in MAO-B probe fluorescence could be prevented by pargyline and other newly developed MAO-B inhibitors, suggesting that it was MAO-B activity-dependent.	Iron	13-17	monoamine oxidase B	Homo sapiens	121-126
28685208-5	2017	In addition, iron-induced increase in MAO-B probe fluorescence could be prevented by pargyline and other newly developed MAO-B inhibitors, suggesting that it was MAO-B activity-dependent.	Iron	13-17	monoamine oxidase B	Homo sapiens	121-126
28685208-5	2017	In addition, iron-induced increase in MAO-B probe fluorescence could be prevented by pargyline and other newly developed MAO-B inhibitors, suggesting that it was MAO-B activity-dependent.	Pargyline	85-94	monoamine oxidase B	Homo sapiens	38-43
28685208-6	2017	These findings may suggest MAO-B is an important sensor in iron-stressed neuronal cells.	Iron	59-63	monoamine oxidase B	Homo sapiens	27-32
28332824-0	2017	Indole-Substituted Benzothiazoles and Benzoxazoles as Selective and Reversible MAO-B Inhibitors for Treatment of Parkinson"s Disease.	indole-substituted benzothiazoles	0-33	monoamine oxidase B	Homo sapiens	79-84
28650165-3	2017	The practical utility of this transition-metal-free approach to 1,3,4-oxadiazole-2(3H)-one is highlighted by the convenient synthesis of a commercial herbicide Oxadiazon and a MAO B inhibitor.	Metals	41-46	monoamine oxidase B	Homo sapiens	176-181
28650165-3	2017	The practical utility of this transition-metal-free approach to 1,3,4-oxadiazole-2(3H)-one is highlighted by the convenient synthesis of a commercial herbicide Oxadiazon and a MAO B inhibitor.	1,3,4-oxadiazol-2-ol	64-90	monoamine oxidase B	Homo sapiens	176-181
28456030-4	2017	An older study reports that 1,4-benzoquinone inhibits MAO-A and MAO-B from human synaptosomes.	quinone	28-44	monoamine oxidase B	Homo sapiens	64-69
28456030-7	2017	The 1,4-benzoquinones were found to be moderately potent MAO inhibitors with IC50 values of 5.03-13.2 muM (MAO-A) and 3.69-23.2 muM (MAO-B).	Benzoquinones	4-21	monoamine oxidase B	Homo sapiens	133-138
28456030-10	2017	MAO-B is much less sensitive to inactivation by the 1,4-benzoquinones.	Benzoquinones	52-69	monoamine oxidase B	Homo sapiens	0-5
28332824-0	2017	Indole-Substituted Benzothiazoles and Benzoxazoles as Selective and Reversible MAO-B Inhibitors for Treatment of Parkinson"s Disease.	Benzoxazoles	38-50	monoamine oxidase B	Homo sapiens	79-84
28332824-1	2017	To develop novel, selective, and reversible MAO-B inhibitors for safer treatment of Parkinson"s disease, benzothiazole and benzoxazole derivatives with indole moiety were designed and synthesized.	benzothiazole	105-118	monoamine oxidase B	Homo sapiens	44-49
28332824-1	2017	To develop novel, selective, and reversible MAO-B inhibitors for safer treatment of Parkinson"s disease, benzothiazole and benzoxazole derivatives with indole moiety were designed and synthesized.	Benzoxazoles	123-134	monoamine oxidase B	Homo sapiens	44-49
28332824-1	2017	To develop novel, selective, and reversible MAO-B inhibitors for safer treatment of Parkinson"s disease, benzothiazole and benzoxazole derivatives with indole moiety were designed and synthesized.	indole	152-158	monoamine oxidase B	Homo sapiens	44-49
28377303-6	2017	Nile blue also represents a potent MAO-B inhibitor with an IC50 value of 0.012muM.	Nile Blue	0-9	monoamine oxidase B	Homo sapiens	35-40
28629145-0	2017	Synthesis and Evaluation of Phenylxanthine Derivatives as Potential Dual A2AR Antagonists/MAO-B Inhibitors for Parkinson"s Disease.	phenylxanthine	28-42	monoamine oxidase B	Homo sapiens	90-95
28629145-1	2017	The aim of this research was to prove the speculation that phenylxanthine (PX) derivatives possess adenosine A2A receptor (A2AR)-blocking properties and to screening and evaluate these PX derivatives as dual A2AR antagonists/MAO-B inhibitors for Parkinson"s disease.	phenylxanthine	59-73	monoamine oxidase B	Homo sapiens	225-230
28629145-1	2017	The aim of this research was to prove the speculation that phenylxanthine (PX) derivatives possess adenosine A2A receptor (A2AR)-blocking properties and to screening and evaluate these PX derivatives as dual A2AR antagonists/MAO-B inhibitors for Parkinson"s disease.	Pentoxifylline	75-77	monoamine oxidase B	Homo sapiens	225-230
28629145-5	2017	Further, the compounds PX-D-P6 and PX-E-P8 displayed efficacious antiparkinsonian properties in haloperidol-induced catalepsy experiments, verifying that these two compounds were potent A2AR antagonists and MAO-B inhibitors.	px-d-p6	23-30	monoamine oxidase B	Homo sapiens	207-212
28629145-5	2017	Further, the compounds PX-D-P6 and PX-E-P8 displayed efficacious antiparkinsonian properties in haloperidol-induced catalepsy experiments, verifying that these two compounds were potent A2AR antagonists and MAO-B inhibitors.	px-e-p8	35-42	monoamine oxidase B	Homo sapiens	207-212
28487125-3	2017	The most promising compound TM-33 showed potent and balance inhibitory activities toward ChE and MAO (eeAChE, eqBuChE, hMAO-A and hMAO-B with IC50 values of 0.56muM, 2.3muM, 0.3muM and 1.4muM, respectively) but low selectivity.	tm-33	28-33	monoamine oxidase B	Homo sapiens	130-136
28537214-4	2017	Areas covered: This invited review suggests safinamide as an ideal compound for therapy of Parkinson"s disease, as its pharmacological profile includes reversible monoamine oxidase B inhibition, blockage of voltage-dependent sodium channels, modulation of calcium channels and abnormal glutamate release.	safinamide	44-54	monoamine oxidase B	Homo sapiens	163-182
28550482-1	2017	Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD).	Selegiline	53-63	monoamine oxidase B	Homo sapiens	0-24
28550482-1	2017	Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD).	Selegiline	53-63	monoamine oxidase B	Homo sapiens	26-31
28550482-1	2017	Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD).	rasagiline	68-78	monoamine oxidase B	Homo sapiens	0-24
28550482-1	2017	Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD).	rasagiline	68-78	monoamine oxidase B	Homo sapiens	26-31
28550482-1	2017	Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD).	Levodopa	130-138	monoamine oxidase B	Homo sapiens	0-24
28550482-1	2017	Monoamine oxidase type B (MAO-B) inhibitors, such as selegiline and rasagiline, can be used as monotherapy or adjuvant therapy to levodopa in Parkinson"s disease (PD).	Levodopa	130-138	monoamine oxidase B	Homo sapiens	26-31
28550482-8	2017	However, MAO-B inhibitor use was associated with ~2-fold lower change in daily dose of levodopa (p < 0.001) and lower dyskinesia scores (p = 0.028) than non-users.	Levodopa	87-95	monoamine oxidase B	Homo sapiens	9-14
28550482-10	2017	Long-term use of MAO-B inhibitors resulted in a significant reduction in levodopa requirements and a lower frequency of dyskinesias in patients with PD.	Levodopa	73-81	monoamine oxidase B	Homo sapiens	17-22
28291352-1	2017	Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of aryalkylamines neurotransmitters with concomitant reduction of oxygen to hydrogen peroxide.	Hydrogen Peroxide	140-157	monoamine oxidase B	Homo sapiens	0-19
28068665-4	2017	The piloquinone 4,7-dihydroxy-3-methyl-2-(4-methyl-1-oxopentyl)-6H-dibenzo[b,d]pyran-6-one (1) was found to be a highly potent inhibitor of human MAO-B, with an IC50 value of 1.21 micro; in addition, it was found to be highly effective against MAO-A, with an IC50 value of 6.47 micro.	Piloquinone	4-15	monoamine oxidase B	Homo sapiens	146-151
28068665-4	2017	The piloquinone 4,7-dihydroxy-3-methyl-2-(4-methyl-1-oxopentyl)-6H-dibenzo[b,d]pyran-6-one (1) was found to be a highly potent inhibitor of human MAO-B, with an IC50 value of 1.21 micro; in addition, it was found to be highly effective against MAO-A, with an IC50 value of 6.47 micro.	4,7-dihydroxy-3-methyl-2-(4-methyl-1-oxopentyl)-6H-dibenzo[b,d]pyran-6-one	16-90	monoamine oxidase B	Homo sapiens	146-151
28068665-6	2017	Compound 1,8-dihydroxy-2-methyl-3-(4-methyl-1-oxopentyl)-9,10-phenanthrenedione (2) was moderately effective for the inhibition of MAO-B (IC50 = 14.50 micro) but not for MAO-A (IC50 > 80 micro).	1,8-dihydroxy-2-methyl-3-(4-methyl-1-oxopentyl)-9,10-phenanthrenedione	9-79	monoamine oxidase B	Homo sapiens	131-136
28299453-4	2017	We confirm with this design, that rasagiline and selegiline inhibit monoamine oxidase-B but not monoamine oxidase-A after single dosing.	rasagiline	34-44	monoamine oxidase B	Homo sapiens	68-87
28299453-4	2017	We confirm with this design, that rasagiline and selegiline inhibit monoamine oxidase-B but not monoamine oxidase-A after single dosing.	Selegiline	49-59	monoamine oxidase B	Homo sapiens	68-87
28301816-8	2017	The reference drugs selegiline (IC50 = 0.040 muM) and rasagiline (IC50 = 0.066 muM) also displayed a significant inhibition against hMAO-B.	Selegiline	20-30	monoamine oxidase B	Homo sapiens	132-138
28301816-8	2017	The reference drugs selegiline (IC50 = 0.040 muM) and rasagiline (IC50 = 0.066 muM) also displayed a significant inhibition against hMAO-B.	rasagiline	54-64	monoamine oxidase B	Homo sapiens	132-138
28291352-0	2017	Understanding the Molecular Determinant of Reversible Human Monoamine Oxidase B Inhibitors Containing 2H-Chromen-2-One Core: Structure-Based and Ligand-Based Derived Three-Dimensional Quantitative Structure-Activity Relationships Predictive Models.	coumarin	102-118	monoamine oxidase B	Homo sapiens	60-79
28291352-1	2017	Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of aryalkylamines neurotransmitters with concomitant reduction of oxygen to hydrogen peroxide.	aryalkylamines	67-81	monoamine oxidase B	Homo sapiens	0-19
28291352-1	2017	Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of aryalkylamines neurotransmitters with concomitant reduction of oxygen to hydrogen peroxide.	aryalkylamines	67-81	monoamine oxidase B	Homo sapiens	21-26
28291352-1	2017	Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of aryalkylamines neurotransmitters with concomitant reduction of oxygen to hydrogen peroxide.	Oxygen	130-136	monoamine oxidase B	Homo sapiens	0-19
28291352-1	2017	Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of aryalkylamines neurotransmitters with concomitant reduction of oxygen to hydrogen peroxide.	Oxygen	130-136	monoamine oxidase B	Homo sapiens	21-26
28291352-1	2017	Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of aryalkylamines neurotransmitters with concomitant reduction of oxygen to hydrogen peroxide.	Hydrogen Peroxide	140-157	monoamine oxidase B	Homo sapiens	21-26
28251489-3	2017	The aim of this study was to determine the effectiveness of eckol and dieckol isolated from the methanolic extract of E. bicyclis against PD by the inhibition of human MAO-A and MAO-B (hMAO-A and hMAO-B).	dieckol	70-77	monoamine oxidase B	Homo sapiens	178-183
28273563-0	2017	Discovery of highly selective and potent monoamine oxidase B inhibitors: Contribution of additional phenyl rings introduced into 2-aryl-1,3,4-oxadiazin-5(6H)-one.	2-aryl-1,3,4-oxadiazin-5(6h)-one	129-161	monoamine oxidase B	Homo sapiens	41-60
28273563-1	2017	Monoamine oxidase B (MAO-B) is a flavin adenine dinucleotide (FAD)-containing enzyme that plays a major role in the oxidative deamination of biogenic amines and neurotransmitters.	Flavin-Adenine Dinucleotide	33-60	monoamine oxidase B	Homo sapiens	0-19
28273563-1	2017	Monoamine oxidase B (MAO-B) is a flavin adenine dinucleotide (FAD)-containing enzyme that plays a major role in the oxidative deamination of biogenic amines and neurotransmitters.	Flavin-Adenine Dinucleotide	33-60	monoamine oxidase B	Homo sapiens	21-26
28273563-1	2017	Monoamine oxidase B (MAO-B) is a flavin adenine dinucleotide (FAD)-containing enzyme that plays a major role in the oxidative deamination of biogenic amines and neurotransmitters.	Flavin-Adenine Dinucleotide	62-65	monoamine oxidase B	Homo sapiens	0-19
28273563-1	2017	Monoamine oxidase B (MAO-B) is a flavin adenine dinucleotide (FAD)-containing enzyme that plays a major role in the oxidative deamination of biogenic amines and neurotransmitters.	Flavin-Adenine Dinucleotide	62-65	monoamine oxidase B	Homo sapiens	21-26
28273563-3	2017	Here, we report a series of 2-aryl-1,3,4-oxadiazin-5(6H)-one derivatives as highly selective and potent MAO-B inhibitors.	2-aryl-1,3,4-oxadiazin-5(6h)-one	28-60	monoamine oxidase B	Homo sapiens	104-109
28273563-7	2017	Docking results suggest that an optimal linker between two aromatic rings on the 2-aryl-1,3,4-oxadiazin-5(6H)-one scaffold is a key element in the binding and inhibition of MAO-B.	2-aryl-1,3,4-oxadiazin-5(6h)-one	81-113	monoamine oxidase B	Homo sapiens	173-178
28251489-6	2017	The results suggested that methanolic extract of E. bicyclis and its isolated phlorotannins, eckol and dieckol, have potent inhibitory activity against hMAO-A and hMAO-B.	methanolic	27-37	monoamine oxidase B	Homo sapiens	163-169
28251489-6	2017	The results suggested that methanolic extract of E. bicyclis and its isolated phlorotannins, eckol and dieckol, have potent inhibitory activity against hMAO-A and hMAO-B.	phlorotannins	78-91	monoamine oxidase B	Homo sapiens	163-169
28251489-3	2017	The aim of this study was to determine the effectiveness of eckol and dieckol isolated from the methanolic extract of E. bicyclis against PD by the inhibition of human MAO-A and MAO-B (hMAO-A and hMAO-B).	dieckol	70-77	monoamine oxidase B	Homo sapiens	196-202
28251489-6	2017	The results suggested that methanolic extract of E. bicyclis and its isolated phlorotannins, eckol and dieckol, have potent inhibitory activity against hMAO-A and hMAO-B.	dieckol	103-110	monoamine oxidase B	Homo sapiens	163-169
28251489-8	2017	Molecular docking simulation predicted that eckol and dieckol exhibit higher binding affinity towards hMAO-A and hMAO-B through hydrogen bonding and hydrophobic interactions.	dieckol	54-61	monoamine oxidase B	Homo sapiens	113-119
27665574-3	2017	The pharmacological profile of safinamide includes reversible monoamine oxidase B inhibition, blockage of voltage-dependent Na+ channels, modulation of Ca2+ channels, and inhibition of glutamate release.	safinamide	31-41	monoamine oxidase B	Homo sapiens	62-81
28251489-8	2017	Molecular docking simulation predicted that eckol and dieckol exhibit higher binding affinity towards hMAO-A and hMAO-B through hydrogen bonding and hydrophobic interactions.	Hydrogen	128-136	monoamine oxidase B	Homo sapiens	113-119
28359327-0	2017	Monoamine oxidase B inhibitor, selegiline, reduces 18F-THK5351 uptake in the human brain.	Selegiline	31-41	monoamine oxidase B	Homo sapiens	0-19
28359327-0	2017	Monoamine oxidase B inhibitor, selegiline, reduces 18F-THK5351 uptake in the human brain.	THK5351	55-62	monoamine oxidase B	Homo sapiens	0-19
28359327-3	2017	Here, we tested the effects of MAO-B inhibition on 18F-THK5351 brain uptake using PET and autoradiography.	THK5351	55-62	monoamine oxidase B	Homo sapiens	31-36
28359327-14	2017	Tissue autoradiography confirmed the effects of MAO-B inhibition on 18F-THK5351 uptake.	THK5351	68-79	monoamine oxidase B	Homo sapiens	48-53
28267984-0	2017	Pyridoxine-resveratrol hybrids Mannich base derivatives as novel dual inhibitors of AChE and MAO-B with antioxidant and metal-chelating properties for the treatment of Alzheimer"s disease.	Pyridoxine	0-10	monoamine oxidase B	Homo sapiens	93-98
28267984-0	2017	Pyridoxine-resveratrol hybrids Mannich base derivatives as novel dual inhibitors of AChE and MAO-B with antioxidant and metal-chelating properties for the treatment of Alzheimer"s disease.	Resveratrol	11-22	monoamine oxidase B	Homo sapiens	93-98
28267984-0	2017	Pyridoxine-resveratrol hybrids Mannich base derivatives as novel dual inhibitors of AChE and MAO-B with antioxidant and metal-chelating properties for the treatment of Alzheimer"s disease.	Mannich Bases	31-43	monoamine oxidase B	Homo sapiens	93-98
28267984-0	2017	Pyridoxine-resveratrol hybrids Mannich base derivatives as novel dual inhibitors of AChE and MAO-B with antioxidant and metal-chelating properties for the treatment of Alzheimer"s disease.	Metals	120-125	monoamine oxidase B	Homo sapiens	93-98
28188911-2	2017	To uncover the molecular rationale of hMAOs selectivity, two recently prepared 2H-chromene-2-ones, namely compounds 1 and 2, were herein chosen as molecular probes being highly selective toward hMAO-A and hMAO-B, respectively.	hmaos	38-43	monoamine oxidase B	Homo sapiens	205-211
28188911-2	2017	To uncover the molecular rationale of hMAOs selectivity, two recently prepared 2H-chromene-2-ones, namely compounds 1 and 2, were herein chosen as molecular probes being highly selective toward hMAO-A and hMAO-B, respectively.	2h-chromene-2-ones	79-97	monoamine oxidase B	Homo sapiens	205-211
28435530-2	2017	The most potent compound, (2-chloropyridin-4-yl)methanamine 20 (hLOXL2 IC50 = 126 nM), was shown to be selective for LOXL2 over LOX and three other amine oxidases (MAO-A, MAO-B, and SSAO).	(2-chloropyridin-4-yl)methanamine	26-59	monoamine oxidase B	Homo sapiens	171-176
27926950-4	2017	Based on our interest in discovering reversible inhibitors with specificity for MAO-B, we have recently reported that, among a series of 10 3,4-dihydro-2(1H)-quinolinone derivatives, are high potency MAO-B inhibitors, with a number of homologues displaying good selectivities for MAO-B over the MAO-A isoform.	3,4-dihydro-2(1H)-quinolinone	140-169	monoamine oxidase B	Homo sapiens	200-205
27926950-4	2017	Based on our interest in discovering reversible inhibitors with specificity for MAO-B, we have recently reported that, among a series of 10 3,4-dihydro-2(1H)-quinolinone derivatives, are high potency MAO-B inhibitors, with a number of homologues displaying good selectivities for MAO-B over the MAO-A isoform.	3,4-dihydro-2(1H)-quinolinone	140-169	monoamine oxidase B	Homo sapiens	80-85
27926950-4	2017	Based on our interest in discovering reversible inhibitors with specificity for MAO-B, we have recently reported that, among a series of 10 3,4-dihydro-2(1H)-quinolinone derivatives, are high potency MAO-B inhibitors, with a number of homologues displaying good selectivities for MAO-B over the MAO-A isoform.	3,4-dihydro-2(1H)-quinolinone	140-169	monoamine oxidase B	Homo sapiens	200-205
27926950-8	2017	Conclusions: It may thus be concluded that substitution of 3,4-dihydro-2(1H)-quinolinone on C6 and C7 with a variety of side chains yields highly potent and selective MAO-B inhibitors, compounds with existing and prospective therapeutic applications.	3,4-dihydro-2(1H)-quinolinone	59-88	monoamine oxidase B	Homo sapiens	167-172
27633250-0	2017	Positron emission tomography measurement of brain MAO-B inhibition in patients with Alzheimer"s disease and elderly controls after oral administration of sembragiline.	sembragiline	154-166	monoamine oxidase B	Homo sapiens	50-55
27633250-1	2017	PURPOSE: In Alzheimer"s disease (AD), increased metabolism of monoamines by monoamine oxidase type B (MAO-B) leads to the production of toxic reactive oxygen species (ROS), which are thought to contribute to disease pathogenesis.	Reactive Oxygen Species	142-165	monoamine oxidase B	Homo sapiens	76-100
27633250-1	2017	PURPOSE: In Alzheimer"s disease (AD), increased metabolism of monoamines by monoamine oxidase type B (MAO-B) leads to the production of toxic reactive oxygen species (ROS), which are thought to contribute to disease pathogenesis.	Reactive Oxygen Species	142-165	monoamine oxidase B	Homo sapiens	102-107
27633250-1	2017	PURPOSE: In Alzheimer"s disease (AD), increased metabolism of monoamines by monoamine oxidase type B (MAO-B) leads to the production of toxic reactive oxygen species (ROS), which are thought to contribute to disease pathogenesis.	Reactive Oxygen Species	167-170	monoamine oxidase B	Homo sapiens	76-100
27633250-1	2017	PURPOSE: In Alzheimer"s disease (AD), increased metabolism of monoamines by monoamine oxidase type B (MAO-B) leads to the production of toxic reactive oxygen species (ROS), which are thought to contribute to disease pathogenesis.	Reactive Oxygen Species	167-170	monoamine oxidase B	Homo sapiens	102-107
27633250-2	2017	Inhibition of the MAO-B enzyme may restore brain levels of monoaminergic neurotransmitters, reduce the formation of toxic ROS and reduce neuroinflammation (reactive astrocytosis), potentially leading to neuroprotection.	Reactive Oxygen Species	122-125	monoamine oxidase B	Homo sapiens	18-23
27633250-3	2017	Sembragiline (also referred as RO4602522, RG1577 and EVT 302 in previous communications) is a potent, selective and reversible inhibitor of MAO-B developed as a potential treatment for AD.	sembragiline	0-12	monoamine oxidase B	Homo sapiens	140-145
27633250-3	2017	Sembragiline (also referred as RO4602522, RG1577 and EVT 302 in previous communications) is a potent, selective and reversible inhibitor of MAO-B developed as a potential treatment for AD.	sembragiline	31-40	monoamine oxidase B	Homo sapiens	140-145
27633250-3	2017	Sembragiline (also referred as RO4602522, RG1577 and EVT 302 in previous communications) is a potent, selective and reversible inhibitor of MAO-B developed as a potential treatment for AD.	sembragiline	42-48	monoamine oxidase B	Homo sapiens	140-145
27633250-3	2017	Sembragiline (also referred as RO4602522, RG1577 and EVT 302 in previous communications) is a potent, selective and reversible inhibitor of MAO-B developed as a potential treatment for AD.	EVT	53-56	monoamine oxidase B	Homo sapiens	140-145
27633250-4	2017	METHODS: This study assessed the relationship between plasma concentration of sembragiline and brain MAO-B inhibition in patients with AD and in healthy elderly control (EC) subjects.	sembragiline	78-90	monoamine oxidase B	Homo sapiens	101-106
27633250-6	2017	RESULTS: At steady state, the relationship between sembragiline plasma concentration and MAO-B inhibition resulted in an Emax of ~80-90 % across brain regions of interest and in an EC50 of 1-2 ng/mL.	sembragiline	51-63	monoamine oxidase B	Homo sapiens	89-94
27633250-7	2017	Data in patients with AD and EC subjects showed that near-maximal inhibition of brain MAO-B was achieved with 1 mg sembragiline daily, regardless of the population, whereas lower doses resulted in lower and variable brain MAO-B inhibition.	sembragiline	115-127	monoamine oxidase B	Homo sapiens	86-91
27633250-8	2017	CONCLUSIONS: This PET study confirmed that daily treatment of at least 1 mg sembragiline resulted in near-maximal inhibition of brain MAO-B enzyme in patients with AD.	sembragiline	76-88	monoamine oxidase B	Homo sapiens	134-139
28052533-0	2017	What a Difference a Methyl Group Makes: The Selectivity of Monoamine Oxidase B Towards Histamine and N-Methylhistamine.	Histamine	87-96	monoamine oxidase B	Homo sapiens	59-78
28052533-0	2017	What a Difference a Methyl Group Makes: The Selectivity of Monoamine Oxidase B Towards Histamine and N-Methylhistamine.	N-methylhistamine	101-118	monoamine oxidase B	Homo sapiens	59-78
28052533-3	2017	Inhibitors that act on MAO A are used to treat depression, due to their ability to raise serotonin concentrations, whereas MAO B inhibitors decrease dopamine degradation and improve motor control in patients with Parkinson disease.	Dopamine	149-157	monoamine oxidase B	Homo sapiens	123-128
28084742-0	2017	Pharmacophore-Based 3D-QSAR Analysis of Thienyl Chalcones as a New Class of Human MAO-B Inhibitors: Investigation of Combined Quantum Chemical and Molecular Dynamics Approach.	thienyl chalcones	40-57	monoamine oxidase B	Homo sapiens	82-87
28084742-2	2017	Herein, we describe the pharmacophore generation and atom-based three-dimensional quantitative structure-activity relationship (3D-QSAR) analyses of previously reported thiophene-based hMAO-B inhibitors by our research group.	Thiophenes	169-178	monoamine oxidase B	Homo sapiens	185-191
27806193-10	2017	DHC12 inhibited MAO-A and MAO-B activity.	dhc12	0-5	monoamine oxidase B	Homo sapiens	26-31
28107736-0	2017	Crystal structures, binding interactions, and ADME evaluation of brain penetrant N-substituted indazole-5-carboxamides as subnanomolar, selective monoamine oxidase B and dual MAO-A/B inhibitors.	n-substituted indazole-5-carboxamides	81-118	monoamine oxidase B	Homo sapiens	146-165
28107736-6	2017	The binding modes of 12a,b and 13a,b confirmed that the major interactions with hMAO-B were established via the flexible carbonyl group of the carboxamide linkage and the electron-donating nitrogens N1 or N2 of the indazole moiety, allowing further exploration of the alkyl side chain for next step lead optimization efforts.	carboxamide	143-154	monoamine oxidase B	Homo sapiens	80-86
28107736-6	2017	The binding modes of 12a,b and 13a,b confirmed that the major interactions with hMAO-B were established via the flexible carbonyl group of the carboxamide linkage and the electron-donating nitrogens N1 or N2 of the indazole moiety, allowing further exploration of the alkyl side chain for next step lead optimization efforts.	Nitrogen	189-198	monoamine oxidase B	Homo sapiens	80-86
28107736-6	2017	The binding modes of 12a,b and 13a,b confirmed that the major interactions with hMAO-B were established via the flexible carbonyl group of the carboxamide linkage and the electron-donating nitrogens N1 or N2 of the indazole moiety, allowing further exploration of the alkyl side chain for next step lead optimization efforts.	Indazoles	215-223	monoamine oxidase B	Homo sapiens	80-86
28148284-4	2017	Recently, her Stalevo had been changed to rasagiline (a monoamine oxidase B inhibitor).	rasagiline	42-52	monoamine oxidase B	Homo sapiens	56-75
28011206-5	2017	In addition, 6c inhibited self-induced Abeta1-42 aggregation and Cu2+-induced Abeta1-42 aggregation by 89.5% and 79.7% at 25muM respectively, as well as acted as a selective monoamine oxidase B inhibitor (IC50=0.29muM) and a selective biometal chelator.	Carbon	13-15	monoamine oxidase B	Homo sapiens	174-193
28108387-0	2017	Inhibition of monoamine oxidase-B by selegiline reduces cigarette smoke-induced oxidative stress and inflammation in airway epithelial cells.	Selegiline	37-47	monoamine oxidase B	Homo sapiens	14-33
28108387-4	2017	Pretreatment with MAO-B selective inhibitor selegiline reversed the CSM-induced changes in MAO-B activity, ROS levels and IL-8 release in a dose-dependent manner.	Selegiline	44-54	monoamine oxidase B	Homo sapiens	18-23
28108387-4	2017	Pretreatment with MAO-B selective inhibitor selegiline reversed the CSM-induced changes in MAO-B activity, ROS levels and IL-8 release in a dose-dependent manner.	Selegiline	44-54	monoamine oxidase B	Homo sapiens	91-96
28108387-4	2017	Pretreatment with MAO-B selective inhibitor selegiline reversed the CSM-induced changes in MAO-B activity, ROS levels and IL-8 release in a dose-dependent manner.	ros	107-110	monoamine oxidase B	Homo sapiens	18-23
28108387-8	2017	Our study demonstrated that in AECs, inhibition of MAO-B using selegiline reversed the CSM-induced oxidative stress and inflammation.	Selegiline	63-73	monoamine oxidase B	Homo sapiens	51-56
27863747-3	2017	The bis-iminothiazolidinone compounds were investigated in vitro for their inhibition of monoamine oxidase (MAO-A &amp; MAO-B) enzymes with the aim to identify new and distinct pharmacophores for the treatment of neurodegenerative disorders like Parkinson"s disease.	bis-iminothiazolidinone	4-27	monoamine oxidase B	Homo sapiens	120-125
28110399-1	2017	Safinamide (Xadago ) is an orally active, selective, reversible monoamine oxidase-B inhibitor with both dopaminergic and non-dopaminergic (glutamatergic) properties.	safinamide	0-10	monoamine oxidase B	Homo sapiens	64-83
28110399-1	2017	Safinamide (Xadago ) is an orally active, selective, reversible monoamine oxidase-B inhibitor with both dopaminergic and non-dopaminergic (glutamatergic) properties.	safinamide	12-18	monoamine oxidase B	Homo sapiens	64-83
27806193-12	2017	Taken together, our results support the concept that DHC12 is a mitochondrial-targeted neuroprotective iron-copper chelator and MAO-B inhibitor with potent antioxidant and mitochondria protective activities.	dhc12	53-58	monoamine oxidase B	Homo sapiens	128-133
28124620-6	2017	RESULTS: MAO-B inhibitors have a favorable pharmacokinetic profile, improve the dopamine deficient state and may have neuroprotective properties.	Dopamine	80-88	monoamine oxidase B	Homo sapiens	9-14
27744252-0	2017	Synthesis and evaluation of 7-substituted coumarin derivatives as multimodal monoamine oxidase-B and cholinesterase inhibitors for the treatment of Alzheimer"s disease.	coumarin	42-50	monoamine oxidase B	Homo sapiens	77-96
27744252-1	2017	A series of 7-substituted coumarin derivatives were designed and synthesised to display ChE and MAO-B inhibitory activity.	coumarin	26-34	monoamine oxidase B	Homo sapiens	96-101
27744252-6	2017	Within the N-benzylpiperidine (16-19) and p-bromo-N-benzylpiperizine (21-24) series the compounds in general showed moderate ChE and MAO-B inhibitory activity.	1-benzylpiperidine	11-29	monoamine oxidase B	Homo sapiens	133-138
27744252-6	2017	Within the N-benzylpiperidine (16-19) and p-bromo-N-benzylpiperizine (21-24) series the compounds in general showed moderate ChE and MAO-B inhibitory activity.	p-bromo-n-benzylpiperizine	42-68	monoamine oxidase B	Homo sapiens	133-138
27666135-4	2017	The most potent flavone MAO inhibitor studied is Az2k19 (1.6 mum for MAO-A, 2.1 mum for MAO-B), while Az1k15 and Az2k15 displayed better selectivity toward MAO-B (SI &gt; 10).	flavone	16-23	monoamine oxidase B	Homo sapiens	88-93
27923535-0	2017	Multitarget drug design strategy against Alzheimer"s disease: Homoisoflavonoid Mannich base derivatives serve as acetylcholinesterase and monoamine oxidase B dual inhibitors with multifunctional properties.	homoisoflavonoid	62-78	monoamine oxidase B	Homo sapiens	138-157
27923535-0	2017	Multitarget drug design strategy against Alzheimer"s disease: Homoisoflavonoid Mannich base derivatives serve as acetylcholinesterase and monoamine oxidase B dual inhibitors with multifunctional properties.	Mannich Bases	79-91	monoamine oxidase B	Homo sapiens	138-157
27855360-0	2017	Benzyloxynitrostyrene analogues - A novel class of selective and highly potent inhibitors of monoamine oxidase B.	benzyloxynitrostyrene	0-21	monoamine oxidase B	Homo sapiens	93-112
27855360-3	2017	This study shows that the 3-benzyloxy-beta-nitrostyrene analogues are potent inhibitors of the MAO-B isoform with IC50 values in the nanomolar range (39-565 nM).	3-benzyloxy-beta-nitrostyrene	26-55	monoamine oxidase B	Homo sapiens	95-100
27855360-5	2017	Since some of the 3-benzyloxy-beta-nitrostyrene analogues possess potencies that are comparable to that of the reversible inhibitor, safinamide (IC50 = 0.080 muM), it may be concluded that this class may be promising leads for the development of reversible and selective MAO-B inhibitors, that may be useful for the management of Parkinson"s disease.	3-benzyloxy-beta-nitrostyrene	18-47	monoamine oxidase B	Homo sapiens	271-276
27855360-5	2017	Since some of the 3-benzyloxy-beta-nitrostyrene analogues possess potencies that are comparable to that of the reversible inhibitor, safinamide (IC50 = 0.080 muM), it may be concluded that this class may be promising leads for the development of reversible and selective MAO-B inhibitors, that may be useful for the management of Parkinson"s disease.	safinamide	133-143	monoamine oxidase B	Homo sapiens	271-276
30108765-4	2017	In addition, the structure-activity relationships for MAO-B inhibition indicated that electron-withdrawing groups in the open small molecules were more suitable for MAO-B inhibition, and substitutions at the benzyloxy of the open small molecules, particularly with the halogen substituted benzyloxy, were more favorable for MAO-B inhibition.	Halogens	269-276	monoamine oxidase B	Homo sapiens	54-59
28245770-0	2017	Structural Exploration of Synthetic Chromones as Selective MAO-B Inhibitors: A Mini Review.	Chromones	36-45	monoamine oxidase B	Homo sapiens	59-64
28245770-3	2017	MATERIALS AND METHODS: Among these, chromone (4H-1-benzopyran-4-one) derivatives have recently emerged as a chemotype with specific and high potency MAO-B inhibition.	Chromones	36-44	monoamine oxidase B	Homo sapiens	149-154
28245770-3	2017	MATERIALS AND METHODS: Among these, chromone (4H-1-benzopyran-4-one) derivatives have recently emerged as a chemotype with specific and high potency MAO-B inhibition.	4-chromone	46-67	monoamine oxidase B	Homo sapiens	149-154
28245770-4	2017	Chromones are structurally related to a series of coumarins and chalcones, which are well-known inhibitors of MAO-B.	Chromones	0-9	monoamine oxidase B	Homo sapiens	110-115
28245770-4	2017	Chromones are structurally related to a series of coumarins and chalcones, which are well-known inhibitors of MAO-B.	Coumarins	50-59	monoamine oxidase B	Homo sapiens	110-115
28294055-8	2017	The selective MAO-B inhibitors are used with L-DOPA and/or dopamine agonists in the symptomatic treatment of Parkinson"s disease.	Levodopa	45-51	monoamine oxidase B	Homo sapiens	14-19
28294055-8	2017	The selective MAO-B inhibitors are used with L-DOPA and/or dopamine agonists in the symptomatic treatment of Parkinson"s disease.	Dopamine	59-67	monoamine oxidase B	Homo sapiens	14-19
28245770-4	2017	Chromones are structurally related to a series of coumarins and chalcones, which are well-known inhibitors of MAO-B.	Chalcones	64-73	monoamine oxidase B	Homo sapiens	110-115
28124620-8	2017	When applied as monotherapy, MAO-B inhibitors provide a modest, but significant improvement of motor function and delay the need for levodopa.	Levodopa	133-141	monoamine oxidase B	Homo sapiens	29-34
28245770-6	2017	CONCLUSION: The current review focuses on the MAO-B inhibitory properties of various synthetically derived chromones with specific emphasis on the structure-activity relationships and molecular recognition of MAO-B inhibition by this class.	Chromones	107-116	monoamine oxidase B	Homo sapiens	46-51
28245770-6	2017	CONCLUSION: The current review focuses on the MAO-B inhibitory properties of various synthetically derived chromones with specific emphasis on the structure-activity relationships and molecular recognition of MAO-B inhibition by this class.	Chromones	107-116	monoamine oxidase B	Homo sapiens	209-214
28124620-10	2017	As add-on to levodopa, MAO-B inhibitors significantly reduced off-time and were comparable in efficacy to COMT inhibitors.	Levodopa	13-21	monoamine oxidase B	Homo sapiens	23-28
28245770-7	2017	This review covers the recent updates present in the literature and will certainly provide a greater insight for the design and development of new class of potent chromone based selective MAO-B inhibitors.	Chromones	163-171	monoamine oxidase B	Homo sapiens	188-193
27658798-0	2016	8-Substituted 1,3-dimethyltetrahydropyrazino[2,1-f]purinediones: Water-soluble adenosine receptor antagonists and monoamine oxidase B inhibitors.	8-substituted 1,3-dimethyltetrahydropyrazino[2,1-f]purinediones	0-63	monoamine oxidase B	Homo sapiens	114-133
26648064-5	2017	The discovery of crystal structure of MAO-A &amp; MAO-B isoforms helped in understanding the drug-receptor interactions at the molecular level and designing of ligands with selectivity for either of the isoforms.	Adenosine Monophosphate	45-48	monoamine oxidase B	Homo sapiens	50-55
28550255-1	2017	BACKGROUND: Sembragiline is a potent, selective, long-acting, and reversible MAO-B inhibitor developed as a potential treatment for Alzheimer"s disease (AD).	sembragiline	12-24	monoamine oxidase B	Homo sapiens	77-82
28777756-2	2017	Safinamide is a drug with an innovative mechanism of action, dopaminergic and non-dopaminergic, that includes the reversible inhibition of the monoamine oxidase-B (MAO-B) enzyme and the modulation of excessive glutamate release through the use- and state-dependent blockade of the sodium channels.	safinamide	0-10	monoamine oxidase B	Homo sapiens	143-162
28777756-2	2017	Safinamide is a drug with an innovative mechanism of action, dopaminergic and non-dopaminergic, that includes the reversible inhibition of the monoamine oxidase-B (MAO-B) enzyme and the modulation of excessive glutamate release through the use- and state-dependent blockade of the sodium channels.	safinamide	0-10	monoamine oxidase B	Homo sapiens	164-169
28777756-2	2017	Safinamide is a drug with an innovative mechanism of action, dopaminergic and non-dopaminergic, that includes the reversible inhibition of the monoamine oxidase-B (MAO-B) enzyme and the modulation of excessive glutamate release through the use- and state-dependent blockade of the sodium channels.	Glutamic Acid	210-219	monoamine oxidase B	Homo sapiens	164-169
28777756-2	2017	Safinamide is a drug with an innovative mechanism of action, dopaminergic and non-dopaminergic, that includes the reversible inhibition of the monoamine oxidase-B (MAO-B) enzyme and the modulation of excessive glutamate release through the use- and state-dependent blockade of the sodium channels.	Sodium	281-287	monoamine oxidase B	Homo sapiens	164-169
28777756-8	2017	CONCLUSION: The favorable effect of safinamide on mood may be explained by the improvement in wearing off and by its modulation of glutamatergic hyperactivity and reversible MAO-B inhibition.	safinamide	36-46	monoamine oxidase B	Homo sapiens	174-179
30566289-3	2017	Novel dopamine agonists, catecholmethyltransferase inhibitors, and monoamine oxidase B inhibitors offered more continuous dopamine delivery that can attenuate motor complications.	Dopamine	122-130	monoamine oxidase B	Homo sapiens	67-86
30566307-9	2017	Rasagiline is a widely used MAO-B inhibitor in many countries.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	28-33
28546851-6	2017	MAOs" expression substantially increases with ageing (6-fold MAO-A in the heart and 4-fold MAO-B in neuronal tissue), and their involvement in cardiac diseases is supposedly related to the formation of ROS, via the hydrogen peroxide produced during the substrate degradation.	Reactive Oxygen Species	202-205	monoamine oxidase B	Homo sapiens	91-96
27845365-5	2016	The drug ethoxzolamide and the natural compound piperlongumine, present in Piper longum L, showed hMAO-B activity with IC50 values of 25 and 65 muM respectively.	Ethoxzolamide	9-22	monoamine oxidase B	Homo sapiens	98-104
27845365-5	2016	The drug ethoxzolamide and the natural compound piperlongumine, present in Piper longum L, showed hMAO-B activity with IC50 values of 25 and 65 muM respectively.	piperlonguminine	48-62	monoamine oxidase B	Homo sapiens	98-104
28035939-0	2017	Could MAO-B Inhibitor Withdrawal Rather than Nilotinib Benefit Explain the Dopamine Metabolite Increase in Parkinsonian Study Subjects?	Dopamine	75-83	monoamine oxidase B	Homo sapiens	6-11
27902880-1	2016	Numerous studies have shown that chalcones are promising scaffolds for the development of new monoamine oxidase-B (MAO-B) inhibitors.	Chalcones	33-42	monoamine oxidase B	Homo sapiens	94-113
27902880-1	2016	Numerous studies have shown that chalcones are promising scaffolds for the development of new monoamine oxidase-B (MAO-B) inhibitors.	Chalcones	33-42	monoamine oxidase B	Homo sapiens	115-120
27662218-2	2016	These compounds are structurally related to series of heterocyclic chalcone derivatives which have previously been shown to act as MAO-B specific inhibitors.	Chalcone	67-75	monoamine oxidase B	Homo sapiens	131-136
27028260-4	2016	The inhibitory activity of the compounds against MAO-A and MAO-B enzymes was evaluated by using in vitro flurometric method in which kynuramine was used as a substrate.	Kynuramine	133-143	monoamine oxidase B	Homo sapiens	59-64
27381555-0	2016	Genetic variants of MAOB affect serotonin level and specific behavioral attributes to increase autism spectrum disorder (ASD) susceptibility in males.	Serotonin	32-41	monoamine oxidase B	Homo sapiens	20-24
30351802-10	2016	But, monoamine oxidase B (MAO-B) inhibitor should be discontinued at least two weeks before surgery because of severe drug interactions with pethidine.	Meperidine	141-150	monoamine oxidase B	Homo sapiens	5-24
27882077-2	2016	MPP+ is the toxic metabolite of MPTP and is generated by the enzymatic activity of monoamine oxidase B, which is predominantly located in astrocytes.	mangion-purified polysaccharide (Candida albicans)	0-4	monoamine oxidase B	Homo sapiens	83-102
27882077-2	2016	MPP+ is the toxic metabolite of MPTP and is generated by the enzymatic activity of monoamine oxidase B, which is predominantly located in astrocytes.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	32-36	monoamine oxidase B	Homo sapiens	83-102
27523294-2	2016	MPTP is activated by monoamine oxidase-B (MAO-B) to MPP+ that inhibits mitochondrial function.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	21-40
27523294-2	2016	MPTP is activated by monoamine oxidase-B (MAO-B) to MPP+ that inhibits mitochondrial function.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	42-47
27523294-2	2016	MPTP is activated by monoamine oxidase-B (MAO-B) to MPP+ that inhibits mitochondrial function.	mangion-purified polysaccharide (Candida albicans)	52-56	monoamine oxidase B	Homo sapiens	21-40
27523294-2	2016	MPTP is activated by monoamine oxidase-B (MAO-B) to MPP+ that inhibits mitochondrial function.	mangion-purified polysaccharide (Candida albicans)	52-56	monoamine oxidase B	Homo sapiens	42-47
30351802-10	2016	But, monoamine oxidase B (MAO-B) inhibitor should be discontinued at least two weeks before surgery because of severe drug interactions with pethidine.	Meperidine	141-150	monoamine oxidase B	Homo sapiens	26-31
27754693-4	2016	The potency of MAO inhibition by acacetin was &gt;5-fold higher for MAO-A (0.121 muM vs 0.640 muM) and &gt;22-fold higher for MAO-B (0.049 muM vs 1.12 muM) as compared to apigenin, the closest flavone structural analogue.	acacetin	33-41	monoamine oxidase B	Homo sapiens	126-131
27480491-1	2016	Deprenyl/Selegiline (DEP), created by Joseph Knoll in the 1960s, registered in more than 60 countries to treat Parkinson"s disease, Alzheimer"s disease, major depressive disorder; and used as an anti-aging drug, achieved its place in research and therapy as the first selective inhibitor of B-type monoamine oxidase (MAO-B).	dep	21-24	monoamine oxidase B	Homo sapiens	317-322
27480491-1	2016	Deprenyl/Selegiline (DEP), created by Joseph Knoll in the 1960s, registered in more than 60 countries to treat Parkinson"s disease, Alzheimer"s disease, major depressive disorder; and used as an anti-aging drug, achieved its place in research and therapy as the first selective inhibitor of B-type monoamine oxidase (MAO-B).	deprenyl/selegiline	0-19	monoamine oxidase B	Homo sapiens	317-322
27754693-7	2016	Acacetin showed more preference toward MAO-B than to MAO-A, suggesting its potential for eliciting selective pharmacological effects that might be useful in the treatment of neurological and psychiatric disorders.	acacetin	0-8	monoamine oxidase B	Homo sapiens	39-44
27575476-1	2016	Monoamine oxidase (MAO) catalyzes the oxidation of monoamines and its two isoforms, MAO-A and MAO-B, break down neurotransmitter amines.	monoamines	51-61	monoamine oxidase B	Homo sapiens	94-99
27605388-0	2016	ONIOM calculations on serotonin degradation by monoamine oxidase B: insight into the oxidation mechanism and covalent reversible inhibition.	Serotonin	22-31	monoamine oxidase B	Homo sapiens	47-66
27803666-5	2016	The irreversible inhibitors of MAO-B, selegiline and rasagiline, are used clinically in treatment of Parkinson"s disease, and a recently introduced reversible MAO-B inhibitor, safinamide, has also been found efficacious.	safinamide	176-186	monoamine oxidase B	Homo sapiens	31-36
27803666-5	2016	The irreversible inhibitors of MAO-B, selegiline and rasagiline, are used clinically in treatment of Parkinson"s disease, and a recently introduced reversible MAO-B inhibitor, safinamide, has also been found efficacious.	safinamide	176-186	monoamine oxidase B	Homo sapiens	159-164
27396685-1	2016	Different azides and alkynes have been coupled via Cu-catalyzed 1,3-dipolar Huisgen cycloaddition to afford a novel family of N1- and C5-substituted 1,2,3-triazole derivatives that feature the propargylamine group typical of irreversible MAO-B inhibitors at the C4-side chain of the triazole ring.	Azides	10-16	monoamine oxidase B	Homo sapiens	238-243
27396685-1	2016	Different azides and alkynes have been coupled via Cu-catalyzed 1,3-dipolar Huisgen cycloaddition to afford a novel family of N1- and C5-substituted 1,2,3-triazole derivatives that feature the propargylamine group typical of irreversible MAO-B inhibitors at the C4-side chain of the triazole ring.	Alkynes	21-28	monoamine oxidase B	Homo sapiens	238-243
27396685-1	2016	Different azides and alkynes have been coupled via Cu-catalyzed 1,3-dipolar Huisgen cycloaddition to afford a novel family of N1- and C5-substituted 1,2,3-triazole derivatives that feature the propargylamine group typical of irreversible MAO-B inhibitors at the C4-side chain of the triazole ring.	Copper	51-53	monoamine oxidase B	Homo sapiens	238-243
27396685-1	2016	Different azides and alkynes have been coupled via Cu-catalyzed 1,3-dipolar Huisgen cycloaddition to afford a novel family of N1- and C5-substituted 1,2,3-triazole derivatives that feature the propargylamine group typical of irreversible MAO-B inhibitors at the C4-side chain of the triazole ring.	1,3-dipolar huisgen	64-83	monoamine oxidase B	Homo sapiens	238-243
27396685-1	2016	Different azides and alkynes have been coupled via Cu-catalyzed 1,3-dipolar Huisgen cycloaddition to afford a novel family of N1- and C5-substituted 1,2,3-triazole derivatives that feature the propargylamine group typical of irreversible MAO-B inhibitors at the C4-side chain of the triazole ring.	3-triazole	153-163	monoamine oxidase B	Homo sapiens	238-243
27396685-1	2016	Different azides and alkynes have been coupled via Cu-catalyzed 1,3-dipolar Huisgen cycloaddition to afford a novel family of N1- and C5-substituted 1,2,3-triazole derivatives that feature the propargylamine group typical of irreversible MAO-B inhibitors at the C4-side chain of the triazole ring.	propargylamine	193-207	monoamine oxidase B	Homo sapiens	238-243
27396685-1	2016	Different azides and alkynes have been coupled via Cu-catalyzed 1,3-dipolar Huisgen cycloaddition to afford a novel family of N1- and C5-substituted 1,2,3-triazole derivatives that feature the propargylamine group typical of irreversible MAO-B inhibitors at the C4-side chain of the triazole ring.	Triazoles	155-163	monoamine oxidase B	Homo sapiens	238-243
27396685-6	2016	Overall, the results support the suitability of the 4-triazolylalkyl propargylamine scaffold for exploring the design of multipotent anti-Alzheimer compounds endowed with irreversible MAO-B inhibitory activity.	4-triazolylalkyl propargylamine	52-83	monoamine oxidase B	Homo sapiens	184-189
27575476-1	2016	Monoamine oxidase (MAO) catalyzes the oxidation of monoamines and its two isoforms, MAO-A and MAO-B, break down neurotransmitter amines.	Amines	55-61	monoamine oxidase B	Homo sapiens	94-99
27575476-2	2016	Of the compounds isolated from the roots of Sophora flavescens, (-)-maackiain (4), a pterocarpan, was found to potently and selectively inhibit human MAO-B, with an IC50 of 0.68muM, and to have a selectivity index of 126.2 for MAO-B.	inermin	64-77	monoamine oxidase B	Homo sapiens	150-155
27575476-2	2016	Of the compounds isolated from the roots of Sophora flavescens, (-)-maackiain (4), a pterocarpan, was found to potently and selectively inhibit human MAO-B, with an IC50 of 0.68muM, and to have a selectivity index of 126.2 for MAO-B.	inermin	64-77	monoamine oxidase B	Homo sapiens	227-232
27575476-2	2016	Of the compounds isolated from the roots of Sophora flavescens, (-)-maackiain (4), a pterocarpan, was found to potently and selectively inhibit human MAO-B, with an IC50 of 0.68muM, and to have a selectivity index of 126.2 for MAO-B.	Pterocarpans	85-96	monoamine oxidase B	Homo sapiens	150-155
27575476-4	2016	Genistein (1) highly, effectively and non-selectively inhibited MAO-A and MAO-B with IC50 values of 3.9muM and 4.1muM, respectively.	Genistein	0-9	monoamine oxidase B	Homo sapiens	74-79
27575476-5	2016	(-)-4-Hydroxy-3-methoxy-8,9-methylenedioxypterocarpan (2) effectively and non-selectively inhibited MAO-A and MAO-B with IC50 values of 20.3muM and 10.3muM, respectively.	(-)-4-hydroxy-3-methoxy-8,9-methylenedioxypterocarpan	0-53	monoamine oxidase B	Homo sapiens	110-115
27575476-8	2016	Furthermore, Cys172 of MAO-B was found to be a key residue for hydrogen bonding with compound 4.	Hydrogen	63-71	monoamine oxidase B	Homo sapiens	23-28
27578245-2	2016	The 2-benzylidene-1-indanone derivatives are structurally related to a series of benzylideneindanone derivatives which has previously been found to be MAO-B inhibitors.	2-benzylidene-1-indanone	4-28	monoamine oxidase B	Homo sapiens	151-156
27578245-2	2016	The 2-benzylidene-1-indanone derivatives are structurally related to a series of benzylideneindanone derivatives which has previously been found to be MAO-B inhibitors.	benzylideneindanone	81-100	monoamine oxidase B	Homo sapiens	151-156
27578245-3	2016	This study finds that the 2-benzylidene-1-indanones are MAO-B specific inhibitors with IC50 values &lt;2.74muM.	2-benzylidene-1-indanone	26-51	monoamine oxidase B	Homo sapiens	56-61
27262516-7	2016	Molecular docking and molecular dynamics simulation studies were carried out using Autodock-4.2 and Amber 14 to understand the molecular level interaction and energy relation of MAO isoforms with selective MAO-B inhibitor TC6.	TC6	222-225	monoamine oxidase B	Homo sapiens	206-211
27318273-2	2016	Based on this rational, a new class of cholinesterase (ChE)-monoamine oxidase (MAO) inhibitors were designed and synthesized by amalgamating the propargyl moiety of the irreversible selective MAO-B inhibitor, neuroprotective/neurorestorative anti-Parkinsonian drug, rasagiline, into the "N-methyl" position of the ChE inhibitor, anti-AD drug rivastigmine.	rasagiline	266-276	monoamine oxidase B	Homo sapiens	192-197
27262516-0	2016	Exploration of chlorinated thienyl chalcones: A new class of monoamine oxidase-B inhibitors.	chlorinated thienyl chalcones	15-44	monoamine oxidase B	Homo sapiens	61-80
27262516-5	2016	The most potent compound (2E)-1-(4-chlorocyclopenta-1,3-dien-1-yl)-3-(4-ethylphenyl)prop-2-en-1-one (TC6) was found to be the best activity and higher selectivity towards hMAO-B with Ki and SI values of 0.31+-0.02muM and 16.84, respectively.	(2e)-1-(4-chlorocyclopenta-1,3-dien-1-yl)-3-(4-ethylphenyl)prop-2-en-1-one	25-99	monoamine oxidase B	Homo sapiens	171-177
27262516-5	2016	The most potent compound (2E)-1-(4-chlorocyclopenta-1,3-dien-1-yl)-3-(4-ethylphenyl)prop-2-en-1-one (TC6) was found to be the best activity and higher selectivity towards hMAO-B with Ki and SI values of 0.31+-0.02muM and 16.84, respectively.	TC6	101-104	monoamine oxidase B	Homo sapiens	171-177
27318273-2	2016	Based on this rational, a new class of cholinesterase (ChE)-monoamine oxidase (MAO) inhibitors were designed and synthesized by amalgamating the propargyl moiety of the irreversible selective MAO-B inhibitor, neuroprotective/neurorestorative anti-Parkinsonian drug, rasagiline, into the "N-methyl" position of the ChE inhibitor, anti-AD drug rivastigmine.	Rivastigmine	342-354	monoamine oxidase B	Homo sapiens	192-197
27597816-1	2016	HIGHLIGHTS Compounds that interact with multiple targets but minimally with the cytochrome P450 system (CYP) address the many factors leading to neurodegeneration.Acetyl- and Butyryl-cholineEsterases (AChE, BChE) and Monoamine Oxidases A/B (MAO A, MAO B) are targets for Multi-Target Designed Ligands (MTDL).ASS234 is an irreversible inhibitor of MAO A &gt;MAO B and has micromolar potency against the cholinesterases.ASS234 is a poor CYP substrate in human liver, yielding the depropargylated metabolite.SMe1EC2, a stobadine derivative, showed high radical scavenging property, in vitro and in vivo giving protection in head trauma and diabetic damage of endothelium.Control of mitochondrial function and morphology by manipulating fission and fusion is emerging as a target area for therapeutic strategies to decrease the pathological outcome of neurodegenerative diseases.	dicarbine	516-525	monoamine oxidase B	Homo sapiens	248-253
27729794-1	2016	INTRODUCTION: Rasagiline is a selective, irreversible monoamine oxidase B inhibitor that ameliorates the symptoms of Parkinson"s disease (PD) by inhibiting striatal dopamine metabolism.	rasagiline	14-24	monoamine oxidase B	Homo sapiens	54-73
27729794-1	2016	INTRODUCTION: Rasagiline is a selective, irreversible monoamine oxidase B inhibitor that ameliorates the symptoms of Parkinson"s disease (PD) by inhibiting striatal dopamine metabolism.	Dopamine	165-173	monoamine oxidase B	Homo sapiens	54-73
27729794-2	2016	There is also evidence that monoamine oxidase B inhibitors increase melatonin levels in the pineal gland and may have a beneficial effect on sleep disorders, which are a common feature in patients with PD.	Melatonin	68-77	monoamine oxidase B	Homo sapiens	28-47
27597816-1	2016	HIGHLIGHTS Compounds that interact with multiple targets but minimally with the cytochrome P450 system (CYP) address the many factors leading to neurodegeneration.Acetyl- and Butyryl-cholineEsterases (AChE, BChE) and Monoamine Oxidases A/B (MAO A, MAO B) are targets for Multi-Target Designed Ligands (MTDL).ASS234 is an irreversible inhibitor of MAO A &gt;MAO B and has micromolar potency against the cholinesterases.ASS234 is a poor CYP substrate in human liver, yielding the depropargylated metabolite.SMe1EC2, a stobadine derivative, showed high radical scavenging property, in vitro and in vivo giving protection in head trauma and diabetic damage of endothelium.Control of mitochondrial function and morphology by manipulating fission and fusion is emerging as a target area for therapeutic strategies to decrease the pathological outcome of neurodegenerative diseases.	dicarbine	516-525	monoamine oxidase B	Homo sapiens	357-362
27536120-6	2016	Therefore, safinamide is an ideal candidate for treatment of patients with PD, since its pharmacological profile includes reversible monoamine oxidase-B inhibition, blockade of voltage-dependent sodium channels, modulation of calcium channels, and inhibition of glutamate release.	safinamide	11-21	monoamine oxidase B	Homo sapiens	133-152
27402375-0	2016	Potent and Selective Monoamine Oxidase-B Inhibitory Activity: Fluoro- vs. Trifluoromethyl-4-hydroxylated Chalcone Derivatives.	trifluoromethyl-4-hydroxylated chalcone	74-113	monoamine oxidase B	Homo sapiens	21-40
27373997-0	2016	Identification of Indole-Based Chalcones: Discovery of a Potent, Selective, and Reversible Class of MAO-B Inhibitors.	indole-based chalcones	18-40	monoamine oxidase B	Homo sapiens	100-105
27373997-5	2016	It was found to be better than the standard drug, selegiline (hMAO-B with Ki  = 0.20 +- 0.020 muM) with a selectivity index of 30.55.	Selegiline	50-60	monoamine oxidase B	Homo sapiens	62-68
27373997-7	2016	Moreover, the most potent MAO-B inhibitor, IC9, was nontoxic at 5 and 25 muM, with 95.20 and 69.17% viable cells, respectively.	IC9	43-46	monoamine oxidase B	Homo sapiens	26-31
27402375-2	2016	In our previous study, we have shown that a series of methoxylated chalcones with F functional group exhibited high binding affinity toward human monoamine oxidase-B (hMAO-B).	Chalcones	67-76	monoamine oxidase B	Homo sapiens	146-165
27402375-2	2016	In our previous study, we have shown that a series of methoxylated chalcones with F functional group exhibited high binding affinity toward human monoamine oxidase-B (hMAO-B).	Chalcones	67-76	monoamine oxidase B	Homo sapiens	167-173
27402375-5	2016	The most active compound, (2E)-1-(4-hydroxyphenyl)-3-[4-(trifluoromethyl)phenyl]prop-2-en-1-one, exhibited a Ki value of 0.33 +- 0.01 mum toward hMAO-B with a selectivity index of 26.36.	(2e)-1-(4-hydroxyphenyl)-3-[4-(trifluoromethyl)phenyl]prop-2-en-1-one	26-95	monoamine oxidase B	Homo sapiens	145-151
27402375-6	2016	A molecular docking study revealed that the presence of a H-bond network in hydroxylated chalcone with the N(5) atom of FAD is crucial for MAO-B selectivity and potency.	Chalcone	89-97	monoamine oxidase B	Homo sapiens	139-144
27402375-6	2016	A molecular docking study revealed that the presence of a H-bond network in hydroxylated chalcone with the N(5) atom of FAD is crucial for MAO-B selectivity and potency.	8-dehydroxythienamycin	107-111	monoamine oxidase B	Homo sapiens	139-144
27402375-6	2016	A molecular docking study revealed that the presence of a H-bond network in hydroxylated chalcone with the N(5) atom of FAD is crucial for MAO-B selectivity and potency.	Flavin-Adenine Dinucleotide	120-123	monoamine oxidase B	Homo sapiens	139-144
27089850-0	2016	Free-water and BOLD imaging changes in Parkinson"s disease patients chronically treated with a MAO-B inhibitor.	Water	5-10	monoamine oxidase B	Homo sapiens	95-100
27089850-1	2016	Rasagiline is a monoamine oxidase type B inhibitor that possesses no amphetamine-like properties, and provides symptomatic relief in early and late stages of Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	16-40
27341797-3	2016	Monoamine oxidase A (MAOA) and B (MAOB), two isoenzymes bound to the outer membrane of mitochondria, are involved in the degradation of monoamines and were explored for association with ADHD in different ethnic groups.	monoamines	136-146	monoamine oxidase B	Homo sapiens	34-38
27135371-0	2016	(E)-3-Heteroarylidenechroman-4-ones as potent and selective monoamine oxidase-B inhibitors.	(e)-3-heteroarylidenechroman-4-ones	0-35	monoamine oxidase B	Homo sapiens	60-79
27135371-1	2016	A series of (E)-3-heteroarylidenechroman-4-ones (1a-r) was designed, synthesized and investigated in vitro for their ability to inhibit the enzymatic activity of both human monoamine oxidase (hMAO) isoforms, hMAO-A and hMAO-B.	(e)-3-heteroarylidenechroman-4-ones	12-47	monoamine oxidase B	Homo sapiens	219-225
27135371-3	2016	(E)-5,7-Dichloro-3-{[(2-(dimethylamino)pyrimidin-5-yl]methylene}chroman-4-one (1c) was the most interesting compound identified in this study, endowed with higher hMAO-B potency (IC50 = 10.58 nM) and selectivity (SI &gt; 9452) with respect to the reference selective inhibitor selegiline (IC50 = 19.60 nM, IC50 &gt; 3431).	(e)-5,7-dichloro-3-{[(2-(dimethylamino)pyrimidin-5-yl]methylene}chroman-4-one	0-77	monoamine oxidase B	Homo sapiens	163-169
27245668-6	2016	Moreover, chrysin markedly inhibited monoamine oxidase-B activity in vitro and in vivo.	chrysin	10-17	monoamine oxidase B	Homo sapiens	37-56
27230855-2	2016	The MAO-B inhibitor rasagiline has shown neuroprotective effects in preclinical models of neurodegeneration.	rasagiline	20-30	monoamine oxidase B	Homo sapiens	4-9
26891670-4	2016	The need to inhibit MAO B to combat decreased brain amines continues to drive the search for new drugs.	Amines	52-58	monoamine oxidase B	Homo sapiens	20-25
26891670-6	2016	Multi-target ligands designed to combat the elevated activity of MAO B in Alzheimer"s and Parkinson"s Diseases incorporate MAO inhibition (usually irreversible) as well as iron chelation, antioxidant or neuroprotective properties.	Iron	172-176	monoamine oxidase B	Homo sapiens	65-70
26891670-7	2016	The main focus of drug design is the catalytic activity of MAO, but the imidazoline I2 site in the entrance cavity of MAO B is also a pharmacological target.	Imidazolines	72-83	monoamine oxidase B	Homo sapiens	118-123
26964906-3	2016	Most of the studies converge in associating MAO-A and MAO-B with impulsive, aggressive or antisocial personality traits or behaviours, including alcohol-related problems, and for MAO-A available evidence strongly supports interaction with adverse environmental exposures in childhood.	Alcohols	145-152	monoamine oxidase B	Homo sapiens	54-59
27347731-0	2016	Exploring Basic Tail Modifications of Coumarin-Based Dual Acetylcholinesterase-Monoamine Oxidase B Inhibitors: Identification of Water-Soluble, Brain-Permeant Neuroprotective Multitarget Agents.	coumarin	38-46	monoamine oxidase B	Homo sapiens	79-98
27347731-0	2016	Exploring Basic Tail Modifications of Coumarin-Based Dual Acetylcholinesterase-Monoamine Oxidase B Inhibitors: Identification of Water-Soluble, Brain-Permeant Neuroprotective Multitarget Agents.	Water	129-134	monoamine oxidase B	Homo sapiens	79-98
27347731-1	2016	Aiming at modulating two key enzymatic targets for Alzheimer"s disease (AD), i.e., acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), a series of multitarget ligands was properly designed by linking the 3,4-dimethylcoumarin scaffold to 1,3- and 1,4-substituted piperidine moieties, thus modulating the basicity to improve the hydrophilic/lipophilic balance.	3,4-DIMETHYL-CHROMEN-2-ONE	213-233	monoamine oxidase B	Homo sapiens	136-141
27347731-1	2016	Aiming at modulating two key enzymatic targets for Alzheimer"s disease (AD), i.e., acetylcholinesterase (AChE) and monoamine oxidase B (MAO B), a series of multitarget ligands was properly designed by linking the 3,4-dimethylcoumarin scaffold to 1,3- and 1,4-substituted piperidine moieties, thus modulating the basicity to improve the hydrophilic/lipophilic balance.	,4-substituted piperidine	256-281	monoamine oxidase B	Homo sapiens	136-141
27332045-1	2016	A series of 2-amino-6-nitrobenzothiazole-derived extended hydrazones were designed, synthesized, and investigated for their ability to inhibit monoamine oxidase A and B (MAO-A/MAO-B).	2-AMINO-6-NITROBENZOTHIAZOLE	12-40	monoamine oxidase B	Homo sapiens	176-181
27332045-1	2016	A series of 2-amino-6-nitrobenzothiazole-derived extended hydrazones were designed, synthesized, and investigated for their ability to inhibit monoamine oxidase A and B (MAO-A/MAO-B).	extended	49-57	monoamine oxidase B	Homo sapiens	176-181
27332045-1	2016	A series of 2-amino-6-nitrobenzothiazole-derived extended hydrazones were designed, synthesized, and investigated for their ability to inhibit monoamine oxidase A and B (MAO-A/MAO-B).	Hydrazones	58-68	monoamine oxidase B	Homo sapiens	176-181
27471444-8	2016	Inhibitors that act mainly on MAO A are used in the treatment of depression, due to their ability to raise serotonin concentrations, while MAO B inhibitors decrease dopamine degradation and improve motor control in patients with Parkinson disease.	Dopamine	165-173	monoamine oxidase B	Homo sapiens	139-144
27159243-0	2016	Synthesis, Biochemistry, and Computational Studies of Brominated Thienyl Chalcones: A New Class of Reversible MAO-B Inhibitors.	thienyl chalcones	65-82	monoamine oxidase B	Homo sapiens	110-115
27244485-2	2016	Therefore, a small library of chromone derivatives was synthesized and screened toward human monoamine oxidase isoforms (hMAO-A and hMAO-B).	Chromones	30-38	monoamine oxidase B	Homo sapiens	132-138
27244485-4	2016	The most potent MAO-B inhibitors were N-(3"-chlorophenyl)-4-oxo-4H-chromene-3-carboxamide (20) (IC50 = 403 pM) and N-(3",4"-dimethylphenyl)-4-oxo-4H-chromene-3-carboxamide (27) (IC50 = 669 pM), acting as competitive and noncompetitive reversible inhibitors, respectively.	n-(3"-chlorophenyl)-4-oxo-4h-chromene-3-carboxamide	38-89	monoamine oxidase B	Homo sapiens	16-21
27244485-4	2016	The most potent MAO-B inhibitors were N-(3"-chlorophenyl)-4-oxo-4H-chromene-3-carboxamide (20) (IC50 = 403 pM) and N-(3",4"-dimethylphenyl)-4-oxo-4H-chromene-3-carboxamide (27) (IC50 = 669 pM), acting as competitive and noncompetitive reversible inhibitors, respectively.	n-(3",4"-dimethylphenyl)-4-oxo-4h-chromene-3-carboxamide	115-171	monoamine oxidase B	Homo sapiens	16-21
27135466-3	2016	Compound 16, 1-(2,6-dichlorobenzylidene)-4-(benzo[1,3]dioxol-5-yl)semicarbazide presented a balanced multifunctional profile of MAO-A (IC50 =4.52+-0.032 mum), MAO-B (IC50 =0.059+-0.002 mum), and AChE (IC50 =0.0087+-0.0002 mum) inhibition without neurotoxicity.	16, 1-(2,6-dichlorobenzylidene)-4-(benzo[1,3]dioxol-5-yl)semicarbazide	9-79	monoamine oxidase B	Homo sapiens	159-164
27060436-1	2016	Rasagiline is a selective, irreversible inhibitor of monoamine oxidase type-B (MAO-B) and has been used both as a monotherapy and in addition to levodopa in the treatment of Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	53-77
27060436-1	2016	Rasagiline is a selective, irreversible inhibitor of monoamine oxidase type-B (MAO-B) and has been used both as a monotherapy and in addition to levodopa in the treatment of Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	79-84
27079124-5	2016	However the 6-methoxyl aurones 15a-c revealed excellent selectivity toward MAO-B.	6-methoxyl aurones	12-30	monoamine oxidase B	Homo sapiens	75-80
26974383-0	2016	Design and synthesis of novel chalcones as potent selective monoamine oxidase-B inhibitors.	Chalcones	30-39	monoamine oxidase B	Homo sapiens	60-79
26974383-1	2016	A novel series of substituted chalcones were designed and synthesized to be evaluated as selective human MAO-B inhibitors.	Chalcones	30-39	monoamine oxidase B	Homo sapiens	105-110
27252617-1	2016	HIGHLIGHTS ASS234 is a MTDL compound containing a moiety from Donepezil and the propargyl group from the PF 9601N, a potent and selective MAO B inhibitor.	Donepezil	62-71	monoamine oxidase B	Homo sapiens	138-143
27152414-0	2016	Why p-OMe- and p-Cl-beta-Methylphenethylamines Display Distinct Activities upon MAO-B Binding.	p-ome	4-9	monoamine oxidase B	Homo sapiens	80-85
27152414-0	2016	Why p-OMe- and p-Cl-beta-Methylphenethylamines Display Distinct Activities upon MAO-B Binding.	p-cl-beta-methylphenethylamines	15-46	monoamine oxidase B	Homo sapiens	80-85
27152414-1	2016	Despite their structural and chemical commonalities, p-chloro-beta-methylphenethylamine and p-methoxy-beta-methylphenethylamine display distinct inhibitory and substrate activities upon MAO-B binding.	p-chloro-beta-methylphenethylamine	53-87	monoamine oxidase B	Homo sapiens	186-191
27152414-1	2016	Despite their structural and chemical commonalities, p-chloro-beta-methylphenethylamine and p-methoxy-beta-methylphenethylamine display distinct inhibitory and substrate activities upon MAO-B binding.	p-methoxy-beta-methylphenethylamine	92-127	monoamine oxidase B	Homo sapiens	186-191
27052821-4	2016	All tested compounds were selective MAO-B inhibitors, although only the substituted isoquinoline derivative 2b showed IC50 lower than the concentration of 100 muM (IC50 = 82.41 muM).	isoquinoline	84-96	monoamine oxidase B	Homo sapiens	36-41
26684482-4	2016	Of these, 5,8-dihydroxy-1,4-naphthoquinone was found to be the most potent inhibitor with an IC50 value of 0.860 mum for the inhibition of MAO-B.	naphthazarin	10-42	monoamine oxidase B	Homo sapiens	139-144
26684482-5	2016	A related compound, shikonin, inhibits both the MAO-A and MAO-B isoforms with IC50 values of 1.50 and 1.01 mum, respectively.	shikonin	20-28	monoamine oxidase B	Homo sapiens	58-63
27052821-0	2016	4-Organoseleno-Isoquinolines Selectively and Reversibly Inhibit the Cerebral Monoamine Oxidase B Activity.	4-organoseleno-isoquinolines	0-28	monoamine oxidase B	Homo sapiens	77-96
27020523-3	2016	Among the active compounds two pyrrolo[3,4-f]indole-5,7-dione derivatives inhibited MAO-A (4 g) and MAO-B (4d) with IC50 values of 0.250 and 0.581 muM, respectively.	pyrrolo[3,4-f]indole-5,7-dione	31-61	monoamine oxidase B	Homo sapiens	100-105
26964672-0	2016	Novel tricyclic pyrazolo[1,5-d][1,4]benzoxazepin-5(6H)-one: Design, synthesis, model and use as hMAO-B inhibitors.	tricyclic pyrazolo[1,5-d][1,4]benzoxazepin-5(6h)-one	6-58	monoamine oxidase B	Homo sapiens	96-102
27341283-1	2016	AIMS: Monoamine oxidase-B inhibitors (MAO-BIs) are used for the initial therapy of Parkinson"s disease.	mao-bis	38-45	monoamine oxidase B	Homo sapiens	6-25
27052821-1	2016	Isoquinolines are formed endogenously as metabolites of neurotransmitters and are studied because they have structures similar to neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and selegiline, a selective inhibitor of MAO-B.	Isoquinolines	0-13	monoamine oxidase B	Homo sapiens	227-232
27058977-0	2016	High-throughput screening and radioligand binding studies reveal monoamine oxidase-B as the primary binding target for d-deprenyl.	Selegiline	119-129	monoamine oxidase B	Homo sapiens	65-84
27058977-7	2016	KEY FINDINGS: Our high-throughput investigation identified monoamine oxidase-B, monoamine oxidase-A and angiotensin converting enzyme as potential targets for d-deprenyl.	Selegiline	159-169	monoamine oxidase B	Homo sapiens	59-78
27058977-8	2016	Further competitive [(3)H]d-deprenyl binding studies with specific inhibitors identified monoamine oxidase-B as the major binding site.	[(3)h]d-deprenyl	20-36	monoamine oxidase B	Homo sapiens	89-108
27058977-11	2016	It verified 249 candidate proteins and confirmed the role of monoamine oxidase - B in d-deprenyl binding.	Selegiline	86-96	monoamine oxidase B	Homo sapiens	61-82
26964672-2	2016	A series of selective hMAO-B inhibitors (3a-3u) with novel scaffold of tricyclic pyrazolo[1,5-d][1,4]benzoxazepin-5(6H)-one were designed and synthesized.	tricyclic pyrazolo[1,5-d][1,4]benzoxazepin-5(6h)-one	71-123	monoamine oxidase B	Homo sapiens	22-28
26964672-3	2016	Compound 3u (IC50=221 nM) exhibited the best inhibitory activity and isoform selectivity against hMAO-B, superior to selegiline (IC50=321 nM), which is a commercial selective hMAO-B inhibitor used to Parkinson"s disease.	Selegiline	117-127	monoamine oxidase B	Homo sapiens	175-181
26964672-4	2016	Modeling study indicated that the selectivity of our compounds to hMAO-B is determined by at least two residues, i.e., Ile 199 and Cys 172 (or corresponded Phe 208 and Asn 181 of hMAO-A).	Isoleucine	119-122	monoamine oxidase B	Homo sapiens	66-72
26964672-4	2016	Modeling study indicated that the selectivity of our compounds to hMAO-B is determined by at least two residues, i.e., Ile 199 and Cys 172 (or corresponded Phe 208 and Asn 181 of hMAO-A).	Cysteine	131-134	monoamine oxidase B	Homo sapiens	66-72
26964672-4	2016	Modeling study indicated that the selectivity of our compounds to hMAO-B is determined by at least two residues, i.e., Ile 199 and Cys 172 (or corresponded Phe 208 and Asn 181 of hMAO-A).	Phenylalanine	156-159	monoamine oxidase B	Homo sapiens	66-72
26964672-4	2016	Modeling study indicated that the selectivity of our compounds to hMAO-B is determined by at least two residues, i.e., Ile 199 and Cys 172 (or corresponded Phe 208 and Asn 181 of hMAO-A).	Asparagine	168-171	monoamine oxidase B	Homo sapiens	66-72
27010708-0	2016	Path Integral Simulation of the H/D Kinetic Isotope Effect in Monoamine Oxidase B Catalyzed Decomposition of Dopamine.	Dopamine	109-117	monoamine oxidase B	Homo sapiens	62-81
27010708-2	2016	A starting point to address challenges raised by the increasing burden of brain diseases is to understand, at atomistic level, the catalytic mechanism of an essential amine metabolic enzyme-monoamine oxidase B (MAO B).	essential amine	157-172	monoamine oxidase B	Homo sapiens	183-209
27010708-2	2016	A starting point to address challenges raised by the increasing burden of brain diseases is to understand, at atomistic level, the catalytic mechanism of an essential amine metabolic enzyme-monoamine oxidase B (MAO B).	essential amine	157-172	monoamine oxidase B	Homo sapiens	211-216
27010708-3	2016	Recently, we demonstrated that the rate-limiting step of MAO B catalyzed conversion of amines into imines represents the hydride anion transfer from the substrate alpha-CH2 group to the N5 atom of the flavin cofactor moiety.	Amines	87-93	monoamine oxidase B	Homo sapiens	57-62
27010708-3	2016	Recently, we demonstrated that the rate-limiting step of MAO B catalyzed conversion of amines into imines represents the hydride anion transfer from the substrate alpha-CH2 group to the N5 atom of the flavin cofactor moiety.	Imines	99-105	monoamine oxidase B	Homo sapiens	57-62
27010708-3	2016	Recently, we demonstrated that the rate-limiting step of MAO B catalyzed conversion of amines into imines represents the hydride anion transfer from the substrate alpha-CH2 group to the N5 atom of the flavin cofactor moiety.	4,6-dinitro-o-cresol	201-207	monoamine oxidase B	Homo sapiens	57-62
27010708-4	2016	In this article we simulated for MAO B catalyzed dopamine decomposition the effects of nuclear tunneling by the calculation of the H/D kinetic isotope effect.	Dopamine	49-57	monoamine oxidase B	Homo sapiens	33-38
26917219-1	2016	Combining N-benzylpiperidine moiety of donepezil and coumarin into in a single molecule, novel hybrids with ChE and MAO-B inhibitory activity were designed and synthesized.	1-benzylpiperidine	10-28	monoamine oxidase B	Homo sapiens	116-121
27061066-0	2016	Rotigotine in Combination with the MAO-B Inhibitor Selegiline in Early Parkinson"s Disease: A Post Hoc Analysis.	Selegiline	51-61	monoamine oxidase B	Homo sapiens	35-40
27061066-12	2016	CONCLUSIONS: In these post hoc analyses, adjunctive treatment with rotigotine in patients already receiving an MAO-B inhibitor improved UPDRS II+III score; this appeared to be largely driven by improvements in the motor aspects of PD.	rotigotine	67-77	monoamine oxidase B	Homo sapiens	111-116
26917219-1	2016	Combining N-benzylpiperidine moiety of donepezil and coumarin into in a single molecule, novel hybrids with ChE and MAO-B inhibitory activity were designed and synthesized.	Donepezil	39-48	monoamine oxidase B	Homo sapiens	116-121
26917219-1	2016	Combining N-benzylpiperidine moiety of donepezil and coumarin into in a single molecule, novel hybrids with ChE and MAO-B inhibitory activity were designed and synthesized.	coumarin	53-61	monoamine oxidase B	Homo sapiens	116-121
26999091-0	2016	Searching for Multi-Targeting Neurotherapeutics against Alzheimer"s: Discovery of Potent AChE-MAO B Inhibitors through the Decoration of the 2H-Chromen-2-one Structural Motif.	2h-chromen-2-	141-154	monoamine oxidase B	Homo sapiens	94-99
26897020-0	2016	Erratum to: Prescribing pattern and resource utilization of monoamine oxidase-B inhibitors in Parkinson treatment: comparison between rasagiline and selegiline.	rasagiline	134-144	monoamine oxidase B	Homo sapiens	60-79
26999091-3	2016	Compounds bearing a propargylamine moiety at position 3 displayed the highest in vitro inhibitory activities against MAO-B.	propargylamine	20-34	monoamine oxidase B	Homo sapiens	117-122
26873265-0	2016	Pharmacophore generation, atom-based 3D-QSAR, HQSAR and activity cliff analyses of benzothiazine and deazaxanthine derivatives as dual A2A antagonists/MAO-B inhibitors.	benzothiazine	83-96	monoamine oxidase B	Homo sapiens	151-156
26873265-0	2016	Pharmacophore generation, atom-based 3D-QSAR, HQSAR and activity cliff analyses of benzothiazine and deazaxanthine derivatives as dual A2A antagonists/MAO-B inhibitors.	7-deazaxanthine	101-114	monoamine oxidase B	Homo sapiens	151-156
26917951-3	2016	SAF inhibits monoamine oxidase B and dopamine reuptake and glutamate release, blocks voltage-dependent sodium channels, and modulates calcium channels.	safinamide	0-3	monoamine oxidase B	Homo sapiens	13-32
26821818-4	2016	The results show that the benzoxathiolones are potent MAO-B inhibitors with IC50 values ranging from 0.003 to 0.051 muM.	benzoxathiolones	26-42	monoamine oxidase B	Homo sapiens	54-59
26821818-5	2016	Although the benzoxathiolones are selective for the MAO-B isoform, two compounds display good MAO-A inhibition with IC50 values of 0.189 and 0.424 muM.	benzoxathiolones	13-29	monoamine oxidase B	Homo sapiens	52-57
26821818-7	2016	It may thus be concluded that the benzoxathiolone class is suitable for the design and development of MAO-B inhibitors, and that in some instances good MAO-A inhibition may also be achieved.	benzoxathiolone	34-49	monoamine oxidase B	Homo sapiens	102-107
25604428-3	2016	It has been suggested that the irreversible MAO-B inhibitors selegiline and rasagiline exert a neuroprotective effect in Parkinson"s and Alzheimer"s diseases.	Selegiline	61-71	monoamine oxidase B	Homo sapiens	44-49
26590367-0	2016	The MAO-B inhibitor deprenyl reduces the oral tremor and the dopamine depletion induced by the VMAT-2 inhibitor tetrabenazine.	Dopamine	61-69	monoamine oxidase B	Homo sapiens	4-9
26590367-0	2016	The MAO-B inhibitor deprenyl reduces the oral tremor and the dopamine depletion induced by the VMAT-2 inhibitor tetrabenazine.	Tetrabenazine	112-125	monoamine oxidase B	Homo sapiens	4-9
26590367-6	2016	Deprenyl is a selective and irreversible inhibitor of monoamine oxidase-B, and administration of deprenyl produced a dose-related suppression of TBZ-induced TJMs.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	54-73
25604428-3	2016	It has been suggested that the irreversible MAO-B inhibitors selegiline and rasagiline exert a neuroprotective effect in Parkinson"s and Alzheimer"s diseases.	rasagiline	76-86	monoamine oxidase B	Homo sapiens	44-49
25604428-5	2016	There is increasing evidence that MAO-A activity, but not that of MAO-B, is implicated in the pathophysiology of neurodegenerative disorders, but also in gene induction by MAO-B inhibitors; on the other hand, selegiline and rasagiline increase MAO-A mRNA, protein, and enzyme activity levels.	rasagiline	224-234	monoamine oxidase B	Homo sapiens	172-177
26429556-4	2016	CONCLUSION: Many of the studies clearly revealed that most of the chalcones showed selective, reversible and potent MAO-B inhibition compared to MAO-A.	Chalcones	66-75	monoamine oxidase B	Homo sapiens	116-121
26585057-0	2016	In Vivo and In Vitro Characterization of a Novel MAO-B Inhibitor Radioligand, 18F-Labeled Deuterated Fluorodeprenyl.	deuterated fluorodeprenyl	90-115	monoamine oxidase B	Homo sapiens	49-54
26585057-1	2016	UNLABELLED: The aim of this study was to radiolabel a novel bis-deuterium substituted l-deprenyl analog (fluorodeprenyl-D2) with (18)F and to evaluate its potential to visualize and quantify monoamine oxidase (MAO) B activity in vivo.	bis-deuterium	60-73	monoamine oxidase B	Homo sapiens	191-216
26585057-1	2016	UNLABELLED: The aim of this study was to radiolabel a novel bis-deuterium substituted l-deprenyl analog (fluorodeprenyl-D2) with (18)F and to evaluate its potential to visualize and quantify monoamine oxidase (MAO) B activity in vivo.	Selegiline	86-96	monoamine oxidase B	Homo sapiens	191-216
26585057-1	2016	UNLABELLED: The aim of this study was to radiolabel a novel bis-deuterium substituted l-deprenyl analog (fluorodeprenyl-D2) with (18)F and to evaluate its potential to visualize and quantify monoamine oxidase (MAO) B activity in vivo.	fluorodeprenyl-d2	105-122	monoamine oxidase B	Homo sapiens	191-216
26585057-10	2016	The autoradiography binding density of (18)F-fluorodeprenyl-D2 was consistent with known MAO-B expression in the human brain.	f-fluorodeprenyl-d2	43-62	monoamine oxidase B	Homo sapiens	89-94
26585057-13	2016	Administration of a 1 mg/kg dose of l-deprenyl yielded 70% inhibition of MAO-B in all regions.	Selegiline	36-46	monoamine oxidase B	Homo sapiens	73-78
26585057-16	2016	CONCLUSION: The results suggest that (18)F-fluorodeprenyl-D2 is a suitable PET radioligand for visualization of MAO-B activity in the human brain.	f-fluorodeprenyl-d2	41-60	monoamine oxidase B	Homo sapiens	112-117
26796202-5	2016	Scopoletin occupied the hydrophobic aromatic pockets showing favorable interactions for MAO-B; experimental Ki agreed with the predicted Ki.	Scopoletin	0-10	monoamine oxidase B	Homo sapiens	88-93
26796202-8	2016	Overall, scopoletin is a partially selective MAO-B inhibitor that increases brain dopamine level.	Scopoletin	9-19	monoamine oxidase B	Homo sapiens	45-50
26796202-8	2016	Overall, scopoletin is a partially selective MAO-B inhibitor that increases brain dopamine level.	Dopamine	82-90	monoamine oxidase B	Homo sapiens	45-50
26592858-6	2016	In case of compounds having an aromatic nucleus at the amino terminus, increasing the carbon number between N and the aromatic ring increases the potency as well as selectivity toward hMAO-B.	Carbon	86-92	monoamine oxidase B	Homo sapiens	184-190
25687583-4	2016	The R and S form of thiophene based pyrazolines-carboxamides showed a binding energy and inhibition constant between 7.93 to -8.76 and 1.54 to 0.38 muM toward MAO-A and -6.39 to -8.51 and 20.84 to 0.57 muM toward MAO-B respectively.	Thiophenes	20-29	monoamine oxidase B	Homo sapiens	213-218
25687583-4	2016	The R and S form of thiophene based pyrazolines-carboxamides showed a binding energy and inhibition constant between 7.93 to -8.76 and 1.54 to 0.38 muM toward MAO-A and -6.39 to -8.51 and 20.84 to 0.57 muM toward MAO-B respectively.	pyrazolines-carboxamides	36-60	monoamine oxidase B	Homo sapiens	213-218
25788143-0	2016	Pharmacophore Modeling, 3D-QSAR and Molecular Docking of Furanochalcones as Inhibitors of Monoamine Oxidase-B.	furanochalcones	57-72	monoamine oxidase B	Homo sapiens	90-109
25788143-2	2016	Herein described is pharmacophore generation and atom-based 3D-QSAR analysis of previously reported furan based MAO-B inhibitors in order to get insight into their structural requirements responsible for high affinity.	furan	100-105	monoamine oxidase B	Homo sapiens	112-117
26717204-1	2016	With the aim to identify new, potent and selective monoamine oxidase B (MAO-B) inhibitors, molecular interaction field analysis has been applied to a MAO-B complex with 3-acetyl-2,5-diaryl-2,3-dihydro-1,3,4-oxadiazole chemical structure, known as a privileged scaffold for this target.	3-acetyl-2,5-diaryl-2,3-dihydro-1,3,4-oxadiazole	169-217	monoamine oxidase B	Homo sapiens	51-70
26717204-1	2016	With the aim to identify new, potent and selective monoamine oxidase B (MAO-B) inhibitors, molecular interaction field analysis has been applied to a MAO-B complex with 3-acetyl-2,5-diaryl-2,3-dihydro-1,3,4-oxadiazole chemical structure, known as a privileged scaffold for this target.	3-acetyl-2,5-diaryl-2,3-dihydro-1,3,4-oxadiazole	169-217	monoamine oxidase B	Homo sapiens	72-77
26717204-1	2016	With the aim to identify new, potent and selective monoamine oxidase B (MAO-B) inhibitors, molecular interaction field analysis has been applied to a MAO-B complex with 3-acetyl-2,5-diaryl-2,3-dihydro-1,3,4-oxadiazole chemical structure, known as a privileged scaffold for this target.	3-acetyl-2,5-diaryl-2,3-dihydro-1,3,4-oxadiazole	169-217	monoamine oxidase B	Homo sapiens	150-155
26592797-4	2016	Kinetic studies revealed that compounds 18 and 16 (1-benzyl-3-hydroxy-3-(4"-bromophenacyl)oxindole) exhibit competitive inhibition against MAO-A and MAO-B, respectively.	1-benzyl-3-hydroxy-3-(4"-bromophenacyl)oxindole	51-98	monoamine oxidase B	Homo sapiens	149-154
26299850-2	2016	Leflunomide inhibits human MAO-A and MAO-B and exhibits IC&amp;lt;sub&amp;gt;50&amp;lt;/sub&amp;gt; values of 19.1 muM and 13.7 muM, respectively.	Leflunomide	0-11	monoamine oxidase B	Homo sapiens	37-42
26299850-3	2016	The corresponding K&amp;lt;sub&amp;gt;i&amp;lt;/sub&amp;gt; values are 17.7 muM (MAO-A) and 10.1 muM (MAO-B).	k&amp	18-23	monoamine oxidase B	Homo sapiens	102-107
26299850-3	2016	The corresponding K&amp;lt;sub&amp;gt;i&amp;lt;/sub&amp;gt; values are 17.7 muM (MAO-A) and 10.1 muM (MAO-B).	Adenosine Monophosphate	20-23	monoamine oxidase B	Homo sapiens	102-107
26299850-3	2016	The corresponding K&amp;lt;sub&amp;gt;i&amp;lt;/sub&amp;gt; values are 17.7 muM (MAO-A) and 10.1 muM (MAO-B).	Adenosine Monophosphate	31-34	monoamine oxidase B	Homo sapiens	102-107
26299850-3	2016	The corresponding K&amp;lt;sub&amp;gt;i&amp;lt;/sub&amp;gt; values are 17.7 muM (MAO-A) and 10.1 muM (MAO-B).	Adenosine Monophosphate	31-34	monoamine oxidase B	Homo sapiens	102-107
26561069-2	2016	1.4.3.4) is a flavin-adenine type of enzyme with two isoforms referred to MAO-A and MAO-B that function for oxidation of monoamines.	flavin adenine	14-28	monoamine oxidase B	Homo sapiens	84-89
26561069-2	2016	1.4.3.4) is a flavin-adenine type of enzyme with two isoforms referred to MAO-A and MAO-B that function for oxidation of monoamines.	monoamines	121-131	monoamine oxidase B	Homo sapiens	84-89
25798687-2	2016	In this context, we focused on the design, synthesis and evaluation of homoisoflavonoid derivatives as dual acetyl cholinesterase (AChE) and monoamine oxidase (MAO-B) inhibitors.	homoisoflavonoid	71-87	monoamine oxidase B	Homo sapiens	160-165
26849427-1	2016	Safinamide (brand name Xadago , Zambon S.p.A) is a third-generation reversible MAO-B inhibitor, which also blocks sodium voltage-sensitive channels and modulates stimulated release of glutamate.	safinamide	0-10	monoamine oxidase B	Homo sapiens	79-84
26849427-1	2016	Safinamide (brand name Xadago , Zambon S.p.A) is a third-generation reversible MAO-B inhibitor, which also blocks sodium voltage-sensitive channels and modulates stimulated release of glutamate.	zambon	32-38	monoamine oxidase B	Homo sapiens	79-84
26849427-1	2016	Safinamide (brand name Xadago , Zambon S.p.A) is a third-generation reversible MAO-B inhibitor, which also blocks sodium voltage-sensitive channels and modulates stimulated release of glutamate.	Sodium	114-120	monoamine oxidase B	Homo sapiens	79-84
27118978-3	2016	As finding safer and reversible MAOIs is our target, we characterized the recombinant human (h) MAO-A and MAO-B inhibition potentials of two common natural isoflavones, genistein (GST) and daidzein (DZ) using luminescence assay.	Genistein	169-178	monoamine oxidase B	Homo sapiens	106-111
27118978-7	2016	GST also inhibited hMAO-B tyramine oxidation and hydrogen peroxide production more than hMAO-A.	Tyramine	26-34	monoamine oxidase B	Homo sapiens	19-25
27118978-8	2016	Docking studies conducted indicated that the GST reversibility and hMAO-B selectivity of inhibition may relate to C5-OH effects on its orientation and its interactions with the threonine 201 residue of the active site.	Threonine	177-186	monoamine oxidase B	Homo sapiens	67-73
27366756-4	2016	Additionally, the expression of monoamine-oxidase type B (Maob) seems to be lower in islets from humans and mice with diabetes compared to nondiabetic islets, which may lead to increased monoamine concentrations.	monoamine	32-41	monoamine oxidase B	Homo sapiens	58-62
26536532-10	2015	In general, the 5-(hydroxamic acid)methyl oxazolidinone derivatives demonstrated moderate but selective MAO-B inhibitory activity.	5-(hydroxamic acid)methyl oxazolidinone	16-55	monoamine oxidase B	Homo sapiens	104-109
26478315-0	2016	Monoamine oxidase B layer-by-layer film fabrication and characterization toward dopamine detection.	Dopamine	80-88	monoamine oxidase B	Homo sapiens	0-19
26478315-1	2016	In this work nanostructured film composites of the monoamine oxidase B (MAO-B) enzyme, free or encapsulated in liposomes, were fabricated by the layer-by-layer (LbL) self-assembly technique, employing polyethylene imine (PEI) as polycation.	polyethylene imine	201-219	monoamine oxidase B	Homo sapiens	51-70
26478315-1	2016	In this work nanostructured film composites of the monoamine oxidase B (MAO-B) enzyme, free or encapsulated in liposomes, were fabricated by the layer-by-layer (LbL) self-assembly technique, employing polyethylene imine (PEI) as polycation.	polyethylene imine	201-219	monoamine oxidase B	Homo sapiens	72-77
26478315-1	2016	In this work nanostructured film composites of the monoamine oxidase B (MAO-B) enzyme, free or encapsulated in liposomes, were fabricated by the layer-by-layer (LbL) self-assembly technique, employing polyethylene imine (PEI) as polycation.	pei	221-224	monoamine oxidase B	Homo sapiens	51-70
26478315-1	2016	In this work nanostructured film composites of the monoamine oxidase B (MAO-B) enzyme, free or encapsulated in liposomes, were fabricated by the layer-by-layer (LbL) self-assembly technique, employing polyethylene imine (PEI) as polycation.	pei	221-224	monoamine oxidase B	Homo sapiens	72-77
26478315-5	2016	The biosensor fabricated by MAO-B incorporated into liposomes composed of DPPG:POPG in the ratio (1:4) (w/w) showed the best performance with a sensitivity of 0.86 (muA cm(-2))/(mmol L(-1)) and a detection limit of 0.33 mmol L(-1).	1,2-dipalmitoylphosphatidylglycerol	74-78	monoamine oxidase B	Homo sapiens	28-33
28635937-0	2016	[A role of the MAO-B inhibitor rasagiline in treatment of Parkinson"s disease].	rasagiline	31-41	monoamine oxidase B	Homo sapiens	15-20
28635937-4	2016	Rasagiline (azilect), a new generation MAO-B inhibitor, helps to solve the problems at different stages of PD.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	39-44
28635937-4	2016	Rasagiline (azilect), a new generation MAO-B inhibitor, helps to solve the problems at different stages of PD.	rasagiline	12-19	monoamine oxidase B	Homo sapiens	39-44
25807300-2	2015	Most of them had an inhibitory effect in the low micromolar/high nanomolar range, being derivatives of 4-acetylpyridine selective hMAO-B inhibitors also at low nanomolar concentrations.	4-acetylpyridine	103-119	monoamine oxidase B	Homo sapiens	130-136
26189013-0	2015	Development of fluorinated methoxylated chalcones as selective monoamine oxidase-B inhibitors: Synthesis, biochemistry and molecular docking studies.	fluorinated methoxylated chalcones	15-49	monoamine oxidase B	Homo sapiens	63-82
27004312-3	2015	CASE REPORT: The authors reported a case of serotonin syndrome associated with combined therapy of monoamine oxidase-B inhibitors and selective serotonin reuptake inhibitor A 77-year-old Thai man had been taking escitalopram for depression for three years.	Serotonin	44-53	monoamine oxidase B	Homo sapiens	99-118
27004312-3	2015	CASE REPORT: The authors reported a case of serotonin syndrome associated with combined therapy of monoamine oxidase-B inhibitors and selective serotonin reuptake inhibitor A 77-year-old Thai man had been taking escitalopram for depression for three years.	Citalopram	212-224	monoamine oxidase B	Homo sapiens	99-118
26432037-2	2015	Of particular importance to the present study is a report that a series of furanochalcones acts as MAO-B selective inhibitors.	furanochalcones	75-90	monoamine oxidase B	Homo sapiens	99-104
26432037-6	2015	The most potent MAO-B inhibitor (4h) displays an IC50 value of 0.067 muM while the most potent MAO-A inhibitor (4e) exhibits an IC50 value of 3.81 muM.	4h	33-35	monoamine oxidase B	Homo sapiens	16-21
26432037-8	2015	4h, however, may exhibit tight-binding to MAO-B, a property linked to its thiophene moiety.	4h	0-2	monoamine oxidase B	Homo sapiens	42-47
26432037-8	2015	4h, however, may exhibit tight-binding to MAO-B, a property linked to its thiophene moiety.	Thiophenes	74-83	monoamine oxidase B	Homo sapiens	42-47
26432037-9	2015	We conclude that high potency chalcones such as 4h represent suitable leads for the development of MAO-B inhibitors for the treatment of Parkinson"s disease and possibly other neurodegenerative disorders.	Chalcones	30-39	monoamine oxidase B	Homo sapiens	99-104
26432037-9	2015	We conclude that high potency chalcones such as 4h represent suitable leads for the development of MAO-B inhibitors for the treatment of Parkinson"s disease and possibly other neurodegenerative disorders.	4h	48-50	monoamine oxidase B	Homo sapiens	99-104
26263056-7	2015	The developed method was successfully applied for detection of the MAO-A and MAO-B inhibitive activities by model drugs, including pargyline, clorgyline, as well as beta-carboline alkaloids from Peganum harmala.	Pargyline	131-140	monoamine oxidase B	Homo sapiens	77-82
26263056-7	2015	The developed method was successfully applied for detection of the MAO-A and MAO-B inhibitive activities by model drugs, including pargyline, clorgyline, as well as beta-carboline alkaloids from Peganum harmala.	Clorgyline	142-152	monoamine oxidase B	Homo sapiens	77-82
26263056-7	2015	The developed method was successfully applied for detection of the MAO-A and MAO-B inhibitive activities by model drugs, including pargyline, clorgyline, as well as beta-carboline alkaloids from Peganum harmala.	beta-carboline alkaloids	165-189	monoamine oxidase B	Homo sapiens	77-82
26337020-2	2015	Among them, compound 10b including alpha,beta-unsaturated ketone group showed the most potent and selective MAO-B inhibitory activity (IC50 human MAO-B 16 nM, &gt;6000-fold selective vs MAO-A) and compound 10b exhibited good reversibility compared with selegiline, a well-known irreversible MAO-B inhibitor.	alpha,beta-unsaturated ketone	35-64	monoamine oxidase B	Homo sapiens	108-113
26744740-3	2015	Ideal candidates for the balance of these neurotransmitter deficits are compounds like safinamide with broad mechanisms of action such as reversible monoamine oxidase type B inhibition, blockage of voltage-dependent sodium channels, modulation of calcium channels and of glutamate release.	safinamide	87-97	monoamine oxidase B	Homo sapiens	149-173
26352677-3	2015	The most potent selective hMAO-B inhibitor D7 has a selectivity ratio of 20.93, with an IC50 value of 2.78 muM, similar or better than selegiline (IC50 = 2.89 muM), a selective hMAO-B inhibitor currently in the market for the treatment of Parkinson"s disease.	Selegiline	135-145	monoamine oxidase B	Homo sapiens	26-32
26352677-4	2015	Our modeling study indicates that Tyr 326 of hMAO-B (or corresponded Ile 335 of hMAO-A) may be the determinant for the specificity of these compounds.	Tyrosine	34-37	monoamine oxidase B	Homo sapiens	45-51
26491258-2	2015	The 3-coumaranone derivatives are structurally related to series of alpha-tetralone and 1-indanone derivatives, which have recently been shown to potently inhibit MAO, with selectivity for MAO-B (in preference to the MAO-A isoform).	3-coumaranone	4-17	monoamine oxidase B	Homo sapiens	189-194
26491258-2	2015	The 3-coumaranone derivatives are structurally related to series of alpha-tetralone and 1-indanone derivatives, which have recently been shown to potently inhibit MAO, with selectivity for MAO-B (in preference to the MAO-A isoform).	Tetralones	68-83	monoamine oxidase B	Homo sapiens	189-194
26491258-2	2015	The 3-coumaranone derivatives are structurally related to series of alpha-tetralone and 1-indanone derivatives, which have recently been shown to potently inhibit MAO, with selectivity for MAO-B (in preference to the MAO-A isoform).	indacrinone	88-98	monoamine oxidase B	Homo sapiens	189-194
26491258-7	2015	On the basis of the selectivity profiles and potent action, it may be concluded that the 3-coumaranone derivatives are suitable leads for the development of selective MAO-B inhibitors as potential treatment for disorders such as Parkinson"s disease and Alzheimer"s disease.	3-coumaranone	89-102	monoamine oxidase B	Homo sapiens	167-172
26594490-0	2015	A comparison of the structures of some 2- and 3-substituted chromone derivatives: a structural study on the importance of the secondary carboxamide backbone for the inhibitory activity of MAO-B.	Chromones	60-68	monoamine oxidase B	Homo sapiens	188-193
26594490-0	2015	A comparison of the structures of some 2- and 3-substituted chromone derivatives: a structural study on the importance of the secondary carboxamide backbone for the inhibitory activity of MAO-B.	carboxamide	136-147	monoamine oxidase B	Homo sapiens	188-193
26293971-8	2015	Compound 6h showed hMAO-B inhibitory activity whereas the others potently inhibited hMAO-A.	compound 6h	0-11	monoamine oxidase B	Homo sapiens	19-25
26337020-1	2015	We have synthesized three categories of alpha,beta-unsaturated carbonyl derivatives and evaluated their MAO-A and MAO-B inhibitory activities.	alpha,beta-unsaturated carbonyl derivatives	40-83	monoamine oxidase B	Homo sapiens	114-119
26337020-2	2015	Among them, compound 10b including alpha,beta-unsaturated ketone group showed the most potent and selective MAO-B inhibitory activity (IC50 human MAO-B 16 nM, &gt;6000-fold selective vs MAO-A) and compound 10b exhibited good reversibility compared with selegiline, a well-known irreversible MAO-B inhibitor.	alpha,beta-unsaturated ketone	35-64	monoamine oxidase B	Homo sapiens	146-151
26337020-2	2015	Among them, compound 10b including alpha,beta-unsaturated ketone group showed the most potent and selective MAO-B inhibitory activity (IC50 human MAO-B 16 nM, &gt;6000-fold selective vs MAO-A) and compound 10b exhibited good reversibility compared with selegiline, a well-known irreversible MAO-B inhibitor.	alpha,beta-unsaturated ketone	35-64	monoamine oxidase B	Homo sapiens	146-151
26337020-2	2015	Among them, compound 10b including alpha,beta-unsaturated ketone group showed the most potent and selective MAO-B inhibitory activity (IC50 human MAO-B 16 nM, &gt;6000-fold selective vs MAO-A) and compound 10b exhibited good reversibility compared with selegiline, a well-known irreversible MAO-B inhibitor.	Selegiline	253-263	monoamine oxidase B	Homo sapiens	108-113
26189013-4	2015	The most potent compound (2E)-1-(4-methoxyphenyl)-3-[4-(trifluoromethyl)phenyl] prop-2-en-1-one showed the best activity and higher selectivity towards hMAO-B with Ki and SI values of 0.22+-0.01muM and 0.05 comparable to that standard drug, Selegiline Ki and SI values were found as 0.33+-0.03muM and 0.04, respectively.	(2e)-1-(4-methoxyphenyl)-3-[4-(trifluoromethyl)phenyl] prop-2-en-1-one	25-95	monoamine oxidase B	Homo sapiens	152-158
26189013-4	2015	The most potent compound (2E)-1-(4-methoxyphenyl)-3-[4-(trifluoromethyl)phenyl] prop-2-en-1-one showed the best activity and higher selectivity towards hMAO-B with Ki and SI values of 0.22+-0.01muM and 0.05 comparable to that standard drug, Selegiline Ki and SI values were found as 0.33+-0.03muM and 0.04, respectively.	Selegiline	241-251	monoamine oxidase B	Homo sapiens	152-158
26519278-2	2015	Glucocorticoid receptor antagonist RU38486 prevented increase in monoamine oxidase B activity and content of LPO products of in brain cortex typical of anxiogenic stress.	Mifepristone	35-42	monoamine oxidase B	Homo sapiens	65-84
26337020-3	2015	However, both alpha,beta-unsaturated amide and ester derivatives exhibited weaker MAO-B inhibition potencies.	alpha,beta-unsaturated amide	14-42	monoamine oxidase B	Homo sapiens	82-87
26337020-3	2015	However, both alpha,beta-unsaturated amide and ester derivatives exhibited weaker MAO-B inhibition potencies.	Esters	47-52	monoamine oxidase B	Homo sapiens	82-87
25581511-2	2015	Arylalkyloxy substitution on C7 of the alpha-tetralone moiety yielded compounds with high inhibition potencies toward the human monoamine oxidase-B isoform with all compounds possessing IC50 values in the submicromolar range (0.00089-0.047 mum).	Tetralones	39-54	monoamine oxidase B	Homo sapiens	128-147
25581511-4	2015	The alpha-tetralones were, however, in each instance selective for monoamine oxidase-B over the monoamine oxidase-A isoform.	alpha-tetralones	4-20	monoamine oxidase B	Homo sapiens	67-86
25572450-2	2015	A potential pharmaceutical treatment for smoking cessation is selegiline, a selective and irreversible monoamine oxidase B inhibitor.	Selegiline	62-72	monoamine oxidase B	Homo sapiens	103-122
25863936-1	2015	Rasagiline and selegiline, inhibitors of type B monoamine oxidase (MAO-B), protect neurons from cell death in cellular and animal models.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	67-72
25863936-1	2015	Rasagiline and selegiline, inhibitors of type B monoamine oxidase (MAO-B), protect neurons from cell death in cellular and animal models.	Selegiline	15-25	monoamine oxidase B	Homo sapiens	67-72
26293004-6	2015	Positive results were also obtained with a new monoamine oxidase B (MAO-B) inhibitor (safinamide) and a catechol-O-methyltransferase COMT inhibitor (opicapone).	safinamide	86-96	monoamine oxidase B	Homo sapiens	68-73
25755053-6	2015	After pre-incubation of the cyclopropylamine with the enzyme, the inhibition was irreversible for both MAO A and MAO B, and the activity was not restored by dilution.	cyclopropylamine	28-44	monoamine oxidase B	Homo sapiens	113-118
25891478-1	2015	Isatin is an endogenous inhibitor of monoamine oxidase B and is found in human blood and tissue.	Isatin	0-6	monoamine oxidase B	Homo sapiens	37-56
25755053-9	2015	The best inhibitor was cis-N-benzyl-2-methoxycyclopropylamine, with an IC50 of 5 nm for MAO B and 170 nm for MAO A after 30 min pre-incubation.	cis-N-benzyl-2-methoxycyclopropylamine	23-61	monoamine oxidase B	Homo sapiens	88-93
25755053-10	2015	This cis-cyclopropylamine is over 20-fold more effective than tranylcypromine, so may be studied as a lead for selective inhibitors of MAO B that do not inhibit LSD1.	cis-cyclopropylamine	5-25	monoamine oxidase B	Homo sapiens	135-140
25755053-10	2015	This cis-cyclopropylamine is over 20-fold more effective than tranylcypromine, so may be studied as a lead for selective inhibitors of MAO B that do not inhibit LSD1.	Tranylcypromine	62-77	monoamine oxidase B	Homo sapiens	135-140
26091526-2	2015	The Quantum Chemical Cluster Approach was used to obtain transition states of MAO B complexed with phenylethylamine (PEA), benzylamine (BA), and p-nitrobenzylamine (NBA).	Phenethylamines	99-115	monoamine oxidase B	Homo sapiens	78-83
26091526-2	2015	The Quantum Chemical Cluster Approach was used to obtain transition states of MAO B complexed with phenylethylamine (PEA), benzylamine (BA), and p-nitrobenzylamine (NBA).	Phenethylamines	117-120	monoamine oxidase B	Homo sapiens	78-83
26087676-0	2015	Catalytic Amine Oxidation under Ambient Aerobic Conditions: Mimicry of Monoamine Oxidase B.	Amines	10-15	monoamine oxidase B	Homo sapiens	71-90
26091526-2	2015	The Quantum Chemical Cluster Approach was used to obtain transition states of MAO B complexed with phenylethylamine (PEA), benzylamine (BA), and p-nitrobenzylamine (NBA).	benzylamine	123-134	monoamine oxidase B	Homo sapiens	78-83
26091526-2	2015	The Quantum Chemical Cluster Approach was used to obtain transition states of MAO B complexed with phenylethylamine (PEA), benzylamine (BA), and p-nitrobenzylamine (NBA).	benzylamine	136-138	monoamine oxidase B	Homo sapiens	78-83
26091526-2	2015	The Quantum Chemical Cluster Approach was used to obtain transition states of MAO B complexed with phenylethylamine (PEA), benzylamine (BA), and p-nitrobenzylamine (NBA).	4-nitrobenzylamine	145-163	monoamine oxidase B	Homo sapiens	78-83
26091526-2	2015	The Quantum Chemical Cluster Approach was used to obtain transition states of MAO B complexed with phenylethylamine (PEA), benzylamine (BA), and p-nitrobenzylamine (NBA).	nba	165-168	monoamine oxidase B	Homo sapiens	78-83
26091526-3	2015	The choice of these amines relies on their importance to address MAO B catalytic mechanisms so as to help us to answer questions such as why BA is a better substrate than NBA or how para-substitution affects substrate"s reactivity.	Amines	20-26	monoamine oxidase B	Homo sapiens	65-70
26091526-3	2015	The choice of these amines relies on their importance to address MAO B catalytic mechanisms so as to help us to answer questions such as why BA is a better substrate than NBA or how para-substitution affects substrate"s reactivity.	benzylamine	141-143	monoamine oxidase B	Homo sapiens	65-70
26091526-5	2015	From a theoretical point of view, and according to the our reported transition states, their calculated barriers and structural and orbital differences obtained by us among these compounds, we propose that good substrates such as BA and PEA might follow the hydride transfer pathway while poor substrates such as NBA prefer the polar nucleophilic mechanism, which might suggest that MAO B can act by both mechanisms.	benzylamine	230-232	monoamine oxidase B	Homo sapiens	383-388
26091526-6	2015	The low free energy barriers for BA and PEA reflect the preference that MAO B has for hydride transfer over the polar nucleophilic mechanism when catalyzing the oxidative deamination of neurotransmitters.	benzylamine	33-35	monoamine oxidase B	Homo sapiens	72-77
25368372-1	2015	OBJECTIVE: The current study examined the efficacy and safety of rasagiline, a selective MAO-B inhibitor, for the treatment of persistent negative symptoms.	rasagiline	65-75	monoamine oxidase B	Homo sapiens	89-94
26203229-4	2015	Analyses of the structure-activity relationships for MAO inhibition show that substitution on the C5 position of the 2-acetylphenol moiety is a requirement for MAO-B inhibition, and the benzyloxy substituent is particularly favorable in this regard.	2'-hydroxyacetophenone	117-131	monoamine oxidase B	Homo sapiens	160-165
26203229-5	2015	This study concludes that C5-substituted 2-acetylphenol analogs are potent and selective MAO-B inhibitors, appropriate for the design of therapies for neurodegenerative disorders such as Parkinson"s disease.	2'-hydroxyacetophenone	41-55	monoamine oxidase B	Homo sapiens	89-94
25934229-2	2015	The in vitro assay shows that most target compounds exhibit good MAO-B activities with submicromolar IC50 values and antioxidant activity (1.49-5.67 ORAC-FL values).	orac	149-153	monoamine oxidase B	Homo sapiens	65-70
25934229-2	2015	The in vitro assay shows that most target compounds exhibit good MAO-B activities with submicromolar IC50 values and antioxidant activity (1.49-5.67 ORAC-FL values).	Fluorides	154-156	monoamine oxidase B	Homo sapiens	65-70
26107513-3	2015	Highly flexible N-benzyl-N-alkyloxy coumarins 2-12 showed good inhibitory activities at MAO-B, AChE, and BChE but low selectivity.	n-benzyl-n-alkyloxy coumarins	16-45	monoamine oxidase B	Homo sapiens	88-93
25346381-5	2015	Furthermore, compound XZ09 exhibited less inhibition against the homologous monoamine oxidase A (MAO-A) and B (MAO-B) displaying its moderate selectivity.	XZ09	22-26	monoamine oxidase B	Homo sapiens	111-116
25820651-2	2015	Based on the structural similarity between alpha-tetralone and 1-indanone, the present study involved synthesis of 34 1-indanone and related indane derivatives as potential inhibitors of recombinant human MAO-A and MAO-B.	Tetralones	43-58	monoamine oxidase B	Homo sapiens	215-220
25725114-8	2015	Our findings could be verified on a sample of human male volunteers treated for infertility, because human organism tolerate higher doses of R-(-)-deprenyl, which is a selective inhibitor of monoamine oxidase B employed in our experiment and used in the therapy of Parkinson s disease, rather well.	r-(-)-deprenyl	141-155	monoamine oxidase B	Homo sapiens	191-210
25820651-4	2015	C5-Substituted indanone and indane derivatives are comparatively weaker MAO-B inhibitors.	c5-substituted indanone	0-23	monoamine oxidase B	Homo sapiens	72-77
26164425-2	2015	Selegiline was the first MAO-B to be used therapeutically, while rasagiline is a second-generation drug with higher potency and selectivity.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	25-30
26164425-3	2015	Safinamide is an investigational MAO-B inhibitor with non-dopaminergic properties that may provide advantages over its predecessors.	safinamide	0-10	monoamine oxidase B	Homo sapiens	33-38
26164425-5	2015	In combination with levodopa, MAO-B inhibitors may improve motor fluctuations and allow for lower total doses of levodopa.	Levodopa	113-121	monoamine oxidase B	Homo sapiens	30-35
25812965-0	2015	Multi-target tacrine-coumarin hybrids: cholinesterase and monoamine oxidase B inhibition properties against Alzheimer"s disease.	Tacrine	13-20	monoamine oxidase B	Homo sapiens	58-77
25812965-0	2015	Multi-target tacrine-coumarin hybrids: cholinesterase and monoamine oxidase B inhibition properties against Alzheimer"s disease.	coumarin	21-29	monoamine oxidase B	Homo sapiens	58-77
25812965-3	2015	Among these compounds, 14c exhibited strong inhibitory activity for AChE (IC50 values of 33.63 nM for eeAChE and 16.11 nM for hAChE) and BuChE (IC50 values of 80.72 nM for eqBuChE and 112.72 nM for hBuChE), and the highest inhibitory activity against hMAO-B (IC50 value of 0.24 muM).	Carbon-14	23-26	monoamine oxidase B	Homo sapiens	251-257
25857942-7	2015	It may be concluded that benzodioxane derivatives are promising leads for the design of selective MAO-B inhibitors for the treatment of Parkinson"s disease.	benzodioxane	25-37	monoamine oxidase B	Homo sapiens	98-103
25820651-4	2015	C5-Substituted indanone and indane derivatives are comparatively weaker MAO-B inhibitors.	indan	28-34	monoamine oxidase B	Homo sapiens	72-77
25820651-5	2015	Although the 1-indanone and indane derivatives are selective inhibitors of the MAO-B isoform, a number of homologues are also potent MAO-A inhibitors, with three homologues possessing IC50 values &lt;0.1 muM.	indacrinone	13-23	monoamine oxidase B	Homo sapiens	79-84
25820651-2	2015	Based on the structural similarity between alpha-tetralone and 1-indanone, the present study involved synthesis of 34 1-indanone and related indane derivatives as potential inhibitors of recombinant human MAO-A and MAO-B.	indacrinone	63-73	monoamine oxidase B	Homo sapiens	215-220
25820651-5	2015	Although the 1-indanone and indane derivatives are selective inhibitors of the MAO-B isoform, a number of homologues are also potent MAO-A inhibitors, with three homologues possessing IC50 values &lt;0.1 muM.	indan	28-34	monoamine oxidase B	Homo sapiens	79-84
25820651-2	2015	Based on the structural similarity between alpha-tetralone and 1-indanone, the present study involved synthesis of 34 1-indanone and related indane derivatives as potential inhibitors of recombinant human MAO-A and MAO-B.	indacrinone	118-128	monoamine oxidase B	Homo sapiens	215-220
25820651-2	2015	Based on the structural similarity between alpha-tetralone and 1-indanone, the present study involved synthesis of 34 1-indanone and related indane derivatives as potential inhibitors of recombinant human MAO-A and MAO-B.	indan	141-147	monoamine oxidase B	Homo sapiens	215-220
25820651-3	2015	The results show that C6-substituted indanones are particularly potent and selective MAO-B inhibitors, with IC50 values ranging from 0.001 to 0.030 muM.	c6-substituted indanones	22-46	monoamine oxidase B	Homo sapiens	85-90
25677185-3	2015	We developed a novel MAO-B-selectively activated prodrug, N,N-bis(2-chloroethyl)-2-(1-methyl-1,2,3,6-tetrahydropyridin-4-yl)propanamide (MP-MUS), for the treatment of gliomas based on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	n,n-bis(2-chloroethyl)-2-(1-methyl-1,2,3,6-tetrahydropyridin-4-yl)propanamide	58-135	monoamine oxidase B	Homo sapiens	21-26
25770611-1	2015	beta-Carbolines are inhibitors of monoamine oxidases (MAO-A and MAO-B) and can be found in foods, hallucinogenic plant or various drugs.	Carbolines	0-15	monoamine oxidase B	Homo sapiens	64-69
25770611-6	2015	The MAO-A is inhibited by all three tested beta-carbolines (harmane, norharmane, and harmaline) while MAO-B is inhibited only by norharmane.	norharman	129-139	monoamine oxidase B	Homo sapiens	102-107
25770611-7	2015	The presence of norharmane in mixtures of beta-carbolines can be identified based on the difference between the cumulative inhibition of MAO-A by all beta-carbolines and MAO-B inhibition.	norharman	16-26	monoamine oxidase B	Homo sapiens	170-175
25770611-7	2015	The presence of norharmane in mixtures of beta-carbolines can be identified based on the difference between the cumulative inhibition of MAO-A by all beta-carbolines and MAO-B inhibition.	Carbolines	42-57	monoamine oxidase B	Homo sapiens	170-175
25746740-0	2015	The adenosine receptor affinities and monoamine oxidase B inhibitory properties of sulfanylphthalimide analogues.	sulfanylphthalimide	83-102	monoamine oxidase B	Homo sapiens	38-57
25746740-3	2015	The results document that the sulfanylphthalimide analogues are selective for the adenosine A1 receptor over the A2A receptor subtype, with a number of compounds also possessing MAO-B inhibitory properties.	sulfanylphthalimide	30-49	monoamine oxidase B	Homo sapiens	178-183
25746740-6	2015	Such dual-target-directed compounds may act synergistic in the treatment of Parkinson"s disease: antagonism of the A1 receptor may facilitate dopamine release, while MAO-B inhibition may reduce dopamine metabolism.	Dopamine	194-202	monoamine oxidase B	Homo sapiens	166-171
25677185-3	2015	We developed a novel MAO-B-selectively activated prodrug, N,N-bis(2-chloroethyl)-2-(1-methyl-1,2,3,6-tetrahydropyridin-4-yl)propanamide (MP-MUS), for the treatment of gliomas based on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	mp-mus	137-143	monoamine oxidase B	Homo sapiens	21-26
25677185-3	2015	We developed a novel MAO-B-selectively activated prodrug, N,N-bis(2-chloroethyl)-2-(1-methyl-1,2,3,6-tetrahydropyridin-4-yl)propanamide (MP-MUS), for the treatment of gliomas based on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	184-228	monoamine oxidase B	Homo sapiens	21-26
25677185-3	2015	We developed a novel MAO-B-selectively activated prodrug, N,N-bis(2-chloroethyl)-2-(1-methyl-1,2,3,6-tetrahydropyridin-4-yl)propanamide (MP-MUS), for the treatment of gliomas based on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	230-234	monoamine oxidase B	Homo sapiens	21-26
25677185-9	2015	Moreover, maturation of MP-MUS is highly dependent on MAO-B, and inhibition of MAO-B activity with selegiline protected human glioma cells from apoptosis.	Selegiline	99-109	monoamine oxidase B	Homo sapiens	79-84
25857233-1	2015	The human cytochrome P450 2A6 (CYP2A6) and monoamine oxidases (MAO-A and MAO-B), catalyzing nicotine and dopamine metabolisms, respectively, are two therapeutic targets of nicotine dependence.	Nicotine	92-100	monoamine oxidase B	Homo sapiens	73-78
25857233-1	2015	The human cytochrome P450 2A6 (CYP2A6) and monoamine oxidases (MAO-A and MAO-B), catalyzing nicotine and dopamine metabolisms, respectively, are two therapeutic targets of nicotine dependence.	Dopamine	105-113	monoamine oxidase B	Homo sapiens	73-78
25857233-1	2015	The human cytochrome P450 2A6 (CYP2A6) and monoamine oxidases (MAO-A and MAO-B), catalyzing nicotine and dopamine metabolisms, respectively, are two therapeutic targets of nicotine dependence.	Nicotine	172-180	monoamine oxidase B	Homo sapiens	73-78
25857233-3	2015	In the present study, we found eight active compounds isolated from V. cinerea that comprise inhibitory activity toward CYP2A6 and MAO-A and MAO-B enzymes using activity-guided assays, with coumarin as substrate of CYP2A6 and kynuramine of MAOs.	coumarin	190-198	monoamine oxidase B	Homo sapiens	141-146
25857233-8	2015	Flavonoids inhibited MAOs with variable degrees and were more prominent in inhibition toward MAO-A than hirsutinolides, while two of hirsutinolides inhibited MAO-B approximately comparable to two flavonoids.	hirsutinolides	133-147	monoamine oxidase B	Homo sapiens	158-163
25883430-6	2015	However, testosterone was negatively correlated with platelet MAO-B (r = -0.315), and 5-HT (r = -.419) in smokers.	Testosterone	9-21	monoamine oxidase B	Homo sapiens	62-67
25883430-8	2015	In conclusion, our study showed that altered testosterone and cortisol levels may aggravate behavior, mood disturbances and symptoms of depression by decreasing platelet 5-HT and MAO-B activity in smokers.	Testosterone	45-57	monoamine oxidase B	Homo sapiens	179-184
25883430-8	2015	In conclusion, our study showed that altered testosterone and cortisol levels may aggravate behavior, mood disturbances and symptoms of depression by decreasing platelet 5-HT and MAO-B activity in smokers.	Hydrocortisone	62-70	monoamine oxidase B	Homo sapiens	179-184
25701250-4	2015	For example, 3-chloro-2-(4-methylphenyl)-1H-indole-5,6-dicarbonitrile inhibited MAO-A and MAO-B with IC50 values of 0.014muM and 0.017muM, respectively.	CHEMBL3398531	13-69	monoamine oxidase B	Homo sapiens	90-95
25701250-6	2015	An analysis of the SARs for MAO inhibition by 3-chloro-1H-indole-5,6-dicarbonitriles showed that methylation of the indole nitrogen eliminates MAO-B inhibition activity, and replacement of the 2-phenyl ring with the thienyl results in a 9-fold reduction of MAO-B inhibition activity.	Nitrogen	123-131	monoamine oxidase B	Homo sapiens	143-148
25701250-6	2015	An analysis of the SARs for MAO inhibition by 3-chloro-1H-indole-5,6-dicarbonitriles showed that methylation of the indole nitrogen eliminates MAO-B inhibition activity, and replacement of the 2-phenyl ring with the thienyl results in a 9-fold reduction of MAO-B inhibition activity.	Nitrogen	123-131	monoamine oxidase B	Homo sapiens	257-262
25600407-1	2015	Monoamine oxidase B (MAO-B) plays a key role in the metabolism of dopamine, a neurotransmitter critical for the maintenance of cognitive function.	Dopamine	66-74	monoamine oxidase B	Homo sapiens	0-19
25978392-2	2015	MAO, catalyzing the reaction of oxidative deamination of major neurotransmitter monoamines, exists in two highly homologous forms, MAO A and MAO B, distinguished by substrate specificity and inhibitor selectivity.	monoamines	80-90	monoamine oxidase B	Homo sapiens	141-146
25671411-7	2015	In this paper, we report on an in-depth computational analysis concerning the role of the enzymatic environment for the reaction mechanism of human MAO-B with different p-substituted benzylamines as substrates.	p-substituted benzylamines	169-195	monoamine oxidase B	Homo sapiens	148-153
25514361-1	2015	Rasagiline (N-propargyl-1-R-aminoindan) and selegiline (1-deprenyl) are MAO-B inhibitors which are used in the treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	72-77
25514361-1	2015	Rasagiline (N-propargyl-1-R-aminoindan) and selegiline (1-deprenyl) are MAO-B inhibitors which are used in the treatment of Parkinson"s disease.	n-propargyl-1-r-aminoindan	12-38	monoamine oxidase B	Homo sapiens	72-77
25514361-1	2015	Rasagiline (N-propargyl-1-R-aminoindan) and selegiline (1-deprenyl) are MAO-B inhibitors which are used in the treatment of Parkinson"s disease.	Selegiline	44-54	monoamine oxidase B	Homo sapiens	72-77
25514361-1	2015	Rasagiline (N-propargyl-1-R-aminoindan) and selegiline (1-deprenyl) are MAO-B inhibitors which are used in the treatment of Parkinson"s disease.	1-deprenyl	56-66	monoamine oxidase B	Homo sapiens	72-77
25600407-1	2015	Monoamine oxidase B (MAO-B) plays a key role in the metabolism of dopamine, a neurotransmitter critical for the maintenance of cognitive function.	Dopamine	66-74	monoamine oxidase B	Homo sapiens	21-26
25532905-0	2015	Potent and selective MAO-B inhibitory activity: amino- versus nitro-3-arylcoumarin derivatives.	versus nitro-3-arylcoumarin	55-82	monoamine oxidase B	Homo sapiens	21-26
25592412-1	2015	INTRODUCTION: Selegiline (l-deprenyl) is a selective monoamine oxidase type B inhibitor that has been shown to have neurotrophic and anti-apoptotic properties and to protect neurons in different experimental models of cerebral ischaemia.	Selegiline	14-24	monoamine oxidase B	Homo sapiens	53-77
25592412-1	2015	INTRODUCTION: Selegiline (l-deprenyl) is a selective monoamine oxidase type B inhibitor that has been shown to have neurotrophic and anti-apoptotic properties and to protect neurons in different experimental models of cerebral ischaemia.	Selegiline	26-36	monoamine oxidase B	Homo sapiens	53-77
25579652-2	2015	Herein, we report the discovery of two new classes of potent and selective MAO-B inhibitors based on chromane-2,4-dione and chromone-3-carboxamide scaffolds.	chromane-2,4-dione	101-119	monoamine oxidase B	Homo sapiens	75-80
25579652-2	2015	Herein, we report the discovery of two new classes of potent and selective MAO-B inhibitors based on chromane-2,4-dione and chromone-3-carboxamide scaffolds.	4-oxo-4H-chromene-3-carboxamide	124-146	monoamine oxidase B	Homo sapiens	75-80
25532905-1	2015	In this study we synthesized and evaluated a new series of amino and nitro 3-arylcoumarins as hMAO-A and hMAO-B inhibitors.	amino and nitro 3-arylcoumarins	59-90	monoamine oxidase B	Homo sapiens	105-111
25532905-2	2015	Compounds 2, 3, 5 and 6 presented a better activity and selectivity profile against the hMAO-B isoform (IC50 values between 2 and 6nM) than selegiline.	Selegiline	140-150	monoamine oxidase B	Homo sapiens	88-94
25532905-3	2015	In general, the amino derivatives (4-6) proved to be more selective against MAO-B than the nitro derivatives (1-3).	nitro	91-96	monoamine oxidase B	Homo sapiens	76-81
25546160-13	2015	Compared to MAO-B inhibitors, the HR for switching to levodopa was 0.38 (CI 0.34-0.43; p<0.001) for anticholinergics and 0.85 (CI 0.75-0.97; p=0.017) for nonergot DA.	Levodopa	54-62	monoamine oxidase B	Homo sapiens	12-17
25249059-0	2015	Evidence that formulations of the selective MAO-B inhibitor, selegiline, which bypass first-pass metabolism, also inhibit MAO-A in the human brain.	Selegiline	61-71	monoamine oxidase B	Homo sapiens	44-49
25249059-1	2015	Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	66-85
25249059-1	2015	Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	87-92
25249059-1	2015	Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson"s disease.	Selegiline	12-22	monoamine oxidase B	Homo sapiens	66-85
25249059-1	2015	Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson"s disease.	Selegiline	12-22	monoamine oxidase B	Homo sapiens	87-92
25249059-4	2015	Although there is indirect evidence that Zydis selegiline at high doses loses its selectivity for MAO-B, there is no direct evidence that it also inhibits brain MAO-A in humans.	Selegiline hydrochloride	41-57	monoamine oxidase B	Homo sapiens	98-103
26557867-5	2015	BNN showed selective hMAO-B inhibition (IC50 ~ 8.82 muM) more than hMAO-A (IC502009;~ 189.28 muM).	bavachinin	0-3	monoamine oxidase B	Homo sapiens	21-27
25261037-1	2015	Zonisamide has been reported to have protective effects on epilepsy and Parkinson s disease and to work via various mechanisms of action, such as inhibition of monoamine oxidase-B and enhancement of tyrosine hydroxylase.	Zonisamide	0-10	monoamine oxidase B	Homo sapiens	160-179
25544641-4	2015	MAO-B inhibitors are established therapy of Parkinson"s disease and inhibit the MAO-B-catalysed metabolism of dopamine in the brain.	Dopamine	110-118	monoamine oxidase B	Homo sapiens	0-5
25544641-4	2015	MAO-B inhibitors are established therapy of Parkinson"s disease and inhibit the MAO-B-catalysed metabolism of dopamine in the brain.	Dopamine	110-118	monoamine oxidase B	Homo sapiens	80-85
25544641-7	2015	Interestingly, caffeine, a known adenosine receptor antagonist, has been recently considered as a lead compound for the design and discovery of A2A antagonists and MAO-B inhibitors.	Caffeine	15-23	monoamine oxidase B	Homo sapiens	164-169
26557867-7	2015	BNN competitively inhibited hMAO-A and hMAO-B, with a lower hMAO-B K i than hMAO-A K i by 10.33-fold, and reduced hMAO-B K m /V max efficiency ratio to be comparable to the standard selegiline.	bavachinin	0-3	monoamine oxidase B	Homo sapiens	39-45
26557867-7	2015	BNN competitively inhibited hMAO-A and hMAO-B, with a lower hMAO-B K i than hMAO-A K i by 10.33-fold, and reduced hMAO-B K m /V max efficiency ratio to be comparable to the standard selegiline.	bavachinin	0-3	monoamine oxidase B	Homo sapiens	60-66
26557867-7	2015	BNN competitively inhibited hMAO-A and hMAO-B, with a lower hMAO-B K i than hMAO-A K i by 10.33-fold, and reduced hMAO-B K m /V max efficiency ratio to be comparable to the standard selegiline.	bavachinin	0-3	monoamine oxidase B	Homo sapiens	60-66
26557867-9	2015	These findings suggest that BNN, which is known to be a potent PPAR-gamma agonist, is a selective and competitive hMAO-B inhibitor and could be used in the management of PD.	bavachinin	28-31	monoamine oxidase B	Homo sapiens	114-120
26364897-1	2015	INTRODUCTION: Rasagiline is a potent, selective, irreversible Monoamine Oxidase-B (MAO-B) inhibitor, developed to prolong the action of dopamine in the brain.	rasagiline	14-24	monoamine oxidase B	Homo sapiens	62-81
26364897-1	2015	INTRODUCTION: Rasagiline is a potent, selective, irreversible Monoamine Oxidase-B (MAO-B) inhibitor, developed to prolong the action of dopamine in the brain.	rasagiline	14-24	monoamine oxidase B	Homo sapiens	83-88
26364897-1	2015	INTRODUCTION: Rasagiline is a potent, selective, irreversible Monoamine Oxidase-B (MAO-B) inhibitor, developed to prolong the action of dopamine in the brain.	Dopamine	136-144	monoamine oxidase B	Homo sapiens	62-81
26364897-1	2015	INTRODUCTION: Rasagiline is a potent, selective, irreversible Monoamine Oxidase-B (MAO-B) inhibitor, developed to prolong the action of dopamine in the brain.	Dopamine	136-144	monoamine oxidase B	Homo sapiens	83-88
25342080-8	2014	Promising results include the extension of L-dopa action without inducing LID of the novel monoamine oxidase B- and glutamate-release inhibitor safinamide; however, this had no obvious effect on existing LID.	safinamide	144-154	monoamine oxidase B	Homo sapiens	91-110
25420207-3	2015	We report the effects of the addition of a monoamine oxidase B inhibitor, rasagiline, to antidepressant treatment in PD.	rasagiline	74-84	monoamine oxidase B	Homo sapiens	43-62
24964753-13	2015	MAO-B inhibitors of the N-propargylamine type (e.g., selegiline) also counteract the DSP4-induced neurotoxicity with another, yet unknown mechanism.	n-propargylamine	24-40	monoamine oxidase B	Homo sapiens	0-5
24964753-13	2015	MAO-B inhibitors of the N-propargylamine type (e.g., selegiline) also counteract the DSP4-induced neurotoxicity with another, yet unknown mechanism.	Selegiline	53-63	monoamine oxidase B	Homo sapiens	0-5
25314256-1	2014	BACKGROUND: The serotonin toxicity syndrome (STS) is a potential risk with concurrent use of the monoamine oxidase type-B inhibitor rasagiline and antidepressants.	Serotonin	16-25	monoamine oxidase B	Homo sapiens	97-121
25296658-5	2014	The active contaminants were identified by gas chromatography-mass spectroscopy as dodecan-1-ol, dodecyl 3-(3-dodecoxy-3-oxopropyl)sulfanylpropanoate, and dodecanoic acid, and they were found to be selective monoamine oxidase-B inhibitors.	dodecyl 3-(3-dodecoxy-3-oxopropyl)sulfanylpropanoate	97-149	monoamine oxidase B	Homo sapiens	208-227
25314256-1	2014	BACKGROUND: The serotonin toxicity syndrome (STS) is a potential risk with concurrent use of the monoamine oxidase type-B inhibitor rasagiline and antidepressants.	rasagiline	132-142	monoamine oxidase B	Homo sapiens	97-121
25456120-7	2014	Overexpression of wild-type GBA and treatment with MAO-B inhibitors normalized alpha-synuclein and dopamine levels, suggesting a combination therapy for the affected twin.	Dopamine	99-107	monoamine oxidase B	Homo sapiens	51-56
25220264-0	2014	Empirical valence bond simulations of the hydride transfer step in the monoamine oxidase B catalyzed metabolism of dopamine.	Dopamine	115-123	monoamine oxidase B	Homo sapiens	71-90
25220264-2	2014	In this work, we present a comprehensive study of the rate-limiting step of dopamine degradation by MAO B, which consists in the hydride transfer from the methylene group of the substrate to the flavin moiety of the FAD prosthetic group.	Dopamine	76-84	monoamine oxidase B	Homo sapiens	100-105
25220264-2	2014	In this work, we present a comprehensive study of the rate-limiting step of dopamine degradation by MAO B, which consists in the hydride transfer from the methylene group of the substrate to the flavin moiety of the FAD prosthetic group.	4,6-dinitro-o-cresol	195-201	monoamine oxidase B	Homo sapiens	100-105
25220264-2	2014	In this work, we present a comprehensive study of the rate-limiting step of dopamine degradation by MAO B, which consists in the hydride transfer from the methylene group of the substrate to the flavin moiety of the FAD prosthetic group.	Flavin-Adenine Dinucleotide	216-219	monoamine oxidase B	Homo sapiens	100-105
25220264-4	2014	We show that MAO B is specifically tuned to catalyze the hydride transfer step from the substrate to the flavin moiety of the FAD prosthetic group and that it lowers the activation barrier by 12.3 kcal mol-1 compared to the same reaction in aqueous solution, a rate enhancement of more than nine orders of magnitude.	4,6-dinitro-o-cresol	105-111	monoamine oxidase B	Homo sapiens	13-18
25220264-4	2014	We show that MAO B is specifically tuned to catalyze the hydride transfer step from the substrate to the flavin moiety of the FAD prosthetic group and that it lowers the activation barrier by 12.3 kcal mol-1 compared to the same reaction in aqueous solution, a rate enhancement of more than nine orders of magnitude.	Flavin-Adenine Dinucleotide	126-129	monoamine oxidase B	Homo sapiens	13-18
25253656-1	2014	The membrane bound enzyme monoamine oxidase exist in two splice variants designated A and B (MAO-A and MAO-B) and are key players in the oxidative metabolism of monoamines in mammalians.	monoamines	161-171	monoamine oxidase B	Homo sapiens	103-108
25253656-3	2014	In this study we present a systematic study of the MAO-A and MAO-B substrate specificity profile by probing two series of phenethylamine analogs.	phenethylamine	122-136	monoamine oxidase B	Homo sapiens	61-66
25253656-4	2014	Km and kcat values were determined for four N-alkyl analogs 2-5 and four aryl halide analogs 6-9 at MAO-A and MAO-B.	aryl halide	73-84	monoamine oxidase B	Homo sapiens	110-115
25253656-6	2014	This new insight is important for the understanding of the substrate specificity of the MAO-B enzyme and will be relevant for future drug design within the field of monoamines.	monoamines	165-175	monoamine oxidase B	Homo sapiens	88-93
25412041-4	2014	The dichloromethane extract of propolis showed potent inhibition of human MAO-A and MAO-B.	Methylene Chloride	4-19	monoamine oxidase B	Homo sapiens	84-89
25378907-7	2014	For hMAO B, only DPHs 13 and 14 were moderate inhibitors, and compound DPH14 was the most potent (IC50 [MAO B] =3,950+-940 nM).	dph14	71-76	monoamine oxidase B	Homo sapiens	5-10
24452523-3	2014	On the other hand, compounds substituted with 2-naphthyl inhibited MAO-B enzyme with a moderate selectivity index.	2-naphthyl	46-56	monoamine oxidase B	Homo sapiens	67-72
25405283-2	2014	In this paper, a series of 2-phenoxyacetamide analogues were synthesized, and their inhibitory potency towards monoamine oxidases A (MAO-A) and B (MAO-B) were evaluated using enzyme and cancer cell lysate.	2-Phenoxyacetamide	27-45	monoamine oxidase B	Homo sapiens	147-152
25322951-1	2014	Rasagiline (Azilect( )) is an oral, second-generation, selective, irreversible monoamine oxidase-B (MAO-B) inhibitor approved in the US for the treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	79-98
25322951-1	2014	Rasagiline (Azilect( )) is an oral, second-generation, selective, irreversible monoamine oxidase-B (MAO-B) inhibitor approved in the US for the treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	100-105
25322951-1	2014	Rasagiline (Azilect( )) is an oral, second-generation, selective, irreversible monoamine oxidase-B (MAO-B) inhibitor approved in the US for the treatment of Parkinson"s disease.	rasagiline	12-19	monoamine oxidase B	Homo sapiens	79-98
25322951-1	2014	Rasagiline (Azilect( )) is an oral, second-generation, selective, irreversible monoamine oxidase-B (MAO-B) inhibitor approved in the US for the treatment of Parkinson"s disease.	rasagiline	12-19	monoamine oxidase B	Homo sapiens	100-105
25173853-4	2014	The molecules were all found to covalently inhibit KDM1A and to become increasingly selective against human monoamine oxidases MAO A and MAO B through the introduction of bulkier substituents on the cyclopropylamine ring.	cyclopropylamine	199-215	monoamine oxidase B	Homo sapiens	137-142
25035107-4	2014	The results, corrected for multiple testing, revealed increased platelet MAO-B activity in patients with alcohol dependence, subdivided into those with or without alcohol-related liver diseases, compared to control subjects (P&lt;0.001).	Alcohols	105-112	monoamine oxidase B	Homo sapiens	73-78
25196265-1	2014	INTRODUCTION: Oxidative stress reduction via monoamine oxidase-B (MAO-B) inhibition with rasagiline is under investigation to modify the course of Parkinson"s disease (PD) progression.	rasagiline	89-99	monoamine oxidase B	Homo sapiens	45-64
25196265-1	2014	INTRODUCTION: Oxidative stress reduction via monoamine oxidase-B (MAO-B) inhibition with rasagiline is under investigation to modify the course of Parkinson"s disease (PD) progression.	rasagiline	89-99	monoamine oxidase B	Homo sapiens	66-71
25034874-1	2014	BACKGROUND: Catechol-O-Methyltransferase (COMT) and Monoamine oxidase B (MAO-B) are the main enzymes that metabolize dopamine in the brain.	Dopamine	117-125	monoamine oxidase B	Homo sapiens	52-71
25017965-4	2014	We find that upon incubation with hydrogen peroxide or the MAO substrate tyramine myoblasts from patients upregulate MAO-B expression and display a significant rise in reactive oxygen species (ROS) levels, with concomitant mitochondrial depolarization.	Hydrogen Peroxide	34-51	monoamine oxidase B	Homo sapiens	117-122
25017965-4	2014	We find that upon incubation with hydrogen peroxide or the MAO substrate tyramine myoblasts from patients upregulate MAO-B expression and display a significant rise in reactive oxygen species (ROS) levels, with concomitant mitochondrial depolarization.	Tyramine	73-81	monoamine oxidase B	Homo sapiens	117-122
25034874-1	2014	BACKGROUND: Catechol-O-Methyltransferase (COMT) and Monoamine oxidase B (MAO-B) are the main enzymes that metabolize dopamine in the brain.	Dopamine	117-125	monoamine oxidase B	Homo sapiens	73-78
24307270-4	2014	Using recombinant human MAO-A and MAO-B, this study finds that phenformin acts as a moderately potent MAO-A selective inhibitor with an IC50 value of 41 microM.	Phenformin	63-73	monoamine oxidase B	Homo sapiens	34-39
25127869-0	2014	Development of potential selective and reversible pyrazoline based MAO-B inhibitors as MAO-B PET tracer precursors and reference substances for the early detection of Alzheimer"s disease.	pyrazoline	50-60	monoamine oxidase B	Homo sapiens	67-72
25127869-0	2014	Development of potential selective and reversible pyrazoline based MAO-B inhibitors as MAO-B PET tracer precursors and reference substances for the early detection of Alzheimer"s disease.	pyrazoline	50-60	monoamine oxidase B	Homo sapiens	87-92
25127869-3	2014	the aim of this work was the development of a compound library of selective and reversible MAO-B inhibitors by performing bioisosteric modifications of the core structure of 3-(anthracen-9-yl)-5-phenyl-4,5-dihydro-1H-pyrazoles.	3-(anthracen-9-yl)-5-phenyl-4,5-dihydro-1h-pyrazoles	174-226	monoamine oxidase B	Homo sapiens	91-96
25127869-4	2014	In conclusion, 13 new pyrazoline based derivatives have been prepared, which will serve as precursor substances for future radiolabeling as well as reference compounds for the investigation of increased MAO-B levels in AD.	pyrazoline	22-32	monoamine oxidase B	Homo sapiens	203-208
24307270-5	2014	Pentamidine, on the other hand, potently inhibits both MAO-A and MAO-B with IC50 values of 0.61 muM and 0.22 muM, respectively.	Pentamidine	0-11	monoamine oxidase B	Homo sapiens	65-70
24307270-7	2014	A kinetic analysis suggests that pentamidine acts as a competitive inhibitor with estimated Ki values of 0.41 muM and 0.22 muM for the inhibition of MAO-A and MAO-B, respectively.	Pentamidine	33-44	monoamine oxidase B	Homo sapiens	159-164
24449518-6	2014	Bacopaside I and bacoside A mixture inhibited the MAO-A and MAO-B enzymes.	bacopaside I	0-12	monoamine oxidase B	Homo sapiens	60-65
24449518-6	2014	Bacopaside I and bacoside A mixture inhibited the MAO-A and MAO-B enzymes.	bacoside A	17-27	monoamine oxidase B	Homo sapiens	60-65
24955776-0	2014	Indazole- and indole-5-carboxamides: selective and reversible monoamine oxidase B inhibitors with subnanomolar potency.	Indazoles	0-8	monoamine oxidase B	Homo sapiens	62-81
24955776-0	2014	Indazole- and indole-5-carboxamides: selective and reversible monoamine oxidase B inhibitors with subnanomolar potency.	indole-5-carboxamide	14-35	monoamine oxidase B	Homo sapiens	62-81
24955776-4	2014	Replacement of the carboxamide linker with a methanimine spacer leading to (E)-N-(3,4-dichlorophenyl)-1-(1H-indazol-5-yl)methanimine (58) represents a further novel class of highly potent and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, &gt;16000-fold selective versus MAO-A).	(e)-n-(3,4-dichlorophenyl)-1-(1h-indazol-5-yl)methanimine	75-132	monoamine oxidase B	Homo sapiens	202-207
24955776-4	2014	Replacement of the carboxamide linker with a methanimine spacer leading to (E)-N-(3,4-dichlorophenyl)-1-(1H-indazol-5-yl)methanimine (58) represents a further novel class of highly potent and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, &gt;16000-fold selective versus MAO-A).	(e)-n-(3,4-dichlorophenyl)-1-(1h-indazol-5-yl)methanimine	75-132	monoamine oxidase B	Homo sapiens	231-236
24955776-4	2014	Replacement of the carboxamide linker with a methanimine spacer leading to (E)-N-(3,4-dichlorophenyl)-1-(1H-indazol-5-yl)methanimine (58) represents a further novel class of highly potent and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, &gt;16000-fold selective versus MAO-A).	methyleneimine	45-56	monoamine oxidase B	Homo sapiens	231-236
24955776-1	2014	Indazole- and indole-carboxamides were discovered as highly potent, selective, competitive, and reversible inhibitors of monoamine oxidase B (MAO-B).	Indazoles	0-8	monoamine oxidase B	Homo sapiens	121-140
24955776-5	2014	In N-(3,4-difluorophenyl-1H-indazole-5-carboxamide (30, PSB-1434, IC50 human MAO-B 1.59 nM, selectivity versus MAO-A&gt;6000-fold), high potency and selectivity are optimally combined with superior physicochemical properties.	n-(3,4-difluorophenyl-1h-indazole-5-carboxamide	3-50	monoamine oxidase B	Homo sapiens	77-82
24955776-1	2014	Indazole- and indole-carboxamides were discovered as highly potent, selective, competitive, and reversible inhibitors of monoamine oxidase B (MAO-B).	Indazoles	0-8	monoamine oxidase B	Homo sapiens	142-147
24955776-1	2014	Indazole- and indole-carboxamides were discovered as highly potent, selective, competitive, and reversible inhibitors of monoamine oxidase B (MAO-B).	indole-carboxamides	14-33	monoamine oxidase B	Homo sapiens	121-140
24955776-1	2014	Indazole- and indole-carboxamides were discovered as highly potent, selective, competitive, and reversible inhibitors of monoamine oxidase B (MAO-B).	indole-carboxamides	14-33	monoamine oxidase B	Homo sapiens	142-147
24955776-4	2014	Replacement of the carboxamide linker with a methanimine spacer leading to (E)-N-(3,4-dichlorophenyl)-1-(1H-indazol-5-yl)methanimine (58) represents a further novel class of highly potent and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, &gt;16000-fold selective versus MAO-A).	methyleneimine	45-56	monoamine oxidase B	Homo sapiens	202-207
24934993-1	2014	Naturally occurring coumarins, having wide spectrum of activities such as antioxidant, anti-inflammatory, anticancer, MAO-B inhibitory and antimicrobial, are frequently used by the researchers to develop novel synthetic and semisynthetic coumarin based therapeutic agents.	Coumarins	20-29	monoamine oxidase B	Homo sapiens	118-123
24986657-3	2014	With the exception of 5i, which was a selective MAO-B inhibitor, all derivatives inhibited hMAO-A potently and selectively.	carvone	22-24	monoamine oxidase B	Homo sapiens	48-53
24934993-1	2014	Naturally occurring coumarins, having wide spectrum of activities such as antioxidant, anti-inflammatory, anticancer, MAO-B inhibitory and antimicrobial, are frequently used by the researchers to develop novel synthetic and semisynthetic coumarin based therapeutic agents.	coumarin	20-28	monoamine oxidase B	Homo sapiens	118-123
24950010-4	2014	We will also review several investigational treatments that have shown promise for the treatment of early Parkinson"s disease, including a new extended release formulation of carbidopa/levodopa (IPX066), safinamide which inhibits MAO-B, dopamine uptake and glutamate and pardoprunox which is a 5HT-1A agonist and a partial dopamine agonist.	safinamide	204-214	monoamine oxidase B	Homo sapiens	230-235
24782464-3	2014	Here, two series of 3-phenylcoumarin derivatives were synthesized and evaluated against MAO-A and MAO-B.	3-Phenylcoumarin	20-36	monoamine oxidase B	Homo sapiens	98-103
24782464-5	2014	Only 6-chloro-4-hydroxy-3-(2"-hydroxyphenyl)coumarin exhibited activity against the MAO-A isoform, while still retaining good selectivity for MAO-B.	6-chloro-4-hydroxy-3-(2"-hydroxyphenyl)coumarin	5-52	monoamine oxidase B	Homo sapiens	142-147
24782464-6	2014	6-Chloro-3-phenylcoumarins unsubstituted at the 4 position were found to be more active as MAO-B inhibitors than the corresponding 4-hydroxylated coumarins.	6-chloro-3-phenylcoumarins	0-26	monoamine oxidase B	Homo sapiens	91-96
24782464-6	2014	6-Chloro-3-phenylcoumarins unsubstituted at the 4 position were found to be more active as MAO-B inhibitors than the corresponding 4-hydroxylated coumarins.	Coumarins	17-26	monoamine oxidase B	Homo sapiens	91-96
24848125-3	2014	METHODS: The MAO-A and MAO-B inhibition profile of N-(furan-2-ylmethyl)-N-prop-2-yn-1-amine derivates (compounds 1-3) were evaluated by fluorimetric method and their absorption, distribution, metabolism, excretion, and toxicity (ADMET) properties estimated.	n-(furan-2-ylmethyl)-n-prop-2-yn-1-amine	51-91	monoamine oxidase B	Homo sapiens	23-28
24607445-3	2014	More recently, the understanding that: a) potentiation of indirectly-acting sympathomimetic amines is caused by inhibitors of MAO-A but not by inhibitors of MAO-B, and b) that reversible inhibitors of MAO-A cause minimal tyramine potentiation, has led to their re-introduction to clinical use for treatment of depression (reversible MAO-A inhibitors and new dose form MAO-B inhibitor) and treatment of Parkinson"s disease (MAO-B inhibitors).	Amines	92-98	monoamine oxidase B	Homo sapiens	368-373
24607445-4	2014	The profound neuroprotective properties of propargyl-based inhibitors of MAO-B in preclinical experiments have drawn attention to the possibility of employing these drugs for their neuroprotective effect in neurodegenerative diseases, and have raised the question of the involvement of the MAO-mediated reaction as a source of reactive free radicals.	propargyl	43-52	monoamine oxidase B	Homo sapiens	73-78
24607445-4	2014	The profound neuroprotective properties of propargyl-based inhibitors of MAO-B in preclinical experiments have drawn attention to the possibility of employing these drugs for their neuroprotective effect in neurodegenerative diseases, and have raised the question of the involvement of the MAO-mediated reaction as a source of reactive free radicals.	Free Radicals	336-349	monoamine oxidase B	Homo sapiens	73-78
24715707-0	2014	Insight into the functional and structural properties of 3-arylcoumarin as an interesting scaffold in monoamine oxidase B inhibition.	3-arylcoumarin	57-71	monoamine oxidase B	Homo sapiens	102-121
24715707-5	2014	Coumarin 12 (3-(3-bromophenyl)-6-methylcoumarin) is the most active compound (IC50 =134 pM), being 140-fold more active than selegiline and showing the highest specificity for hMAO-B.	coumarin 12	0-11	monoamine oxidase B	Homo sapiens	176-182
24715707-5	2014	Coumarin 12 (3-(3-bromophenyl)-6-methylcoumarin) is the most active compound (IC50 =134 pM), being 140-fold more active than selegiline and showing the highest specificity for hMAO-B.	3-(3-bromophenyl)-6-methylcoumarin	13-47	monoamine oxidase B	Homo sapiens	176-182
25073638-4	2014	METHODS: We have searched for association between 119 SNPs in genes implicated in monoaminergic pathways [tryptophan hydroxylase 1 (TPH1), TPH2, tyrosine hydroxylase (TH), DOPA decarboxylase (DDC), dopamine beta-hydroxylase (DBH), catechol-O-methyltransferase (COMT), monoamine oxidase A (MAOA) and MAOB] and monoamine metabolite concentrations in CSF in 74 patients with psychotic disorder.	monoamine	82-91	monoamine oxidase B	Homo sapiens	299-303
25073638-6	2014	The strongest association (p = 0.0004) was found between MAOB rs5905512, a SNP previously reported to be associated with schizophrenia in men, and MHPG concentrations in men with psychotic disorder.	Methoxyhydroxyphenylglycol	147-151	monoamine oxidase B	Homo sapiens	57-61
24937131-9	2014	The adenosine A2A antagonist MSX-3, the antidepressant and catecholamine uptake inhibitor bupropion, and the MAO-B inhibitor deprenyl, all reversed the impairments induced by tetrabenazine.	Selegiline	125-133	monoamine oxidase B	Homo sapiens	109-114
24937131-9	2014	The adenosine A2A antagonist MSX-3, the antidepressant and catecholamine uptake inhibitor bupropion, and the MAO-B inhibitor deprenyl, all reversed the impairments induced by tetrabenazine.	Tetrabenazine	175-188	monoamine oxidase B	Homo sapiens	109-114
24769350-3	2014	In designing the compounds we focused on the structures of rasagiline and selegiline, two well known MAO-B inhibitors and proposed neuroprotective agents.	rasagiline	59-69	monoamine oxidase B	Homo sapiens	101-106
24794105-2	2014	The alpha-tetralone derivatives examined are structurally related to a series of chromone (1-benzopyran-4-one) derivatives which has previously been shown to act as MAO-B inhibitors.	Tetralones	4-19	monoamine oxidase B	Homo sapiens	165-170
24794105-2	2014	The alpha-tetralone derivatives examined are structurally related to a series of chromone (1-benzopyran-4-one) derivatives which has previously been shown to act as MAO-B inhibitors.	Chromones	81-89	monoamine oxidase B	Homo sapiens	165-170
24794105-2	2014	The alpha-tetralone derivatives examined are structurally related to a series of chromone (1-benzopyran-4-one) derivatives which has previously been shown to act as MAO-B inhibitors.	4-chromone	91-109	monoamine oxidase B	Homo sapiens	165-170
24794105-3	2014	The results document that the alpha-tetralones are highly potent MAO-B inhibitors with all compounds exhibiting IC50 values in the nanomolar range (&lt;78nM).	alpha-tetralones	30-46	monoamine oxidase B	Homo sapiens	65-70
24794105-7	2014	For MAO-B inhibition, alkyl and halogen substituents on the meta and para positions of the benzyloxy ring enhance inhibitory potency.	Halogens	32-39	monoamine oxidase B	Homo sapiens	4-9
24769350-3	2014	In designing the compounds we focused on the structures of rasagiline and selegiline, two well known MAO-B inhibitors and proposed neuroprotective agents.	Selegiline	74-84	monoamine oxidase B	Homo sapiens	101-106
24769350-8	2014	In the MAO-B assay, 8-phenyl-ethynyl-8-hydroxypentacycloundecane (10), exhibited MAO-B inhibition of 73.32% at 300 muM.	8-phenyl-ethynyl-8-hydroxypentacycloundecane	20-64	monoamine oxidase B	Homo sapiens	7-12
24769350-8	2014	In the MAO-B assay, 8-phenyl-ethynyl-8-hydroxypentacycloundecane (10), exhibited MAO-B inhibition of 73.32% at 300 muM.	8-phenyl-ethynyl-8-hydroxypentacycloundecane	20-64	monoamine oxidase B	Homo sapiens	81-86
24746464-0	2014	Identification of the stereochemical requirements in the 4-aryl-2-cycloalkylidenhydrazinylthiazole scaffold for the design of selective human monoamine oxidase B inhibitors.	4-aryl-2-cycloalkylidenhydrazinylthiazole	57-98	monoamine oxidase B	Homo sapiens	142-161
24666288-14	2014	Imidazoline-2 (I-2) receptors interact with monoamine oxidase A and monoamine oxidase B leading to research that has focused on the effect of I-2 receptors and depression and the suggestion of a possible antidepressant action of the imidazolines.	Imidazolines	233-245	monoamine oxidase B	Homo sapiens	68-87
24746464-1	2014	Exploring the effect that substituents on the cycloaliphatic ring had on the inhibitory activity against human monoamine oxidase B of a series of 4-aryl-2-cycloalkylidenhydrazinylthiazoles led to the synthesis of a new series of 2-methylcyclopentyl and 3-methylcyclopentyl derivatives which were tested in vitro as mixtures of diastereoisomers.	methylcyclopentyl	231-248	monoamine oxidase B	Homo sapiens	111-130
24746464-1	2014	Exploring the effect that substituents on the cycloaliphatic ring had on the inhibitory activity against human monoamine oxidase B of a series of 4-aryl-2-cycloalkylidenhydrazinylthiazoles led to the synthesis of a new series of 2-methylcyclopentyl and 3-methylcyclopentyl derivatives which were tested in vitro as mixtures of diastereoisomers.	methylcyclopentyl	255-272	monoamine oxidase B	Homo sapiens	111-130
24746464-3	2014	4-(2,4-Difluorophenyl)-2-(2-(3-methylcyclopentylidene)hydrazinyl)thiazole was chosen as a model to investigate the influence of stereochemical requirements on the inhibitory activity against hMAO-B of these derivatives after a stereoconservative synthesis and semi-preparative HPLC diastereoseparation.	4-(2,4-difluorophenyl)-2-(2-(3-methylcyclopentylidene)hydrazinyl)thiazole	0-73	monoamine oxidase B	Homo sapiens	191-197
24517979-0	2014	Kinetic modeling of the monoamine oxidase B radioligand [11C]SL25.1188 in human brain with high-resolution positron emission tomography.	Carbon-11	57-60	monoamine oxidase B	Homo sapiens	24-43
24517979-1	2014	This article describes the kinetic modeling of [(11)C]SL25.1188 ([(S)-5-methoxymethyl-3-[6-(4,4,4-trifluorobutoxy)-benzo[d]isoxazol-3-yl]-oxazolidin-2-[(11)C]one]) binding to monoamine oxidase B (MAO-B) in the human brain using high-resolution positron emission tomography (PET).	[(s)-5-methoxymethyl-3-[6-(4,4,4-trifluorobutoxy)-benzo[d]isoxazol-3-yl]-oxazolidin-2-[(11)c]one	65-161	monoamine oxidase B	Homo sapiens	175-194
24517979-1	2014	This article describes the kinetic modeling of [(11)C]SL25.1188 ([(S)-5-methoxymethyl-3-[6-(4,4,4-trifluorobutoxy)-benzo[d]isoxazol-3-yl]-oxazolidin-2-[(11)C]one]) binding to monoamine oxidase B (MAO-B) in the human brain using high-resolution positron emission tomography (PET).	[(s)-5-methoxymethyl-3-[6-(4,4,4-trifluorobutoxy)-benzo[d]isoxazol-3-yl]-oxazolidin-2-[(11)c]one	65-161	monoamine oxidase B	Homo sapiens	196-201
24313346-1	2014	OBJECTIVES: Caffeine represents a useful scaffold for the design of monoamine oxidase (MAO) type B inhibitors.	Caffeine	12-20	monoamine oxidase B	Homo sapiens	68-98
24313346-3	2014	To explore the structure-activity relationships of MAO-B inhibition by caffeine-derived compounds, this study examines the MAO inhibitory properties of a series of phenylalkylcaffeine analogues.	Caffeine	71-79	monoamine oxidase B	Homo sapiens	51-56
24313346-4	2014	METHODS: Employing the recombinant human enzymes, the potencies (IC50 values) by which the caffeine analogues inhibit MAO-A and MAO-B were measured.	Caffeine	91-99	monoamine oxidase B	Homo sapiens	128-133
24313346-6	2014	KEY FINDINGS: The results document that the phenylalkylcaffeine analogues are reversible and selective MAO-B inhibitors with a competitive mode of inhibition.	phenylalkylcaffeine	44-63	monoamine oxidase B	Homo sapiens	103-108
24313346-9	2014	CONCLUSIONS: Phenylalkylcaffeines represent a new class of high-potency MAO-B inhibitors with the longer alkyl side chains yielding enhanced inhibitory activity.	phenylalkylcaffeines	13-33	monoamine oxidase B	Homo sapiens	72-77
24720993-0	2014	An automated sequential injection spectrophotometric method for evaluation of tyramine oxidase inhibitory activity of some flavonoids.	Flavonoids	123-133	monoamine oxidase B	Homo sapiens	78-94
24601544-4	2014	Docking and molecular dynamics were used to explore how 2-(2-benzofuranyl)-2-imidazoline hydrochloride (2-BFI) binds to MAO A and to explain why tranylcypromine increases tight binding to MAO B.	2-BFI hydrochloride	56-102	monoamine oxidase B	Homo sapiens	188-193
24601544-4	2014	Docking and molecular dynamics were used to explore how 2-(2-benzofuranyl)-2-imidazoline hydrochloride (2-BFI) binds to MAO A and to explain why tranylcypromine increases tight binding to MAO B.	2-(2-benzofuranyl)-2-imidazoline	104-109	monoamine oxidase B	Homo sapiens	188-193
24601544-4	2014	Docking and molecular dynamics were used to explore how 2-(2-benzofuranyl)-2-imidazoline hydrochloride (2-BFI) binds to MAO A and to explain why tranylcypromine increases tight binding to MAO B.	Tranylcypromine	145-160	monoamine oxidase B	Homo sapiens	188-193
24601544-5	2014	The energy for 2-BFI binding to MAO A was comparable to that for tranylcypromine-modified MAO B, but the location of 2-BFI in the MAO A could be anywhere in the monopartite substrate cavity.	Tranylcypromine	65-80	monoamine oxidase B	Homo sapiens	90-95
24601544-6	2014	Binding to the tranylcypromine-modified MAO B was with high affinity and in the entrance cavity as in the crystal structure, but the energies of interaction with the native MAO B were less favorable.	Tranylcypromine	15-30	monoamine oxidase B	Homo sapiens	40-45
24601544-6	2014	Binding to the tranylcypromine-modified MAO B was with high affinity and in the entrance cavity as in the crystal structure, but the energies of interaction with the native MAO B were less favorable.	Tranylcypromine	15-30	monoamine oxidase B	Homo sapiens	173-178
24601544-7	2014	Molecular dynamics revealed that the entrance cavity of MAO B after tranylcypromine modification is both smaller and less flexible.	Tranylcypromine	68-83	monoamine oxidase B	Homo sapiens	56-61
24601544-8	2014	This change in the presence of tranylcypromine may be responsible for the greater affinity of tranylcypromine-modified MAO B for imidazoline ligands.	Tranylcypromine	31-46	monoamine oxidase B	Homo sapiens	119-124
24601544-8	2014	This change in the presence of tranylcypromine may be responsible for the greater affinity of tranylcypromine-modified MAO B for imidazoline ligands.	Tranylcypromine	94-109	monoamine oxidase B	Homo sapiens	119-124
24601544-8	2014	This change in the presence of tranylcypromine may be responsible for the greater affinity of tranylcypromine-modified MAO B for imidazoline ligands.	Imidazolines	129-140	monoamine oxidase B	Homo sapiens	119-124
24756517-6	2014	RESULTS: Although levodopa is the most effective medication available for treating the motor symptoms of Parkinson disease, in certain instances (eg, mild symptoms, tremor as the only or most prominent symptom, aged <60 years) other medications (eg, monoamine oxidase type B inhibitors [MAOBIs], amantadine, anticholinergics, beta-blockers, or dopamine agonists) may be initiated first to avoid levodopa-related motor complications.	Levodopa	18-26	monoamine oxidase B	Homo sapiens	250-274
24720993-2	2014	The method is based on the inhibition of TOD that catalyzes the oxidation of tyramine substrate to produce aldehyde and hydrogen peroxide (H2O2).	Tyramine	77-85	monoamine oxidase B	Homo sapiens	41-44
24720993-2	2014	The method is based on the inhibition of TOD that catalyzes the oxidation of tyramine substrate to produce aldehyde and hydrogen peroxide (H2O2).	Aldehydes	107-115	monoamine oxidase B	Homo sapiens	41-44
24720993-2	2014	The method is based on the inhibition of TOD that catalyzes the oxidation of tyramine substrate to produce aldehyde and hydrogen peroxide (H2O2).	Hydrogen Peroxide	120-137	monoamine oxidase B	Homo sapiens	41-44
24720993-2	2014	The method is based on the inhibition of TOD that catalyzes the oxidation of tyramine substrate to produce aldehyde and hydrogen peroxide (H2O2).	Hydrogen Peroxide	139-143	monoamine oxidase B	Homo sapiens	41-44
24720993-4	2014	The decrease of the quinoneimine dye is related to an increase of TOD inhibitory activity.	quinoneimine	20-32	monoamine oxidase B	Homo sapiens	66-69
24720993-5	2014	Under the optimum conditions: 1.0 mM tyramine, 8 U mL(-1) TOD, 1.0 mM vanillic acid, 1.0 mM 4-AA and delay time of 10 s, some flavonoid compounds were examined for the TOD inhibitory activity expressed as IC50 value.	Flavonoids	126-135	monoamine oxidase B	Homo sapiens	58-61
24720993-5	2014	Under the optimum conditions: 1.0 mM tyramine, 8 U mL(-1) TOD, 1.0 mM vanillic acid, 1.0 mM 4-AA and delay time of 10 s, some flavonoid compounds were examined for the TOD inhibitory activity expressed as IC50 value.	Flavonoids	126-135	monoamine oxidase B	Homo sapiens	168-171
24720993-6	2014	It was found that flavonols (quercetin and myricetin) and flavans (epicatechin gallate (ECG) and epigallocatechin (EGC)) showed higher TOD inhibitory activity than flavones and flavanones.	Flavonols	18-27	monoamine oxidase B	Homo sapiens	135-138
24720993-6	2014	It was found that flavonols (quercetin and myricetin) and flavans (epicatechin gallate (ECG) and epigallocatechin (EGC)) showed higher TOD inhibitory activity than flavones and flavanones.	Quercetin	29-38	monoamine oxidase B	Homo sapiens	135-138
24720993-6	2014	It was found that flavonols (quercetin and myricetin) and flavans (epicatechin gallate (ECG) and epigallocatechin (EGC)) showed higher TOD inhibitory activity than flavones and flavanones.	myricetin	43-52	monoamine oxidase B	Homo sapiens	135-138
24720993-6	2014	It was found that flavonols (quercetin and myricetin) and flavans (epicatechin gallate (ECG) and epigallocatechin (EGC)) showed higher TOD inhibitory activity than flavones and flavanones.	leucocyanidin	58-65	monoamine oxidase B	Homo sapiens	135-138
24720993-6	2014	It was found that flavonols (quercetin and myricetin) and flavans (epicatechin gallate (ECG) and epigallocatechin (EGC)) showed higher TOD inhibitory activity than flavones and flavanones.	epicatechin gallate	67-86	monoamine oxidase B	Homo sapiens	135-138
24720993-6	2014	It was found that flavonols (quercetin and myricetin) and flavans (epicatechin gallate (ECG) and epigallocatechin (EGC)) showed higher TOD inhibitory activity than flavones and flavanones.	epicatechin gallate	88-91	monoamine oxidase B	Homo sapiens	135-138
24720993-6	2014	It was found that flavonols (quercetin and myricetin) and flavans (epicatechin gallate (ECG) and epigallocatechin (EGC)) showed higher TOD inhibitory activity than flavones and flavanones.	gallocatechol	97-113	monoamine oxidase B	Homo sapiens	135-138
24720993-6	2014	It was found that flavonols (quercetin and myricetin) and flavans (epicatechin gallate (ECG) and epigallocatechin (EGC)) showed higher TOD inhibitory activity than flavones and flavanones.	gallocatechol	115-118	monoamine oxidase B	Homo sapiens	135-138
24393810-1	2014	A series of 6-substituted 3-(pyrrolidin-1-ylmethyl)chromen-2-ones (coumarins) have been synthesized and their inhibitory activity to human monoamine oxidase A (MAO A) and B (MAO B) determined.	6-substituted 3-(pyrrolidin-1-ylmethyl)chromen-2-ones	12-65	monoamine oxidase B	Homo sapiens	174-179
24165164-4	2014	Herein, we demonstrated that certain antitumor 1,4-NQs, including spermidine-1,4-NQ, lapachol, and nor-lapachol display inhibitory activity on human MAO-A and MAO-B.	1,4-naphthoquinone	47-54	monoamine oxidase B	Homo sapiens	159-164
24635520-2	2014	In this study we synthesized and evaluated a new series of compounds, with benzo[f]coumarin structure, as potential inhibitors of MAO-A, MAO-B, AChE and BuChE.	benzo[f]coumarin	75-91	monoamine oxidase B	Homo sapiens	137-142
24447649-0	2014	Cardiac safety of rasagiline, a selective monoamine oxidase type B inhibitor for the treatment of Parkinson"s disease: a thorough QT/QTc study.	rasagiline	18-28	monoamine oxidase B	Homo sapiens	42-66
24447649-1	2014	AIMS: Rasagiline is a selective, irreversible monoamine oxidase type B inhibitor, developed for the treatment of Parkinson"s disease.	rasagiline	6-16	monoamine oxidase B	Homo sapiens	46-70
24165164-4	2014	Herein, we demonstrated that certain antitumor 1,4-NQs, including spermidine-1,4-NQ, lapachol, and nor-lapachol display inhibitory activity on human MAO-A and MAO-B.	spermidine-1,4-nq	66-83	monoamine oxidase B	Homo sapiens	159-164
24165164-4	2014	Herein, we demonstrated that certain antitumor 1,4-NQs, including spermidine-1,4-NQ, lapachol, and nor-lapachol display inhibitory activity on human MAO-A and MAO-B.	lapachol	85-93	monoamine oxidase B	Homo sapiens	159-164
24165164-4	2014	Herein, we demonstrated that certain antitumor 1,4-NQs, including spermidine-1,4-NQ, lapachol, and nor-lapachol display inhibitory activity on human MAO-A and MAO-B.	norlapachol	99-111	monoamine oxidase B	Homo sapiens	159-164
24165164-7	2014	Furthermore, ability to inhibit both MAO-A and MAO-B can be potentialized by the formation of hydrogen bonds between these compounds and FAD and/or the residues in the active site.	Hydrogen	94-102	monoamine oxidase B	Homo sapiens	47-52
24165164-7	2014	Furthermore, ability to inhibit both MAO-A and MAO-B can be potentialized by the formation of hydrogen bonds between these compounds and FAD and/or the residues in the active site.	Flavin-Adenine Dinucleotide	137-140	monoamine oxidase B	Homo sapiens	47-52
24560738-0	2014	Alkynyl-coumarinyl ethers as MAO-B inhibitors.	alkynyl-coumarinyl ethers	0-25	monoamine oxidase B	Homo sapiens	29-34
24560738-1	2014	In this study, alkynyl-coumarinyl ethers were developed as inhibitors of human monoamine oxidase B (MAO-B).	alkynyl-coumarinyl ethers	15-40	monoamine oxidase B	Homo sapiens	79-98
24560738-1	2014	In this study, alkynyl-coumarinyl ethers were developed as inhibitors of human monoamine oxidase B (MAO-B).	alkynyl-coumarinyl ethers	15-40	monoamine oxidase B	Homo sapiens	100-105
24560738-6	2014	Among the 7-hex-5-ynyloxy-coumarins, the 3-methoxycarbonyl derivative 36 was characterized as a dual-acting inhibitor with IC50 values of less than 10 nM towards MAO-A and MAO-B, and the 3-(4-methoxy)phenyl derivative 44 was shown to combine strong anti-MAO-B potency (IC50=3.0 nM) and selectivity for MAO-B over MAO-A (selectivity &gt;3400-fold).	7-hex-5-ynyloxy-coumarins	10-35	monoamine oxidase B	Homo sapiens	172-177
24560738-6	2014	Among the 7-hex-5-ynyloxy-coumarins, the 3-methoxycarbonyl derivative 36 was characterized as a dual-acting inhibitor with IC50 values of less than 10 nM towards MAO-A and MAO-B, and the 3-(4-methoxy)phenyl derivative 44 was shown to combine strong anti-MAO-B potency (IC50=3.0 nM) and selectivity for MAO-B over MAO-A (selectivity &gt;3400-fold).	7-hex-5-ynyloxy-coumarins	10-35	monoamine oxidase B	Homo sapiens	254-259
24560738-6	2014	Among the 7-hex-5-ynyloxy-coumarins, the 3-methoxycarbonyl derivative 36 was characterized as a dual-acting inhibitor with IC50 values of less than 10 nM towards MAO-A and MAO-B, and the 3-(4-methoxy)phenyl derivative 44 was shown to combine strong anti-MAO-B potency (IC50=3.0 nM) and selectivity for MAO-B over MAO-A (selectivity &gt;3400-fold).	7-hex-5-ynyloxy-coumarins	10-35	monoamine oxidase B	Homo sapiens	254-259
24529308-3	2014	Poorly toxic, up to very active, reversible inhibitors of BAO, very selective toward DAO, LO and MAO B, were obtained with benzylamines 10, 11, 12 containing hydrophilic omega-hydroxyalkoxy groups.	Benzylamines	123-135	monoamine oxidase B	Homo sapiens	97-102
24055209-3	2014	Rasagiline is a second generation MAO-B I inducing moderate symptomatic and possibly disease modifying benefits with apparently good tolerability and safety profile in PD patients.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	34-39
24393810-1	2014	A series of 6-substituted 3-(pyrrolidin-1-ylmethyl)chromen-2-ones (coumarins) have been synthesized and their inhibitory activity to human monoamine oxidase A (MAO A) and B (MAO B) determined.	Coumarins	67-76	monoamine oxidase B	Homo sapiens	174-179
23915421-0	2014	The expression of KLF11 (TIEG2), a monoamine oxidase B transcriptional activator in the prefrontal cortex of human alcohol dependence.	Alcohols	115-122	monoamine oxidase B	Homo sapiens	35-54
24247011-5	2014	Similar differences were also found between the binding of dicarbonitrile compounds to MAO A and to MAO B.	dicarbonitrile	59-73	monoamine oxidase B	Homo sapiens	100-105
23915421-2	2014	Monoamine oxidase B (MAO B; an enzyme that catabolizes neurotransmitters such as dopamine) is consistently increased in this psychiatric illness.	Dopamine	81-89	monoamine oxidase B	Homo sapiens	0-19
23915421-2	2014	Monoamine oxidase B (MAO B; an enzyme that catabolizes neurotransmitters such as dopamine) is consistently increased in this psychiatric illness.	Dopamine	81-89	monoamine oxidase B	Homo sapiens	21-26
23915421-3	2014	MAO B has been implicated in the pathogenesis of alcohol dependence and alcohol-induced brain neurotoxicity.	Alcohols	49-56	monoamine oxidase B	Homo sapiens	0-5
23915421-3	2014	MAO B has been implicated in the pathogenesis of alcohol dependence and alcohol-induced brain neurotoxicity.	Alcohols	72-79	monoamine oxidase B	Homo sapiens	0-5
23915421-15	2014	It further supports that the KLF11-MAO B cell death cascade may contribute to chronic alcohol-induced brain damage.	Alcohols	86-93	monoamine oxidase B	Homo sapiens	35-40
23701542-5	2014	The literature is reviewed to document identified degenerative reactions attributed to H2O2 produced by MAO A and by MAO B catalysis.	Hydrogen Peroxide	87-91	monoamine oxidase B	Homo sapiens	117-122
24190245-2	2013	The aim of this investigation was to determine if the MAO-B inhibitor rasagiline can improve olfaction in PD patients.	rasagiline	70-80	monoamine oxidase B	Homo sapiens	54-59
26000219-1	2014	Rasagiline is a monoamine oxidase type-B inhibitor used as monotherapy or in addition to levodopa in the treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	16-40
24169316-0	2013	Chromenylchalcones with inhibitory effects on monoamine oxidase B.	chromenylchalcones	0-18	monoamine oxidase B	Homo sapiens	46-65
24169316-6	2013	The chromenylchalcone scaffold, which is derived from natural products including isoflavonoids and chalcones, had not been previously reported as an MAO-B inhibitor.	chromenylchalcone	4-21	monoamine oxidase B	Homo sapiens	149-154
24169316-6	2013	The chromenylchalcone scaffold, which is derived from natural products including isoflavonoids and chalcones, had not been previously reported as an MAO-B inhibitor.	isoflavonoids	81-94	monoamine oxidase B	Homo sapiens	149-154
24169316-6	2013	The chromenylchalcone scaffold, which is derived from natural products including isoflavonoids and chalcones, had not been previously reported as an MAO-B inhibitor.	Chalcones	99-108	monoamine oxidase B	Homo sapiens	149-154
24522637-4	2014	With no apparent toxicity, U1 may be used to monitor MAO-B activities in small animals during disease development.	Uranium	27-29	monoamine oxidase B	Homo sapiens	53-58
24128814-0	2013	Inhibition of cholinesterase and monoamine oxidase-B activity by Tacrine-Homoisoflavonoid hybrids.	Tacrine	65-72	monoamine oxidase B	Homo sapiens	33-52
24128814-0	2013	Inhibition of cholinesterase and monoamine oxidase-B activity by Tacrine-Homoisoflavonoid hybrids.	homoisoflavonoid	73-89	monoamine oxidase B	Homo sapiens	33-52
24128814-3	2013	Among these hybrids, compound 8b, with a 6 carbon linker between tacrine and (E)-7-hydroxy-3-(4-methoxybenzylidene)chroman-4-one, proved to be the most potent against AChE and MAO-B with IC50 values of 67.9 nM and 0.401 muM, respectively.	(e)-7-hydroxy-3-(4-methoxybenzylidene)chroman-4-one	77-128	monoamine oxidase B	Homo sapiens	176-181
24164690-3	2013	We modeled the reaction of human MAO-B with benzylamine by means of QM/MM calculations based on density functional theory.	benzylamine	44-55	monoamine oxidase B	Homo sapiens	33-38
24012376-0	2013	Development of a novel fluorine-18 labeled deuterated fluororasagiline ([(18)F]fluororasagiline-D2) radioligand for PET studies of monoamino oxidase B (MAO-B).	Fluorine-18	23-34	monoamine oxidase B	Homo sapiens	152-157
24012376-0	2013	Development of a novel fluorine-18 labeled deuterated fluororasagiline ([(18)F]fluororasagiline-D2) radioligand for PET studies of monoamino oxidase B (MAO-B).	deuterated fluororasagiline	43-70	monoamine oxidase B	Homo sapiens	152-157
24012376-0	2013	Development of a novel fluorine-18 labeled deuterated fluororasagiline ([(18)F]fluororasagiline-D2) radioligand for PET studies of monoamino oxidase B (MAO-B).	fluororasagiline-d2	79-98	monoamine oxidase B	Homo sapiens	152-157
24012376-1	2013	The objective of this study was to synthesize and evaluate a novel fluorine-18 labeled deuterium substituted analogue of rasagiline (9, [(18)F]fluororasagiline-D2) as a potential PET radioligand for studies of monoamine oxidase B (MAO-B).	Deuterium	87-96	monoamine oxidase B	Homo sapiens	210-229
24012376-1	2013	The objective of this study was to synthesize and evaluate a novel fluorine-18 labeled deuterium substituted analogue of rasagiline (9, [(18)F]fluororasagiline-D2) as a potential PET radioligand for studies of monoamine oxidase B (MAO-B).	Deuterium	87-96	monoamine oxidase B	Homo sapiens	231-236
24012376-1	2013	The objective of this study was to synthesize and evaluate a novel fluorine-18 labeled deuterium substituted analogue of rasagiline (9, [(18)F]fluororasagiline-D2) as a potential PET radioligand for studies of monoamine oxidase B (MAO-B).	rasagiline	121-131	monoamine oxidase B	Homo sapiens	210-229
24012376-1	2013	The objective of this study was to synthesize and evaluate a novel fluorine-18 labeled deuterium substituted analogue of rasagiline (9, [(18)F]fluororasagiline-D2) as a potential PET radioligand for studies of monoamine oxidase B (MAO-B).	rasagiline	121-131	monoamine oxidase B	Homo sapiens	231-236
24012376-11	2013	An efficient radiolabeling of 9 was successfully established and in the monkey brain 9 binds to MAO-B rich regions and its binding is blocked by the selective MAO-B compound l-deprenyl.	Selegiline	174-184	monoamine oxidase B	Homo sapiens	96-101
24012376-11	2013	An efficient radiolabeling of 9 was successfully established and in the monkey brain 9 binds to MAO-B rich regions and its binding is blocked by the selective MAO-B compound l-deprenyl.	Selegiline	174-184	monoamine oxidase B	Homo sapiens	159-164
24005822-3	2013	Selegiline is a selective and irreversible MAO-B inhibitor and, although clinical trials already shown the beneficial effect of selegiline on cognition of AD patients, its mechanism of action remains to be elucidated.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	43-48
23812646-7	2013	In addition, istradefylline hardly inhibited monoamine oxidase-A, monoamine oxidase-B, or catechol-O-methyl transferase.	istradefylline	13-27	monoamine oxidase B	Homo sapiens	66-85
23860591-3	2013	The results demonstrate that these furan substituted phenylpropenones exhibited moderate to good inhibitory activities towards MAO-B, but showed weak or no inhibition of the MAO-A enzyme.	furan	35-40	monoamine oxidase B	Homo sapiens	127-132
24005822-2	2013	Monoamine oxidase B (MAO-B) activity, involved in the oxidation of biogenic monoamines, is particularly high around the senile plaques and increased in AD patients in middle to late clinical stages of the disease.	monoamines	76-86	monoamine oxidase B	Homo sapiens	0-19
24005822-2	2013	Monoamine oxidase B (MAO-B) activity, involved in the oxidation of biogenic monoamines, is particularly high around the senile plaques and increased in AD patients in middle to late clinical stages of the disease.	monoamines	76-86	monoamine oxidase B	Homo sapiens	21-26
24012182-2	2013	The 3,4-dihydro-2(1H)-quinolinone derivatives are structurally related to a series of coumarin (1-benzopyran-2-one) derivatives which have been reported to act as MAO-B inhibitors.	3,4-dihydro-2(1H)-quinolinone	4-33	monoamine oxidase B	Homo sapiens	163-168
24012182-2	2013	The 3,4-dihydro-2(1H)-quinolinone derivatives are structurally related to a series of coumarin (1-benzopyran-2-one) derivatives which have been reported to act as MAO-B inhibitors.	coumarin	86-94	monoamine oxidase B	Homo sapiens	163-168
24012182-2	2013	The 3,4-dihydro-2(1H)-quinolinone derivatives are structurally related to a series of coumarin (1-benzopyran-2-one) derivatives which have been reported to act as MAO-B inhibitors.	coumarin	96-114	monoamine oxidase B	Homo sapiens	163-168
24012182-3	2013	The results document that the quinolinones are highly potent and selective MAO-B inhibitors with most homologues exhibiting IC50 values in the nanomolar range.	Quinolones	30-42	monoamine oxidase B	Homo sapiens	75-80
24012182-4	2013	The most potent MAO-B inhibitor, 7-(3-bromobenzyloxy)-3,4-dihydro-2(1H)-quinolinone, exhibits an IC50 value of 2.9 nM with a 2750-fold selectivity for MAO-B over the MAO-A isoform.	7-(3-bromobenzyloxy)-3,4-dihydro-2(1h)-quinolinone	33-83	monoamine oxidase B	Homo sapiens	16-21
24012182-4	2013	The most potent MAO-B inhibitor, 7-(3-bromobenzyloxy)-3,4-dihydro-2(1H)-quinolinone, exhibits an IC50 value of 2.9 nM with a 2750-fold selectivity for MAO-B over the MAO-A isoform.	7-(3-bromobenzyloxy)-3,4-dihydro-2(1h)-quinolinone	33-83	monoamine oxidase B	Homo sapiens	151-156
24012182-5	2013	An analysis of the structure-activity relationships for MAO-B inhibition shows that substitution on the C7 position of the 3,4-dihydro-2(1H)-quinolinone scaffold leads to significantly more potent inhibition compared to substitution on C6.	3,4-dihydro-2(1H)-quinolinone	123-152	monoamine oxidase B	Homo sapiens	56-61
23927971-0	2013	Design, synthesis, and in vitro hMAO-B inhibitory evaluation of some 1-methyl-3,5-diphenyl-4,5-dihydro-1H-pyrazoles.	1-methyl-3,5-diphenyl-4,5-dihydro-1H-pyrazole	69-115	monoamine oxidase B	Homo sapiens	32-38
23810676-0	2013	Oxazolopyridines and thiazolopyridines as monoamine oxidase B inhibitors for the treatment of Parkinson"s disease.	oxazolopyridines	0-16	monoamine oxidase B	Homo sapiens	42-61
23810676-0	2013	Oxazolopyridines and thiazolopyridines as monoamine oxidase B inhibitors for the treatment of Parkinson"s disease.	thiazolopyridines	21-38	monoamine oxidase B	Homo sapiens	42-61
23810676-2	2013	Among the enzymes which are involved in the biosynthesis and catabolism of dopamine, monoamine oxidase B (MAO-B) has been a therapeutic target of Parkinson"s disease.	Dopamine	75-83	monoamine oxidase B	Homo sapiens	85-104
23810676-2	2013	Among the enzymes which are involved in the biosynthesis and catabolism of dopamine, monoamine oxidase B (MAO-B) has been a therapeutic target of Parkinson"s disease.	Dopamine	75-83	monoamine oxidase B	Homo sapiens	106-111
23860591-3	2013	The results demonstrate that these furan substituted phenylpropenones exhibited moderate to good inhibitory activities towards MAO-B, but showed weak or no inhibition of the MAO-A enzyme.	phenylpropenones	53-69	monoamine oxidase B	Homo sapiens	127-132
23810676-4	2013	In this study, we designed and synthesized the oxazolopyridine and thiazolopyridine derivatives, and biologically evaluated their inhibitory activities against MAO-B.	OXAZOLO[5,4-B]PYRIDINE	47-62	monoamine oxidase B	Homo sapiens	160-165
23860591-4	2013	The most active compound, 2E-3-(5-chlorofuran-2-yl)-1-(3-chlorophenyl)prop-2-en-1-one, exhibited an IC50 value of 0.174 muM for the inhibition of MAO-B and 28.6 muM for the inhibition of MAO-A.	2e-3-(5-chlorofuran-2-yl)-1-(3-chlorophenyl)prop-2-en-1-one	26-85	monoamine oxidase B	Homo sapiens	146-151
23810676-4	2013	In this study, we designed and synthesized the oxazolopyridine and thiazolopyridine derivatives, and biologically evaluated their inhibitory activities against MAO-B.	Thiazolo[5,4-b]pyridine	67-83	monoamine oxidase B	Homo sapiens	160-165
23810676-7	2013	Molecular docking study showed that van der Waals interaction in the human MAO-B active site could explain the enhanced inhibitory activities of thiazolopyridine derivatives.	Thiazolo[5,4-b]pyridine	145-161	monoamine oxidase B	Homo sapiens	75-80
23735235-1	2013	Rasagiline (Azilect( )) is a selective and irreversible monoamine oxidase B inhibitor, which is well tolerated, safe, improves motor symptoms, and prevents motor complications in Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	56-75
23677700-3	2013	Using recombinant human MAO-A and MAO-B, IC50 values for the inhibition of these enzymes by esomeprazole were experimentally determined.	Esomeprazole	92-104	monoamine oxidase B	Homo sapiens	34-39
23677700-7	2013	The results document that esomeprazole inhibits both MAO-A and MAO-B with IC50 values of 23 microM and 48 microM, respectively.	Esomeprazole	26-38	monoamine oxidase B	Homo sapiens	63-68
23677700-8	2013	The interactions of esomeprazole with MAO-A and MAO-B are reversible and most likely competitive with Ki values for the inhibition of the respective enzymes of 8.99 microM and 31.7 microM.	Esomeprazole	20-32	monoamine oxidase B	Homo sapiens	48-53
24053341-3	2013	Safinamide has a unique pharmacological profile, which combines modulation of dopamine metabolism by reversible, highly specific monoamine oxidase-B inhibition, blockage of voltage-dependent sodium channels, modulation of calcium channels and of glutamate release induced by abnormal neuronal activity.	safinamide	0-10	monoamine oxidase B	Homo sapiens	129-148
23850513-7	2013	KEY FINDINGS: Caffeine acts as a MAO inhibitor with Ki values of 0.70 mM and 3.83 mM for the inhibition of MAO-A and MAO-B, respectively.	Caffeine	14-22	monoamine oxidase B	Homo sapiens	117-122
23850513-9	2013	SIGNIFICANCE: Although structural modifications of caffeine lead to highly potent MAO inhibitors, caffeine is a weak inhibitor of MAO-A and MAO-B.	Caffeine	98-106	monoamine oxidase B	Homo sapiens	140-145
23551956-1	2013	Rasagiline mesylate is a highly potent, selective and irreversible monoamine oxidase type B (MAOB) inhibitor and is effective as monotherapy or adjunct to levodopa for patients with Parkinson"s disease (PD).	Rasagiline mesylate	0-19	monoamine oxidase B	Homo sapiens	67-91
23551956-1	2013	Rasagiline mesylate is a highly potent, selective and irreversible monoamine oxidase type B (MAOB) inhibitor and is effective as monotherapy or adjunct to levodopa for patients with Parkinson"s disease (PD).	Rasagiline mesylate	0-19	monoamine oxidase B	Homo sapiens	93-97
23735235-1	2013	Rasagiline (Azilect( )) is a selective and irreversible monoamine oxidase B inhibitor, which is well tolerated, safe, improves motor symptoms, and prevents motor complications in Parkinson"s disease (PD).	rasagiline	12-19	monoamine oxidase B	Homo sapiens	56-75
23612197-3	2013	In vitro, tedizolid and linezolid were reversible inhibitors of human MAO-A and MAO-B; the 50% inhibitory concentration (IC50) for tedizolid was 8.7 muM for MAO-A and 5.7 muM for MAO-B and 46.0 and 2.1 muM, respectively, with linezolid.	tedizolid	10-19	monoamine oxidase B	Homo sapiens	80-85
23612197-3	2013	In vitro, tedizolid and linezolid were reversible inhibitors of human MAO-A and MAO-B; the 50% inhibitory concentration (IC50) for tedizolid was 8.7 muM for MAO-A and 5.7 muM for MAO-B and 46.0 and 2.1 muM, respectively, with linezolid.	tedizolid	10-19	monoamine oxidase B	Homo sapiens	179-184
23612197-3	2013	In vitro, tedizolid and linezolid were reversible inhibitors of human MAO-A and MAO-B; the 50% inhibitory concentration (IC50) for tedizolid was 8.7 muM for MAO-A and 5.7 muM for MAO-B and 46.0 and 2.1 muM, respectively, with linezolid.	Linezolid	24-33	monoamine oxidase B	Homo sapiens	80-85
23612197-3	2013	In vitro, tedizolid and linezolid were reversible inhibitors of human MAO-A and MAO-B; the 50% inhibitory concentration (IC50) for tedizolid was 8.7 muM for MAO-A and 5.7 muM for MAO-B and 46.0 and 2.1 muM, respectively, with linezolid.	Linezolid	24-33	monoamine oxidase B	Homo sapiens	179-184
23612197-3	2013	In vitro, tedizolid and linezolid were reversible inhibitors of human MAO-A and MAO-B; the 50% inhibitory concentration (IC50) for tedizolid was 8.7 muM for MAO-A and 5.7 muM for MAO-B and 46.0 and 2.1 muM, respectively, with linezolid.	tedizolid	131-140	monoamine oxidase B	Homo sapiens	80-85
23612197-3	2013	In vitro, tedizolid and linezolid were reversible inhibitors of human MAO-A and MAO-B; the 50% inhibitory concentration (IC50) for tedizolid was 8.7 muM for MAO-A and 5.7 muM for MAO-B and 46.0 and 2.1 muM, respectively, with linezolid.	tedizolid	131-140	monoamine oxidase B	Homo sapiens	179-184
23612197-9	2013	In summary, tedizolid is a weak, reversible inhibitor of MAO-A and MAO-B in vitro.	tedizolid	12-21	monoamine oxidase B	Homo sapiens	67-72
23410524-4	2013	l-Deprenyl and rasagiline, both selective MAO-B inhibitors, are used in the management of Parkinson"s disease, but these drugs may be useful in the treatment of other neurodegenerative disorders given that they demonstrate neuroprotective/neurorescue properties in a wide variety of models in vitro and in vivo.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	42-47
23673214-1	2013	In the present work we synthesized a series of hydroxy-3-arylcoumarins (compounds 1-9), some of them previously described as MAO-B selective inhibitors, with the aim of evaluating their antioxidant properties.	hydroxy-3-arylcoumarins	47-70	monoamine oxidase B	Homo sapiens	125-130
23634791-1	2013	INTRODUCTION: Rasagiline (Azilect, AGN 1135) is a selective irreversible inhibitor of monoamine oxidase B (MAO-B).	rasagiline	14-24	monoamine oxidase B	Homo sapiens	86-105
23634791-1	2013	INTRODUCTION: Rasagiline (Azilect, AGN 1135) is a selective irreversible inhibitor of monoamine oxidase B (MAO-B).	rasagiline	14-24	monoamine oxidase B	Homo sapiens	107-112
23634791-1	2013	INTRODUCTION: Rasagiline (Azilect, AGN 1135) is a selective irreversible inhibitor of monoamine oxidase B (MAO-B).	rasagiline	26-33	monoamine oxidase B	Homo sapiens	86-105
23634791-1	2013	INTRODUCTION: Rasagiline (Azilect, AGN 1135) is a selective irreversible inhibitor of monoamine oxidase B (MAO-B).	rasagiline	26-33	monoamine oxidase B	Homo sapiens	107-112
23634791-1	2013	INTRODUCTION: Rasagiline (Azilect, AGN 1135) is a selective irreversible inhibitor of monoamine oxidase B (MAO-B).	rasagiline	35-43	monoamine oxidase B	Homo sapiens	86-105
23634791-1	2013	INTRODUCTION: Rasagiline (Azilect, AGN 1135) is a selective irreversible inhibitor of monoamine oxidase B (MAO-B).	rasagiline	35-43	monoamine oxidase B	Homo sapiens	107-112
23634791-11	2013	In conclusion, rasagiline is a well-tolerated MAO-B inhibitor that may help to achieve the desired level of clinical benefit in Parkinson"s disease.	rasagiline	15-25	monoamine oxidase B	Homo sapiens	46-51
23410524-4	2013	l-Deprenyl and rasagiline, both selective MAO-B inhibitors, are used in the management of Parkinson"s disease, but these drugs may be useful in the treatment of other neurodegenerative disorders given that they demonstrate neuroprotective/neurorescue properties in a wide variety of models in vitro and in vivo.	rasagiline	15-25	monoamine oxidase B	Homo sapiens	42-47
23631427-0	2013	Dual targeting of adenosine A(2A) receptors and monoamine oxidase B by 4H-3,1-benzothiazin-4-ones.	4h-3,1-benzothiazin-4-ones	71-97	monoamine oxidase B	Homo sapiens	48-67
23631427-2	2013	In the present study, benzothiazinones, e.g., 2-(3-chlorophenoxy)-N-(4-oxo-4H-3,1-benzothiazin-2-yl)acetamide (13), were identified as a novel class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).	benzothiazinones	22-38	monoamine oxidase B	Homo sapiens	159-164
23631427-2	2013	In the present study, benzothiazinones, e.g., 2-(3-chlorophenoxy)-N-(4-oxo-4H-3,1-benzothiazin-2-yl)acetamide (13), were identified as a novel class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).	benzothiazinones	22-38	monoamine oxidase B	Homo sapiens	188-193
23631427-2	2013	In the present study, benzothiazinones, e.g., 2-(3-chlorophenoxy)-N-(4-oxo-4H-3,1-benzothiazin-2-yl)acetamide (13), were identified as a novel class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).	2-(3-chlorophenoxy)-n-(4-oxo-4h-3,1-benzothiazin-2-yl)acetamide	46-109	monoamine oxidase B	Homo sapiens	159-164
23631427-2	2013	In the present study, benzothiazinones, e.g., 2-(3-chlorophenoxy)-N-(4-oxo-4H-3,1-benzothiazin-2-yl)acetamide (13), were identified as a novel class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).	2-(3-chlorophenoxy)-n-(4-oxo-4h-3,1-benzothiazin-2-yl)acetamide	46-109	monoamine oxidase B	Homo sapiens	188-193
23631427-4	2013	By optimizing benzothiazinones for both targets, the first potent, dual-acting A2AAR/MAO-B inhibitors with a nonxanthine structure were developed.	benzothiazinones	14-30	monoamine oxidase B	Homo sapiens	85-90
23631427-4	2013	By optimizing benzothiazinones for both targets, the first potent, dual-acting A2AAR/MAO-B inhibitors with a nonxanthine structure were developed.	nonxanthine	109-120	monoamine oxidase B	Homo sapiens	85-90
23631427-5	2013	The best derivative was N-(4-oxo-4H-3,1-benzothiazin-2-yl)-4-phenylbutanamide (17, Ki human A2A, 39.5 nM; IC50 human MAO-B, 34.9 nM; selective versus other AR subtypes and MAO-A), which inhibited A2AAR-induced cAMP accumulation and showed competitive, reversible MAO-B inhibition.	N-(4-oxo-4H-3,1-benzothiazin-2-yl)-4-phenylbutanamide	24-77	monoamine oxidase B	Homo sapiens	117-122
23631427-5	2013	The best derivative was N-(4-oxo-4H-3,1-benzothiazin-2-yl)-4-phenylbutanamide (17, Ki human A2A, 39.5 nM; IC50 human MAO-B, 34.9 nM; selective versus other AR subtypes and MAO-A), which inhibited A2AAR-induced cAMP accumulation and showed competitive, reversible MAO-B inhibition.	N-(4-oxo-4H-3,1-benzothiazin-2-yl)-4-phenylbutanamide	24-77	monoamine oxidase B	Homo sapiens	263-268
23611731-3	2013	In this study, however, we found that selective MAO-A inhibitors, moclobemide and Ro41-1049, and a selective MAO-B inhibitor, selegiline, promoted adiponectin production during adipocyte differentiation in hBM-MSCs, which suggested the anti-diabetic potential of these drugs.	Selegiline	126-136	monoamine oxidase B	Homo sapiens	109-114
23417310-2	2013	The detailed molecular mechanism proposed for the MAO-catalyzed oxidation of amines has been controversial with the basic assumption that both MAO A and MAO B follow the same pathway for the C-H bond cleavage step.	Amines	77-83	monoamine oxidase B	Homo sapiens	153-158
23589499-2	2013	Several 3-arylcoumarin derivatives were previously described as interesting selective MAO-B inhibitors.	3-arylcoumarin	8-22	monoamine oxidase B	Homo sapiens	86-91
23589499-5	2013	5-Nitro-2-(4-methoxyphenyl)benzofuran (8) is the most active compound of the benzofuran series, presenting MAO-B selectivity and reversible inhibition (IC50 =140 nM).	5-nitro-2-(4-methoxyphenyl)benzofuran	0-37	monoamine oxidase B	Homo sapiens	107-112
23589499-5	2013	5-Nitro-2-(4-methoxyphenyl)benzofuran (8) is the most active compound of the benzofuran series, presenting MAO-B selectivity and reversible inhibition (IC50 =140 nM).	benzofuran	27-37	monoamine oxidase B	Homo sapiens	107-112
23589499-6	2013	3-(4"-Methoxyphenyl)-6-nitrocoumarin (15), with the same substitution pattern as that of compound 8, was found to be the most active MAO-B inhibitor of the coumarin series (IC50 =3 nM).	3-(4"-methoxyphenyl)-6-nitrocoumarin	0-36	monoamine oxidase B	Homo sapiens	133-138
23589499-6	2013	3-(4"-Methoxyphenyl)-6-nitrocoumarin (15), with the same substitution pattern as that of compound 8, was found to be the most active MAO-B inhibitor of the coumarin series (IC50 =3 nM).	coumarin	28-36	monoamine oxidase B	Homo sapiens	133-138
23589499-8	2013	Docking experiments for the most active compounds into the MAO-B and MAO-A binding pockets highlighted different interactions between the derivative classes (2-arylbenzofurans and 3-arylcoumarins), and provided new information about the enzyme-inhibitor interaction and the potential therapeutic application of these scaffolds.	2-arylbenzofurans	158-175	monoamine oxidase B	Homo sapiens	59-64
23589499-8	2013	Docking experiments for the most active compounds into the MAO-B and MAO-A binding pockets highlighted different interactions between the derivative classes (2-arylbenzofurans and 3-arylcoumarins), and provided new information about the enzyme-inhibitor interaction and the potential therapeutic application of these scaffolds.	3-arylcoumarins	180-195	monoamine oxidase B	Homo sapiens	59-64
23420173-4	2013	Selegiline, a selective MAO-B inhibitor, known to have beneficial effects in the brain regions which are rich by dopamine receptors, however, studies based on brain targeting of selegiline are limited.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	24-29
23420173-5	2013	Since some recent studies showed the possible Abeta-fibril destabilizing effects of MAO inhibitors, present study was designed to (1) prepare the selective MAO-B inhibitor selegiline-loaded Poly (lactic-co-glycolic acid)-poly (ethylene glycol) (PLGA-b-PEG) nanoparticles (2) to investigate the in vitro Abeta-fibril destabilizing effect of the loaded particles.	Selegiline	172-182	monoamine oxidase B	Homo sapiens	156-161
23420173-5	2013	Since some recent studies showed the possible Abeta-fibril destabilizing effects of MAO inhibitors, present study was designed to (1) prepare the selective MAO-B inhibitor selegiline-loaded Poly (lactic-co-glycolic acid)-poly (ethylene glycol) (PLGA-b-PEG) nanoparticles (2) to investigate the in vitro Abeta-fibril destabilizing effect of the loaded particles.	Polylactic Acid-Polyglycolic Acid Copolymer	190-220	monoamine oxidase B	Homo sapiens	156-161
23417310-3	2013	Using the mechanistic approach of investigation of electronic effects of various benzylamine ring substituents in experiments at pH 9.0, human MAO A exhibits a kinetic behavior characteristic of an H(+) abstraction, while human MAO B exhibits kinetic properties characteristic of a H(-) abstraction.	benzylamine	81-92	monoamine oxidase B	Homo sapiens	228-233
23328949-4	2013	Among the compounds examined, compound 16 was found to be more selective than selegiline, a known MAO-B inhibitor, in respect to the K i values experimentally found.	Selegiline	78-88	monoamine oxidase B	Homo sapiens	98-103
23420173-5	2013	Since some recent studies showed the possible Abeta-fibril destabilizing effects of MAO inhibitors, present study was designed to (1) prepare the selective MAO-B inhibitor selegiline-loaded Poly (lactic-co-glycolic acid)-poly (ethylene glycol) (PLGA-b-PEG) nanoparticles (2) to investigate the in vitro Abeta-fibril destabilizing effect of the loaded particles.	Polyethylene Glycols	221-243	monoamine oxidase B	Homo sapiens	156-161
23420173-5	2013	Since some recent studies showed the possible Abeta-fibril destabilizing effects of MAO inhibitors, present study was designed to (1) prepare the selective MAO-B inhibitor selegiline-loaded Poly (lactic-co-glycolic acid)-poly (ethylene glycol) (PLGA-b-PEG) nanoparticles (2) to investigate the in vitro Abeta-fibril destabilizing effect of the loaded particles.	poly(lactic-glycolic acid)-poly(ethyleneglycol) copolymer	245-256	monoamine oxidase B	Homo sapiens	156-161
23242744-7	2013	The MAO-B inhibition activities of the candidates were compared with the properties of rasagiline which is known to be a selective inhibitor of MAO-B.	rasagiline	87-97	monoamine oxidase B	Homo sapiens	144-149
23499958-1	2013	Resveratrol is known as an activator of SIRT1, which leads to the deacetylation of histone and non-histone protein substrates, but also has other pharmacological profiles such as the inhibition of monoamine oxidase (MAO)-A and MAO-B.	Resveratrol	0-11	monoamine oxidase B	Homo sapiens	227-232
22887993-2	2013	Moreover, MAO-B inhibitors are used in the treatment of idiopathic Parkinson disease as preliminary monotherapy or adjunct therapy with L-dopa.	Levodopa	136-142	monoamine oxidase B	Homo sapiens	10-15
23499958-6	2013	The inhibition of both MAO-A and MAO-B by clorgyline and pargyline, respectively, enhanced the effects of cocaine on DARPP-32 phosphorylation.	Clorgyline	42-52	monoamine oxidase B	Homo sapiens	33-38
23360954-2	2013	Safinamide is a monoamine oxidase B inhibitor with additional non-dopaminergic actions.	safinamide	0-10	monoamine oxidase B	Homo sapiens	16-35
23499958-6	2013	The inhibition of both MAO-A and MAO-B by clorgyline and pargyline, respectively, enhanced the effects of cocaine on DARPP-32 phosphorylation.	Pargyline	57-66	monoamine oxidase B	Homo sapiens	33-38
23499958-6	2013	The inhibition of both MAO-A and MAO-B by clorgyline and pargyline, respectively, enhanced the effects of cocaine on DARPP-32 phosphorylation.	Cocaine	106-113	monoamine oxidase B	Homo sapiens	33-38
23499958-7	2013	The acute effect of resveratrol on cocaine-induced DARPP-32 phosphorylation was occluded with inhibition of MAO-A and MAO-B.	Resveratrol	20-31	monoamine oxidase B	Homo sapiens	118-123
23499958-7	2013	The acute effect of resveratrol on cocaine-induced DARPP-32 phosphorylation was occluded with inhibition of MAO-A and MAO-B.	Cocaine	35-42	monoamine oxidase B	Homo sapiens	118-123
23499958-9	2013	Thus, this study provides pharmacological evidence that acute resveratrol enhances cocaine-induced dopamine neurotransmission and behavioral responses, presumably via mechanisms involving the inhibition of dopamine catabolism by MAO-A and MAO-B.	Resveratrol	62-73	monoamine oxidase B	Homo sapiens	239-244
23499958-9	2013	Thus, this study provides pharmacological evidence that acute resveratrol enhances cocaine-induced dopamine neurotransmission and behavioral responses, presumably via mechanisms involving the inhibition of dopamine catabolism by MAO-A and MAO-B.	Cocaine	83-90	monoamine oxidase B	Homo sapiens	239-244
23673910-2	2013	Monoamine oxidase B inhibitors, dopamine agonists, N-methyl-D-aspartate antagonists and levodopa (LD), with its various formulations and administration modes, mainly improve the motor symptoms in PD, which are thought to be related to decreased dopamine levels in the brain.	Dopamine	245-253	monoamine oxidase B	Homo sapiens	0-19
23474901-0	2013	Novel (coumarin-3-yl)carbamates as selective MAO-B inhibitors: synthesis, in vitro and in vivo assays, theoretical evaluation of ADME properties and docking study.	(coumarin-3-yl)carbamates	6-31	monoamine oxidase B	Homo sapiens	45-50
23474901-1	2013	A series of (coumarin-3-yl)carbamates was synthesized and evaluated in vitro as monoamine oxidase (MAO-A and MAO-B) inhibitors.	(coumarin-3-yl)carbamates	12-37	monoamine oxidase B	Homo sapiens	109-114
23474901-4	2013	Compound 8 (benzyl(coumarin-3-yl)carbamate), which presented the most interesting in vitro MAO-B inhibitory profile (IC50 against MAO-B = 45 nM), was subjected to further studies.	benzyl(coumarin-3-yl)carbamate	12-42	monoamine oxidase B	Homo sapiens	91-96
23474901-4	2013	Compound 8 (benzyl(coumarin-3-yl)carbamate), which presented the most interesting in vitro MAO-B inhibitory profile (IC50 against MAO-B = 45 nM), was subjected to further studies.	benzyl(coumarin-3-yl)carbamate	12-42	monoamine oxidase B	Homo sapiens	130-135
23474901-5	2013	This in vitro MAO-B inhibitory activity is comparable with that of the selegiline, the reference compound (IC50 against MAO-B = 20 nM).	Selegiline	71-81	monoamine oxidase B	Homo sapiens	14-19
23474901-5	2013	This in vitro MAO-B inhibitory activity is comparable with that of the selegiline, the reference compound (IC50 against MAO-B = 20 nM).	Selegiline	71-81	monoamine oxidase B	Homo sapiens	120-125
23506388-4	2013	The selective monoamine oxidase B inhibitor, selegiline , is widely used in the treatment of Parkinson"s disease.	Selegiline	45-55	monoamine oxidase B	Homo sapiens	14-33
22872464-1	2013	Ralfinamide, an original Na(+) channel blocker developed for the treatment of chronic pain, inhibits monoamineoxidase-B with no apparent effect on monoamineoxidase-A.	Ralfinamide	0-11	monoamine oxidase B	Homo sapiens	101-119
22872464-10	2013	These preliminary results give an evidence for the specificity of ralfinamide for MAO-B in comparison with MAO-A, analogously to the observations previously done for safinamide.	Ralfinamide	66-77	monoamine oxidase B	Homo sapiens	82-87
23515972-3	2013	Levodopa still remains the gold standard for the treatment of motor symptoms of PD but dopamine agonists (DAs), catechol-O-methyltransferase (COMT) inhibitors and monoamine oxidase B (MAO-B) inhibitors have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes and decrease the risk of levodopa-induced motor complications.	Levodopa	356-364	monoamine oxidase B	Homo sapiens	184-189
23418798-7	2013	For patients taking carbidopa/levodopa who have motor complications, adjunctive therapy with a dopamine agonist, a monoamine oxidase-B inhibitor, or a catechol O-methyltransferase inhibitor will improve motor symptoms and functional status, but with an increase in dyskinesias.	carbidopa, levodopa drug combination	20-38	monoamine oxidase B	Homo sapiens	115-134
23281824-0	2013	Synthesis of (E)-8-(3-chlorostyryl)caffeine analogues leading to 9-deazaxanthine derivatives as dual A(2A) antagonists/MAO-B inhibitors.	(E)-8-(3-chlorostyryl)caffeine	13-43	monoamine oxidase B	Homo sapiens	119-124
23281824-0	2013	Synthesis of (E)-8-(3-chlorostyryl)caffeine analogues leading to 9-deazaxanthine derivatives as dual A(2A) antagonists/MAO-B inhibitors.	9-deazaxanthine	65-80	monoamine oxidase B	Homo sapiens	119-124
23281824-4	2013	Two analogues of 17f, namely 18b and 19a, inhibit MAO-B with IC(50) of 68 and 48 nM, respectively, being 5-7-fold more potent than the prototypical MAO-B inhibitor deprenyl (IC(50) = 334 nM).	Selegiline	164-172	monoamine oxidase B	Homo sapiens	148-153
23374869-4	2013	In most instances, C6-substituted phthalides exhibit MAO-B specific inhibition.	c6-substituted phthalides	19-44	monoamine oxidase B	Homo sapiens	53-58
22968599-2	2013	MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neuronal cells by direct intervention in mitochondrial death signaling and induction of pro-survival Bcl-2 and neurotrophic factors.	rasagiline	18-28	monoamine oxidase B	Homo sapiens	0-5
22968599-2	2013	MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neuronal cells by direct intervention in mitochondrial death signaling and induction of pro-survival Bcl-2 and neurotrophic factors.	Selegiline	33-43	monoamine oxidase B	Homo sapiens	0-5
22968599-2	2013	MAO-B inhibitors, rasagiline and selegiline [(-)deprenyl], protect neuronal cells by direct intervention in mitochondrial death signaling and induction of pro-survival Bcl-2 and neurotrophic factors.	Selegiline	45-56	monoamine oxidase B	Homo sapiens	0-5
22915483-3	2013	Platelet monoamine oxidase (MAO-B) activity was assayed with [14C]-beta-phenylethylamine as substrate.	[14c]-beta-phenylethylamine	61-88	monoamine oxidase B	Homo sapiens	28-33
23325357-5	2013	Inhibition of the MAO-B enzyme boosts the effect of both endogenous and exogenous DA.	Dopamine	82-84	monoamine oxidase B	Homo sapiens	18-23
23211968-0	2013	Synthesis and biological evaluation of novel propargyl amines as potential fluorine-18 labeled radioligands for detection of MAO-B activity.	propargylamine	45-61	monoamine oxidase B	Homo sapiens	125-130
23065686-0	2013	Synthesis and selective human monoamine oxidase B inhibition of heterocyclic hybrids based on hydrazine and thiazole scaffolds.	hydrazine	94-103	monoamine oxidase B	Homo sapiens	30-49
23065686-0	2013	Synthesis and selective human monoamine oxidase B inhibition of heterocyclic hybrids based on hydrazine and thiazole scaffolds.	Thiazoles	108-116	monoamine oxidase B	Homo sapiens	30-49
23065686-1	2013	A new scaffold of hydrazothiazoles has been designed as monoamine oxidase (MAO) inhibitors combining the hydrazine moiety of iproniazid and the thiazole nucleus of glitazones, a class of peroxisome proliferator-activated receptor (PPAR)gamma agonists recently co-crystallized with human MAO-B.	hydrazothiazoles	18-34	monoamine oxidase B	Homo sapiens	287-292
23065686-1	2013	A new scaffold of hydrazothiazoles has been designed as monoamine oxidase (MAO) inhibitors combining the hydrazine moiety of iproniazid and the thiazole nucleus of glitazones, a class of peroxisome proliferator-activated receptor (PPAR)gamma agonists recently co-crystallized with human MAO-B.	Thiazoles	25-33	monoamine oxidase B	Homo sapiens	287-292
23065686-1	2013	A new scaffold of hydrazothiazoles has been designed as monoamine oxidase (MAO) inhibitors combining the hydrazine moiety of iproniazid and the thiazole nucleus of glitazones, a class of peroxisome proliferator-activated receptor (PPAR)gamma agonists recently co-crystallized with human MAO-B.	Thiazolidinediones	164-174	monoamine oxidase B	Homo sapiens	287-292
23211968-0	2013	Synthesis and biological evaluation of novel propargyl amines as potential fluorine-18 labeled radioligands for detection of MAO-B activity.	Fluorine-18	75-86	monoamine oxidase B	Homo sapiens	125-130
23211968-1	2013	The aim of this project was to synthesize and evaluate three novel fluorine-18 labeled derivatives of propargyl amine as potential PET radioligands to visualize monoamine oxidase B (MAO-B) activity.	Fluorine-18	67-78	monoamine oxidase B	Homo sapiens	161-180
23211968-1	2013	The aim of this project was to synthesize and evaluate three novel fluorine-18 labeled derivatives of propargyl amine as potential PET radioligands to visualize monoamine oxidase B (MAO-B) activity.	Fluorine-18	67-78	monoamine oxidase B	Homo sapiens	182-187
23211968-1	2013	The aim of this project was to synthesize and evaluate three novel fluorine-18 labeled derivatives of propargyl amine as potential PET radioligands to visualize monoamine oxidase B (MAO-B) activity.	propargylamine	102-117	monoamine oxidase B	Homo sapiens	161-180
23211968-1	2013	The aim of this project was to synthesize and evaluate three novel fluorine-18 labeled derivatives of propargyl amine as potential PET radioligands to visualize monoamine oxidase B (MAO-B) activity.	propargylamine	102-117	monoamine oxidase B	Homo sapiens	182-187
23176073-1	2013	OBJECTIVE: Rasagiline is a second-generation, irreversible MAO-B inhibitor (MAOB-I) previously shown to be efficacious and well-tolerated compared to placebo in the treatment of early Parkinson"s disease (PD).	rasagiline	11-21	monoamine oxidase B	Homo sapiens	59-64
24533911-3	2013	Our study identified the detailed structure activity relationship, the structural requirement for enzyme interaction and the effect of chirality on the pyrazoline nucleus towards MAO-A and MAO-B.	pyrazoline	152-162	monoamine oxidase B	Homo sapiens	189-194
23207409-1	2013	Due to their role in the metabolism of monoamine neurotransmitters, MAO-A and MAO-B present a significant pharmacological interest.	monoamine	39-48	monoamine oxidase B	Homo sapiens	78-83
23410161-6	2013	The design strategy for yet another agent, ladostigil, employed the amalgamation of active chemical moieties of the AChE inhibitor rivastigmine, and the monoamine oxidase-B (MAO-B) inhibitor rasagiline, leading to a single compound that targets both enzymes simultaneously.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	43-53	monoamine oxidase B	Homo sapiens	153-172
23410161-6	2013	The design strategy for yet another agent, ladostigil, employed the amalgamation of active chemical moieties of the AChE inhibitor rivastigmine, and the monoamine oxidase-B (MAO-B) inhibitor rasagiline, leading to a single compound that targets both enzymes simultaneously.	rasagiline	191-201	monoamine oxidase B	Homo sapiens	153-172
23410161-6	2013	The design strategy for yet another agent, ladostigil, employed the amalgamation of active chemical moieties of the AChE inhibitor rivastigmine, and the monoamine oxidase-B (MAO-B) inhibitor rasagiline, leading to a single compound that targets both enzymes simultaneously.	rasagiline	191-201	monoamine oxidase B	Homo sapiens	174-179
23410161-11	2013	Finally, compounds derived from the xanthine scaffold afford neuroprotection in Parkinson"s disease through mechanisms that include dual adenosine A2A receptor antagonism and MAO-B inhibition.	Xanthine	36-44	monoamine oxidase B	Homo sapiens	175-180
23116392-1	2013	Flavin-containing monoamine oxidases (MAO A and MAO B) located on the outer membrane of mitochondria oxidise amines and generate hydrogen peroxide.	Amines	109-115	monoamine oxidase B	Homo sapiens	48-53
23116392-1	2013	Flavin-containing monoamine oxidases (MAO A and MAO B) located on the outer membrane of mitochondria oxidise amines and generate hydrogen peroxide.	Hydrogen Peroxide	129-146	monoamine oxidase B	Homo sapiens	48-53
24140951-4	2013	Compound 3, an asymmetric spermine analogue bearing a thiophene ring, acts as a reversible mixed inhibitor, selective for MAO B (K(IE) = 23 muM).	Spermine	26-34	monoamine oxidase B	Homo sapiens	122-127
24140951-4	2013	Compound 3, an asymmetric spermine analogue bearing a thiophene ring, acts as a reversible mixed inhibitor, selective for MAO B (K(IE) = 23 muM).	Thiophenes	54-63	monoamine oxidase B	Homo sapiens	122-127
24140951-1	2013	New polyamine derivatives 1-8, related to the previously reported N(1),N(12)-dibenzyldodecane-1,12-diamine (Bis-Bza-Diado) and N(1)-benzyl-spermine (BD6), have been synthesized and used as "probes" (potential substrates or inhibitors) of the human monoamine oxidases (MAO A and MAO B) and Vascular-Adhesion-protein -1 (VAP-1).	Polyamines	4-13	monoamine oxidase B	Homo sapiens	278-283
24231308-0	2013	Fine molecular tuning at position 4 of 2H-chromen-2-one derivatives in the search of potent and selective monoamine oxidase B inhibitors.	coumarin	39-55	monoamine oxidase B	Homo sapiens	106-125
24231308-4	2013	In particular, the 7-metachlorobenzyloxy-4-oxyacetamido-2H-chromen-2-one (entry 62) showed single digit nanomolar MAO-B potency (IC50 = 3.1 nM) and high selectivity over the MAO-A isoform (selectivity ratio = 7244).	7-metachlorobenzyloxy-4-oxyacetamido-2h-chromen-2-one	19-72	monoamine oxidase B	Homo sapiens	114-119
24231308-5	2013	The great variety of the investigated substituents at C4 of the 2H-chromen-2-one nucleus, combined with binding models generated from docking studies carried out on selected compounds, allowed us to shed light on the main molecular requirements for potent and selective MAO-B inhibition, highlighting the dominant role of the steric effects.	coumarin	64-80	monoamine oxidase B	Homo sapiens	270-275
23620664-8	2013	Monoamine oxidase-B inhibitors (eg, selegiline) inhibit alpha-synuclein nitration, implicated in Lewy body formation, and inhibit 1-methyl 4-phenylpyridinium and 3-morpholinosydnonimine-induced apoptosis in cultured human dopaminergic neurons and mesencephalic fetal stem cells.	Selegiline	36-46	monoamine oxidase B	Homo sapiens	0-19
23207410-0	2013	1,5-Diphenylpenta-2,4-dien-1-ones as potent and selective monoamine oxidase-B inhibitors.	1,5-diphenylpenta-2,4-dien-1-ones	0-33	monoamine oxidase B	Homo sapiens	58-77
23207410-4	2013	Moreover, partial recovery of MAO-B activity was observed after repeated washing in the presence of isatin (reversible inhibitor) and compounds 3g and 3h suggesting a reversible inhibition of the enzyme.	Isatin	100-106	monoamine oxidase B	Homo sapiens	30-35
23620664-8	2013	Monoamine oxidase-B inhibitors (eg, selegiline) inhibit alpha-synuclein nitration, implicated in Lewy body formation, and inhibit 1-methyl 4-phenylpyridinium and 3-morpholinosydnonimine-induced apoptosis in cultured human dopaminergic neurons and mesencephalic fetal stem cells.	4-phenylpyridinium	139-157	monoamine oxidase B	Homo sapiens	0-19
23620664-8	2013	Monoamine oxidase-B inhibitors (eg, selegiline) inhibit alpha-synuclein nitration, implicated in Lewy body formation, and inhibit 1-methyl 4-phenylpyridinium and 3-morpholinosydnonimine-induced apoptosis in cultured human dopaminergic neurons and mesencephalic fetal stem cells.	linsidomine	162-185	monoamine oxidase B	Homo sapiens	0-19
23207410-4	2013	Moreover, partial recovery of MAO-B activity was observed after repeated washing in the presence of isatin (reversible inhibitor) and compounds 3g and 3h suggesting a reversible inhibition of the enzyme.	Tritium	151-153	monoamine oxidase B	Homo sapiens	30-35
23122857-0	2012	Sulfanylphthalonitrile analogues as selective and potent inhibitors of monoamine oxidase B.	sulfanylphthalonitrile	0-22	monoamine oxidase B	Homo sapiens	71-90
24204150-1	2013	We report a case in which selegiline, an irreversible monoamine oxidase B (MAO-B) inhibitor, greatly improved depressive symptoms in an adult with stage 5 treatment-resistant major depressive disorder.	Selegiline	26-36	monoamine oxidase B	Homo sapiens	54-73
24204150-1	2013	We report a case in which selegiline, an irreversible monoamine oxidase B (MAO-B) inhibitor, greatly improved depressive symptoms in an adult with stage 5 treatment-resistant major depressive disorder.	Selegiline	26-36	monoamine oxidase B	Homo sapiens	75-80
22782687-9	2013	MAO-B activity was enhanced after treatment with aggregated peptides and strongly inhibited after soluble Abeta(42) treatment.	UNII-042A8N37WH	106-111	monoamine oxidase B	Homo sapiens	0-5
23122857-1	2012	It has recently been reported that nitrile containing compounds frequently act as potent monoamine oxidase B (MAO-B) inhibitors.	Nitriles	35-42	monoamine oxidase B	Homo sapiens	89-108
23122934-6	2012	The results show that, compared to the corresponding 8-sulfanylcaffeine analogues, the 8-sulfinylcaffeins are weaker MAO-B inhibitors.	8-sulfinylcaffeins	87-105	monoamine oxidase B	Homo sapiens	117-122
23122857-1	2012	It has recently been reported that nitrile containing compounds frequently act as potent monoamine oxidase B (MAO-B) inhibitors.	Nitriles	35-42	monoamine oxidase B	Homo sapiens	110-115
23122857-2	2012	Modelling studies suggest that this high potency inhibition may rely, at least in part, on polar interactions between nitrile functional groups and polar moieties within the MAO-B substrate cavity.	Nitriles	118-125	monoamine oxidase B	Homo sapiens	174-179
23122857-5	2012	In general, the sulfanylphthalonitriles exhibited higher binding affinities for MAO-B than the corresponding sulfanylbenzonitrile homologues.	sulfanylphthalonitriles	16-39	monoamine oxidase B	Homo sapiens	80-85
23122857-5	2012	In general, the sulfanylphthalonitriles exhibited higher binding affinities for MAO-B than the corresponding sulfanylbenzonitrile homologues.	sulfanylbenzonitrile	109-129	monoamine oxidase B	Homo sapiens	80-85
23122857-6	2012	Among the compounds evaluated, 4-[(4-bromobenzyl)sulfanyl]phthalonitrile is a particularly promising inhibitor since it displayed a high degree of selectivity (8720-fold) for MAO-B over MAO-A, and potent MAO-B inhibition (IC(50)=0.025 muM).	CHEMBL2204757	31-72	monoamine oxidase B	Homo sapiens	175-180
23122857-6	2012	Among the compounds evaluated, 4-[(4-bromobenzyl)sulfanyl]phthalonitrile is a particularly promising inhibitor since it displayed a high degree of selectivity (8720-fold) for MAO-B over MAO-A, and potent MAO-B inhibition (IC(50)=0.025 muM).	CHEMBL2204757	31-72	monoamine oxidase B	Homo sapiens	204-209
21992679-3	2012	Oxidation of MPTP by human MAO-B was more efficient than by MAO-A.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	13-17	monoamine oxidase B	Homo sapiens	27-32
23153282-4	2012	The docking experiments carried out on MAO-A and MAO-B structures proved new information about the enzyme-inhibitor interaction and the potential therapeutic application of 7-oxycoumarin scaffold.	7-hydroxycoumarin	173-186	monoamine oxidase B	Homo sapiens	49-54
23064123-4	2012	While the chromone derivatives also exhibit affinities for MAO-A, with IC(50) values ranging from 0.495 to 8.03 muM, they are selective for the MAO-B isoform.	Chromones	10-18	monoamine oxidase B	Homo sapiens	144-149
23064123-5	2012	Structure-activity relationships (SAR) show that 7-benzyloxy substitution of chromone is suitable for MAO-B inhibition with tolerance for a variety of substituents and substitution patterns on the benzyloxy ring.	Chromones	77-85	monoamine oxidase B	Homo sapiens	102-107
23064123-6	2012	It may be concluded that 7-benzyloxychromones are appropriate lead compounds for the design of reversible and selective MAO-B inhibitors.	7-benzyloxychromones	25-45	monoamine oxidase B	Homo sapiens	120-125
23153812-0	2012	Recent advances in the development of selective human MAO-B inhibitors: (hetero)arylidene-(4-substituted-thiazol-2-yl)hydrazines.	(hetero)arylidene-(4-substituted-thiazol-2-yl)hydrazines	72-128	monoamine oxidase B	Homo sapiens	54-59
23153812-4	2012	The substituent on the alpha-carbon to the N1-hydrazine moiety (methyl or hydrogen) had a great influence on the activity and hMAO-B selectivity.	Carbon	29-35	monoamine oxidase B	Homo sapiens	126-132
23153812-4	2012	The substituent on the alpha-carbon to the N1-hydrazine moiety (methyl or hydrogen) had a great influence on the activity and hMAO-B selectivity.	4-(2-(4-isopropylbenzamido)ethoxy)benzoic acid	43-46	monoamine oxidase B	Homo sapiens	126-132
23153812-4	2012	The substituent on the alpha-carbon to the N1-hydrazine moiety (methyl or hydrogen) had a great influence on the activity and hMAO-B selectivity.	hydrazine	46-55	monoamine oxidase B	Homo sapiens	126-132
23153812-4	2012	The substituent on the alpha-carbon to the N1-hydrazine moiety (methyl or hydrogen) had a great influence on the activity and hMAO-B selectivity.	Hydrogen	74-82	monoamine oxidase B	Homo sapiens	126-132
21992679-4	2012	R-Deprenyl, a known neuroprotectant, norharman (beta-carboline), 5-nitroindazole and menadione (vitamin K3) inhibited MAO-B and reduced the formation of toxic pyridinium cations.	r-deprenyl	0-10	monoamine oxidase B	Homo sapiens	118-123
21992679-4	2012	R-Deprenyl, a known neuroprotectant, norharman (beta-carboline), 5-nitroindazole and menadione (vitamin K3) inhibited MAO-B and reduced the formation of toxic pyridinium cations.	norharman	37-46	monoamine oxidase B	Homo sapiens	118-123
21992679-4	2012	R-Deprenyl, a known neuroprotectant, norharman (beta-carboline), 5-nitroindazole and menadione (vitamin K3) inhibited MAO-B and reduced the formation of toxic pyridinium cations.	norharman	48-62	monoamine oxidase B	Homo sapiens	118-123
21992679-4	2012	R-Deprenyl, a known neuroprotectant, norharman (beta-carboline), 5-nitroindazole and menadione (vitamin K3) inhibited MAO-B and reduced the formation of toxic pyridinium cations.	5-nitroindazole	65-80	monoamine oxidase B	Homo sapiens	118-123
21992679-4	2012	R-Deprenyl, a known neuroprotectant, norharman (beta-carboline), 5-nitroindazole and menadione (vitamin K3) inhibited MAO-B and reduced the formation of toxic pyridinium cations.	Vitamin K 3	85-94	monoamine oxidase B	Homo sapiens	118-123
21992679-4	2012	R-Deprenyl, a known neuroprotectant, norharman (beta-carboline), 5-nitroindazole and menadione (vitamin K3) inhibited MAO-B and reduced the formation of toxic pyridinium cations.	Vitamin K 3	96-106	monoamine oxidase B	Homo sapiens	118-123
21992679-6	2012	Cigarette smoke, as well as the naturally occurring beta-carbolines (norharman and harman) isolated from smoke and coffee inhibited the oxidation of MPTP by MAO-B and/or MAO-A, suggesting protective effects against MPTP.	Carbolines	52-67	monoamine oxidase B	Homo sapiens	157-162
21992679-6	2012	Cigarette smoke, as well as the naturally occurring beta-carbolines (norharman and harman) isolated from smoke and coffee inhibited the oxidation of MPTP by MAO-B and/or MAO-A, suggesting protective effects against MPTP.	norharman	69-78	monoamine oxidase B	Homo sapiens	157-162
21992679-6	2012	Cigarette smoke, as well as the naturally occurring beta-carbolines (norharman and harman) isolated from smoke and coffee inhibited the oxidation of MPTP by MAO-B and/or MAO-A, suggesting protective effects against MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	149-153	monoamine oxidase B	Homo sapiens	157-162
22512575-2	2012	Since the I(1) imidazoline receptor is involved in central inhibition of sympathicus that produce hypotensive effect, the I(2) receptor is allosteric modulator of monoamine oxidase B (MAO-B) and the I(3) receptor regulates insulin secretion from pancreatic beta-cells, design and synthesis of selective I(1)/I(2)/I(3) imidazoline ligands are very important for the development of new effective therapeutic agents.	Imidazolines	15-26	monoamine oxidase B	Homo sapiens	184-189
22954444-1	2012	The objective was to investigate the anodal iontophoresis of the MAO-B inhibitors rasagiline (RAS) and selegiline (SEL) across porcine and human skin in vitro.	rasagiline	82-92	monoamine oxidase B	Homo sapiens	65-70
22954444-1	2012	The objective was to investigate the anodal iontophoresis of the MAO-B inhibitors rasagiline (RAS) and selegiline (SEL) across porcine and human skin in vitro.	rasagiline	94-97	monoamine oxidase B	Homo sapiens	65-70
22954444-1	2012	The objective was to investigate the anodal iontophoresis of the MAO-B inhibitors rasagiline (RAS) and selegiline (SEL) across porcine and human skin in vitro.	Selegiline	115-118	monoamine oxidase B	Homo sapiens	65-70
23010267-0	2012	Novel sulfanylphthalimide analogues as highly potent inhibitors of monoamine oxidase B.	sulfanylphthalimide	6-25	monoamine oxidase B	Homo sapiens	67-86
23010267-3	2012	Based on a recent report that the phthalimide moiety may be a useful scaffold for the design of potent MAO-B inhibitors, the present study examines a series of 5-sulfanylphthalimide analogues as potential inhibitors of both human MAO isoforms.	phthalimide	34-45	monoamine oxidase B	Homo sapiens	103-108
23010267-4	2012	The results document that 5-sulfanylphthalimides are highly potent and selective MAO-B inhibitors with all of the examined compounds possessing IC(50) values in the nanomolar range.	5-sulfanylphthalimides	26-48	monoamine oxidase B	Homo sapiens	81-86
23010267-5	2012	The most potent inhibitor, 5-(benzylsulfanyl)phthalimide, exhibits an IC(50) value of 0.0045 muM for the inhibition of MAO-B with a 427-fold selectivity for MAO-B compared to MAO-A.	CHEMBL2158241	27-56	monoamine oxidase B	Homo sapiens	119-124
23010267-5	2012	The most potent inhibitor, 5-(benzylsulfanyl)phthalimide, exhibits an IC(50) value of 0.0045 muM for the inhibition of MAO-B with a 427-fold selectivity for MAO-B compared to MAO-A.	CHEMBL2158241	27-56	monoamine oxidase B	Homo sapiens	157-162
23010267-6	2012	We conclude that 5-sulfanylphthalimides represent an interesting class of MAO-B inhibitors and may serve as lead compounds for the design of antiparkinsonian therapy.	5-sulfanylphthalimides	17-39	monoamine oxidase B	Homo sapiens	74-79
22978824-0	2012	Multitarget-directed benzylideneindanone derivatives: anti-beta-amyloid (Abeta) aggregation, antioxidant, metal chelation, and monoamine oxidase B (MAO-B) inhibition properties against Alzheimer"s disease.	benzylideneindanone	21-40	monoamine oxidase B	Homo sapiens	127-146
23346517-5	2012	Rasagiline is a novel, potent, and irreversible monoamine oxidase type B (MAO-B) inhibitor that has recently been approved by the Food and Drug Administration for treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	48-72
23346517-5	2012	Rasagiline is a novel, potent, and irreversible monoamine oxidase type B (MAO-B) inhibitor that has recently been approved by the Food and Drug Administration for treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	74-79
22974659-1	2012	Monoamine oxidase B (MAO-B) plays an important role in the metabolism of neuroactive and vasoactive amines in the central nervous system and peripheral tissues.	Amines	100-106	monoamine oxidase B	Homo sapiens	0-19
22974659-1	2012	Monoamine oxidase B (MAO-B) plays an important role in the metabolism of neuroactive and vasoactive amines in the central nervous system and peripheral tissues.	Amines	100-106	monoamine oxidase B	Homo sapiens	21-26
22978824-0	2012	Multitarget-directed benzylideneindanone derivatives: anti-beta-amyloid (Abeta) aggregation, antioxidant, metal chelation, and monoamine oxidase B (MAO-B) inhibition properties against Alzheimer"s disease.	benzylideneindanone	21-40	monoamine oxidase B	Homo sapiens	148-153
22978824-2	2012	The in vitro studies showed that most of the molecules exhibited a significant ability to inhibit self-induced beta-amyloid (Abeta(1-42)) aggregation (10.5-80.1%, 20 muM) and MAO-B activity (IC(50) of 7.5-40.5 muM), to act as potential antioxidants (ORAC-FL value of 2.75-9.37), and to function as metal chelators.	Metals	298-303	monoamine oxidase B	Homo sapiens	175-180
22978824-3	2012	In particular, compound 41 had the greatest ability to inhibit Abeta(1-42) aggregation (80.1%), and MAO-B (IC(50) = 7.5 muM) was also an excellent antioxidant and metal chelator.	Metals	163-168	monoamine oxidase B	Homo sapiens	100-105
22948897-5	2012	This study confirms that safinamide is a highly selective monoamine oxidase-B inhibitor, even at supratherapeutic doses, and suggests that it can be administered without tyramine-related dietary restrictions.	safinamide	25-35	monoamine oxidase B	Homo sapiens	58-77
26593027-1	2012	Monoamine oxidase (MAO), which exists in two isozymic forms, MAO A and MAO B, is an important flavoenzyme responsible for the metabolism of amine neurotransmitters such as dopamine, serotonin, and norepinephrine.	Amines	4-9	monoamine oxidase B	Homo sapiens	71-76
26593027-1	2012	Monoamine oxidase (MAO), which exists in two isozymic forms, MAO A and MAO B, is an important flavoenzyme responsible for the metabolism of amine neurotransmitters such as dopamine, serotonin, and norepinephrine.	Dopamine	172-180	monoamine oxidase B	Homo sapiens	71-76
26593027-1	2012	Monoamine oxidase (MAO), which exists in two isozymic forms, MAO A and MAO B, is an important flavoenzyme responsible for the metabolism of amine neurotransmitters such as dopamine, serotonin, and norepinephrine.	Serotonin	182-191	monoamine oxidase B	Homo sapiens	71-76
26593027-1	2012	Monoamine oxidase (MAO), which exists in two isozymic forms, MAO A and MAO B, is an important flavoenzyme responsible for the metabolism of amine neurotransmitters such as dopamine, serotonin, and norepinephrine.	Norepinephrine	197-211	monoamine oxidase B	Homo sapiens	71-76
26593027-4	2012	Therefore, in order to investigate features essential for the modes of action of MAO, we have calculated pKa values of three relevant tyrosine residues in the MAO B active site, with and without dopamine bound as the substrate (as well as the pKa of the dopamine itself in the active site).	Tyrosine	134-142	monoamine oxidase B	Homo sapiens	159-164
22451094-0	2012	A selective reversible monoamine oxidase B inhibitor in smoking cessation: effects on its own and in association with transdermal nicotine patch.	Nicotine	130-138	monoamine oxidase B	Homo sapiens	23-42
22850212-1	2012	A previous study has shown that a series of C6-benzyloxy substituted chromones exhibit high binding affinities for human monoamine oxidase (MAO) B.	-benzyloxy substituted chromones	46-78	monoamine oxidase B	Homo sapiens	121-146
22850212-2	2012	In an attempt to discover additional chromones with potent and selective MAO-B inhibitory potencies and to further examine the structure-activity relationships of MAO-B inhibition by chromones, the series was expanded with homologues containing polar functional groups on C3 of the chromone ring.	Chromones	37-46	monoamine oxidase B	Homo sapiens	73-78
22850212-2	2012	In an attempt to discover additional chromones with potent and selective MAO-B inhibitory potencies and to further examine the structure-activity relationships of MAO-B inhibition by chromones, the series was expanded with homologues containing polar functional groups on C3 of the chromone ring.	Chromones	37-45	monoamine oxidase B	Homo sapiens	73-78
22850212-3	2012	The results demonstrate that 6-[(3-bromobenzyl)oxy]chromones containing acidic and aldehydic functional groups on C3 act as potent reversible MAO-B inhibitors with IC(50) values of 2.8 and 3.7 nM, respectively.	6-[(3-bromobenzyl)oxy]chromones	29-60	monoamine oxidase B	Homo sapiens	142-147
22850212-4	2012	Interestingly, a 2-hydroxy-2,3-dihydro-1-benzopyran-4-one derivative as well as open-ring 2-acetylphenol analogues of the chromones also were potent MAO-B inhibitors with IC(50) values ranging from 4 to 11 nM.	2-hydroxy-2,3-dihydro-1-benzopyran-4-one	17-57	monoamine oxidase B	Homo sapiens	149-154
22850212-4	2012	Interestingly, a 2-hydroxy-2,3-dihydro-1-benzopyran-4-one derivative as well as open-ring 2-acetylphenol analogues of the chromones also were potent MAO-B inhibitors with IC(50) values ranging from 4 to 11 nM.	2'-Hydroxyacetophenone	90-104	monoamine oxidase B	Homo sapiens	149-154
22850212-4	2012	Interestingly, a 2-hydroxy-2,3-dihydro-1-benzopyran-4-one derivative as well as open-ring 2-acetylphenol analogues of the chromones also were potent MAO-B inhibitors with IC(50) values ranging from 4 to 11 nM.	Chromones	122-131	monoamine oxidase B	Homo sapiens	149-154
22850212-5	2012	Chromone derivatives containing the benzyloxy substituent on C5 of the chromone ring, however, exhibit MAO-B inhibition potencies that are several orders of magnitude weaker.	Chromones	0-8	monoamine oxidase B	Homo sapiens	103-108
22850212-5	2012	Chromone derivatives containing the benzyloxy substituent on C5 of the chromone ring, however, exhibit MAO-B inhibition potencies that are several orders of magnitude weaker.	Chromones	71-79	monoamine oxidase B	Homo sapiens	103-108
22451094-2	2012	A MAO-B inhibitor alone or co-administered with nicotine may mimic the effects of smoking and be a candidate drug for smoking cessation.	Nicotine	48-56	monoamine oxidase B	Homo sapiens	2-7
22451094-3	2012	OBJECTIVE: This study aims to determine the efficacy and safety of EVT302, a selective reversible MAO-B inhibitor, alone and on top of nicotine patch (NP) in smoking cessation.	sembragiline	67-73	monoamine oxidase B	Homo sapiens	98-103
22451094-12	2012	CONCLUSIONS: The selective, reversible MAO-B inhibitor EVT302 was not superior to placebo in helping smokers quit, in line with data with selegiline and confirms that MAO-B inhibitors are not effective in smoking cessation.	sembragiline	55-61	monoamine oxidase B	Homo sapiens	39-44
22691758-3	2012	In this review, we focus on recent studies with monoamine oxidase type B inhibitors (selegiline and rasagiline), coenzyme Q10, creatine, and exercise in early Parkinson"s disease.	Selegiline	85-95	monoamine oxidase B	Homo sapiens	48-72
22765918-0	2012	Modulations of brain amines and dopaminergic behavior by a novel, reversible and selective MAO-B inhibitor.	Amines	21-27	monoamine oxidase B	Homo sapiens	91-96
22765918-2	2012	Recently we have reported a few pyrazolines as reversible and selective MAO-B inhibitors.	pyrazolines	32-43	monoamine oxidase B	Homo sapiens	72-77
27186120-3	2012	Currently under investigation for use in the treatment of PD, safinamide has multiple modes of action including monoamine oxidase B inhibition.	safinamide	62-72	monoamine oxidase B	Homo sapiens	112-131
22772874-2	2012	RECENT FINDINGS: This review includes novel approaches to dopaminergic drug delivery such as intraintestinal infusions or new extended-release formulations of levodopa and also intrapulmonary delivery of apomorphine as well as novel dopaminergic agents like the monoamine oxidase-B inhibitor safinamide or novel catechol-O-methyl transferase inhibitors.	Apomorphine	204-215	monoamine oxidase B	Homo sapiens	262-281
22691758-3	2012	In this review, we focus on recent studies with monoamine oxidase type B inhibitors (selegiline and rasagiline), coenzyme Q10, creatine, and exercise in early Parkinson"s disease.	rasagiline	100-110	monoamine oxidase B	Homo sapiens	48-72
22329629-0	2012	Mao-B elevation decreases parkin"s ability to efficiently clear damaged mitochondria: protective effects of rapamycin.	Sirolimus	108-117	monoamine oxidase B	Homo sapiens	0-5
22426510-0	2012	Targeting imidazoline site on monoamine oxidase B through molecular docking simulations.	Imidazolines	10-21	monoamine oxidase B	Homo sapiens	30-49
22426510-3	2012	Furthermore, crystallographic studies identified the imidazoline-binding domain on monoamine oxidase B (MAO-B), which opens the possibility of molecular docking studies focused on this binding site.	Imidazolines	53-64	monoamine oxidase B	Homo sapiens	83-102
22426510-3	2012	Furthermore, crystallographic studies identified the imidazoline-binding domain on monoamine oxidase B (MAO-B), which opens the possibility of molecular docking studies focused on this binding site.	Imidazolines	53-64	monoamine oxidase B	Homo sapiens	104-109
22592509-1	2012	Selegiline at the doses used in Parkinson disease is a selective irreversible monoamine oxidase type B inhibitor, which potentiates dopaminergic function in the brain, and is used as monotherapy in early Parkinson disease or in combination with levodopa in more advanced disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	78-102
22678415-0	2012	5-(5-Aryl-1,3,4-oxadiazole-2-carbonyl)furan-3-carboxylate and new cyclic C-glycoside analogues from carbohydrate precursors with MAO-B, antimicrobial and antifungal activities.	5-(5-aryl-1,3,4-oxadiazole-2-carbonyl)furan-3-carboxylate	0-57	monoamine oxidase B	Homo sapiens	129-134
22678415-0	2012	5-(5-Aryl-1,3,4-oxadiazole-2-carbonyl)furan-3-carboxylate and new cyclic C-glycoside analogues from carbohydrate precursors with MAO-B, antimicrobial and antifungal activities.	cyclic c-glycoside	66-84	monoamine oxidase B	Homo sapiens	129-134
22678415-0	2012	5-(5-Aryl-1,3,4-oxadiazole-2-carbonyl)furan-3-carboxylate and new cyclic C-glycoside analogues from carbohydrate precursors with MAO-B, antimicrobial and antifungal activities.	Carbohydrates	100-112	monoamine oxidase B	Homo sapiens	129-134
22475561-2	2012	It is worth noting that most of the small amine moieties substituted on the piperidine ring proved to be potent and selective inhibitors of MAO-B rather than of MAO-A.	Amines	42-47	monoamine oxidase B	Homo sapiens	140-145
22475561-2	2012	It is worth noting that most of the small amine moieties substituted on the piperidine ring proved to be potent and selective inhibitors of MAO-B rather than of MAO-A.	piperidine	76-86	monoamine oxidase B	Homo sapiens	140-145
22475561-3	2012	5-(3,4-methylenedioxyphenyl)-2E,4E-pentadienoic acid n-propyl amide (3) showed the greatest MAO-B inhibitory activity (IC(50)(MAO-B)=0.045 muM) and good selectivity (IC(50)(MAO-A)=3.66 muM).	5-(3,4-methylenedioxyphenyl)-2e	0-31	monoamine oxidase B	Homo sapiens	92-97
22475561-3	2012	5-(3,4-methylenedioxyphenyl)-2E,4E-pentadienoic acid n-propyl amide (3) showed the greatest MAO-B inhibitory activity (IC(50)(MAO-B)=0.045 muM) and good selectivity (IC(50)(MAO-A)=3.66 muM).	5-(3,4-methylenedioxyphenyl)-2e	0-31	monoamine oxidase B	Homo sapiens	126-131
22475561-3	2012	5-(3,4-methylenedioxyphenyl)-2E,4E-pentadienoic acid n-propyl amide (3) showed the greatest MAO-B inhibitory activity (IC(50)(MAO-B)=0.045 muM) and good selectivity (IC(50)(MAO-A)=3.66 muM).	4e-pentadienoic acid n-propyl amide	32-67	monoamine oxidase B	Homo sapiens	92-97
22475561-3	2012	5-(3,4-methylenedioxyphenyl)-2E,4E-pentadienoic acid n-propyl amide (3) showed the greatest MAO-B inhibitory activity (IC(50)(MAO-B)=0.045 muM) and good selectivity (IC(50)(MAO-A)=3.66 muM).	4e-pentadienoic acid n-propyl amide	32-67	monoamine oxidase B	Homo sapiens	126-131
22890201-2	2012	Both monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) regulate neurochemistry by degrading monoamine neurotransmitters (serotonin, dopamine, and norepinephrine).	Serotonin	131-140	monoamine oxidase B	Homo sapiens	37-56
22890201-2	2012	Both monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) regulate neurochemistry by degrading monoamine neurotransmitters (serotonin, dopamine, and norepinephrine).	Serotonin	131-140	monoamine oxidase B	Homo sapiens	58-63
22890201-2	2012	Both monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) regulate neurochemistry by degrading monoamine neurotransmitters (serotonin, dopamine, and norepinephrine).	Dopamine	142-150	monoamine oxidase B	Homo sapiens	37-56
22890201-2	2012	Both monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) regulate neurochemistry by degrading monoamine neurotransmitters (serotonin, dopamine, and norepinephrine).	Dopamine	142-150	monoamine oxidase B	Homo sapiens	58-63
22890201-2	2012	Both monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) regulate neurochemistry by degrading monoamine neurotransmitters (serotonin, dopamine, and norepinephrine).	Norepinephrine	156-170	monoamine oxidase B	Homo sapiens	37-56
22890201-2	2012	Both monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) regulate neurochemistry by degrading monoamine neurotransmitters (serotonin, dopamine, and norepinephrine).	Norepinephrine	156-170	monoamine oxidase B	Homo sapiens	58-63
22890201-6	2012	Furthermore, KLF11 may influence MAO-B expression and augment glyceraldehyde-3 phosphate dehydrogenase (GAPDH) to upregulate MAO-B transcription upon exposure to ethanol.	Ethanol	162-169	monoamine oxidase B	Homo sapiens	125-130
22436387-0	2012	Synthesis and evaluation of [18F]fluororasagiline, a novel positron emission tomography (PET) radioligand for monoamine oxidase B (MAO-B).	fluororasagiline	32-49	monoamine oxidase B	Homo sapiens	110-129
22436387-0	2012	Synthesis and evaluation of [18F]fluororasagiline, a novel positron emission tomography (PET) radioligand for monoamine oxidase B (MAO-B).	fluororasagiline	32-49	monoamine oxidase B	Homo sapiens	131-136
22436387-1	2012	The aim of this study was to synthesize and evaluate a novel fluorine-18 labeled analogue of rasagiline (6) as a PET radioligand for monoamine oxidase B (MAO-B).	Fluorine-18	61-72	monoamine oxidase B	Homo sapiens	133-152
22436387-1	2012	The aim of this study was to synthesize and evaluate a novel fluorine-18 labeled analogue of rasagiline (6) as a PET radioligand for monoamine oxidase B (MAO-B).	Fluorine-18	61-72	monoamine oxidase B	Homo sapiens	154-159
22436387-1	2012	The aim of this study was to synthesize and evaluate a novel fluorine-18 labeled analogue of rasagiline (6) as a PET radioligand for monoamine oxidase B (MAO-B).	rasagiline	93-103	monoamine oxidase B	Homo sapiens	133-152
22436387-1	2012	The aim of this study was to synthesize and evaluate a novel fluorine-18 labeled analogue of rasagiline (6) as a PET radioligand for monoamine oxidase B (MAO-B).	rasagiline	93-103	monoamine oxidase B	Homo sapiens	154-159
22436387-7	2012	Blocking experiments with pirlindole (MAO-A), L-deprenyl and rasagiline (MAO-B) were conducted to demonstrate the specificity of the binding.	rasagiline	61-71	monoamine oxidase B	Homo sapiens	73-78
22436387-16	2012	Our investigations demonstrated that the new ligand [(18)F]fluororasagiline (6) binds specifically to MAO-B in vitro and has a MAO-B specific binding pattern in vivo.	fluororasagiline	59-75	monoamine oxidase B	Homo sapiens	102-107
22436387-16	2012	Our investigations demonstrated that the new ligand [(18)F]fluororasagiline (6) binds specifically to MAO-B in vitro and has a MAO-B specific binding pattern in vivo.	fluororasagiline	59-75	monoamine oxidase B	Homo sapiens	127-132
21873469-9	2012	RESULTS: Cholangiocarcinoma cells display (1) enhanced HDC and decreased monoamine oxidase B expression resulting in increased histamine secretion; and (2) increased expression of H1-H4 HRs.	Histamine	127-136	monoamine oxidase B	Homo sapiens	73-92
22365943-4	2012	Patients who lack both MAOA and MAOB have the most extreme laboratory values (urine, blood, and CSF serotonin 4-6 times normal, with elevated O-methylated amine metabolites and reduced deaminated metabolites) in addition to severe intellectual deficiency and behavioral problems.	Serotonin	100-109	monoamine oxidase B	Homo sapiens	32-36
22365943-4	2012	Patients who lack both MAOA and MAOB have the most extreme laboratory values (urine, blood, and CSF serotonin 4-6 times normal, with elevated O-methylated amine metabolites and reduced deaminated metabolites) in addition to severe intellectual deficiency and behavioral problems.	Amines	155-160	monoamine oxidase B	Homo sapiens	32-36
22270014-1	2012	Monoamine oxidase-B (Mao-B) catalysing the breakdown of the neurotransmitter dopamine, is known to be involved in the pathophysiology of Parkinson"s (PD) and Alzheimer"s disease (AD).	Dopamine	77-85	monoamine oxidase B	Homo sapiens	0-19
22086140-1	2012	Selegiline (R-deprenyl), a monoamine oxidase-B (MAO-B) inhibitor, has complex pharmacological effect that contributes to treatment of neurodegenerative diseases such as Parkinson"s and presumably Alzheimer"s disease and might work as an inhibitor of tumor growth.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	27-46
22086140-1	2012	Selegiline (R-deprenyl), a monoamine oxidase-B (MAO-B) inhibitor, has complex pharmacological effect that contributes to treatment of neurodegenerative diseases such as Parkinson"s and presumably Alzheimer"s disease and might work as an inhibitor of tumor growth.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	48-53
22086140-1	2012	Selegiline (R-deprenyl), a monoamine oxidase-B (MAO-B) inhibitor, has complex pharmacological effect that contributes to treatment of neurodegenerative diseases such as Parkinson"s and presumably Alzheimer"s disease and might work as an inhibitor of tumor growth.	r-deprenyl	12-22	monoamine oxidase B	Homo sapiens	27-46
22086140-1	2012	Selegiline (R-deprenyl), a monoamine oxidase-B (MAO-B) inhibitor, has complex pharmacological effect that contributes to treatment of neurodegenerative diseases such as Parkinson"s and presumably Alzheimer"s disease and might work as an inhibitor of tumor growth.	r-deprenyl	12-22	monoamine oxidase B	Homo sapiens	48-53
21628600-0	2012	The monoamine oxidase type B inhibitor rasagiline in the treatment of Parkinson disease: is tyramine a challenge?	rasagiline	39-49	monoamine oxidase B	Homo sapiens	4-28
21628600-1	2012	Rasagiline is an irreversible monoamine oxidase type B (MAO-B) inhibitor indicated for the treatment of the signs and symptoms of idiopathic Parkinson disease as initial monotherapy and as adjunct therapy to levodopa.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	30-54
21628600-1	2012	Rasagiline is an irreversible monoamine oxidase type B (MAO-B) inhibitor indicated for the treatment of the signs and symptoms of idiopathic Parkinson disease as initial monotherapy and as adjunct therapy to levodopa.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	56-61
21628600-1	2012	Rasagiline is an irreversible monoamine oxidase type B (MAO-B) inhibitor indicated for the treatment of the signs and symptoms of idiopathic Parkinson disease as initial monotherapy and as adjunct therapy to levodopa.	Levodopa	208-216	monoamine oxidase B	Homo sapiens	56-61
21628600-3	2012	Tyramine challenge studies, conducted to characterize rasagiline selectivity for the MAO-B enzyme and tyramine sensitivity, demonstrate that rasagiline, when used at the recommended dose, is selective for MAO-B and is not associated with heightened tyramine sensitivity.	Tyramine	0-8	monoamine oxidase B	Homo sapiens	85-90
21628600-3	2012	Tyramine challenge studies, conducted to characterize rasagiline selectivity for the MAO-B enzyme and tyramine sensitivity, demonstrate that rasagiline, when used at the recommended dose, is selective for MAO-B and is not associated with heightened tyramine sensitivity.	rasagiline	54-64	monoamine oxidase B	Homo sapiens	85-90
21628600-3	2012	Tyramine challenge studies, conducted to characterize rasagiline selectivity for the MAO-B enzyme and tyramine sensitivity, demonstrate that rasagiline, when used at the recommended dose, is selective for MAO-B and is not associated with heightened tyramine sensitivity.	rasagiline	141-151	monoamine oxidase B	Homo sapiens	85-90
21628600-3	2012	Tyramine challenge studies, conducted to characterize rasagiline selectivity for the MAO-B enzyme and tyramine sensitivity, demonstrate that rasagiline, when used at the recommended dose, is selective for MAO-B and is not associated with heightened tyramine sensitivity.	rasagiline	141-151	monoamine oxidase B	Homo sapiens	205-210
21628600-6	2012	In addition, because rasagiline has been demonstrated to be selective for MAO-B at the approved dose of up to 1 mg/d, contraindications regarding concomitant use with sympathomimetic amines, use of sympathomimetic vasopressors in conjunction with general or local anesthesia, and use in patients with pheochromocytoma also were removed.	rasagiline	21-31	monoamine oxidase B	Homo sapiens	74-79
22270014-1	2012	Monoamine oxidase-B (Mao-B) catalysing the breakdown of the neurotransmitter dopamine, is known to be involved in the pathophysiology of Parkinson"s (PD) and Alzheimer"s disease (AD).	Dopamine	77-85	monoamine oxidase B	Homo sapiens	21-26
22065207-1	2012	Rasagiline and (-)deprenyl (selegiline), irreversible type B monoamine oxidase (MAO-B) inhibitors, protect neuronal cells through gene induction of pro-survival Bcl-2 and neurotrophic factors in the cellular models of neurodegenerative disorders.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	80-85
22065207-1	2012	Rasagiline and (-)deprenyl (selegiline), irreversible type B monoamine oxidase (MAO-B) inhibitors, protect neuronal cells through gene induction of pro-survival Bcl-2 and neurotrophic factors in the cellular models of neurodegenerative disorders.	Selegiline	18-26	monoamine oxidase B	Homo sapiens	80-85
22065207-1	2012	Rasagiline and (-)deprenyl (selegiline), irreversible type B monoamine oxidase (MAO-B) inhibitors, protect neuronal cells through gene induction of pro-survival Bcl-2 and neurotrophic factors in the cellular models of neurodegenerative disorders.	Selegiline	28-38	monoamine oxidase B	Homo sapiens	80-85
22065207-5	2012	MAO-B overexpression inhibited Bcl-2 induction by rasagiline and befloxatone, but did not affect that by (-)deprenyl, suggesting the different mechanisms behind Bcl-2 gene induction by these MAO-B inhibitors.	rasagiline	50-60	monoamine oxidase B	Homo sapiens	0-5
22065207-5	2012	MAO-B overexpression inhibited Bcl-2 induction by rasagiline and befloxatone, but did not affect that by (-)deprenyl, suggesting the different mechanisms behind Bcl-2 gene induction by these MAO-B inhibitors.	befloxatone	65-76	monoamine oxidase B	Homo sapiens	0-5
22287164-0	2012	8-Substituted 3-arylcoumarins as potent and selective MAO-B inhibitors: synthesis, pharmacological evaluation, and docking studies.	8-substituted 3-arylcoumarins	0-29	monoamine oxidase B	Homo sapiens	54-59
22439669-1	2012	Rasagiline (Azilect ), a selective, irreversible, monoamine oxidase-B inhibitor, is available in the EU, the US and in several other countries worldwide, including Canada and Israel.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	50-69
22439669-1	2012	Rasagiline (Azilect ), a selective, irreversible, monoamine oxidase-B inhibitor, is available in the EU, the US and in several other countries worldwide, including Canada and Israel.	rasagiline	12-19	monoamine oxidase B	Homo sapiens	50-69
20641293-2	2004	MAO-A preferentially oxidizes serotonin and noradrenaline, whereas MAO-B preferentially oxidizes phenethylamine.	phenethylamine	97-111	monoamine oxidase B	Homo sapiens	67-72
22287164-3	2012	With the aim of finding new MAO-B-selective inhibitors, we report the synthesis, in vitro evaluation, and docking simulation of a new series of 3-arylcoumarins variously substituted at the 8-position.	3-arylcoumarins	144-159	monoamine oxidase B	Homo sapiens	28-33
22287164-7	2012	Docking experiments were carried out with hMAO-B crystal structures, providing new information about the enzyme-inhibitor interaction and the potential therapeutic application of the new 8-substituted 3-arylcoumarins.	8-substituted 3-arylcoumarins	187-216	monoamine oxidase B	Homo sapiens	42-48
22100142-1	2012	It was recently reported that a series of C5-substituted phthalimides are remarkably potent reversible inhibitors of recombinant human monoamine oxidase (MAO) B.	Phthalimides	57-69	monoamine oxidase B	Homo sapiens	135-160
21895709-3	2012	METHODS: Platelet monoamine oxidase B (MAO-B) protein was quantitated in 2 populations of subjects who had histories of different levels of alcohol consumption.	Alcohols	140-147	monoamine oxidase B	Homo sapiens	18-37
21895709-3	2012	METHODS: Platelet monoamine oxidase B (MAO-B) protein was quantitated in 2 populations of subjects who had histories of different levels of alcohol consumption.	Alcohols	140-147	monoamine oxidase B	Homo sapiens	39-44
21895709-8	2012	In the treatment-seeking population, low MAO-B protein levels at admission are associated with heavy drinking prior to admission, and these protein levels increase over a period of abstinence from alcohol.	Alcohols	197-204	monoamine oxidase B	Homo sapiens	41-46
21895709-9	2012	CONCLUSIONS: The platelet MAO-B protein measurement is particularly effective for male alcohol consumers.	Alcohols	87-94	monoamine oxidase B	Homo sapiens	26-31
22309913-3	2012	The results document that the C6-substituted chromones are potent reversible MAO-B inhibitors with IC(50) values in the low nM range (2-76 nM).	Chromones	45-54	monoamine oxidase B	Homo sapiens	77-82
22309913-5	2012	It may therefore be concluded that C6-substituted chromones are highly potent MAO-B selective inhibitors and promising lead compounds for the development of therapy for neurodegenerative disorders such as Parkinson"s disease.	Chromones	50-59	monoamine oxidase B	Homo sapiens	78-83
22257893-0	2012	Design and synthesis of 8-substituted benzamido-phenylxanthine derivatives as MAO-B inhibitors.	8-substituted benzamido-phenylxanthine	24-62	monoamine oxidase B	Homo sapiens	78-83
22257893-2	2012	We designed and synthesized a class of 8-substituted benzamido-phenylxanthine derivatives as MAO-B inhibitors.	8-substituted benzamido-phenylxanthine	39-77	monoamine oxidase B	Homo sapiens	93-98
21858471-2	2012	The aim of this study was to evaluate the effect of some synthetic polyamines as inhibitors of two new potential targets, human semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 (SSAO/VAP-1) and monoamine oxidases B (MAO B), enzymes involved in various multi-factorial diseases such as Alzheimer"s disease.	Polyamines	67-77	monoamine oxidase B	Homo sapiens	211-231
21858471-2	2012	The aim of this study was to evaluate the effect of some synthetic polyamines as inhibitors of two new potential targets, human semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 (SSAO/VAP-1) and monoamine oxidases B (MAO B), enzymes involved in various multi-factorial diseases such as Alzheimer"s disease.	Polyamines	67-77	monoamine oxidase B	Homo sapiens	233-238
21858471-9	2012	These results indicate ELP 12 and Bis-Bza-Diado as new "skeletons" for the development of novel SSAO/VAP-1 and MAO B inhibitors.	bis-bza-diado	34-47	monoamine oxidase B	Homo sapiens	111-116
22225638-2	2012	In this study, we searched for novel MAO-B inhibitors using a scaffold hopping approach based on our experience with the thiazolidinedione (TZD) class of compounds as MAO-B inhibitors.	2,4-thiazolidinedione	121-138	monoamine oxidase B	Homo sapiens	37-42
22225638-2	2012	In this study, we searched for novel MAO-B inhibitors using a scaffold hopping approach based on our experience with the thiazolidinedione (TZD) class of compounds as MAO-B inhibitors.	2,4-thiazolidinedione	121-138	monoamine oxidase B	Homo sapiens	167-172
22225638-2	2012	In this study, we searched for novel MAO-B inhibitors using a scaffold hopping approach based on our experience with the thiazolidinedione (TZD) class of compounds as MAO-B inhibitors.	2,4-thiazolidinedione	140-143	monoamine oxidase B	Homo sapiens	37-42
22225638-2	2012	In this study, we searched for novel MAO-B inhibitors using a scaffold hopping approach based on our experience with the thiazolidinedione (TZD) class of compounds as MAO-B inhibitors.	2,4-thiazolidinedione	140-143	monoamine oxidase B	Homo sapiens	167-172
22225638-4	2012	We also found that derivatives of the natural product sulfuretin are potent MAO-A and MAO-B inhibitors.	sulfuretin	54-64	monoamine oxidase B	Homo sapiens	86-91
22100142-2	2012	Modeling studies suggested that the phthalimide ring forms numerous polar interactions with the polar region of the MAO-B substrate cavity while the C5 side chain extends to, and interacts via Van der Waals interactions with the hydrophobic regions of the enzyme entrance cavity.	phthalimide	36-47	monoamine oxidase B	Homo sapiens	116-121
22100142-5	2012	The phthalonitriles were found to be highly potent reversible MAO-B inhibitors with most analogs exhibiting IC(50) values in the low nM range.	1,2-benzenedicarbonitrile	4-19	monoamine oxidase B	Homo sapiens	62-67
22100142-7	2012	Modeling studies suggest that the high binding affinities of the phthalonitriles to MAO-B may depend, at least in part, on the formation of polar interactions between the nitrile functional groups and the enzyme substrate cavity.	1,2-benzenedicarbonitrile	65-80	monoamine oxidase B	Homo sapiens	84-89
22361882-7	2012	Finally, recombinant human monoamine oxidase (MAO)-B, but not MAO-A catalyzed oxidation of GGOH to GGal.	ggoh	91-95	monoamine oxidase B	Homo sapiens	27-52
22100142-7	2012	Modeling studies suggest that the high binding affinities of the phthalonitriles to MAO-B may depend, at least in part, on the formation of polar interactions between the nitrile functional groups and the enzyme substrate cavity.	Nitriles	72-79	monoamine oxidase B	Homo sapiens	84-89
22100142-8	2012	Examination of a homologs series of benzonitriles established that the phthalonitrile moiety is more optimal for MAO-B inhibition than the corresponding benzonitrile moiety, and that C3-substituted benzonitriles are better MAO-B inhibitors than C4-substituted benzonitriles.	benzonitrile	36-49	monoamine oxidase B	Homo sapiens	113-118
22361882-7	2012	Finally, recombinant human monoamine oxidase (MAO)-B, but not MAO-A catalyzed oxidation of GGOH to GGal.	ggal	99-103	monoamine oxidase B	Homo sapiens	27-52
22100142-8	2012	Examination of a homologs series of benzonitriles established that the phthalonitrile moiety is more optimal for MAO-B inhibition than the corresponding benzonitrile moiety, and that C3-substituted benzonitriles are better MAO-B inhibitors than C4-substituted benzonitriles.	1,2-benzenedicarbonitrile	71-85	monoamine oxidase B	Homo sapiens	113-118
22100142-8	2012	Examination of a homologs series of benzonitriles established that the phthalonitrile moiety is more optimal for MAO-B inhibition than the corresponding benzonitrile moiety, and that C3-substituted benzonitriles are better MAO-B inhibitors than C4-substituted benzonitriles.	1,2-benzenedicarbonitrile	71-85	monoamine oxidase B	Homo sapiens	223-228
22100142-8	2012	Examination of a homologs series of benzonitriles established that the phthalonitrile moiety is more optimal for MAO-B inhibition than the corresponding benzonitrile moiety, and that C3-substituted benzonitriles are better MAO-B inhibitors than C4-substituted benzonitriles.	benzonitrile	36-48	monoamine oxidase B	Homo sapiens	113-118
22100142-8	2012	Examination of a homologs series of benzonitriles established that the phthalonitrile moiety is more optimal for MAO-B inhibition than the corresponding benzonitrile moiety, and that C3-substituted benzonitriles are better MAO-B inhibitors than C4-substituted benzonitriles.	benzonitrile	198-211	monoamine oxidase B	Homo sapiens	223-228
22100142-8	2012	Examination of a homologs series of benzonitriles established that the phthalonitrile moiety is more optimal for MAO-B inhibition than the corresponding benzonitrile moiety, and that C3-substituted benzonitriles are better MAO-B inhibitors than C4-substituted benzonitriles.	benzonitrile	198-211	monoamine oxidase B	Homo sapiens	223-228
22100142-9	2012	Since elimination of the nitrile functional group yielded compounds with only moderate MAO-B inhibition potencies, it may be concluded that this functional group is privileged for MAO-B inhibition.	Nitriles	25-32	monoamine oxidase B	Homo sapiens	180-185
22222137-0	2012	Synthesis and biological assessment of novel 2-thiazolylhydrazones and computational analysis of their recognition by monoamine oxidase B.	2-thiazolylhydrazones	45-66	monoamine oxidase B	Homo sapiens	118-137
21819487-1	2012	BACKGROUND: Rasagiline, an MAO-B inhibitor, is indicated for the treatment of Parkinson"s disease (PD).	rasagiline	12-22	monoamine oxidase B	Homo sapiens	27-32
22197611-8	2012	Azure B also reversibly inhibits the MAO-B isozyme with an IC50 value of 968 nM.	Boron	6-7	monoamine oxidase B	Homo sapiens	37-42
23093014-3	2012	Herein, we aimed to test the possible influence of MAOB and COMT genetic polymorphisms on the effective daily dose of levodopa administered in the fifth year of treatment.	Levodopa	118-126	monoamine oxidase B	Homo sapiens	51-55
23093014-13	2012	The present data suggest that pharmacokinetic or pharmacodynamic factors other than the investigated genetic variants of the MAOB and COMT enzymes seem to determine the response to levodopa in the Iranian PD patients.	Levodopa	181-189	monoamine oxidase B	Homo sapiens	125-129
22124705-1	2012	The aim of this study was to determine the correlation between total nitrite/nitrate concentrations (NOx) and the kinetic parameters of monoamine oxidase enzymes (MAO-A and MAO-B) and semicarbazide-sensitive amine oxidase (SSAO) in human mesenteric arteries.	Nitrites	69-76	monoamine oxidase B	Homo sapiens	173-178
22137786-0	2012	Hydroxycoumarins as selective MAO-B inhibitors.	hydroxycoumarins	0-16	monoamine oxidase B	Homo sapiens	30-35
22137786-5	2012	Moreover, the presence of a chloro atom in the six position of the moiety (compound 7) improved the inhibitor activity as well as its selectivity against MAO-B compared with iproniazide, used as reference compound.	Sodium Hypochlorite	28-34	monoamine oxidase B	Homo sapiens	154-159
22137786-5	2012	Moreover, the presence of a chloro atom in the six position of the moiety (compound 7) improved the inhibitor activity as well as its selectivity against MAO-B compared with iproniazide, used as reference compound.	Iproniazid	174-185	monoamine oxidase B	Homo sapiens	154-159
22124705-5	2012	In the non-diabetic group, there was a positive correlation between NOx concentrations and MAO-B parameters: Km (r = 0.612, P = 0.034) and Vmax (r = 0.593, P = 0.042), and a negative correlation with the SSAO parameters: Km (r = -0.625, P = 0.029) and Vmax (r = -0.754, P = 0.005).	nicotine 1-N-oxide	68-71	monoamine oxidase B	Homo sapiens	91-96
23030609-0	2012	QSAR and molecular docking techniques for the discovery of potent monoamine oxidase B inhibitors: computer-aided generation of new rasagiline bioisosteres.	rasagiline	131-141	monoamine oxidase B	Homo sapiens	66-85
22382421-0	2012	Design, synthesis and inhibitory activities of 8-(substituted styrol-formamido)phenyl-xanthine derivatives on monoamine oxidase B.	8-(substituted styrol-formamido)phenyl-xanthine	47-94	monoamine oxidase B	Homo sapiens	110-129
22382421-3	2012	It was observed that compound 9b displayed significant MAO-B inhibition activity and selectivity, fluorine substitution plays a key role in the selectivity of MAO-B inhibition, and the styrol-formamido group at position-3" may enhance the activity and selectivity of 8-phenyl-xanthine analogues.	Fluorine	98-106	monoamine oxidase B	Homo sapiens	159-164
23030609-6	2012	We also give a brief overview about one of the most potent MAO-B inhibitor drugs: rasagiline.	rasagiline	82-92	monoamine oxidase B	Homo sapiens	59-64
23030609-8	2012	By realizing a careful inspection of the meaning of the variables in the QSAR-ANN model, new rasagiline bioisosteres were suggested as possible potent MAO-B inhibitors.	rasagiline	93-103	monoamine oxidase B	Homo sapiens	151-156
22055712-4	2011	The results document that the sulfanylcaffeine analogues are reversible competitive MAO-B inhibitors with potencies comparable to those of the oxycaffeines.	sulfanylcaffeine	30-46	monoamine oxidase B	Homo sapiens	84-89
23231391-5	2012	Despite all the recent research, there are only a few classes of drugs approved for the treatment of motor related symptoms of PD which primarily act on the dopaminergic neurons system: L-dopa, dopamine agonists, monoamine oxidase-B (MAO-B) and catechol-O-methyl transferase (COMT) inhibitors.	Dopamine	157-165	monoamine oxidase B	Homo sapiens	213-232
23231391-5	2012	Despite all the recent research, there are only a few classes of drugs approved for the treatment of motor related symptoms of PD which primarily act on the dopaminergic neurons system: L-dopa, dopamine agonists, monoamine oxidase-B (MAO-B) and catechol-O-methyl transferase (COMT) inhibitors.	Dopamine	157-165	monoamine oxidase B	Homo sapiens	234-239
23231391-9	2012	Different families of nitrogen and oxygen heterocycles, such as pyrazoles, hydrazinylthiazoles, xanthones, coumarins or chromones have also been extensively used as scaffolds in medicinal chemistry programs for searching novel MAO-B inhibitors.	Nitrogen	22-30	monoamine oxidase B	Homo sapiens	227-232
23231391-9	2012	Different families of nitrogen and oxygen heterocycles, such as pyrazoles, hydrazinylthiazoles, xanthones, coumarins or chromones have also been extensively used as scaffolds in medicinal chemistry programs for searching novel MAO-B inhibitors.	Oxygen	35-41	monoamine oxidase B	Homo sapiens	227-232
23231391-9	2012	Different families of nitrogen and oxygen heterocycles, such as pyrazoles, hydrazinylthiazoles, xanthones, coumarins or chromones have also been extensively used as scaffolds in medicinal chemistry programs for searching novel MAO-B inhibitors.	Pyrazoles	64-73	monoamine oxidase B	Homo sapiens	227-232
23231391-9	2012	Different families of nitrogen and oxygen heterocycles, such as pyrazoles, hydrazinylthiazoles, xanthones, coumarins or chromones have also been extensively used as scaffolds in medicinal chemistry programs for searching novel MAO-B inhibitors.	hydrazinylthiazoles	75-94	monoamine oxidase B	Homo sapiens	227-232
23231391-9	2012	Different families of nitrogen and oxygen heterocycles, such as pyrazoles, hydrazinylthiazoles, xanthones, coumarins or chromones have also been extensively used as scaffolds in medicinal chemistry programs for searching novel MAO-B inhibitors.	Xanthones	96-105	monoamine oxidase B	Homo sapiens	227-232
23231391-9	2012	Different families of nitrogen and oxygen heterocycles, such as pyrazoles, hydrazinylthiazoles, xanthones, coumarins or chromones have also been extensively used as scaffolds in medicinal chemistry programs for searching novel MAO-B inhibitors.	Coumarins	107-116	monoamine oxidase B	Homo sapiens	227-232
23231391-9	2012	Different families of nitrogen and oxygen heterocycles, such as pyrazoles, hydrazinylthiazoles, xanthones, coumarins or chromones have also been extensively used as scaffolds in medicinal chemistry programs for searching novel MAO-B inhibitors.	Chromones	120-129	monoamine oxidase B	Homo sapiens	227-232
23231391-10	2012	Nitrogen derivatives play a key role in this subject with several studies pointing out hydrazines, thiazoles or indoles as important scaffolds for the development of novel MAO-B inhibitors.	Nitrogen	0-8	monoamine oxidase B	Homo sapiens	172-177
23231391-10	2012	Nitrogen derivatives play a key role in this subject with several studies pointing out hydrazines, thiazoles or indoles as important scaffolds for the development of novel MAO-B inhibitors.	Hydrazines	87-97	monoamine oxidase B	Homo sapiens	172-177
23231391-10	2012	Nitrogen derivatives play a key role in this subject with several studies pointing out hydrazines, thiazoles or indoles as important scaffolds for the development of novel MAO-B inhibitors.	Thiazoles	99-108	monoamine oxidase B	Homo sapiens	172-177
23231391-10	2012	Nitrogen derivatives play a key role in this subject with several studies pointing out hydrazines, thiazoles or indoles as important scaffolds for the development of novel MAO-B inhibitors.	Indoles	112-119	monoamine oxidase B	Homo sapiens	172-177
23231391-11	2012	This review comprises an overview of the state of the art on the actual pharmacological therapy for PD followed by a specific focus on the discovery and development of nitrogen-based heterocyclic compounds analogues as promising MAO-B inhibitors.	Nitrogen	168-176	monoamine oxidase B	Homo sapiens	229-234
23231391-11	2012	This review comprises an overview of the state of the art on the actual pharmacological therapy for PD followed by a specific focus on the discovery and development of nitrogen-based heterocyclic compounds analogues as promising MAO-B inhibitors.	Heterocyclic Compounds	183-205	monoamine oxidase B	Homo sapiens	229-234
23231395-1	2012	In neurodegenerative disorders, including Parkinson"s and Alzheimer"s diseases, type B monoamine oxidase (MAO-B) has been proposed to play a primary role though generating reactive oxygen species in oxidation of monoamine substrates.	Oxygen	181-187	monoamine oxidase B	Homo sapiens	106-111
23231395-2	2012	MAO-B oxidizes MPTP into MPP+, and an MAO-B inhibitor, deprenyl, prevents the MPTP oxidation and also MPP+neutotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	15-19	monoamine oxidase B	Homo sapiens	0-5
23231395-2	2012	MAO-B oxidizes MPTP into MPP+, and an MAO-B inhibitor, deprenyl, prevents the MPTP oxidation and also MPP+neutotoxicity.	mangion-purified polysaccharide (Candida albicans)	25-29	monoamine oxidase B	Homo sapiens	0-5
23231395-2	2012	MAO-B oxidizes MPTP into MPP+, and an MAO-B inhibitor, deprenyl, prevents the MPTP oxidation and also MPP+neutotoxicity.	Selegiline	55-63	monoamine oxidase B	Homo sapiens	38-43
23231395-2	2012	MAO-B oxidizes MPTP into MPP+, and an MAO-B inhibitor, deprenyl, prevents the MPTP oxidation and also MPP+neutotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	78-82	monoamine oxidase B	Homo sapiens	38-43
23231395-4	2012	On the other hand, deprenyl and rasagiline, selective MAO-B inhibitors, have been proved to protect neuronal cells in cellular and animal models of neurodegeneration.	Selegiline	19-27	monoamine oxidase B	Homo sapiens	54-59
23231395-4	2012	On the other hand, deprenyl and rasagiline, selective MAO-B inhibitors, have been proved to protect neuronal cells in cellular and animal models of neurodegeneration.	rasagiline	32-42	monoamine oxidase B	Homo sapiens	54-59
23231397-4	2012	Differently substituted coumarins have been synthesized and evaluated as MAO-A and MAO-B inhibitors.	Coumarins	24-33	monoamine oxidase B	Homo sapiens	83-88
23231398-7	2012	For this reason, multiple scaffolds, such as substituted coumarins, indolylmethylamine or pyridazine derivatives were synthesized and assayed toward MAO-A and MAO-B inhibition.	pyridazine	90-100	monoamine oxidase B	Homo sapiens	159-164
22213821-3	2012	A multitracer PET investigation was conducted for patients with mild cognitive impairment (MCI), patients with mild AD, and healthy controls using (11)C-deuterium-L-deprenyl ((11)C-DED) to measure monoamine oxidase B located in astrocytes.	c-deuterium-l-deprenyl	151-173	monoamine oxidase B	Homo sapiens	197-216
22071524-5	2011	Herein we show that MAO-B was inhibited competitively by 1,4-NQ (K(i)=1.4 muM) whereas MAO-A was inhibited by non-competitive mechanism (K(i)=7.7 muM).	1,4-naphthoquinone	57-63	monoamine oxidase B	Homo sapiens	20-25
22071524-6	2011	Contrasting with TMN and 1,4-NQ, menadione exhibited a 60-fold selectivity for MAO-B (K(i)=0.4 muM) in comparison with MAO-A (K(i)=26 muM), which makes it as selective as rasagiline.	Vitamin K 3	33-42	monoamine oxidase B	Homo sapiens	79-84
22071524-8	2011	Additionally, docking studies suggest the phenyl side groups of Tyr407 and Tyr444 (for MAO-A) or Tyr398 and Tyr435 (for MAO-B) play an important role in the interaction of the enzyme with 1,4-NQ scaffold through forces of dispersion as verified for menadione, TMN and 1,4-NQ.	1,4-naphthoquinone	188-194	monoamine oxidase B	Homo sapiens	120-125
23231391-1	2012	Part II- discovery of MAO-B inhibitors based on nitrogen heterocycles and analogues.	Nitrogen	48-56	monoamine oxidase B	Homo sapiens	22-27
22572099-3	2012	METHODS: With the use of quantitative real-time polymerase chain reaction and ELISA the expression of genes connected to the dopamine pathway (PAH, PCD, TH, DDC, DBH, PNMT, GPX1, MAOA, MAOB, COMT, DRD1-DRD5, VMAT1 and VMAT2) was observed in vitiligo patients" and control subjects" skin and blood.	Dopamine	125-133	monoamine oxidase B	Homo sapiens	185-189
22572099-6	2012	We provide new data about changes of expression profile of the dopamine-synthesizing enzyme DDC, the dopamine-degrading enzymes MAOA and MAOB and the D1-like family dopamine receptors in vitiligo skin and blood sera.	Dopamine	101-109	monoamine oxidase B	Homo sapiens	137-141
22505887-3	2012	MAO-B was altered in male cerebellum by MeHg, PCB153, and their combination (35%, 45%, and 25% decrease, resp.).	2,4,5,2',4',5'-hexachlorobiphenyl	46-52	monoamine oxidase B	Homo sapiens	0-5
22071524-8	2011	Additionally, docking studies suggest the phenyl side groups of Tyr407 and Tyr444 (for MAO-A) or Tyr398 and Tyr435 (for MAO-B) play an important role in the interaction of the enzyme with 1,4-NQ scaffold through forces of dispersion as verified for menadione, TMN and 1,4-NQ.	Vitamin K 3	249-258	monoamine oxidase B	Homo sapiens	120-125
22071524-8	2011	Additionally, docking studies suggest the phenyl side groups of Tyr407 and Tyr444 (for MAO-A) or Tyr398 and Tyr435 (for MAO-B) play an important role in the interaction of the enzyme with 1,4-NQ scaffold through forces of dispersion as verified for menadione, TMN and 1,4-NQ.	1,4-naphthoquinone	268-274	monoamine oxidase B	Homo sapiens	120-125
22078410-2	2011	Eleven structurally similar tetrahydropyridine derivatives were synthesized and evaluated as inhibitors of MAO-A and MAO-B.	Pyrrolidines	28-46	monoamine oxidase B	Homo sapiens	117-122
22055712-4	2011	The results document that the sulfanylcaffeine analogues are reversible competitive MAO-B inhibitors with potencies comparable to those of the oxycaffeines.	oxycaffeines	143-155	monoamine oxidase B	Homo sapiens	84-89
22055712-5	2011	The most potent inhibitor, 8-{[(4-bromophenyl)methyl]sulfanyl}caffeine, exhibited an IC(50) value of 0.167 muM towards MAO-B.	CHEMBL1927670	27-70	monoamine oxidase B	Homo sapiens	119-124
22055712-6	2011	While the sulfanylcaffeine analogues also exhibit affinities for MAO-A, they display in general a high degree of MAO-B selectivity.	sulfanylcaffeine	10-26	monoamine oxidase B	Homo sapiens	113-118
22055712-9	2011	MAO-B selective sulfanylcaffeine derived inhibitors may act as lead compounds for the design of antiparkinsonian therapies.	sulfanylcaffeine	16-32	monoamine oxidase B	Homo sapiens	0-5
21978362-1	2011	The major structural difference between human monoamine oxidases A (MAO A) and B (MAO B) is that MAO A has a monopartite substrate cavity of ~550 A(3) volume and MAO B contains a dipartite cavity structure with volumes of ~290 A(3) (entrance cavity) and ~400 A(3) (substrate cavity).	dipartite	179-188	monoamine oxidase B	Homo sapiens	82-87
22133327-3	2011	Monoamine oxidase B (MAO-B) inhibitors are used in the symptomatic treatment of Parkinson"s disease as they increase synaptic dopamine by blocking its degradation.	Dopamine	126-134	monoamine oxidase B	Homo sapiens	0-19
22133327-3	2011	Monoamine oxidase B (MAO-B) inhibitors are used in the symptomatic treatment of Parkinson"s disease as they increase synaptic dopamine by blocking its degradation.	Dopamine	126-134	monoamine oxidase B	Homo sapiens	21-26
22133327-4	2011	Two MAO-B inhibitors, selegiline and rasagiline, are currently licensed in Europe and North America for the symptomatic improvement of early Parkinson"s disease and to reduce off-time in patients with more advanced Parkinson"s disease and motor fluctuations related to levodopa.	Selegiline	22-32	monoamine oxidase B	Homo sapiens	4-9
22133327-4	2011	Two MAO-B inhibitors, selegiline and rasagiline, are currently licensed in Europe and North America for the symptomatic improvement of early Parkinson"s disease and to reduce off-time in patients with more advanced Parkinson"s disease and motor fluctuations related to levodopa.	rasagiline	37-47	monoamine oxidase B	Homo sapiens	4-9
22133327-4	2011	Two MAO-B inhibitors, selegiline and rasagiline, are currently licensed in Europe and North America for the symptomatic improvement of early Parkinson"s disease and to reduce off-time in patients with more advanced Parkinson"s disease and motor fluctuations related to levodopa.	Levodopa	269-277	monoamine oxidase B	Homo sapiens	4-9
22133327-5	2011	A third MAO-B inhibitor (safinamide), which also combines additional non-dopaminergic properties of potential benefit to Parkinson"s disease, is currently under development in phase III clinical trials as adjuvant therapy to either a dopamine agonist or levodopa.	safinamide	25-35	monoamine oxidase B	Homo sapiens	8-13
22133327-5	2011	A third MAO-B inhibitor (safinamide), which also combines additional non-dopaminergic properties of potential benefit to Parkinson"s disease, is currently under development in phase III clinical trials as adjuvant therapy to either a dopamine agonist or levodopa.	Dopamine	73-81	monoamine oxidase B	Homo sapiens	8-13
22133327-5	2011	A third MAO-B inhibitor (safinamide), which also combines additional non-dopaminergic properties of potential benefit to Parkinson"s disease, is currently under development in phase III clinical trials as adjuvant therapy to either a dopamine agonist or levodopa.	Levodopa	254-262	monoamine oxidase B	Homo sapiens	8-13
22018876-1	2011	Previous studies on 5H-indeno[1,2-c]pyridazin-5-one derivatives as inhibitors of MAO-B revealed that it was possible to increase the MAO-B inhibitory potency of 5H-indeno[1,2-c]pyridazin-5-ones by substituting the central heterocycle in the 3-position or C-8 with lipophilic groups which occupy the substrate cavity or the entrance of the binding site, respectively.	5h-indeno[1,2-c]pyridazin-5-one	20-51	monoamine oxidase B	Homo sapiens	81-86
22018876-1	2011	Previous studies on 5H-indeno[1,2-c]pyridazin-5-one derivatives as inhibitors of MAO-B revealed that it was possible to increase the MAO-B inhibitory potency of 5H-indeno[1,2-c]pyridazin-5-ones by substituting the central heterocycle in the 3-position or C-8 with lipophilic groups which occupy the substrate cavity or the entrance of the binding site, respectively.	5h-indeno[1,2-c]pyridazin-5-one	20-51	monoamine oxidase B	Homo sapiens	133-138
22018876-1	2011	Previous studies on 5H-indeno[1,2-c]pyridazin-5-one derivatives as inhibitors of MAO-B revealed that it was possible to increase the MAO-B inhibitory potency of 5H-indeno[1,2-c]pyridazin-5-ones by substituting the central heterocycle in the 3-position or C-8 with lipophilic groups which occupy the substrate cavity or the entrance of the binding site, respectively.	5h-indeno[1,2-c]pyridazin-5-ones	161-193	monoamine oxidase B	Homo sapiens	81-86
22018876-1	2011	Previous studies on 5H-indeno[1,2-c]pyridazin-5-one derivatives as inhibitors of MAO-B revealed that it was possible to increase the MAO-B inhibitory potency of 5H-indeno[1,2-c]pyridazin-5-ones by substituting the central heterocycle in the 3-position or C-8 with lipophilic groups which occupy the substrate cavity or the entrance of the binding site, respectively.	5h-indeno[1,2-c]pyridazin-5-ones	161-193	monoamine oxidase B	Homo sapiens	133-138
22018876-1	2011	Previous studies on 5H-indeno[1,2-c]pyridazin-5-one derivatives as inhibitors of MAO-B revealed that it was possible to increase the MAO-B inhibitory potency of 5H-indeno[1,2-c]pyridazin-5-ones by substituting the central heterocycle in the 3-position or C-8 with lipophilic groups which occupy the substrate cavity or the entrance of the binding site, respectively.	1-octene	255-258	monoamine oxidase B	Homo sapiens	81-86
22018876-1	2011	Previous studies on 5H-indeno[1,2-c]pyridazin-5-one derivatives as inhibitors of MAO-B revealed that it was possible to increase the MAO-B inhibitory potency of 5H-indeno[1,2-c]pyridazin-5-ones by substituting the central heterocycle in the 3-position or C-8 with lipophilic groups which occupy the substrate cavity or the entrance of the binding site, respectively.	1-octene	255-258	monoamine oxidase B	Homo sapiens	133-138
22018876-7	2011	Molecular docking studies of 9a within MAO-B suggest that the 5H-indeno[1,2-c]pyridazin-5-one scaffold is well stabilized into the substrate cavity with the meta-chlorobenzyloxy side chain extending towards a rather hydrophobic pocket at the entrance cavity.	5h-indeno[1,2-c]pyridazin-5-one	62-93	monoamine oxidase B	Homo sapiens	39-44
21978362-1	2011	The major structural difference between human monoamine oxidases A (MAO A) and B (MAO B) is that MAO A has a monopartite substrate cavity of ~550 A(3) volume and MAO B contains a dipartite cavity structure with volumes of ~290 A(3) (entrance cavity) and ~400 A(3) (substrate cavity).	dipartite	179-188	monoamine oxidase B	Homo sapiens	162-167
21978362-4	2011	Structural data on the Ile199Ala MAO B mutant show no alterations in active site geometries compared with wild-type enzyme while the Ile199Ala-Tyr326Ala MAO B mutant exhibits alterations in residues 100-103 which are part of the loop gating the entrance to the active site.	ile199ala	133-142	monoamine oxidase B	Homo sapiens	153-158
21978362-9	2011	The Ile199Ala-Tyr326Ala double mutant exhibits inhibitor binding properties more similar to those of MAO A than to MAO B.	ile199ala	4-13	monoamine oxidase B	Homo sapiens	115-120
21953831-5	2011	Monoamine oxidase B (MAO-B) located in the outer mitochondrial membrane controls dopamine metabolism in early PD, and this is the likely location for the symptomatic action of rasagiline.	Dopamine	81-89	monoamine oxidase B	Homo sapiens	0-19
22093536-4	2011	Dopamine agonists, catechol-O-methyltransferase inhibitors and monoamine oxidase-B inhibitors are anti-parkinsonian (anti-PD) drugs that have been found to further improve the potency of l-dopa and prevent the onset of motor complications.	Levodopa	187-193	monoamine oxidase B	Homo sapiens	63-82
22039878-7	2011	In particular, safinamide, a MAO B selective inhibitor in clinical trials for Parkinson"s disease, is neuroprotective by blocking the voltage-dependent Na+ and Ca2+ channels and the Ca2+-mediated glutamate release processes.	safinamide	15-25	monoamine oxidase B	Homo sapiens	29-34
21850574-11	2011	Safinamide, which inhibits monoamine oxidase (MAO)-B, does not affect oral tyramine metabolism mediated mostly by the intestinal MAO-A.	safinamide	0-10	monoamine oxidase B	Homo sapiens	27-52
21953831-5	2011	Monoamine oxidase B (MAO-B) located in the outer mitochondrial membrane controls dopamine metabolism in early PD, and this is the likely location for the symptomatic action of rasagiline.	Dopamine	81-89	monoamine oxidase B	Homo sapiens	21-26
21953831-5	2011	Monoamine oxidase B (MAO-B) located in the outer mitochondrial membrane controls dopamine metabolism in early PD, and this is the likely location for the symptomatic action of rasagiline.	rasagiline	176-186	monoamine oxidase B	Homo sapiens	0-19
21953831-5	2011	Monoamine oxidase B (MAO-B) located in the outer mitochondrial membrane controls dopamine metabolism in early PD, and this is the likely location for the symptomatic action of rasagiline.	rasagiline	176-186	monoamine oxidase B	Homo sapiens	21-26
21953831-8	2011	Thus, the functional neuroprotective actions of rasagiline may not be dependent on MAO-B inhibition, but rather may involve actions of the propargylamine moiety and the aminoindan metabolite.	rasagiline	48-58	monoamine oxidase B	Homo sapiens	83-88
21923181-0	2011	Synthesis and study of a series of 3-arylcoumarins as potent and selective monoamine oxidase B inhibitors.	3-arylcoumarins	35-50	monoamine oxidase B	Homo sapiens	75-94
22045282-1	2011	OBJECTIVE: Rasagiline, a monoamine oxidase type B inhibitor, is indicated for both the initial treatment of Parkinson disease (PD) and as adjunctive (add-on) treatment for patients already taking dopaminergic therapy.	rasagiline	11-21	monoamine oxidase B	Homo sapiens	25-49
21923181-1	2011	New series of 6-substituted-3-arylcoumarins displaying several alkyl, hydroxyl, halogen, and alkoxy groups in the two benzene rings have been designed, synthesized, and evaluated in vitro as human monoamine oxidase A and B (hMAO-A and hMAO-B) inhibitors.	6-substituted-3-arylcoumarins	14-43	monoamine oxidase B	Homo sapiens	235-241
21923181-4	2011	Coumarin 7 is the most active compound of this series, being 64 times more active than selegiline and also showing the highest hMAO-B specificity.	coumarin 7	0-10	monoamine oxidase B	Homo sapiens	127-133
21923198-0	2011	Synthesis of three novel fluorine-18 labeled analogues of L-deprenyl for positron emission tomography (PET) studies of monoamine oxidase B (MAO-B).	Fluorine-18	25-36	monoamine oxidase B	Homo sapiens	119-138
21923198-0	2011	Synthesis of three novel fluorine-18 labeled analogues of L-deprenyl for positron emission tomography (PET) studies of monoamine oxidase B (MAO-B).	Fluorine-18	25-36	monoamine oxidase B	Homo sapiens	140-145
21923198-0	2011	Synthesis of three novel fluorine-18 labeled analogues of L-deprenyl for positron emission tomography (PET) studies of monoamine oxidase B (MAO-B).	Selegiline	58-68	monoamine oxidase B	Homo sapiens	119-138
21923198-0	2011	Synthesis of three novel fluorine-18 labeled analogues of L-deprenyl for positron emission tomography (PET) studies of monoamine oxidase B (MAO-B).	Selegiline	58-68	monoamine oxidase B	Homo sapiens	140-145
21923198-1	2011	The aim in this project was to synthesize and to study fluorine-18 labeled analogues of l-deprenyl which bind selectively to the enzyme monoamine oxidase B (MAO-B).	Fluorine-18	55-66	monoamine oxidase B	Homo sapiens	136-155
21923198-1	2011	The aim in this project was to synthesize and to study fluorine-18 labeled analogues of l-deprenyl which bind selectively to the enzyme monoamine oxidase B (MAO-B).	Fluorine-18	55-66	monoamine oxidase B	Homo sapiens	157-162
21923198-1	2011	The aim in this project was to synthesize and to study fluorine-18 labeled analogues of l-deprenyl which bind selectively to the enzyme monoamine oxidase B (MAO-B).	Selegiline	88-98	monoamine oxidase B	Homo sapiens	136-155
21923198-1	2011	The aim in this project was to synthesize and to study fluorine-18 labeled analogues of l-deprenyl which bind selectively to the enzyme monoamine oxidase B (MAO-B).	Selegiline	88-98	monoamine oxidase B	Homo sapiens	157-162
21923198-5	2011	In addition, the corresponding nonradioactive fluorine-19 compound (13) inhibited recombinant human MAO-B with an IC(50) of 170.5 +- 29 nM but did not inhibit recombinant human MAO-A (IC(50) &gt; 2000 nM), demonstrating its specificity.	Fluorine	46-54	monoamine oxidase B	Homo sapiens	100-105
22282722-0	2011	Molecular Insights into Human Monoamine Oxidase B Inhibition by the Glitazone Anti-Diabetes Drugs.	Thiazolidinediones	68-77	monoamine oxidase B	Homo sapiens	30-49
22282722-5	2011	Rosiglitazone (Avandia) and troglitazone, other members of the glitazone class, are less selective in that they are weaker inhibitors of both MAO A and MAO B These results suggest that pioglitazone may have utility as a "re-purposed" neuro-protectant drug in retarding the progression of disease in Parkinson"s patients.	Rosiglitazone	0-13	monoamine oxidase B	Homo sapiens	152-157
22282722-5	2011	Rosiglitazone (Avandia) and troglitazone, other members of the glitazone class, are less selective in that they are weaker inhibitors of both MAO A and MAO B These results suggest that pioglitazone may have utility as a "re-purposed" neuro-protectant drug in retarding the progression of disease in Parkinson"s patients.	Troglitazone	28-40	monoamine oxidase B	Homo sapiens	152-157
22282722-1	2011	The widely employed anti-diabetic drug pioglitazone (Actos) is shown to be a specific and reversible inhibitor of human monoamine oxidase B (MAO B).	Pioglitazone	39-51	monoamine oxidase B	Homo sapiens	120-139
22282722-5	2011	Rosiglitazone (Avandia) and troglitazone, other members of the glitazone class, are less selective in that they are weaker inhibitors of both MAO A and MAO B These results suggest that pioglitazone may have utility as a "re-purposed" neuro-protectant drug in retarding the progression of disease in Parkinson"s patients.	Thiazolidinediones	4-13	monoamine oxidase B	Homo sapiens	152-157
22282722-5	2011	Rosiglitazone (Avandia) and troglitazone, other members of the glitazone class, are less selective in that they are weaker inhibitors of both MAO A and MAO B These results suggest that pioglitazone may have utility as a "re-purposed" neuro-protectant drug in retarding the progression of disease in Parkinson"s patients.	Pioglitazone	185-197	monoamine oxidase B	Homo sapiens	152-157
22282722-1	2011	The widely employed anti-diabetic drug pioglitazone (Actos) is shown to be a specific and reversible inhibitor of human monoamine oxidase B (MAO B).	Pioglitazone	39-51	monoamine oxidase B	Homo sapiens	141-146
22087552-7	2011	Other therapies, including dopamine agonists and monoamine oxidase type-B (MAO-B) inhibitors, may limit the rate of dyskinesia relative to levodopa-based regimens.	Levodopa	139-147	monoamine oxidase B	Homo sapiens	75-80
22087552-8	2011	It appears that early treatment with the MAO-B inhibitor rasagiline (1 mg), as compared with late treatment, delays the onset of worsened UPDRS score, especially the nonmotor activities of daily living subscore.	rasagiline	57-67	monoamine oxidase B	Homo sapiens	41-46
21899930-5	2011	Among these were (2E)-N-(3-chlorophenyl)-3-(4-hydroxyphenyl)prop-2-enamide (7c) and (2E)-N-(3-bromophenyl)-3-(4-hydroxyphenyl)prop-2-enamide (7d) which inhibited MAO-B selectively and reversibly with IC(50) values of 0.032 muM and 0.026 muM, respectively.	(2e)-n-(3-chlorophenyl)-3-(4-hydroxyphenyl)prop-2-enamide	17-74	monoamine oxidase B	Homo sapiens	162-167
21899930-5	2011	Among these were (2E)-N-(3-chlorophenyl)-3-(4-hydroxyphenyl)prop-2-enamide (7c) and (2E)-N-(3-bromophenyl)-3-(4-hydroxyphenyl)prop-2-enamide (7d) which inhibited MAO-B selectively and reversibly with IC(50) values of 0.032 muM and 0.026 muM, respectively.	(2e)-n-(3-bromophenyl)-3-(4-hydroxyphenyl)prop-2-enamide	84-140	monoamine oxidase B	Homo sapiens	162-167
21899930-7	2011	This study concludes that N,3-diphenylprop-2-enamide is a suitable scaffold for the design of selective MAO-B inhibitors and structural modifications to enhance the binding affinities of the inhibitors for the MAO-B active site include substitution with halogens on the N-phenyl ring and substitution with hydroxyl and nitrile functional groups on the para and meta positions, respectively, of the C3 phenyl ring.	MLS002637516	26-52	monoamine oxidase B	Homo sapiens	104-109
21899930-7	2011	This study concludes that N,3-diphenylprop-2-enamide is a suitable scaffold for the design of selective MAO-B inhibitors and structural modifications to enhance the binding affinities of the inhibitors for the MAO-B active site include substitution with halogens on the N-phenyl ring and substitution with hydroxyl and nitrile functional groups on the para and meta positions, respectively, of the C3 phenyl ring.	MLS002637516	26-52	monoamine oxidase B	Homo sapiens	210-215
21899930-7	2011	This study concludes that N,3-diphenylprop-2-enamide is a suitable scaffold for the design of selective MAO-B inhibitors and structural modifications to enhance the binding affinities of the inhibitors for the MAO-B active site include substitution with halogens on the N-phenyl ring and substitution with hydroxyl and nitrile functional groups on the para and meta positions, respectively, of the C3 phenyl ring.	Hydroxyl Radical	306-314	monoamine oxidase B	Homo sapiens	104-109
21899930-7	2011	This study concludes that N,3-diphenylprop-2-enamide is a suitable scaffold for the design of selective MAO-B inhibitors and structural modifications to enhance the binding affinities of the inhibitors for the MAO-B active site include substitution with halogens on the N-phenyl ring and substitution with hydroxyl and nitrile functional groups on the para and meta positions, respectively, of the C3 phenyl ring.	Hydroxyl Radical	306-314	monoamine oxidase B	Homo sapiens	210-215
21899930-7	2011	This study concludes that N,3-diphenylprop-2-enamide is a suitable scaffold for the design of selective MAO-B inhibitors and structural modifications to enhance the binding affinities of the inhibitors for the MAO-B active site include substitution with halogens on the N-phenyl ring and substitution with hydroxyl and nitrile functional groups on the para and meta positions, respectively, of the C3 phenyl ring.	Nitriles	319-326	monoamine oxidase B	Homo sapiens	104-109
21899930-7	2011	This study concludes that N,3-diphenylprop-2-enamide is a suitable scaffold for the design of selective MAO-B inhibitors and structural modifications to enhance the binding affinities of the inhibitors for the MAO-B active site include substitution with halogens on the N-phenyl ring and substitution with hydroxyl and nitrile functional groups on the para and meta positions, respectively, of the C3 phenyl ring.	Nitriles	319-326	monoamine oxidase B	Homo sapiens	210-215
21899930-8	2011	Possible binding modes of these structures within the MAO-B active site are proposed with the emphasis on the interactions of the inhibitor halogens and the hydroxyl and nitrile functional groups with active site residues and water molecules.	Hydroxyl Radical	157-165	monoamine oxidase B	Homo sapiens	54-59
21899930-8	2011	Possible binding modes of these structures within the MAO-B active site are proposed with the emphasis on the interactions of the inhibitor halogens and the hydroxyl and nitrile functional groups with active site residues and water molecules.	Nitriles	170-177	monoamine oxidase B	Homo sapiens	54-59
21899930-8	2011	Possible binding modes of these structures within the MAO-B active site are proposed with the emphasis on the interactions of the inhibitor halogens and the hydroxyl and nitrile functional groups with active site residues and water molecules.	Water	226-231	monoamine oxidase B	Homo sapiens	54-59
21939547-2	2011	Due to marked advances in PD treatment during the last decades, physicians are nowadays fortunately equipped with a variety of substances that can effectively ameliorate emerging motor symptoms of the disease, among them levodopa, dopamine agonists and monoamine oxidase type B (MAO-B) inhibitors.	Levodopa	221-229	monoamine oxidase B	Homo sapiens	279-284
21939547-4	2011	DISCUSSION: In multiple studies, MAO-B inhibitors, such as selegiline and rasagiline, have shown to provide mild symptomatic effects, delay the need for levodopa, and to reduce the incidence of motor fluctuations.	Selegiline	59-69	monoamine oxidase B	Homo sapiens	33-38
21939547-4	2011	DISCUSSION: In multiple studies, MAO-B inhibitors, such as selegiline and rasagiline, have shown to provide mild symptomatic effects, delay the need for levodopa, and to reduce the incidence of motor fluctuations.	Levodopa	153-161	monoamine oxidase B	Homo sapiens	33-38
21777011-0	2011	3-Acetyl-2,5-diaryl-2,3-dihydro-1,3,4-oxadiazoles: a new scaffold for the selective inhibition of monoamine oxidase B.	3-acetyl-2,5-diaryl-2,3-dihydro-1,3,4-oxadiazoles	0-49	monoamine oxidase B	Homo sapiens	98-117
21777011-6	2011	We conclude that these 1,3,4-oxadiazoles derivatives are promising reversible and selective MAO-B inhibitors.	1,3,4-oxadiazole	23-40	monoamine oxidase B	Homo sapiens	92-97
21939547-4	2011	DISCUSSION: In multiple studies, MAO-B inhibitors, such as selegiline and rasagiline, have shown to provide mild symptomatic effects, delay the need for levodopa, and to reduce the incidence of motor fluctuations.	rasagiline	74-84	monoamine oxidase B	Homo sapiens	33-38
21786798-0	2011	Nitrogen kinetic isotope effects for the monoamine oxidase B-catalyzed oxidation of benzylamine and (1,1-(2)H2)benzylamine: nitrogen rehybridization and CH bond cleavage are not concerted.	Nitrogen	0-8	monoamine oxidase B	Homo sapiens	41-60
21858609-1	2011	Selegiline, the irreversible inhibitor of monoamine oxidase B (MAO-B), is currently used to treat Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	63-68
21858609-2	2011	However, the mechanism of action of selegiline is complex and cannot be explained solely by its MAO-B inhibitory action.	Selegiline	36-46	monoamine oxidase B	Homo sapiens	96-101
21858609-10	2011	The peak response was in a dose of selegiline significantly lower than required for MAO-B inhibition.	Selegiline	35-45	monoamine oxidase B	Homo sapiens	84-89
21858609-0	2011	Effects of selegiline, a monoamine oxidase B inhibitor, on differentiation of P19 embryonal carcinoma stem cells, into neuron-like cells.	Selegiline	11-21	monoamine oxidase B	Homo sapiens	25-44
21858609-1	2011	Selegiline, the irreversible inhibitor of monoamine oxidase B (MAO-B), is currently used to treat Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	42-61
21786798-0	2011	Nitrogen kinetic isotope effects for the monoamine oxidase B-catalyzed oxidation of benzylamine and (1,1-(2)H2)benzylamine: nitrogen rehybridization and CH bond cleavage are not concerted.	benzylamine	84-95	monoamine oxidase B	Homo sapiens	41-60
21786798-0	2011	Nitrogen kinetic isotope effects for the monoamine oxidase B-catalyzed oxidation of benzylamine and (1,1-(2)H2)benzylamine: nitrogen rehybridization and CH bond cleavage are not concerted.	(1,1-(2)h2)benzylamine	100-122	monoamine oxidase B	Homo sapiens	41-60
21786798-0	2011	Nitrogen kinetic isotope effects for the monoamine oxidase B-catalyzed oxidation of benzylamine and (1,1-(2)H2)benzylamine: nitrogen rehybridization and CH bond cleavage are not concerted.	Nitrogen	124-132	monoamine oxidase B	Homo sapiens	41-60
21786798-1	2011	Nitrogen kinetic isotope effects for the oxidation of benzylamine and (1,1-(2)H(2))benzylamine by recombinant human monoamine oxidase B show that cleavage of the CH bond is not concerted with rehybridization of the nitrogen atom.	Nitrogen	0-8	monoamine oxidase B	Homo sapiens	116-135
21786798-1	2011	Nitrogen kinetic isotope effects for the oxidation of benzylamine and (1,1-(2)H(2))benzylamine by recombinant human monoamine oxidase B show that cleavage of the CH bond is not concerted with rehybridization of the nitrogen atom.	benzylamine	54-65	monoamine oxidase B	Homo sapiens	116-135
21786798-1	2011	Nitrogen kinetic isotope effects for the oxidation of benzylamine and (1,1-(2)H(2))benzylamine by recombinant human monoamine oxidase B show that cleavage of the CH bond is not concerted with rehybridization of the nitrogen atom.	(1,1-(2)h(2))benzylamine	70-94	monoamine oxidase B	Homo sapiens	116-135
21786798-1	2011	Nitrogen kinetic isotope effects for the oxidation of benzylamine and (1,1-(2)H(2))benzylamine by recombinant human monoamine oxidase B show that cleavage of the CH bond is not concerted with rehybridization of the nitrogen atom.	Nitrogen	215-223	monoamine oxidase B	Homo sapiens	116-135
21500280-2	2011	Rasagiline is a selective monoamine oxidase type-B inhibitor that enhances central dopaminergic transmission.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	26-50
21778064-2	2011	In general, C5- and C6-substitution of isatin leads to enhanced binding affinity to both MAO isozymes compared to isatin and in most instances result in selective binding to the MAO-B isoform.	Isatin	39-45	monoamine oxidase B	Homo sapiens	178-183
21500280-13	2011	The monoamine oxidase type-B inhibitor rasagiline may exert beneficial effects on certain aspects of attention and executive functions in nondemented patients with Parkinson"s disease with cognitive impairment.	rasagiline	39-49	monoamine oxidase B	Homo sapiens	4-28
21697081-1	2011	Monoamine oxidases (MAO-A, MAO-B) metabolize biogenic amines and have been implicated in neuronal apoptosis.	Amines	54-60	monoamine oxidase B	Homo sapiens	27-32
21812497-12	2011	Of the three delayed-start design clinical trials, two have investigated early versus later start of rasagiline, a specific irreversible monoamine oxidase B inhibitor.	rasagiline	101-111	monoamine oxidase B	Homo sapiens	137-156
21621312-7	2011	For example, the most potent MAO-B inhibitor of the present series is 8-[2-(4-bromophenoxy)ethoxy]caffeine with an IC(50) value of 0.166 muM.	8-[2-(4-bromophenoxy)ethoxy]caffeine	70-106	monoamine oxidase B	Homo sapiens	29-34
21621312-8	2011	This study also reports possible binding orientations of selected oxy caffeines within the active site cavities of MAO-A and MAO-B.	oxy caffeines	66-79	monoamine oxidase B	Homo sapiens	125-130
20479760-7	2011	Hum Mol Genet 2008) and the monoamine degradation enzyme monoamine oxidase B were found in ASD and SCZ, respectively.	monoamine	28-37	monoamine oxidase B	Homo sapiens	57-76
21554916-7	2011	Oxidation of MPTP in mitochondria was performed by human MAO-B and the above active compounds were also inhibitors of this isozyme.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	13-17	monoamine oxidase B	Homo sapiens	57-62
21554916-8	2011	Norharman and 5-nitroindazole were competitive inhibitors of MAO-B whereas methylene blue inhibited MPTP oxidation (IC50 of 50 nM) under a mixed type and predominantly uncompetitive mechanism.	norharman	0-9	monoamine oxidase B	Homo sapiens	61-66
21554916-8	2011	Norharman and 5-nitroindazole were competitive inhibitors of MAO-B whereas methylene blue inhibited MPTP oxidation (IC50 of 50 nM) under a mixed type and predominantly uncompetitive mechanism.	5-nitroindazole	14-29	monoamine oxidase B	Homo sapiens	61-66
21554916-9	2011	Methylene blue, 5-nitroindazole, norharman, 9-methylnorharman and menadione inhibit MAO-B in mitochondria and afford protective effects, as suggested by a reduced conversion of MPTP to neurotoxic species.	Methylene Blue	0-14	monoamine oxidase B	Homo sapiens	84-89
21554916-9	2011	Methylene blue, 5-nitroindazole, norharman, 9-methylnorharman and menadione inhibit MAO-B in mitochondria and afford protective effects, as suggested by a reduced conversion of MPTP to neurotoxic species.	5-nitroindazole	16-31	monoamine oxidase B	Homo sapiens	84-89
21554916-9	2011	Methylene blue, 5-nitroindazole, norharman, 9-methylnorharman and menadione inhibit MAO-B in mitochondria and afford protective effects, as suggested by a reduced conversion of MPTP to neurotoxic species.	norharman	33-42	monoamine oxidase B	Homo sapiens	84-89
21554916-9	2011	Methylene blue, 5-nitroindazole, norharman, 9-methylnorharman and menadione inhibit MAO-B in mitochondria and afford protective effects, as suggested by a reduced conversion of MPTP to neurotoxic species.	9-methyl-beta-carboline	44-61	monoamine oxidase B	Homo sapiens	84-89
21554916-9	2011	Methylene blue, 5-nitroindazole, norharman, 9-methylnorharman and menadione inhibit MAO-B in mitochondria and afford protective effects, as suggested by a reduced conversion of MPTP to neurotoxic species.	Vitamin K 3	66-75	monoamine oxidase B	Homo sapiens	84-89
21554916-9	2011	Methylene blue, 5-nitroindazole, norharman, 9-methylnorharman and menadione inhibit MAO-B in mitochondria and afford protective effects, as suggested by a reduced conversion of MPTP to neurotoxic species.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	177-181	monoamine oxidase B	Homo sapiens	84-89
21453201-2	2011	Other dopaminergic agents, such as dopamine agonists, catechol-O-methyl transferase inhibitors and monoamine oxidase B enzyme inhibitors (MAO-B I) have also been developed to treat patients with PD.	Dopamine	6-14	monoamine oxidase B	Homo sapiens	99-118
21696156-2	2011	The SAR data indicate that chromone derivatives with substituents in position 3 of gamma-pyrone nucleus act preferably as MAO-B inhibitors, with IC(50) values in the nanomolar to micromolar range.	Chromones	27-35	monoamine oxidase B	Homo sapiens	122-127
21696156-2	2011	The SAR data indicate that chromone derivatives with substituents in position 3 of gamma-pyrone nucleus act preferably as MAO-B inhibitors, with IC(50) values in the nanomolar to micromolar range.	4H-PYRAN-4-ONE	83-95	monoamine oxidase B	Homo sapiens	122-127
21696156-3	2011	Almost all chromone 3-carboxamides display selectivity toward MAO-B.	Chromones	11-19	monoamine oxidase B	Homo sapiens	62-67
21696156-3	2011	Almost all chromone 3-carboxamides display selectivity toward MAO-B.	3-carboxamides	20-34	monoamine oxidase B	Homo sapiens	62-67
21696156-5	2011	Notably, chromone (19) exhibits an MAO-B IC(50) of 63 nM, greater than 1000-fold selectivity over MAO-A, and behaves as a quasi-reversible inhibitor.	Chromones	9-17	monoamine oxidase B	Homo sapiens	35-40
21684743-4	2011	The presence or absence of a carbonyl group between the coumarin and the phenyl substituent in 3 position remarks, respectively, the MAO-A or MAO-B inhibitory activity.	coumarin	56-64	monoamine oxidase B	Homo sapiens	142-147
21626552-2	2011	A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson"s disease.	Selegiline	61-71	monoamine oxidase B	Homo sapiens	30-49
21359973-1	2011	Monoamine oxidase (MAO) A and MAO B are a crucial pair of isoenzymes, which oxidatively deaminate monoamine neurotransmitters and dietary amines with a production of hydrogen peroxide.	monoamine	98-107	monoamine oxidase B	Homo sapiens	30-35
21359973-1	2011	Monoamine oxidase (MAO) A and MAO B are a crucial pair of isoenzymes, which oxidatively deaminate monoamine neurotransmitters and dietary amines with a production of hydrogen peroxide.	Amines	138-144	monoamine oxidase B	Homo sapiens	30-35
21359973-1	2011	Monoamine oxidase (MAO) A and MAO B are a crucial pair of isoenzymes, which oxidatively deaminate monoamine neurotransmitters and dietary amines with a production of hydrogen peroxide.	Hydrogen Peroxide	166-183	monoamine oxidase B	Homo sapiens	30-35
21354322-2	2011	zMAO oxidizes the neurotransmitter amines (serotonin, dopamine and tyramine) with k(cat) values that exceed those of hMAO A or of hMAO B.	zmao	0-4	monoamine oxidase B	Homo sapiens	130-136
21354322-2	2011	zMAO oxidizes the neurotransmitter amines (serotonin, dopamine and tyramine) with k(cat) values that exceed those of hMAO A or of hMAO B.	Amines	35-41	monoamine oxidase B	Homo sapiens	130-136
21354322-7	2011	zMAO differs from hMAO A or hMAO B in benzylamine analog binding correlations where an electronic effect (rho=+1.29+-0.31) is observed.	benzylamine	38-49	monoamine oxidase B	Homo sapiens	28-34
21626552-5	2011	Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes.	rasagiline	150-160	monoamine oxidase B	Homo sapiens	118-137
21405131-3	2011	In general, the (E)-3-benzylidenechroman-4-ones 1a-w showed activities in the nano- or micromolar range coupled with high selectivity against hMAO-B.	(e)-3-benzylidenechroman-4-ones	16-47	monoamine oxidase B	Homo sapiens	142-148
21424576-8	2011	Plasma vitamin B(12) concentration was increased by the HP diet and correlates inversely with platelet MaoB expression (r = -0.35; P &lt; 0.02).	Niacinamide	7-16	monoamine oxidase B	Homo sapiens	103-107
21405131-6	2011	(E)-3-(4-(Dimethylamino)benzylidene)chroman-4-one (1l) and (E)-5,7-dihydroxy-3-(4-hydroxybenzylidene)chroman-4-one (1h) were the most interesting compounds of the entire series of inhibitors, showing hMAO-B affinity better than the selective inhibitor selegiline.	CHEMBL452001	0-49	monoamine oxidase B	Homo sapiens	200-206
21405131-0	2011	Homoisoflavonoids: natural scaffolds with potent and selective monoamine oxidase-B inhibition properties.	homoisoflavonoids	0-17	monoamine oxidase B	Homo sapiens	63-82
21405131-6	2011	(E)-3-(4-(Dimethylamino)benzylidene)chroman-4-one (1l) and (E)-5,7-dihydroxy-3-(4-hydroxybenzylidene)chroman-4-one (1h) were the most interesting compounds of the entire series of inhibitors, showing hMAO-B affinity better than the selective inhibitor selegiline.	4'-Demethyleucomin	59-114	monoamine oxidase B	Homo sapiens	200-206
21341713-1	2011	TEMPO-substituted pargyline analogues differentially inhibit recombinant human monoamine oxidase A (MAO A) and B (MAO B) in intact yeast mitochondria, suggesting these membrane-bound enzymes are located on differing faces of the mitochondrial outer membrane [Upadhyay, A., and Edmondson, D. E. (2009) Biochemistry 48, 3928].	Pargyline	18-27	monoamine oxidase B	Homo sapiens	114-119
25205926-5	2011	Other pharmacological measures like catechol-O-methyltrasferase (COMT) inhibitors like entacopone, telcapone and monoamine oxidase B (MAO-B) inhibitors like selegiline and rasagiline are also useful, while L-dopa remains the gold standard in the treatment of PD.	Selegiline	157-167	monoamine oxidase B	Homo sapiens	134-139
25205926-5	2011	Other pharmacological measures like catechol-O-methyltrasferase (COMT) inhibitors like entacopone, telcapone and monoamine oxidase B (MAO-B) inhibitors like selegiline and rasagiline are also useful, while L-dopa remains the gold standard in the treatment of PD.	Levodopa	206-212	monoamine oxidase B	Homo sapiens	113-132
22110357-4	2011	For the treatment of akinesia and motor fluctuations selective irreversible MAO-B inhibitors selegiline and rasagiline are recommended.	Selegiline	93-103	monoamine oxidase B	Homo sapiens	76-81
21377879-0	2011	Development of selective and reversible pyrazoline based MAO-B inhibitors: virtual screening, synthesis and biological evaluation.	pyrazoline	40-50	monoamine oxidase B	Homo sapiens	57-62
21377879-3	2011	All the compounds were found selective, reversible and active in nM range (100 times more potent than selegeline) towards MAO-B.	selegeline	102-112	monoamine oxidase B	Homo sapiens	122-127
21316817-5	2011	According to our results, docking experiments could be an interesting approach to try to predict the activity of this class of coumarins against MAO-B receptors.	Coumarins	127-136	monoamine oxidase B	Homo sapiens	145-150
22110357-4	2011	For the treatment of akinesia and motor fluctuations selective irreversible MAO-B inhibitors selegiline and rasagiline are recommended.	rasagiline	108-118	monoamine oxidase B	Homo sapiens	76-81
21277784-7	2011	Additionally these model examinations provide evidence that oxidations of N-cyclopropyl derivatives of MPTP catalyzed by MAO-B may not be consistent with a pure SET pathway.	n-cyclopropyl derivatives	74-99	monoamine oxidase B	Homo sapiens	121-126
21360301-3	2011	Although Moussa Youdim succeeded in exploring the novel anti-Parkinsonian, selective MAO-B inhibitor drug, rasagiline (Azilect, Teva Pharmaceutical Co.), he did not stop searching for superior therapeutic approaches for neurodegenerative disorders.	rasagiline	107-117	monoamine oxidase B	Homo sapiens	85-90
21277784-7	2011	Additionally these model examinations provide evidence that oxidations of N-cyclopropyl derivatives of MPTP catalyzed by MAO-B may not be consistent with a pure SET pathway.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	103-107	monoamine oxidase B	Homo sapiens	121-126
21971007-2	2011	The MAO-B inhibitor rasagiline has neuroprotective effects in animal models, mediated partly by its antiapoptotic activity.	rasagiline	20-30	monoamine oxidase B	Homo sapiens	4-9
21175212-0	2011	Interactions of monoamine oxidases with the antiepileptic drug zonisamide: specificity of inhibition and structure of the human monoamine oxidase B complex.	Zonisamide	63-73	monoamine oxidase B	Homo sapiens	128-147
21423589-4	2011	This review focuses on rasagiline and selegiline, two medications that belong to a class of antiparkinsonian drugs called monoamine oxidase B (MAO-B) inhibitors.	rasagiline	23-33	monoamine oxidase B	Homo sapiens	122-141
21423589-4	2011	This review focuses on rasagiline and selegiline, two medications that belong to a class of antiparkinsonian drugs called monoamine oxidase B (MAO-B) inhibitors.	rasagiline	23-33	monoamine oxidase B	Homo sapiens	143-148
21423589-4	2011	This review focuses on rasagiline and selegiline, two medications that belong to a class of antiparkinsonian drugs called monoamine oxidase B (MAO-B) inhibitors.	Selegiline	38-48	monoamine oxidase B	Homo sapiens	122-141
21423589-4	2011	This review focuses on rasagiline and selegiline, two medications that belong to a class of antiparkinsonian drugs called monoamine oxidase B (MAO-B) inhibitors.	Selegiline	38-48	monoamine oxidase B	Homo sapiens	143-148
21194943-0	2011	Chromone 3-phenylcarboxamides as potent and selective MAO-B inhibitors.	chromone 3-phenylcarboxamides	0-29	monoamine oxidase B	Homo sapiens	54-59
21194943-6	2011	The chromone-3-carboxamides show high selectivity to hMAO-B, with compounds 9 and 12 displaying IC(50) values at nanomolar range.	chromone-3-carboxamides	4-27	monoamine oxidase B	Homo sapiens	53-59
21183355-11	2011	However, several compounds show a better inhibition on MAO-B compared to harmine.	Harmine	73-80	monoamine oxidase B	Homo sapiens	55-60
21224199-2	2011	The first monoamine oxidase (MAO-B) inhibitor for PD, selegiline (Eldepryl), was approved by the Food and Drug Administration (FDA) in 1996, and rasagiline (Azilect) received FDA approval in 2006.	Selegiline	54-64	monoamine oxidase B	Homo sapiens	29-34
21224199-2	2011	The first monoamine oxidase (MAO-B) inhibitor for PD, selegiline (Eldepryl), was approved by the Food and Drug Administration (FDA) in 1996, and rasagiline (Azilect) received FDA approval in 2006.	Selegiline	66-74	monoamine oxidase B	Homo sapiens	29-34
21224199-8	2011	It also says, "the selectivity of selegiline for MAO B may not be absolute, even at the recommended daily dose."	Selegiline	34-44	monoamine oxidase B	Homo sapiens	49-54
21971003-1	2011	Selegiline, the R-optical enantiomer of deprenyl (phenyl-isopropyl-methyl-propargylamine), was almost exclusively used MAO-B inhibitor during the past decades to treat Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	119-124
21971004-1	2011	In Parkinson"s disease, type B monoamine oxidase (MAO-B) is proposed to play an important role in the pathogenesis through production of reactive oxygen species and neurotoxins from protoxicants, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	Oxygen	146-152	monoamine oxidase B	Homo sapiens	50-55
21971004-1	2011	In Parkinson"s disease, type B monoamine oxidase (MAO-B) is proposed to play an important role in the pathogenesis through production of reactive oxygen species and neurotoxins from protoxicants, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	204-248	monoamine oxidase B	Homo sapiens	50-55
21971006-2	2011	Rasagiline (N-propargyl-1-(R)-aminoindan) is a novel, highly potent irreversible MAO-B inhibitor in the treatment of Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	81-86
21134756-2	2011	Both homologues are reported to exhibit selective binding to the MAO-B isoform with (E)-5-styrylisatin being the most potent inhibitor.	(E)-5-Styrylisatin	84-102	monoamine oxidase B	Homo sapiens	65-70
21134756-4	2011	With the exception of 5-phenylisatin, all of the analogues examined were selective MAO-B inhibitors.	5-Phenylisatin	22-36	monoamine oxidase B	Homo sapiens	83-88
21134756-5	2011	The C5-substituted isatins exhibited higher binding affinities to MAO-B than the corresponding C6-substituted homologues.	Isatin	19-26	monoamine oxidase B	Homo sapiens	66-71
21134756-6	2011	The most potent MAO-B inhibitor, 5-(4-phenylbutyl)isatin, exhibited an IC(50) value of 0.66nM, approximately 13-fold more potent than (E)-5-styrylisatin and 18,500-fold more potent than isatin.	5-(4-Phenylbutyl)Isatin	33-56	monoamine oxidase B	Homo sapiens	16-21
21134756-6	2011	The most potent MAO-B inhibitor, 5-(4-phenylbutyl)isatin, exhibited an IC(50) value of 0.66nM, approximately 13-fold more potent than (E)-5-styrylisatin and 18,500-fold more potent than isatin.	(E)-5-Styrylisatin	134-152	monoamine oxidase B	Homo sapiens	16-21
21134756-6	2011	The most potent MAO-B inhibitor, 5-(4-phenylbutyl)isatin, exhibited an IC(50) value of 0.66nM, approximately 13-fold more potent than (E)-5-styrylisatin and 18,500-fold more potent than isatin.	Isatin	50-56	monoamine oxidase B	Homo sapiens	16-21
21134756-8	2011	The results document that substitution at C5 with a variety of substituents is a general strategy for enhancing the MAO-B inhibition potency of isatin.	Isatin	144-150	monoamine oxidase B	Homo sapiens	116-121
21134756-9	2011	Possible binding orientations of selected isatin analogues within the active site cavities of MAO-A and MAO-B are proposed.	Isatin	42-48	monoamine oxidase B	Homo sapiens	104-109
22035027-6	2011	Although treatment for each patient should be individualized and based on their specific symptoms, severity, and lifestyle, in general MAO-B inhibitors may be used initially to treat mild symptoms, adding a dopamine agonist in younger patients or levodopa in older patients, as symptoms become more severe.	Dopamine	207-215	monoamine oxidase B	Homo sapiens	135-140
22035027-6	2011	Although treatment for each patient should be individualized and based on their specific symptoms, severity, and lifestyle, in general MAO-B inhibitors may be used initially to treat mild symptoms, adding a dopamine agonist in younger patients or levodopa in older patients, as symptoms become more severe.	Levodopa	247-255	monoamine oxidase B	Homo sapiens	135-140
22035029-10	2011	In patients treated with selective MAO-B inhibitors, the risk of serotonin toxicity (ST) due to a concomitant serotonergic agent (e.g., antidepressants, dextromethorphan, serotonergic analgesics) or hypertensive crisis due to dietary tyramine or sympathomimetic amines appears to be minimal and is based on isolated case reports and overgeneralizations from nonselective MAO inhibitor pharmacology.	Serotonin	65-74	monoamine oxidase B	Homo sapiens	35-40
21971010-0	2011	Novel MAO-B inhibitors: potential therapeutic use of the selective MAO-B inhibitor PF9601N in Parkinson"s disease.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	83-90	monoamine oxidase B	Homo sapiens	6-11
21971006-2	2011	Rasagiline (N-propargyl-1-(R)-aminoindan) is a novel, highly potent irreversible MAO-B inhibitor in the treatment of Parkinson"s disease (PD).	n-propargyl-1-(r)-aminoindan	12-40	monoamine oxidase B	Homo sapiens	81-86
21971010-0	2011	Novel MAO-B inhibitors: potential therapeutic use of the selective MAO-B inhibitor PF9601N in Parkinson"s disease.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	83-90	monoamine oxidase B	Homo sapiens	67-72
21971006-3	2011	It has been demonstrated to be neuroprotective in PD model systems by preventing the formation of reactive oxygen species derived from prevention of derived from oxidation of dopamine by MAO-B and via an antiapoptotic action, which appears to be independent of MAO-B inhibition and related to its embedded N-propargyl moiety.	Oxygen	107-113	monoamine oxidase B	Homo sapiens	187-192
21971006-3	2011	It has been demonstrated to be neuroprotective in PD model systems by preventing the formation of reactive oxygen species derived from prevention of derived from oxidation of dopamine by MAO-B and via an antiapoptotic action, which appears to be independent of MAO-B inhibition and related to its embedded N-propargyl moiety.	Dopamine	175-183	monoamine oxidase B	Homo sapiens	187-192
21971010-3	2011	Among them, PF9601N, [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine], showed high potency and selectivity as a MAO-BI (monoamine oxidase type B inhibitor) and also demonstrated remarkable neuroprotective properties in several in vivo and cellular models of PD.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	12-19	monoamine oxidase B	Homo sapiens	124-148
21971010-3	2011	Among them, PF9601N, [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine], showed high potency and selectivity as a MAO-BI (monoamine oxidase type B inhibitor) and also demonstrated remarkable neuroprotective properties in several in vivo and cellular models of PD.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	22-72	monoamine oxidase B	Homo sapiens	124-148
21971010-3	2011	Among them, PF9601N, [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine], showed high potency and selectivity as a MAO-BI (monoamine oxidase type B inhibitor) and also demonstrated remarkable neuroprotective properties in several in vivo and cellular models of PD.	mao-bi	116-122	monoamine oxidase B	Homo sapiens	124-148
21034404-1	2011	A number of studies have identified differential kavalactone activity against a variety of molecular targets, including P-glycoprotein (Pgp), platelet monoamine oxidase (MAO-B), transcription factor binding domains, pregnane X (PXR) and GABA receptors, and cytochrome P450 and cyclo-oxygenase (COX) enzymes.	kavalactone	49-60	monoamine oxidase B	Homo sapiens	170-175
20934874-0	2010	Synthesis and molecular modelling studies of prenylated pyrazolines as MAO-B inhibitors.	pyrazolines	56-67	monoamine oxidase B	Homo sapiens	71-76
21075154-0	2011	Activated MAO-B in the brain of Alzheimer patients, demonstrated by [11C]-L-deprenyl using whole hemisphere autoradiography.	[11c]-l-deprenyl	68-84	monoamine oxidase B	Homo sapiens	10-15
21075154-2	2011	As astrocyte activity and, consequently, the activity of the MAO-B enzyme, is up-regulated in neuroinflammatory processes, radiolabelled analogues of deprenyl may serve as an imaging biomarker in neuroinflammation and neurodegeneration, including Alzheimer"s disease.	Selegiline	150-158	monoamine oxidase B	Homo sapiens	61-66
21075154-3	2011	In the present study [(11)C]-L-deprenyl, the PET radioligand version of L-deprenyl or selegiline , a selective irreversible MAO-B inhibitor was used in whole hemisphere autoradiographic experiments in human brain sections in order to test the radioligand"s binding to the MAO-B enzyme in human brain tissue, with an eye on exploring the radioligand"s applicability as a molecular imaging biomarker in human PET studies, with special regard to diagnostic detection of reactive astrogliosis.	[(11)c]-l-deprenyl	21-39	monoamine oxidase B	Homo sapiens	124-129
21075154-3	2011	In the present study [(11)C]-L-deprenyl, the PET radioligand version of L-deprenyl or selegiline , a selective irreversible MAO-B inhibitor was used in whole hemisphere autoradiographic experiments in human brain sections in order to test the radioligand"s binding to the MAO-B enzyme in human brain tissue, with an eye on exploring the radioligand"s applicability as a molecular imaging biomarker in human PET studies, with special regard to diagnostic detection of reactive astrogliosis.	Selegiline	29-39	monoamine oxidase B	Homo sapiens	124-129
21075154-3	2011	In the present study [(11)C]-L-deprenyl, the PET radioligand version of L-deprenyl or selegiline , a selective irreversible MAO-B inhibitor was used in whole hemisphere autoradiographic experiments in human brain sections in order to test the radioligand"s binding to the MAO-B enzyme in human brain tissue, with an eye on exploring the radioligand"s applicability as a molecular imaging biomarker in human PET studies, with special regard to diagnostic detection of reactive astrogliosis.	Selegiline	29-39	monoamine oxidase B	Homo sapiens	272-277
21075154-3	2011	In the present study [(11)C]-L-deprenyl, the PET radioligand version of L-deprenyl or selegiline , a selective irreversible MAO-B inhibitor was used in whole hemisphere autoradiographic experiments in human brain sections in order to test the radioligand"s binding to the MAO-B enzyme in human brain tissue, with an eye on exploring the radioligand"s applicability as a molecular imaging biomarker in human PET studies, with special regard to diagnostic detection of reactive astrogliosis.	Selegiline	86-96	monoamine oxidase B	Homo sapiens	124-129
21075154-10	2011	Deprenyl itself as well as the MAO-B antagonist rasagiline did effectively block the binding of the radioligand, whereas the MAO-A antagonist pirlindole did not affect it.	rasagiline	48-58	monoamine oxidase B	Homo sapiens	31-36
21075154-11	2011	Compounds with high affinity for the PBR system did not block the radioligand binding either, providing evidence for the specificity of [(11)C]-L-deprenyl for the MAO-B enzyme.	Selegiline	142-154	monoamine oxidase B	Homo sapiens	163-168
21075154-12	2011	In conclusion, the present observations indicate that [(11)C]-L-deprenyl may be a promising and selective imaging biomarker of increased MAO-B activity in the human brain and can therefore serve as a prospective PET tracer targeting neuroinflammation and neurodegeneration.	[(11)c]-l-deprenyl	54-72	monoamine oxidase B	Homo sapiens	137-142
21947069-0	2011	[The role of the MAO-B inhibitor razagiline in the treatment of Parkinson"s disease].	razagiline	33-43	monoamine oxidase B	Homo sapiens	17-22
21947069-1	2011	The features of the new selective MAO-B inhibitor razagiline (azilect) are reviewed against the background of latest advances in the field of treatment of Parkinson"s disease (PD).	razagiline	50-60	monoamine oxidase B	Homo sapiens	34-39
21947069-1	2011	The features of the new selective MAO-B inhibitor razagiline (azilect) are reviewed against the background of latest advances in the field of treatment of Parkinson"s disease (PD).	rasagiline	62-69	monoamine oxidase B	Homo sapiens	34-39
20832472-0	2010	On the formation and nature of the imidazoline I2 binding site on human monoamine oxidase-B.	imidazoline i2	35-49	monoamine oxidase B	Homo sapiens	72-91
20832472-1	2010	An allosteric binding site with high affinity for imidazoline I(2) ligands has been proposed to exist on monoamine oxidase-B (MAO-B).	Imidazolines	50-61	monoamine oxidase B	Homo sapiens	105-124
20832472-1	2010	An allosteric binding site with high affinity for imidazoline I(2) ligands has been proposed to exist on monoamine oxidase-B (MAO-B).	Imidazolines	50-61	monoamine oxidase B	Homo sapiens	126-131
20832472-3	2010	We here confirm previous reports that inactivation of recombinant human MAO-B with tranylcypromine results in the formation of a high affinity I(2) site on the enzyme, measured as an increase in binding of [(3)H]2-BFI.	Tranylcypromine	83-98	monoamine oxidase B	Homo sapiens	72-77
20832472-4	2010	Incubation of MAO-B with 2-phenylethylamine, an endogenous trace amine and MAO-B substrate, resulted in a progressive loss of enzyme activity, increased enzyme mass, distinct spectral changes and, as was observed with tranylcypromine, a parallel increase in high affinity binding of [(3)H]2-BFI.	phenethylamine	25-43	monoamine oxidase B	Homo sapiens	14-19
20832472-4	2010	Incubation of MAO-B with 2-phenylethylamine, an endogenous trace amine and MAO-B substrate, resulted in a progressive loss of enzyme activity, increased enzyme mass, distinct spectral changes and, as was observed with tranylcypromine, a parallel increase in high affinity binding of [(3)H]2-BFI.	phenethylamine	25-43	monoamine oxidase B	Homo sapiens	75-80
20832472-4	2010	Incubation of MAO-B with 2-phenylethylamine, an endogenous trace amine and MAO-B substrate, resulted in a progressive loss of enzyme activity, increased enzyme mass, distinct spectral changes and, as was observed with tranylcypromine, a parallel increase in high affinity binding of [(3)H]2-BFI.	Amines	38-43	monoamine oxidase B	Homo sapiens	14-19
20832472-4	2010	Incubation of MAO-B with 2-phenylethylamine, an endogenous trace amine and MAO-B substrate, resulted in a progressive loss of enzyme activity, increased enzyme mass, distinct spectral changes and, as was observed with tranylcypromine, a parallel increase in high affinity binding of [(3)H]2-BFI.	Amines	38-43	monoamine oxidase B	Homo sapiens	75-80
20832472-4	2010	Incubation of MAO-B with 2-phenylethylamine, an endogenous trace amine and MAO-B substrate, resulted in a progressive loss of enzyme activity, increased enzyme mass, distinct spectral changes and, as was observed with tranylcypromine, a parallel increase in high affinity binding of [(3)H]2-BFI.	Tranylcypromine	218-233	monoamine oxidase B	Homo sapiens	14-19
20832472-4	2010	Incubation of MAO-B with 2-phenylethylamine, an endogenous trace amine and MAO-B substrate, resulted in a progressive loss of enzyme activity, increased enzyme mass, distinct spectral changes and, as was observed with tranylcypromine, a parallel increase in high affinity binding of [(3)H]2-BFI.	2-(2-benzofuranyl)-2-imidazoline	289-294	monoamine oxidase B	Homo sapiens	14-19
20832472-5	2010	Kinetic studies of the mechanism by which 2-BFI inhibits MAO-B activity suggested binding of 2-BFI, at micromolar concentrations, to a site distinct from the active site on at least two forms of the pure enzyme, probably corresponding to oxidised and reduced enzyme states.	2-(2-benzofuranyl)-2-imidazoline	42-47	monoamine oxidase B	Homo sapiens	57-62
20832472-5	2010	Kinetic studies of the mechanism by which 2-BFI inhibits MAO-B activity suggested binding of 2-BFI, at micromolar concentrations, to a site distinct from the active site on at least two forms of the pure enzyme, probably corresponding to oxidised and reduced enzyme states.	2-(2-benzofuranyl)-2-imidazoline	93-98	monoamine oxidase B	Homo sapiens	57-62
20832472-6	2010	Studies with mutant enzymes revealed a pattern of changes consistent with binding of 2-BFI to the substrate entrance channel of human MAO-B.	2-(2-benzofuranyl)-2-imidazoline	85-90	monoamine oxidase B	Homo sapiens	134-139
20832472-8	2010	High affinity I(2) sites may form in vivo due to inactivation of a portion of MAO-B during amine oxidation, while the low affinity I(2) site on active enzyme is a target for novel MAO-B inhibitor drugs.	Amines	91-96	monoamine oxidase B	Homo sapiens	78-83
20832472-8	2010	High affinity I(2) sites may form in vivo due to inactivation of a portion of MAO-B during amine oxidation, while the low affinity I(2) site on active enzyme is a target for novel MAO-B inhibitor drugs.	Amines	91-96	monoamine oxidase B	Homo sapiens	180-185
20855894-1	2010	Crystallographic and biochemical studies have been employed to identify the binding site and mechanism for potentiation of imidazoline binding in human monoamine oxidase B (MAO B).	Imidazolines	123-134	monoamine oxidase B	Homo sapiens	152-171
20855894-1	2010	Crystallographic and biochemical studies have been employed to identify the binding site and mechanism for potentiation of imidazoline binding in human monoamine oxidase B (MAO B).	Imidazolines	123-134	monoamine oxidase B	Homo sapiens	173-178
20855894-2	2010	2-(2-Benzofuranyl)-2-imidazoline (2-BFI) inhibits recombinant human MAO B with a K(i) of 8.3 +- 0.6 muM, whereas tranylcypromine-inhibited MAO B binds 2-BFI with a K(d) of 9 +- 2 nM, representing an increase in binding energy Delta(DeltaG) of -3.9 kcal/mol.	2-(2-benzofuranyl)-2-imidazoline	0-32	monoamine oxidase B	Homo sapiens	68-73
20855894-2	2010	2-(2-Benzofuranyl)-2-imidazoline (2-BFI) inhibits recombinant human MAO B with a K(i) of 8.3 +- 0.6 muM, whereas tranylcypromine-inhibited MAO B binds 2-BFI with a K(d) of 9 +- 2 nM, representing an increase in binding energy Delta(DeltaG) of -3.9 kcal/mol.	2-(2-benzofuranyl)-2-imidazoline	34-39	monoamine oxidase B	Homo sapiens	68-73
20855894-2	2010	2-(2-Benzofuranyl)-2-imidazoline (2-BFI) inhibits recombinant human MAO B with a K(i) of 8.3 +- 0.6 muM, whereas tranylcypromine-inhibited MAO B binds 2-BFI with a K(d) of 9 +- 2 nM, representing an increase in binding energy Delta(DeltaG) of -3.9 kcal/mol.	2-(2-benzofuranyl)-2-imidazoline	34-39	monoamine oxidase B	Homo sapiens	139-144
20855894-5	2010	Data with the I199A mutant of human MAO B and failure to observe a similar binding potentiation with rat MAO B, where Ile(316) is replaced with a Val residue, support an allosteric mechanism where the increased binding affinity of 2-BFI results from a cooperative increase in H-bond strength through formation of a more hydrophobic milieu.	2-(2-benzofuranyl)-2-imidazoline	231-236	monoamine oxidase B	Homo sapiens	36-41
20445015-0	2010	Clinical pharmacology tyramine challenge study to determine the selectivity of the monoamine oxidase type B (MAO-B) inhibitor rasagiline.	Tyramine	22-30	monoamine oxidase B	Homo sapiens	83-107
20445015-0	2010	Clinical pharmacology tyramine challenge study to determine the selectivity of the monoamine oxidase type B (MAO-B) inhibitor rasagiline.	rasagiline	126-136	monoamine oxidase B	Homo sapiens	83-107
20445015-0	2010	Clinical pharmacology tyramine challenge study to determine the selectivity of the monoamine oxidase type B (MAO-B) inhibitor rasagiline.	rasagiline	126-136	monoamine oxidase B	Homo sapiens	109-114
20445015-1	2010	Rasagiline is a selective, monoamine oxidase (MAO)-B inhibitor indicated for treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	27-52
20445015-9	2010	Results demonstrate that rasagiline selectively inhibits MAO-B and is not associated with increased tyramine sensitivity at the indicated dose (1 mg/d).	rasagiline	25-35	monoamine oxidase B	Homo sapiens	57-62
20725780-2	2010	The R-enantiomer of deprenyl (selegiline) is a selective and irreversible inhibitor of the B-isoform of monoamine oxidase (MAO-B) enzyme.	Selegiline	20-28	monoamine oxidase B	Homo sapiens	123-128
20725780-2	2010	The R-enantiomer of deprenyl (selegiline) is a selective and irreversible inhibitor of the B-isoform of monoamine oxidase (MAO-B) enzyme.	Selegiline	30-40	monoamine oxidase B	Homo sapiens	123-128
20725780-4	2010	By inhibiting MAO-B enzyme, R-deprenyl decreases the formation of hydrogen peroxide, alleviating the oxidative stress also reduced by increased expression of antioxidant enzymes (superoxide dismutases and catalase) reported during chronic treatment.	r-deprenyl	28-38	monoamine oxidase B	Homo sapiens	14-19
20725780-4	2010	By inhibiting MAO-B enzyme, R-deprenyl decreases the formation of hydrogen peroxide, alleviating the oxidative stress also reduced by increased expression of antioxidant enzymes (superoxide dismutases and catalase) reported during chronic treatment.	Hydrogen Peroxide	66-83	monoamine oxidase B	Homo sapiens	14-19
20725780-6	2010	R-Deprenyl elicits neuroprotective and neuronal rescue activities in concentrations too low to inhibit MAO-B.	r-deprenyl	0-10	monoamine oxidase B	Homo sapiens	103-108
20934874-2	2010	Structure-activity relationships and molecular modelling showed that some substitutions, such as benzyloxy or chlorine atom, improve the best interaction with active site of hMAO-B.	Chlorine	110-118	monoamine oxidase B	Homo sapiens	174-180
20679667-5	2010	Affected males in this family showed an inherited hemizygous deletion restricted to NDP and two immediately telomeric genes, monoamine oxidase-B (MAO-B) and monoamine oxidase-A (MAO-A), which encode closely related enzymes that metabolize biogenic amines including serotonin, dopamine, and norepinephrine.	Amines	248-254	monoamine oxidase B	Homo sapiens	125-144
21103012-5	2010	Cellular treatment with the synthetic glucocorticoid, dexamethasone (a cellular stressor), has been reported to markedly increase both MAO A and MAO B catalytic activities, as well as apoptosis.	Dexamethasone	54-67	monoamine oxidase B	Homo sapiens	145-150
20839183-4	2010	The versatility of this new nitrogen protecting group is illustrated with a new synthesis of Selegiline, a monoamine oxidase-B inhibitor marketed for the treatment of Parkinson"s disease.	Nitrogen	28-36	monoamine oxidase B	Homo sapiens	107-126
20839183-4	2010	The versatility of this new nitrogen protecting group is illustrated with a new synthesis of Selegiline, a monoamine oxidase-B inhibitor marketed for the treatment of Parkinson"s disease.	Selegiline	93-103	monoamine oxidase B	Homo sapiens	107-126
20843688-3	2010	Docking study was carried out to demonstrate the binding mode between a9 and MAO-A/B, and the result reveals that a9 localized in the "aromatic cage" and oriented to establish pi-pi stacking interactions with Tyr407, Tyr444 and FAD in MAO-A rather than in MAO-B.	Flavin-Adenine Dinucleotide	228-231	monoamine oxidase B	Homo sapiens	256-261
20679667-5	2010	Affected males in this family showed an inherited hemizygous deletion restricted to NDP and two immediately telomeric genes, monoamine oxidase-B (MAO-B) and monoamine oxidase-A (MAO-A), which encode closely related enzymes that metabolize biogenic amines including serotonin, dopamine, and norepinephrine.	Amines	248-254	monoamine oxidase B	Homo sapiens	146-151
20679667-5	2010	Affected males in this family showed an inherited hemizygous deletion restricted to NDP and two immediately telomeric genes, monoamine oxidase-B (MAO-B) and monoamine oxidase-A (MAO-A), which encode closely related enzymes that metabolize biogenic amines including serotonin, dopamine, and norepinephrine.	Serotonin	265-274	monoamine oxidase B	Homo sapiens	125-144
20679667-5	2010	Affected males in this family showed an inherited hemizygous deletion restricted to NDP and two immediately telomeric genes, monoamine oxidase-B (MAO-B) and monoamine oxidase-A (MAO-A), which encode closely related enzymes that metabolize biogenic amines including serotonin, dopamine, and norepinephrine.	Serotonin	265-274	monoamine oxidase B	Homo sapiens	146-151
20679667-5	2010	Affected males in this family showed an inherited hemizygous deletion restricted to NDP and two immediately telomeric genes, monoamine oxidase-B (MAO-B) and monoamine oxidase-A (MAO-A), which encode closely related enzymes that metabolize biogenic amines including serotonin, dopamine, and norepinephrine.	Dopamine	276-284	monoamine oxidase B	Homo sapiens	125-144
20679667-5	2010	Affected males in this family showed an inherited hemizygous deletion restricted to NDP and two immediately telomeric genes, monoamine oxidase-B (MAO-B) and monoamine oxidase-A (MAO-A), which encode closely related enzymes that metabolize biogenic amines including serotonin, dopamine, and norepinephrine.	Dopamine	276-284	monoamine oxidase B	Homo sapiens	146-151
20679667-5	2010	Affected males in this family showed an inherited hemizygous deletion restricted to NDP and two immediately telomeric genes, monoamine oxidase-B (MAO-B) and monoamine oxidase-A (MAO-A), which encode closely related enzymes that metabolize biogenic amines including serotonin, dopamine, and norepinephrine.	Norepinephrine	290-304	monoamine oxidase B	Homo sapiens	125-144
20679667-5	2010	Affected males in this family showed an inherited hemizygous deletion restricted to NDP and two immediately telomeric genes, monoamine oxidase-B (MAO-B) and monoamine oxidase-A (MAO-A), which encode closely related enzymes that metabolize biogenic amines including serotonin, dopamine, and norepinephrine.	Norepinephrine	290-304	monoamine oxidase B	Homo sapiens	146-151
20624440-1	2010	Rasagiline is a propargylamine and irreversible monoamine oxidase (MAO) B inhibitor used for the treatment of Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	48-73
20674099-4	2010	The most potent MAO-B inhibitor, 3,4-dichloro-N-(2-methyl-1H-indol-5-yl)benzamide, exhibited a K(i) value of 0.03 microM and was 99 fold more selective for the B isoform.	CHEMBL1254552	33-81	monoamine oxidase B	Homo sapiens	16-21
20979033-4	2010	DEVELOPMENT: Rasagiline is a monoamine oxidase-B inhibitor whose dopaminergic stimulation has proved to be effective in monotherapy or in combined therapy for improving the motor symptoms in patients with PD in the initial and advanced phases.	rasagiline	13-23	monoamine oxidase B	Homo sapiens	29-48
20600573-0	2010	Rasagiline: a novel anti-Parkinsonian monoamine oxidase-B inhibitor with neuroprotective activity.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	38-57
20600573-1	2010	Rasagiline (N-propargyl-1-(R)-aminoindan) is a novel, highly potent irreversible monoamine oxidase (MAO)-B inhibitor, anti-Parkinsonian drug.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	81-106
20600573-1	2010	Rasagiline (N-propargyl-1-(R)-aminoindan) is a novel, highly potent irreversible monoamine oxidase (MAO)-B inhibitor, anti-Parkinsonian drug.	n-propargyl-1-(r)-aminoindan	12-40	monoamine oxidase B	Homo sapiens	81-106
20600573-3	2010	Its S-isomer, TVP1022 is thousand times less potent as an MAO-B inhibitor.	rasagiline	14-21	monoamine oxidase B	Homo sapiens	58-63
20600573-4	2010	However, both compounds have similar molecular mechanisms of neuroprotection in neuronal cell cultures and animal neurodegenerative models, indicating that the neuroprotective effect of rasagiline does not depend on inhibition of MAO-B, but rather is associated with the N-propargyl moiety, which promotes mitochondrial viability and stabilizes permeability transition by regulating Bcl-2 family proteins.	rasagiline	186-196	monoamine oxidase B	Homo sapiens	230-235
20485326-1	2010	Monoamine oxidases (MAO-A and MAO-B) have a key role in the degradation of amine neurotransmitters, such as dopamine, norepinephrine and serotonin.	Amines	4-9	monoamine oxidase B	Homo sapiens	30-35
20485326-1	2010	Monoamine oxidases (MAO-A and MAO-B) have a key role in the degradation of amine neurotransmitters, such as dopamine, norepinephrine and serotonin.	Dopamine	108-116	monoamine oxidase B	Homo sapiens	30-35
20485326-1	2010	Monoamine oxidases (MAO-A and MAO-B) have a key role in the degradation of amine neurotransmitters, such as dopamine, norepinephrine and serotonin.	Norepinephrine	118-132	monoamine oxidase B	Homo sapiens	30-35
20485326-1	2010	Monoamine oxidases (MAO-A and MAO-B) have a key role in the degradation of amine neurotransmitters, such as dopamine, norepinephrine and serotonin.	Serotonin	137-146	monoamine oxidase B	Homo sapiens	30-35
20674099-5	2010	We conclude that these indole and benzofuran derivatives are promising reversible MAO-B inhibitors with a possible role in the treatment of neurodegenerative diseases such as Parkinson"s disease (PD).	indole	23-29	monoamine oxidase B	Homo sapiens	82-87
20674099-5	2010	We conclude that these indole and benzofuran derivatives are promising reversible MAO-B inhibitors with a possible role in the treatment of neurodegenerative diseases such as Parkinson"s disease (PD).	benzofuran	34-44	monoamine oxidase B	Homo sapiens	82-87
20073575-7	2010	As shown by enzyme assays using [14C]serotonin or [14C]beta-phenylethylamine as selective MAO-A or MAO-B substrates, MAO-A is largely predominant in MSCs.	phenethylamine	55-76	monoamine oxidase B	Homo sapiens	99-104
20659799-0	2010	New halogenated 3-phenylcoumarins as potent and selective MAO-B inhibitors.	3-phenylcoumarins	16-33	monoamine oxidase B	Homo sapiens	58-63
20650633-3	2010	Docking studies were initiated to investigate pioglitazone"s interactions within the substrate cavity of MAO-B.	Pioglitazone	46-58	monoamine oxidase B	Homo sapiens	105-110
20715818-0	2010	Synthesis, stereochemical separation, and biological evaluation of selective inhibitors of human MAO-B: 1-(4-arylthiazol-2-yl)-2-(3-methylcyclohexylidene)hydrazines.	1-(4-arylthiazol-2-yl)-2-(3-methylcyclohexylidene)hydrazines	104-164	monoamine oxidase B	Homo sapiens	97-102
20650633-4	2010	Modeling studies indicated that the thiazolidinedione (TZD) moiety was a likely candidate for its specificity to MAO-B.	2,4-thiazolidinedione	36-53	monoamine oxidase B	Homo sapiens	113-118
20659799-4	2010	Compounds 4 (IC(50)=11.05 nM), 5 (IC(50)=3.23 nM) and 6 (IC(50)=7.12 nM) show higher activity than selegiline (IC(50)=19.60 nM) and higher MAO-B selectivity, with more than 9050-fold, 30,960-fold and 14,045-fold inhibition levels, with respect to the MAO-A isoform.	Selegiline	99-109	monoamine oxidase B	Homo sapiens	139-144
20650633-4	2010	Modeling studies indicated that the thiazolidinedione (TZD) moiety was a likely candidate for its specificity to MAO-B.	2,4-thiazolidinedione	55-58	monoamine oxidase B	Homo sapiens	113-118
20236308-1	2010	BACKGROUND: The MAO-B inhibitor rasagiline is indicated for the treatment of idiopathic Parkinson"s disease (PD), and its use is supported by evidence from large-scale, controlled clinical studies.	rasagiline	32-42	monoamine oxidase B	Homo sapiens	16-21
20650633-6	2010	Our search identified eight novel compounds containing the TZD-moiety that allowed for a limited study to identify structural requirements for binding to MAO-B.	2,4-thiazolidinedione	59-62	monoamine oxidase B	Homo sapiens	154-159
20505872-3	2010	In this paper, we report a direct continuous fluorescence turn-on assay for MAO-B and its inhibitor-screening with the ensemble of silole 1, heptylamine and HSO(3)(-), which are either easily accessible or commercially available.	Heptylamine	141-152	monoamine oxidase B	Homo sapiens	76-81
20644207-3	2010	This study examined reported changes in smoking beliefs during an 8-week smoking cessation trial, which evaluated the safety and efficacy of the monoamine oxidase B inhibitor selegiline hydrochloride versus placebo.	Selegiline	175-199	monoamine oxidase B	Homo sapiens	145-164
20568732-3	2010	In this study, we designed and synthesized several candidate compounds to inhibit LSD1, based on the structures of LSD1 and monoamine oxidase B (MAO-B), in complex with an antidepressant tranylcypromine (2-PCPA) derivative.	Tranylcypromine	187-202	monoamine oxidase B	Homo sapiens	124-143
20568732-3	2010	In this study, we designed and synthesized several candidate compounds to inhibit LSD1, based on the structures of LSD1 and monoamine oxidase B (MAO-B), in complex with an antidepressant tranylcypromine (2-PCPA) derivative.	Tranylcypromine	187-202	monoamine oxidase B	Homo sapiens	145-150
20568732-3	2010	In this study, we designed and synthesized several candidate compounds to inhibit LSD1, based on the structures of LSD1 and monoamine oxidase B (MAO-B), in complex with an antidepressant tranylcypromine (2-PCPA) derivative.	2-phenylcyclopropan-1-amine	204-210	monoamine oxidase B	Homo sapiens	124-143
20568732-3	2010	In this study, we designed and synthesized several candidate compounds to inhibit LSD1, based on the structures of LSD1 and monoamine oxidase B (MAO-B), in complex with an antidepressant tranylcypromine (2-PCPA) derivative.	2-phenylcyclopropan-1-amine	204-210	monoamine oxidase B	Homo sapiens	145-150
20615716-3	2010	The most active and selective derivative (20), bearing a pyridine moiety on the CN, displayed IC(50)=3.81+/-0.12 nM and selectivity ratio=119 toward hMAO-B.	pyridine	57-65	monoamine oxidase B	Homo sapiens	149-155
20579890-0	2010	Synthesis, semipreparative HPLC separation, biological evaluation, and 3D-QSAR of hydrazothiazole derivatives as human monoamine oxidase B inhibitors.	hydrazothiazole	82-97	monoamine oxidase B	Homo sapiens	119-138
20579890-2	2010	Most of the synthesized compounds proved to be potent and selective inhibitors of hMAO-B isoform in the micromolar or nanomolar range, thus demonstrating that hydrazothiazole could be considered a good pharmacophore to design new hMAO-B inhibitors.	hydrazothiazole	159-174	monoamine oxidase B	Homo sapiens	82-88
20579890-2	2010	Most of the synthesized compounds proved to be potent and selective inhibitors of hMAO-B isoform in the micromolar or nanomolar range, thus demonstrating that hydrazothiazole could be considered a good pharmacophore to design new hMAO-B inhibitors.	hydrazothiazole	159-174	monoamine oxidase B	Homo sapiens	230-236
23908775-0	2010	Pharmacology of Rasagiline, a New MAO-B Inhibitor Drug for the Treatment of Parkinson"s Disease with Neuroprotective Potential.	rasagiline	16-26	monoamine oxidase B	Homo sapiens	34-39
23908775-1	2010	Rasagiline (Azilect) is a highly selective and potent propargylamine inhibitor of monoamine oxidase (MAO) type B.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	82-112
23908775-1	2010	Rasagiline (Azilect) is a highly selective and potent propargylamine inhibitor of monoamine oxidase (MAO) type B.	rasagiline	12-19	monoamine oxidase B	Homo sapiens	82-112
23908775-1	2010	Rasagiline (Azilect) is a highly selective and potent propargylamine inhibitor of monoamine oxidase (MAO) type B.	propargylamine	54-68	monoamine oxidase B	Homo sapiens	82-112
23908775-6	2010	Although the exact distribution of MAO isoforms in different neurons and tissues is not known, dopamine behaves largely as a MAO-A substrate in vivo, but following loss of dopaminergic axonal varicosities from the striatum, metabolism by glial MAO-B becomes increasingly important.	Dopamine	95-103	monoamine oxidase B	Homo sapiens	244-249
20707760-5	2010	WHAT THE READER WILL GAIN: The reader will gain an understanding of safinamide and its mechanisms of action, including reversible MAOB inhibition and reduced dopamine reuptake with antiglutamatergic effects, and how it may potentially provide improvement of PD motor symptoms with an antidyskinetic effect through its effect on glutamate release.	safinamide	68-78	monoamine oxidase B	Homo sapiens	130-134
21171285-1	2010	Monoamine oxidase B (MAOB) was purified from porcine liver by solubilization with lysis buffer containing 1% Triton X-100, precipitation with 20%-50% ammonium sulfate, isolation with hydrophobic chromatography and anion exchange chromatography.	Octoxynol	109-121	monoamine oxidase B	Homo sapiens	0-19
21171285-1	2010	Monoamine oxidase B (MAOB) was purified from porcine liver by solubilization with lysis buffer containing 1% Triton X-100, precipitation with 20%-50% ammonium sulfate, isolation with hydrophobic chromatography and anion exchange chromatography.	Octoxynol	109-121	monoamine oxidase B	Homo sapiens	21-25
21171285-1	2010	Monoamine oxidase B (MAOB) was purified from porcine liver by solubilization with lysis buffer containing 1% Triton X-100, precipitation with 20%-50% ammonium sulfate, isolation with hydrophobic chromatography and anion exchange chromatography.	Ammonium Sulfate	150-166	monoamine oxidase B	Homo sapiens	0-19
21171285-1	2010	Monoamine oxidase B (MAOB) was purified from porcine liver by solubilization with lysis buffer containing 1% Triton X-100, precipitation with 20%-50% ammonium sulfate, isolation with hydrophobic chromatography and anion exchange chromatography.	Ammonium Sulfate	150-166	monoamine oxidase B	Homo sapiens	21-25
21171285-6	2010	As MAOB is a membrane enzyme, a key step to the successful purification was the use of Phenyl-Sepharose CL-4B with phenyl density of 75.7 micromol/mL.	Phenyl-Sepharose CL-4B	87-109	monoamine oxidase B	Homo sapiens	3-7
20642018-2	2004	MAO-A preferentially oxidizes serotonin and noradrenaline, whereas MAO-B preferentially oxidizes phenethylamine.	phenethylamine	97-111	monoamine oxidase B	Homo sapiens	67-72
20642018-6	2004	In the human brain, MAO-B predominates and is present in both glial cells and neurons (6), most abundantly in serotonin and histamine neurons (7).	Serotonin	110-119	monoamine oxidase B	Homo sapiens	20-25
20642018-6	2004	In the human brain, MAO-B predominates and is present in both glial cells and neurons (6), most abundantly in serotonin and histamine neurons (7).	Histamine	124-133	monoamine oxidase B	Homo sapiens	20-25
20642018-7	2004	(S)-5-Methoxymethyl-3-[6-(4,4,4-trifluorobutoxy)-benzo[d]isoxazol-3-yl]-oxazolidin-2-one (SL25.1188) is a selective and reversible MAO-B inhibitor (8).	SL25.1188	0-88	monoamine oxidase B	Homo sapiens	131-136
20642018-8	2004	For measurements of MAO-B activity, (S)-5-methoxymethyl-3-[6-(4,4,4-trifluorobutoxy)benzo[d]isoxazol-3-yl]-oxazolidin-2-[(11)C]one ([(11)C]SL25.1188) has been prepared for use in positron emission tomography (PET) studies.	(s)-5-methoxymethyl-3-[6-(4,4,4-trifluorobutoxy)benzo[d]isoxazol-3-yl]-oxazolidin-2-[(11)c]one	36-130	monoamine oxidase B	Homo sapiens	20-25
20505872-5	2010	Moreover, the ensemble of silole 1, heptylamine, HSO(3)(-) and MAO-B can be employed to screen the inhibitors of MAO-B.	Heptylamine	36-47	monoamine oxidase B	Homo sapiens	113-118
20505872-5	2010	Moreover, the ensemble of silole 1, heptylamine, HSO(3)(-) and MAO-B can be employed to screen the inhibitors of MAO-B.	hydrogen sulfite	49-55	monoamine oxidase B	Homo sapiens	113-118
20368333-12	2010	The H(2)S-releasing L-DOPA hybrid molecules also inhibited MAO B activity.	Levodopa	20-26	monoamine oxidase B	Homo sapiens	59-64
20685489-0	2010	Application of an immobilised amylose-based chiral stationary phase to the development of new monoamine oxidase B inhibitors.	Amylose	30-37	monoamine oxidase B	Homo sapiens	94-113
20685489-1	2010	A direct HPLC enantioseparation of three new chiral oxadiazoline derivatives endowed with potential MAO-B inhibitory activity was accomplished on the immobilised Chiralpak IA chiral stationary phase.	oxadiazoline	52-64	monoamine oxidase B	Homo sapiens	100-105
20022592-10	2010	Knockdown expression of GAPDH or treatment with MAO B inhibitors selegiline (deprenyl) and rasagiline (Azilect) can block this cascade.	Selegiline	65-75	monoamine oxidase B	Homo sapiens	48-53
20522954-0	2010	Two polymorphs of safinamide, a selective and reversible inhibitor of monoamine oxidase B.	safinamide	18-28	monoamine oxidase B	Homo sapiens	70-89
20522954-1	2010	Two polymorphs of safinamide {systematic name: (2S)-2-[4-(3-fluorobenzyloxy)benzylamino]propionamide}, C(17)H(19)FN(2)O(2), a potent selective and reversible monoamine oxidase B (MAO-B) inhibitor, are described.	safinamide	18-28	monoamine oxidase B	Homo sapiens	158-177
20522954-1	2010	Two polymorphs of safinamide {systematic name: (2S)-2-[4-(3-fluorobenzyloxy)benzylamino]propionamide}, C(17)H(19)FN(2)O(2), a potent selective and reversible monoamine oxidase B (MAO-B) inhibitor, are described.	safinamide	18-28	monoamine oxidase B	Homo sapiens	179-184
20522954-1	2010	Two polymorphs of safinamide {systematic name: (2S)-2-[4-(3-fluorobenzyloxy)benzylamino]propionamide}, C(17)H(19)FN(2)O(2), a potent selective and reversible monoamine oxidase B (MAO-B) inhibitor, are described.	safinamide	47-100	monoamine oxidase B	Homo sapiens	158-177
20522954-1	2010	Two polymorphs of safinamide {systematic name: (2S)-2-[4-(3-fluorobenzyloxy)benzylamino]propionamide}, C(17)H(19)FN(2)O(2), a potent selective and reversible monoamine oxidase B (MAO-B) inhibitor, are described.	safinamide	47-100	monoamine oxidase B	Homo sapiens	179-184
20517484-3	2010	Rasagiline is a novel, potent, and irreversible monoamine oxidase type B (MAO-B) inhibitor which has been approved for treatment of PD.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	48-72
20517484-3	2010	Rasagiline is a novel, potent, and irreversible monoamine oxidase type B (MAO-B) inhibitor which has been approved for treatment of PD.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	74-79
20517484-4	2010	Rasagiline inhibits MAO-B more potently than selegiline and has the advantage of once-daily dosing.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	20-25
20022592-0	2010	A novel role for glyceraldehyde-3-phosphate dehydrogenase and monoamine oxidase B cascade in ethanol-induced cellular damage.	Ethanol	93-100	monoamine oxidase B	Homo sapiens	62-81
20022592-3	2010	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and monoamine oxidase B (MAO B) reportedly play a role in cellular dysfunction under stressful conditions and might contribute to EtOH-induced cell damage.	Ethanol	179-183	monoamine oxidase B	Homo sapiens	53-72
20022592-3	2010	Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and monoamine oxidase B (MAO B) reportedly play a role in cellular dysfunction under stressful conditions and might contribute to EtOH-induced cell damage.	Ethanol	179-183	monoamine oxidase B	Homo sapiens	74-79
20022592-4	2010	METHODS: Expression of GAPDH and MAO B protein was studied in human glioblastoma and neuroblastoma cell lines exposed to physiological concentrations of EtOH.	Ethanol	153-157	monoamine oxidase B	Homo sapiens	33-38
20022592-8	2010	RESULTS: Ethanol significantly increases levels of GAPDH, especially nuclear GAPDH, and MAO B in neuronal cells as well as in human and rat brains.	Ethanol	9-16	monoamine oxidase B	Homo sapiens	88-93
20022592-9	2010	Nuclear GAPDH interacts with the transcriptional activator, transforming growth factor-beta-inducible early gene 2 (TIEG2), and augments TIEG2-mediated MAO B transactivation, which results in cell damage in neuronal cells exposed to EtOH.	Ethanol	233-237	monoamine oxidase B	Homo sapiens	152-157
20022592-10	2010	Knockdown expression of GAPDH or treatment with MAO B inhibitors selegiline (deprenyl) and rasagiline (Azilect) can block this cascade.	Selegiline	77-85	monoamine oxidase B	Homo sapiens	48-53
20022592-10	2010	Knockdown expression of GAPDH or treatment with MAO B inhibitors selegiline (deprenyl) and rasagiline (Azilect) can block this cascade.	rasagiline	91-101	monoamine oxidase B	Homo sapiens	48-53
20022592-10	2010	Knockdown expression of GAPDH or treatment with MAO B inhibitors selegiline (deprenyl) and rasagiline (Azilect) can block this cascade.	rasagiline	103-110	monoamine oxidase B	Homo sapiens	48-53
20022592-11	2010	CONCLUSIONS: Ethanol-elicited nuclear GAPDH augments TIEG2-mediated MAO B, which might play a role in brain damage in subjects with alcoholism.	Ethanol	13-20	monoamine oxidase B	Homo sapiens	68-73
20195940-3	2010	The MAO B inhibitors selegiline and rasagiline are in use for PD pharmacotherapy; for rasagiline, studies have demonstrated a possible disease-modifying effect.	Selegiline	21-31	monoamine oxidase B	Homo sapiens	4-9
19939587-1	2010	AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers.	sel, l-deprenyl	147-162	monoamine oxidase B	Homo sapiens	104-109
19939587-1	2010	AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers.	Selegiline	164-172	monoamine oxidase B	Homo sapiens	83-102
19939587-1	2010	AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers.	Selegiline	164-172	monoamine oxidase B	Homo sapiens	104-109
20002521-1	2010	The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities.	rasagiline	28-38	monoamine oxidase B	Homo sapiens	176-195
20002521-1	2010	The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities.	rasagiline	28-38	monoamine oxidase B	Homo sapiens	197-202
20002521-1	2010	The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities.	n-propargyl-1-(r)-aminoindan	40-68	monoamine oxidase B	Homo sapiens	176-195
20002521-1	2010	The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities.	n-propargyl-1-(r)-aminoindan	40-68	monoamine oxidase B	Homo sapiens	197-202
20002521-1	2010	The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities.	benzylamine	105-116	monoamine oxidase B	Homo sapiens	176-195
20002521-1	2010	The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities.	benzylamine	105-116	monoamine oxidase B	Homo sapiens	197-202
20002521-1	2010	The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities.	indan	121-127	monoamine oxidase B	Homo sapiens	176-195
20002521-1	2010	The anti-parkinsonian drug, rasagiline [N-propargyl-1-(R)-aminoindan; Azilect(R)], is a secondary cyclic benzylamine and indane derivative, which provides irreversible, potent monoamine oxidase-B (MAO-B) inhibition and possesses neuroprotective and neurorestorative activities.	indan	121-127	monoamine oxidase B	Homo sapiens	197-202
20002521-3	2010	Rasagiline is primarily metabolized by hepatic cytochrome P-450 to form its major metabolite, 1-(R)-aminoindan, a non-amphetamine, weak reversible MAO-B inhibitor compound.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	147-152
20382016-1	2010	Chromone carboxylic acids were evaluated as human monoamine oxidase A and B (hMAO-A and hMAO-B) inhibitors.	chromone-2-carboxylic acid	0-25	monoamine oxidase B	Homo sapiens	88-94
20382016-2	2010	The biological data indicated that only chromone-3-carboxylic acid is a potent hMAO-B inhibitor, with a high degree of selectivity for hMAO-B compared to hMAO-A.	Chromone-3-carboxylic acid	40-66	monoamine oxidase B	Homo sapiens	79-85
20382016-2	2010	The biological data indicated that only chromone-3-carboxylic acid is a potent hMAO-B inhibitor, with a high degree of selectivity for hMAO-B compared to hMAO-A.	Chromone-3-carboxylic acid	40-66	monoamine oxidase B	Homo sapiens	135-141
20297870-5	2010	Monoamine oxidase type B (MAO-B) inhibitors provide mild symptomatic benefit, delay the need for levodopa, are very well tolerated, and may provide long-term disease-modifying effects.	Levodopa	97-105	monoamine oxidase B	Homo sapiens	0-24
20297870-5	2010	Monoamine oxidase type B (MAO-B) inhibitors provide mild symptomatic benefit, delay the need for levodopa, are very well tolerated, and may provide long-term disease-modifying effects.	Levodopa	97-105	monoamine oxidase B	Homo sapiens	26-31
20297872-3	2010	Early treatment of PD with other agents such as dopamine agonists and monoamine oxidase type B inhibitors can provide symptomatic benefit and delay initiation of levodopa therapy.	Levodopa	162-170	monoamine oxidase B	Homo sapiens	70-94
19939587-1	2010	AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers.	Selegiline	121-145	monoamine oxidase B	Homo sapiens	83-102
19939587-1	2010	AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers.	Selegiline	121-145	monoamine oxidase B	Homo sapiens	104-109
19939587-1	2010	AIM: The primary aim of this study was to determine the safety and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers.	sel, l-deprenyl	147-162	monoamine oxidase B	Homo sapiens	83-102
20002521-3	2010	Rasagiline is primarily metabolized by hepatic cytochrome P-450 to form its major metabolite, 1-(R)-aminoindan, a non-amphetamine, weak reversible MAO-B inhibitor compound.	(R)-(-)-1-Aminoindan	94-110	monoamine oxidase B	Homo sapiens	147-152
20195940-3	2010	The MAO B inhibitors selegiline and rasagiline are in use for PD pharmacotherapy; for rasagiline, studies have demonstrated a possible disease-modifying effect.	rasagiline	36-46	monoamine oxidase B	Homo sapiens	4-9
20022119-2	2010	The enzyme monoamine oxidase, type B (MAO-B), is expressed in platelets, and metabolizes endogenous amines.	Amines	100-106	monoamine oxidase B	Homo sapiens	11-36
20022119-2	2010	The enzyme monoamine oxidase, type B (MAO-B), is expressed in platelets, and metabolizes endogenous amines.	Amines	100-106	monoamine oxidase B	Homo sapiens	38-43
20093036-5	2010	A quantitative structure-activity relationship (QSAR) study indicated that the MAO-B inhibition potencies of the 8-benzyloxycaffeinyl analogues are dependent on the Hansch lipophilicity (pi) and Hammett electronic (sigma) constants of the substituents at C-3 of the benzyloxy ring.	8-benzyloxycaffeinyl	113-133	monoamine oxidase B	Homo sapiens	79-84
20117937-4	2010	2-Bromo-N-(2-morpholinoethyl)nicotinamide (3) was the most potent MAO-B inhibitor with the IC(50) value of 0.32 microM, but it was not selective.	2-Bromo-N-(2-morpholinoethyl)nicotinamide	0-41	monoamine oxidase B	Homo sapiens	66-71
20123154-0	2010	2-Arylthiomorpholine derivatives as potent and selective monoamine oxidase B inhibitors.	2-arylthiomorpholine	0-20	monoamine oxidase B	Homo sapiens	57-76
20123154-3	2010	Making the phenylethylamine scaffold rigid by fixing the amine chain in an extended six-membered ring conformation increased MAO-B (but not MAO-A) inhibitory activity relative to the more flexible alpha-methylated derivative.	Phenethylamines	11-27	monoamine oxidase B	Homo sapiens	125-130
20123154-3	2010	Making the phenylethylamine scaffold rigid by fixing the amine chain in an extended six-membered ring conformation increased MAO-B (but not MAO-A) inhibitory activity relative to the more flexible alpha-methylated derivative.	Amines	22-27	monoamine oxidase B	Homo sapiens	125-130
21389939-1	2010	An open observational 3-month study of efficacy and safety of selective MAO B inhibitor rasagiline (AZIlect) in advanced Parkinson"s disease (PD) patients with motor fluctuations on the long-term levodopa therapy (the "AZIMUT" study) has been conducted.	rasagiline	88-98	monoamine oxidase B	Homo sapiens	72-77
19006188-0	2010	Selective MAO-B inhibitors have low potential for the tyramine effect.	Tyramine	54-62	monoamine oxidase B	Homo sapiens	10-15
20045650-0	2010	A new series of flavones, thioflavones, and flavanones as selective monoamine oxidase-B inhibitors.	Flavones	16-24	monoamine oxidase B	Homo sapiens	68-87
20045650-0	2010	A new series of flavones, thioflavones, and flavanones as selective monoamine oxidase-B inhibitors.	thioflavone	26-38	monoamine oxidase B	Homo sapiens	68-87
20045650-2	2010	The most active series is the flavanone one with higher selective inhibitory activity against MAO-B.	flavanone	30-39	monoamine oxidase B	Homo sapiens	94-99
19948168-5	2010	We also discovered that zonisamide inhibited monoamine oxidase B (MAO-B) activity in vitro with an IC(50) of 25 muM, a concentration that is well within the therapeutic range used for treating epilepsy in humans.	Zonisamide	24-34	monoamine oxidase B	Homo sapiens	45-64
19948168-5	2010	We also discovered that zonisamide inhibited monoamine oxidase B (MAO-B) activity in vitro with an IC(50) of 25 muM, a concentration that is well within the therapeutic range used for treating epilepsy in humans.	Zonisamide	24-34	monoamine oxidase B	Homo sapiens	66-71
19948168-9	2010	The potency and reversibility with which zonisamide blocks MAO-B may contribute to the ability of the drug to improve clinical symptoms in PD patients.	Zonisamide	41-51	monoamine oxidase B	Homo sapiens	59-64
20410615-3	2010	(3,5-Dimethyl-1H-pyrrol-2-ylmethylene)-prop-2-ynyl-amine (1, SI=58.96) and compound (2, SI=0.34) were proved to be the superior selective inhibitors toward MAO-A and MAO-B respectively.	(3,5-dimethyl-1h-pyrrol-2-ylmethylene)-prop-2-ynyl-amine	0-56	monoamine oxidase B	Homo sapiens	166-171
20977789-1	2010	Rasagiline is a MAO-B inhibitor that is currently registered for the symptomatic treatment of Parkinson disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	16-21
20197647-1	2010	BACKGROUND: The anti-Parkinson monoamine oxidase B inhibitor rasagiline appears to be the first neuroprotective disease-modifying therapy in early-stage Parkinson"s disease (PD).	rasagiline	61-71	monoamine oxidase B	Homo sapiens	31-50
21389939-1	2010	An open observational 3-month study of efficacy and safety of selective MAO B inhibitor rasagiline (AZIlect) in advanced Parkinson"s disease (PD) patients with motor fluctuations on the long-term levodopa therapy (the "AZIMUT" study) has been conducted.	rasagiline	100-107	monoamine oxidase B	Homo sapiens	72-77
19650872-6	2009	Substitution of the homologous serine in the MAO-B isoform, i.e. Ser200, with either Glu or Ala does not affect the catalytic activity of the corresponding over-expressed proteins.	Serine	31-37	monoamine oxidase B	Homo sapiens	45-50
19733607-5	2009	The MAO-A-dependent catecholamine metabolite DHPG levels did not change significantly during the study suggesting that rasagiline"s MAO-B selectivity was preserved.	rasagiline	119-129	monoamine oxidase B	Homo sapiens	132-137
19804982-0	2009	Synthesis and in vitro evaluation of pteridine analogues as monoamine oxidase B and nitric oxide synthase inhibitors.	Pteridines	37-46	monoamine oxidase B	Homo sapiens	60-79
19804982-4	2009	The pteridine-2,4-dione analogues thus show promise as scaffolds for the development of potent reversible MAO-B inhibitors and as observed in earlier studies, the most potent inhibitors were obtained with 3-chlorostyryl substitution.	lumazine	4-23	monoamine oxidase B	Homo sapiens	106-111
19821381-15	2009	AUTHORS" CONCLUSIONS: MAO-B inhibitors are one option for the early treatment of PD although they have weaker symptomatic effects than levodopa and dopamine agonists.	Dopamine	148-156	monoamine oxidase B	Homo sapiens	22-27
20150659-6	2009	However, Knoll demonstrated in his later work that (-)-deprenyl has enhancing qualities already in femto-picomolar concentrations, which leave MAO-B activity unchanged, and the activity of the catecholaminergic neurons in the brain stem and this previously unknown "enhancer effect" is responsible for the peculiar therapeutic benefits caused by (-)-deprenyl.	Selegiline	51-63	monoamine oxidase B	Homo sapiens	143-148
19506579-1	2009	We present a pharmacogenetic study of acute antipsychotic (AP)-induced extrapyramidal symptoms (EPS) using an extensive linkage disequilibrium mapping approach in seven-candidate genes with a well-established link to dopamine (DRD2, DRD3, ACE, COMT, DAT, MAO-A, MAO-B).	Dopamine	217-225	monoamine oxidase B	Homo sapiens	262-267
19810674-0	2009	Discovery of a novel class of potent coumarin monoamine oxidase B inhibitors: development and biopharmacological profiling of 7-[(3-chlorobenzyl)oxy]-4-[(methylamino)methyl]-2H-chromen-2-one methanesulfonate (NW-1772) as a highly potent, selective, reversible, and orally active monoamine oxidase B inhibitor.	NW-1772	126-207	monoamine oxidase B	Homo sapiens	46-65
19810674-0	2009	Discovery of a novel class of potent coumarin monoamine oxidase B inhibitors: development and biopharmacological profiling of 7-[(3-chlorobenzyl)oxy]-4-[(methylamino)methyl]-2H-chromen-2-one methanesulfonate (NW-1772) as a highly potent, selective, reversible, and orally active monoamine oxidase B inhibitor.	NW-1772	126-207	monoamine oxidase B	Homo sapiens	279-298
19810674-4	2009	Furthermore, computational and experimental studies led to the identification and biopharmacological characterization of 7-[(3-chlorobenzyl)oxy]-4-[(methylamino)methyl]-2H-chromen-2-one methanesulfonate 22b (NW-1772) as an in vitro and in vivo potent and selective MAO-B inhibitor, with rapid blood-brain barrier penetration, short-acting and reversible inhibitory activity, slight inhibition of selected cytochrome P450s, and low in vitro toxicity.	7-[(3-chlorobenzyl)oxy]-4-[(methylamino)methyl]-2h	121-171	monoamine oxidase B	Homo sapiens	265-270
19810674-4	2009	Furthermore, computational and experimental studies led to the identification and biopharmacological characterization of 7-[(3-chlorobenzyl)oxy]-4-[(methylamino)methyl]-2H-chromen-2-one methanesulfonate 22b (NW-1772) as an in vitro and in vivo potent and selective MAO-B inhibitor, with rapid blood-brain barrier penetration, short-acting and reversible inhibitory activity, slight inhibition of selected cytochrome P450s, and low in vitro toxicity.	chromen-2-one methanesulfonate	172-202	monoamine oxidase B	Homo sapiens	265-270
19669997-1	2009	Monoamine oxidase (MAO) B is a mitochondrial enzyme selectively involved in the oxidative activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to toxic pyridinium cations producing Parkinsonism in animal models.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	104-148	monoamine oxidase B	Homo sapiens	0-25
19669997-1	2009	Monoamine oxidase (MAO) B is a mitochondrial enzyme selectively involved in the oxidative activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to toxic pyridinium cations producing Parkinsonism in animal models.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	150-154	monoamine oxidase B	Homo sapiens	0-25
19669997-1	2009	Monoamine oxidase (MAO) B is a mitochondrial enzyme selectively involved in the oxidative activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to toxic pyridinium cations producing Parkinsonism in animal models.	pyridine	176-186	monoamine oxidase B	Homo sapiens	0-25
19669997-3	2009	The oxidation of MPTP by human MAO-B and mitochondria was assessed by HPLC.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	17-21	monoamine oxidase B	Homo sapiens	31-36
19669997-5	2009	5-Nitroindazole (IC(50)=0.99 microM, K(i)=0.102 microM) and 6-nitroindazole (IC(50)=2.5 microM) were better inhibitors of human MAO-B than 7-nitroindazole (IC(50)=27.8 microM).	5-nitroindazole	0-15	monoamine oxidase B	Homo sapiens	128-133
19669997-5	2009	5-Nitroindazole (IC(50)=0.99 microM, K(i)=0.102 microM) and 6-nitroindazole (IC(50)=2.5 microM) were better inhibitors of human MAO-B than 7-nitroindazole (IC(50)=27.8 microM).	6-nitroindazole	60-75	monoamine oxidase B	Homo sapiens	128-133
19669997-5	2009	5-Nitroindazole (IC(50)=0.99 microM, K(i)=0.102 microM) and 6-nitroindazole (IC(50)=2.5 microM) were better inhibitors of human MAO-B than 7-nitroindazole (IC(50)=27.8 microM).	7-nitroindazole	139-154	monoamine oxidase B	Homo sapiens	128-133
19669997-9	2009	5-Nitro- and 6-nitroindazole, previously reported as weak NOS inhibitors, were better inhibitors of human MAO-B and more active against MPTP neurotoxin oxidation (lower MPDP(+) and MPP(+) levels) than 7-nitroindazole and acted as good radical scavengers and could be potential neuroprotective agents in addition to MAO-B inhibitors.	5-nitro	0-7	monoamine oxidase B	Homo sapiens	106-111
19669997-9	2009	5-Nitro- and 6-nitroindazole, previously reported as weak NOS inhibitors, were better inhibitors of human MAO-B and more active against MPTP neurotoxin oxidation (lower MPDP(+) and MPP(+) levels) than 7-nitroindazole and acted as good radical scavengers and could be potential neuroprotective agents in addition to MAO-B inhibitors.	5-nitro	0-7	monoamine oxidase B	Homo sapiens	315-320
19669997-9	2009	5-Nitro- and 6-nitroindazole, previously reported as weak NOS inhibitors, were better inhibitors of human MAO-B and more active against MPTP neurotoxin oxidation (lower MPDP(+) and MPP(+) levels) than 7-nitroindazole and acted as good radical scavengers and could be potential neuroprotective agents in addition to MAO-B inhibitors.	and 6-nitroindazole	9-28	monoamine oxidase B	Homo sapiens	106-111
19669997-9	2009	5-Nitro- and 6-nitroindazole, previously reported as weak NOS inhibitors, were better inhibitors of human MAO-B and more active against MPTP neurotoxin oxidation (lower MPDP(+) and MPP(+) levels) than 7-nitroindazole and acted as good radical scavengers and could be potential neuroprotective agents in addition to MAO-B inhibitors.	and 6-nitroindazole	9-28	monoamine oxidase B	Homo sapiens	315-320
19669997-9	2009	5-Nitro- and 6-nitroindazole, previously reported as weak NOS inhibitors, were better inhibitors of human MAO-B and more active against MPTP neurotoxin oxidation (lower MPDP(+) and MPP(+) levels) than 7-nitroindazole and acted as good radical scavengers and could be potential neuroprotective agents in addition to MAO-B inhibitors.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	136-140	monoamine oxidase B	Homo sapiens	315-320
19657584-8	2009	For MAOB the 4-SNP haplotype GACG formed from rs1799836, rs10521432, rs6651806 and rs590551 was significantly related to lower Negative Emotionality scores (p &lt; 0.002).	gacg	29-33	monoamine oxidase B	Homo sapiens	4-8
19650872-6	2009	Substitution of the homologous serine in the MAO-B isoform, i.e. Ser200, with either Glu or Ala does not affect the catalytic activity of the corresponding over-expressed proteins.	Glutamic Acid	85-88	monoamine oxidase B	Homo sapiens	45-50
19650872-6	2009	Substitution of the homologous serine in the MAO-B isoform, i.e. Ser200, with either Glu or Ala does not affect the catalytic activity of the corresponding over-expressed proteins.	Alanine	92-95	monoamine oxidase B	Homo sapiens	45-50
19789505-3	2009	MATERIAL/METHODS: We investigated MAO labeling with mechanism-based inhibitor [3H]pargyline activities of MAO A, MAO B, and SSAO in healthy and inflamed human dental pulp.	Tritium	79-81	monoamine oxidase B	Homo sapiens	113-118
19789505-3	2009	MATERIAL/METHODS: We investigated MAO labeling with mechanism-based inhibitor [3H]pargyline activities of MAO A, MAO B, and SSAO in healthy and inflamed human dental pulp.	Pargyline	82-91	monoamine oxidase B	Homo sapiens	113-118
19789505-5	2009	MAO activity assayed with 100 microM [14C]5HT or 10 microM [14C]PEA was sensitive to selective inhibitors of MAO A and MAO B, respectively.	14c]5ht	38-45	monoamine oxidase B	Homo sapiens	119-124
19789505-5	2009	MAO activity assayed with 100 microM [14C]5HT or 10 microM [14C]PEA was sensitive to selective inhibitors of MAO A and MAO B, respectively.	Carbon-14	38-41	monoamine oxidase B	Homo sapiens	119-124
19526285-2	2009	MAO-B mediated increases in H(2)O(2) also appeared to result in direct oxidative inhibition of both mitochondrial complex I and aconitase.	Hydrogen Peroxide	28-36	monoamine oxidase B	Homo sapiens	0-5
19526285-1	2009	We previously demonstrated that spare respiratory capacity of the TCA cycle enzyme alpha-ketoglutarate dehydrogenase (KGDH) was completely abolished upon increasing levels of MAO-B activity in a dopaminergic cell model system (Kumar et al., J Biol Chem 278:46432-46439, 2003).	Trichloroacetic Acid	66-69	monoamine oxidase B	Homo sapiens	175-180
19697948-5	2009	Increased nitration of Tyr-39 on endogenous alpha-synuclein via elevations in MAO-B levels could be abrogated by the addition of deprenyl, a specific MAO-B inhibitor.	Tyrosine	23-27	monoamine oxidase B	Homo sapiens	78-83
19697948-5	2009	Increased nitration of Tyr-39 on endogenous alpha-synuclein via elevations in MAO-B levels could be abrogated by the addition of deprenyl, a specific MAO-B inhibitor.	Tyrosine	23-27	monoamine oxidase B	Homo sapiens	150-155
19697948-5	2009	Increased nitration of Tyr-39 on endogenous alpha-synuclein via elevations in MAO-B levels could be abrogated by the addition of deprenyl, a specific MAO-B inhibitor.	Selegiline	129-137	monoamine oxidase B	Homo sapiens	78-83
19697948-5	2009	Increased nitration of Tyr-39 on endogenous alpha-synuclein via elevations in MAO-B levels could be abrogated by the addition of deprenyl, a specific MAO-B inhibitor.	Selegiline	129-137	monoamine oxidase B	Homo sapiens	150-155
19508883-1	2009	We present a schizophrenia association study using an extensive linkage disequilibrium (LD) mapping approach in seven candidate genes with a well established link to dopamine, including receptors (DRD2, DRD3) and genes involved in its metabolism and transport (ACE, COMT, DAT, MAO-A, MAO-B).	Dopamine	166-174	monoamine oxidase B	Homo sapiens	284-289
19628387-0	2009	Synthesis and evaluation of 6-methyl-3-phenylcoumarins as potent and selective MAO-B inhibitors.	6-methyl-3-phenylcoumarins	28-54	monoamine oxidase B	Homo sapiens	79-84
19628387-1	2009	A series of 6-methyl-3-phenylcoumarins 3-6 were synthesized and evaluated as monoamine oxidase A and B (MAO-A and MAO-B) inhibitors.	6-methyl-3-phenylcoumarins	12-38	monoamine oxidase B	Homo sapiens	114-119
19646280-1	2009	BACKGROUND: The selective MAO-B inhibitor selegiline has been evaluated in clinical trials as a potential medication for the treatment of cocaine dependence.	Selegiline	42-52	monoamine oxidase B	Homo sapiens	26-31
19673610-5	2009	Rasagiline-related MAOB-Is prevent mitochondrial permeability transition induced by various insults and activation of subsequent apoptotic cascades: cytochrome c release, casapase activation, and condensation and fragmentation of nuclear DNA.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	19-23
19687003-3	2009	Moclobemide is a reversible inhibitor of monoamine oxidase (MAO)-A, selegiline is an irreversible selective inhibitor of MAO-B, and paroxetine is a selective serotonin reuptake inhibitor.	Selegiline	68-78	monoamine oxidase B	Homo sapiens	121-126
19526291-0	2009	Glyceraldehyde-3-phosphate dehydrogenase-monoamine oxidase B-mediated cell death-induced by ethanol is prevented by rasagiline and 1-R-aminoindan.	Ethanol	92-99	monoamine oxidase B	Homo sapiens	41-60
19259810-6	2009	Parkinson"s cases treated with L-DOPA and MAO-B inhibitor exhibited decreased platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone.	Levodopa	31-37	monoamine oxidase B	Homo sapiens	87-92
19526291-0	2009	Glyceraldehyde-3-phosphate dehydrogenase-monoamine oxidase B-mediated cell death-induced by ethanol is prevented by rasagiline and 1-R-aminoindan.	rasagiline	116-126	monoamine oxidase B	Homo sapiens	41-60
19259810-6	2009	Parkinson"s cases treated with L-DOPA and MAO-B inhibitor exhibited decreased platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone.	Levodopa	157-163	monoamine oxidase B	Homo sapiens	42-47
19259810-7	2009	Interestingly, Parkinson"s cases treated with L-DOPA and amantadine also had lower platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone.	Levodopa	46-52	monoamine oxidase B	Homo sapiens	92-97
19526291-0	2009	Glyceraldehyde-3-phosphate dehydrogenase-monoamine oxidase B-mediated cell death-induced by ethanol is prevented by rasagiline and 1-R-aminoindan.	1-r-aminoindan	131-145	monoamine oxidase B	Homo sapiens	41-60
19259810-7	2009	Interestingly, Parkinson"s cases treated with L-DOPA and amantadine also had lower platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone.	Amantadine	57-67	monoamine oxidase B	Homo sapiens	92-97
19259810-8	2009	Activity of platelet MAO-B in Parkinson"s patients was increased in naive cases and those treated with L-DOPA alone or in combination with other drugs compared to controls.	Levodopa	103-109	monoamine oxidase B	Homo sapiens	21-26
19526291-3	2009	Here, we provide evidence that GAPDH potentiates the ethanol-induced activity of MAO B and brain cell toxicity.	Ethanol	53-60	monoamine oxidase B	Homo sapiens	81-86
19526291-4	2009	The levels of nuclear GAPDH and MAO B activity are significantly increased in brain-derived cell lines upon 75 mM ethanol-induced cell death.	Ethanol	114-121	monoamine oxidase B	Homo sapiens	32-37
19526291-5	2009	Over-expression of GAPDH in cells enhances ethanol-induced cell death, and also increases the ethanol-induced activation of MAO B.	Ethanol	94-101	monoamine oxidase B	Homo sapiens	124-129
19526291-6	2009	In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death.	rasagiline	34-44	monoamine oxidase B	Homo sapiens	17-22
19526291-6	2009	In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death.	rasagiline	34-44	monoamine oxidase B	Homo sapiens	154-159
19526291-6	2009	In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death.	Selegiline	49-59	monoamine oxidase B	Homo sapiens	17-22
19526291-6	2009	In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death.	Selegiline	49-59	monoamine oxidase B	Homo sapiens	154-159
19526291-6	2009	In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death.	rasagiline	78-88	monoamine oxidase B	Homo sapiens	154-159
19526291-6	2009	In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death.	1-r-aminoindan	101-115	monoamine oxidase B	Homo sapiens	154-159
19526291-6	2009	In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death.	Ethanol	138-145	monoamine oxidase B	Homo sapiens	17-22
19526291-6	2009	In contrast, the MAO B inhibitors rasagiline and selegiline (0.25 nM) and the rasagiline metabolite, 1-R-aminoindan (1 muM) decreases the ethanol-induced MAO B, prevents nuclear translocation of GAPDH and reduces cell death.	Ethanol	138-145	monoamine oxidase B	Homo sapiens	154-159
19526291-7	2009	In addition, GAPDH interacts with transforming growth factor-beta-inducible early gene (TIEG2), a transcriptional activator for MAO B, and this interaction is increased in the nucleus by ethanol but reduced by MAO B inhibitors and 1-R-aminoindan.	1-r-aminoindan	231-245	monoamine oxidase B	Homo sapiens	128-133
19526291-9	2009	In summary, ethanol-induced cell death, attenuated by MAO B inhibitors, may result from disrupting the movement of GAPDH with the transcriptional activator into the nucleus and secondly inhibit MAO B gene expression.	Ethanol	12-19	monoamine oxidase B	Homo sapiens	54-59
19526291-9	2009	In summary, ethanol-induced cell death, attenuated by MAO B inhibitors, may result from disrupting the movement of GAPDH with the transcriptional activator into the nucleus and secondly inhibit MAO B gene expression.	Ethanol	12-19	monoamine oxidase B	Homo sapiens	194-199
19526291-10	2009	Thus, the neuroprotective effects of rasagiline or 1-R-aminoindan on ethanol-induced cell death mediated by a novel GAPDH-MAO B pathway may provide a new insight in the treatment of neurobiological diseases including alcohol-use disorders.	rasagiline	37-47	monoamine oxidase B	Homo sapiens	122-127
19526291-10	2009	Thus, the neuroprotective effects of rasagiline or 1-R-aminoindan on ethanol-induced cell death mediated by a novel GAPDH-MAO B pathway may provide a new insight in the treatment of neurobiological diseases including alcohol-use disorders.	1-r-aminoindan	51-65	monoamine oxidase B	Homo sapiens	122-127
19526291-10	2009	Thus, the neuroprotective effects of rasagiline or 1-R-aminoindan on ethanol-induced cell death mediated by a novel GAPDH-MAO B pathway may provide a new insight in the treatment of neurobiological diseases including alcohol-use disorders.	Ethanol	69-76	monoamine oxidase B	Homo sapiens	122-127
19526291-10	2009	Thus, the neuroprotective effects of rasagiline or 1-R-aminoindan on ethanol-induced cell death mediated by a novel GAPDH-MAO B pathway may provide a new insight in the treatment of neurobiological diseases including alcohol-use disorders.	Alcohols	217-224	monoamine oxidase B	Homo sapiens	122-127
19423346-0	2009	A new series of 3-phenylcoumarins as potent and selective MAO-B inhibitors.	3-phenylcoumarins	16-33	monoamine oxidase B	Homo sapiens	58-63
19753135-1	2009	Rasagiline is a second generation, selective, irreversible monoamine oxidase type B (MAO-B) inhibitor.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	59-83
19753135-1	2009	Rasagiline is a second generation, selective, irreversible monoamine oxidase type B (MAO-B) inhibitor.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	85-90
19753135-4	2009	The lack of amphetamine metabolites provides an advantage over the first generation MAO-B inhibitor selegiline.	Selegiline	100-110	monoamine oxidase B	Homo sapiens	84-89
19527191-3	2009	Oral selegiline, at low doses, is a selective monoamine oxidase B (MAO-B) inhibitor, but at higher doses it loses its selectivity and can potentially interact with tyramine.	Selegiline	5-15	monoamine oxidase B	Homo sapiens	46-65
19527191-3	2009	Oral selegiline, at low doses, is a selective monoamine oxidase B (MAO-B) inhibitor, but at higher doses it loses its selectivity and can potentially interact with tyramine.	Selegiline	5-15	monoamine oxidase B	Homo sapiens	67-72
19527191-5	2009	The selegiline transdermal system was developed to deliver sustained selegiline blood concentrations sufficient to selectively inhibit MAO-A and MAO-B in the brain, producing antidepressant effects, without substantially inhibiting MAO-A in the gastrointestinal tract, thereby reducing the risk of hypertensive crisis.	Selegiline	4-14	monoamine oxidase B	Homo sapiens	145-150
19527191-5	2009	The selegiline transdermal system was developed to deliver sustained selegiline blood concentrations sufficient to selectively inhibit MAO-A and MAO-B in the brain, producing antidepressant effects, without substantially inhibiting MAO-A in the gastrointestinal tract, thereby reducing the risk of hypertensive crisis.	Selegiline	69-79	monoamine oxidase B	Homo sapiens	145-150
19401466-0	2009	Retinoic acid activates monoamine oxidase B promoter in human neuronal cells.	Tretinoin	0-13	monoamine oxidase B	Homo sapiens	24-43
19401466-1	2009	Monoamine oxidase (MAO) B deaminates a number of biogenic and dietary amines and plays an important role in many biological processes.	Amines	70-76	monoamine oxidase B	Homo sapiens	0-25
19401466-2	2009	Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human neuroblastoma BE(2)C cell line.	Tretinoin	65-78	monoamine oxidase B	Homo sapiens	30-35
19401466-2	2009	Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human neuroblastoma BE(2)C cell line.	Tretinoin	65-78	monoamine oxidase B	Homo sapiens	113-118
19401466-2	2009	Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human neuroblastoma BE(2)C cell line.	Tretinoin	80-82	monoamine oxidase B	Homo sapiens	30-35
19401466-2	2009	Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human neuroblastoma BE(2)C cell line.	Tretinoin	80-82	monoamine oxidase B	Homo sapiens	113-118
19401466-4	2009	There are four retinoic acid response elements (RAREs) as identified in the MAO B 2-kb promoter, and mutation of the third RARE reduced RA-induced MAO B promoter activation by 50%, suggesting this element is important.	Tretinoin	15-28	monoamine oxidase B	Homo sapiens	76-81
19401466-9	2009	Taken together, this study provides evidence for the first time showing the stimulating effect of RA on MAO B and new insight into the molecular mechanisms of MAO B regulation by hormones.	Tretinoin	98-100	monoamine oxidase B	Homo sapiens	104-109
19401466-9	2009	Taken together, this study provides evidence for the first time showing the stimulating effect of RA on MAO B and new insight into the molecular mechanisms of MAO B regulation by hormones.	Tretinoin	98-100	monoamine oxidase B	Homo sapiens	159-164
19423346-1	2009	6-Methyl-3-phenylcoumarins 3-6 were designed, synthesized and evaluated as monoamine oxidase A and B (MAO-A and MAO-B) inhibitors.	6-methyl-3-phenylcoumarins	0-26	monoamine oxidase B	Homo sapiens	112-117
19378991-1	2009	A large series of substituted chalcones have been synthesized and tested in vitro for their ability to inhibit human monoamine oxidases A and B (hMAO-A and hMAO-B).	Chalcones	30-39	monoamine oxidase B	Homo sapiens	156-162
19324554-0	2009	Inhibition of monoamine oxidase B by N-methyl-2-phenylmaleimides.	n-methyl-2-phenylmaleimides	37-64	monoamine oxidase B	Homo sapiens	14-33
19342233-4	2009	The (E)-5-styrylisatin analogues bound more tightly than the (E)-6 analogue although the latter exhibits the highest MAO-B selectivity.	(E)-5-Styrylisatin	4-22	monoamine oxidase B	Homo sapiens	117-122
19342233-5	2009	Molecular docking studies with MAO-B indicate that the increased binding affinity exhibited by the (E)-styrylisatin analogues, in comparison to isatin, is best explained by the ability of the styrylisatins to bridge both the entrance cavity and the substrate cavity of the enzyme.	(e)-styrylisatin	99-115	monoamine oxidase B	Homo sapiens	31-36
19342233-5	2009	Molecular docking studies with MAO-B indicate that the increased binding affinity exhibited by the (E)-styrylisatin analogues, in comparison to isatin, is best explained by the ability of the styrylisatins to bridge both the entrance cavity and the substrate cavity of the enzyme.	Isatin	109-115	monoamine oxidase B	Homo sapiens	31-36
19342233-5	2009	Molecular docking studies with MAO-B indicate that the increased binding affinity exhibited by the (E)-styrylisatin analogues, in comparison to isatin, is best explained by the ability of the styrylisatins to bridge both the entrance cavity and the substrate cavity of the enzyme.	styrylisatins	192-205	monoamine oxidase B	Homo sapiens	31-36
19342233-6	2009	Experimental support for this model is shown by the weaker binding of the analogues to the Ile199Ala mutant of human MAO-B.	ile199ala	91-100	monoamine oxidase B	Homo sapiens	117-122
19342233-7	2009	The lower selectivity of the (E)-styrylisatin analogues between MAO-A and MAO-B, in contrast to CSC, is best explained by the differing relative geometries of the aromatic rings for these two classes of inhibitors.	(e)-styrylisatin	29-45	monoamine oxidase B	Homo sapiens	74-79
19129751-0	2009	Assessment of MAO-B occupancy in the brain with PET and [11C]-L-deprenyl-D2: a dose-finding study with a novel MAO-B inhibitor, EVT 301.	[11c]-l-deprenyl-d2	56-75	monoamine oxidase B	Homo sapiens	14-19
19129751-0	2009	Assessment of MAO-B occupancy in the brain with PET and [11C]-L-deprenyl-D2: a dose-finding study with a novel MAO-B inhibitor, EVT 301.	N-(4-(3-fluorobenzyloxy)phenyl)malonamide	128-135	monoamine oxidase B	Homo sapiens	111-116
19129751-2	2009	We performed a dose-selection and validation study of a novel, reversible MAO-B inhibitor, EVT 301.	EVT	91-94	monoamine oxidase B	Homo sapiens	74-79
19129751-4	2009	MAO-B occupancy in the brain was assessed using positron emission tomography (PET) with [11C]-L-deprenyl-D2.	[11c]-l-deprenyl-d2	88-107	monoamine oxidase B	Homo sapiens	0-5
19129751-5	2009	EVT 301 was found to dose-dependently occupy MAO-B in the human brain, with occupancy ranging from 58-78% at a dose of 25 mg to 73-90% at a dose of 150 mg.	N-(4-(3-fluorobenzyloxy)phenyl)malonamide	0-7	monoamine oxidase B	Homo sapiens	45-50
19129751-7	2009	Determination of MAO-B inhibition in blood platelets underestimated the actual brain occupancy achieved with EVT 301.	EVT	109-112	monoamine oxidase B	Homo sapiens	17-22
19386233-0	2009	PF9601N [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine] confers MAO-B independent neuroprotection in ER stress-induced cell death.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	0-7	monoamine oxidase B	Homo sapiens	69-74
19386233-0	2009	PF9601N [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine] confers MAO-B independent neuroprotection in ER stress-induced cell death.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	9-59	monoamine oxidase B	Homo sapiens	69-74
19386233-3	2009	Therefore, we have studied the potential usefulness of PF9601N, a non-amphetamine-like MAO-B inhibitor, in preventing cell death in a cell culture model of ER stress.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	55-62	monoamine oxidase B	Homo sapiens	87-92
19324554-1	2009	Based on a recent report that 1-methyl-3-phenylpyrrolyl analogues are moderately potent reversible inhibitors of the enzyme monoamine oxidase B (MAO-B), a series of structurally related N-methyl-2-phenylmaleimidyl analogues has been prepared and evaluated as inhibitors of MAO-B.	1-methyl-3-phenylpyrrolyl	30-55	monoamine oxidase B	Homo sapiens	124-143
19324554-1	2009	Based on a recent report that 1-methyl-3-phenylpyrrolyl analogues are moderately potent reversible inhibitors of the enzyme monoamine oxidase B (MAO-B), a series of structurally related N-methyl-2-phenylmaleimidyl analogues has been prepared and evaluated as inhibitors of MAO-B.	1-methyl-3-phenylpyrrolyl	30-55	monoamine oxidase B	Homo sapiens	145-150
19324554-1	2009	Based on a recent report that 1-methyl-3-phenylpyrrolyl analogues are moderately potent reversible inhibitors of the enzyme monoamine oxidase B (MAO-B), a series of structurally related N-methyl-2-phenylmaleimidyl analogues has been prepared and evaluated as inhibitors of MAO-B.	n-methyl-2-phenylmaleimidyl	186-213	monoamine oxidase B	Homo sapiens	124-143
19324554-5	2009	This is in correspondence with literature reports which suggest that hydrogen bond formation is involved in stabilizing inhibitor-MAO-B complexes.	Hydrogen	69-77	monoamine oxidase B	Homo sapiens	130-135
19384601-10	2009	Rasagiline exhibited highest inhibition on MAO B enzymatic activity and prevention on DNA damage as compared to selegiline and 1-R-aminoindan.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	43-48
19330584-1	2009	Experimental evidence suggests that monoamine oxidase B (MAO-B) and muscarinic cholinergic receptors (mAChRs) are involved in the pathogenesis of neurotoxicity caused by methylmercury and polychlorinated biphenyls (PCBs).	Polychlorinated Biphenyls	188-213	monoamine oxidase B	Homo sapiens	36-55
19330584-1	2009	Experimental evidence suggests that monoamine oxidase B (MAO-B) and muscarinic cholinergic receptors (mAChRs) are involved in the pathogenesis of neurotoxicity caused by methylmercury and polychlorinated biphenyls (PCBs).	Polychlorinated Biphenyls	188-213	monoamine oxidase B	Homo sapiens	57-62
19330584-1	2009	Experimental evidence suggests that monoamine oxidase B (MAO-B) and muscarinic cholinergic receptors (mAChRs) are involved in the pathogenesis of neurotoxicity caused by methylmercury and polychlorinated biphenyls (PCBs).	Polychlorinated Biphenyls	215-219	monoamine oxidase B	Homo sapiens	36-55
19330584-1	2009	Experimental evidence suggests that monoamine oxidase B (MAO-B) and muscarinic cholinergic receptors (mAChRs) are involved in the pathogenesis of neurotoxicity caused by methylmercury and polychlorinated biphenyls (PCBs).	Polychlorinated Biphenyls	215-219	monoamine oxidase B	Homo sapiens	57-62
18937611-1	2008	BACKGROUND: The role of monoamine oxidase type B inhibitors in the treatment of Parkinson"s disease has expanded with the new monoamine oxidase B inhibitor rasagiline and a new formulation, selegiline oral disintegrating tablets.	rasagiline	156-166	monoamine oxidase B	Homo sapiens	24-48
19091581-0	2009	New pyrazoline bearing 4(3H)-quinazolinone inhibitors of monoamine oxidase: synthesis, biological evaluation, and structural determinants of MAO-A and MAO-B selectivity.	pyrazoline	4-14	monoamine oxidase B	Homo sapiens	151-156
19091581-0	2009	New pyrazoline bearing 4(3H)-quinazolinone inhibitors of monoamine oxidase: synthesis, biological evaluation, and structural determinants of MAO-A and MAO-B selectivity.	4-hydroxyquinazoline	23-42	monoamine oxidase B	Homo sapiens	151-156
19091581-11	2009	The very high MAO-B selectivity for 4i can be also explained in terms of the distance between the FAD and the compound, which was greater in the complex of MAO-A-4i as compared to the corresponding MAO-B complex.	Flavin-Adenine Dinucleotide	98-101	monoamine oxidase B	Homo sapiens	14-19
19091581-11	2009	The very high MAO-B selectivity for 4i can be also explained in terms of the distance between the FAD and the compound, which was greater in the complex of MAO-A-4i as compared to the corresponding MAO-B complex.	Flavin-Adenine Dinucleotide	98-101	monoamine oxidase B	Homo sapiens	198-203
19110205-7	2009	When used in combination with levodopa, inhibitors of MAO-B may enhance the elevation of dopamine levels after levodopa treatment, particularly when used in early stages of the disease when dopamine production may not be so severely compromised.	Levodopa	30-38	monoamine oxidase B	Homo sapiens	54-59
19110205-7	2009	When used in combination with levodopa, inhibitors of MAO-B may enhance the elevation of dopamine levels after levodopa treatment, particularly when used in early stages of the disease when dopamine production may not be so severely compromised.	Dopamine	89-97	monoamine oxidase B	Homo sapiens	54-59
19110205-7	2009	When used in combination with levodopa, inhibitors of MAO-B may enhance the elevation of dopamine levels after levodopa treatment, particularly when used in early stages of the disease when dopamine production may not be so severely compromised.	Levodopa	111-119	monoamine oxidase B	Homo sapiens	54-59
19110205-7	2009	When used in combination with levodopa, inhibitors of MAO-B may enhance the elevation of dopamine levels after levodopa treatment, particularly when used in early stages of the disease when dopamine production may not be so severely compromised.	Dopamine	190-198	monoamine oxidase B	Homo sapiens	54-59
19110205-8	2009	Furthermore, MAO-B inhibitors may also possess neuroprotective properties in part by reducing the damaging effect of dopamine turnover in the brain.	Dopamine	117-125	monoamine oxidase B	Homo sapiens	13-18
19110207-2	2009	Ladostigil combines, in a single molecule, the neuroprotective/neurorestorative effects of the novel anti-Parkinsonian drug and selective monoamine oxidase (MAO)-B inhibitor, rasagiline (Azilect, Teva Pharmaceutical Co.) with the cholinesterase (ChE) inhibitory activity of rivastigmine.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	0-10	monoamine oxidase B	Homo sapiens	138-163
19110207-2	2009	Ladostigil combines, in a single molecule, the neuroprotective/neurorestorative effects of the novel anti-Parkinsonian drug and selective monoamine oxidase (MAO)-B inhibitor, rasagiline (Azilect, Teva Pharmaceutical Co.) with the cholinesterase (ChE) inhibitory activity of rivastigmine.	rasagiline	175-185	monoamine oxidase B	Homo sapiens	138-163
19131039-2	2009	The dose of l-dopa can be reduced by the combined administration of inhibitors of peripheral l-amino acid decarboxylase (AADC), catechol O-methyltransferase (COMT), or monoamine oxidase B (MAO B).	Levodopa	12-18	monoamine oxidase B	Homo sapiens	168-187
19131039-2	2009	The dose of l-dopa can be reduced by the combined administration of inhibitors of peripheral l-amino acid decarboxylase (AADC), catechol O-methyltransferase (COMT), or monoamine oxidase B (MAO B).	Levodopa	12-18	monoamine oxidase B	Homo sapiens	189-194
18951902-4	2008	MAO-N exists as a homotetramer with a large channel at its centre and shares some structural features with human MAO B (MAO-B).	mao-n	0-5	monoamine oxidase B	Homo sapiens	113-118
18951902-4	2008	MAO-N exists as a homotetramer with a large channel at its centre and shares some structural features with human MAO B (MAO-B).	mao-n	0-5	monoamine oxidase B	Homo sapiens	120-125
18951902-6	2008	A molecule of l-proline was observed near the FAD, and this ligand superimposed well with isatin, a reversible inhibitor of MAO-B, when the structures of MAO-N proline and MAO-B-isatin were overlaid.	Proline	14-23	monoamine oxidase B	Homo sapiens	124-129
18951902-6	2008	A molecule of l-proline was observed near the FAD, and this ligand superimposed well with isatin, a reversible inhibitor of MAO-B, when the structures of MAO-N proline and MAO-B-isatin were overlaid.	Proline	14-23	monoamine oxidase B	Homo sapiens	172-177
18951902-6	2008	A molecule of l-proline was observed near the FAD, and this ligand superimposed well with isatin, a reversible inhibitor of MAO-B, when the structures of MAO-N proline and MAO-B-isatin were overlaid.	Isatin	90-96	monoamine oxidase B	Homo sapiens	124-129
18951902-6	2008	A molecule of l-proline was observed near the FAD, and this ligand superimposed well with isatin, a reversible inhibitor of MAO-B, when the structures of MAO-N proline and MAO-B-isatin were overlaid.	Isatin	90-96	monoamine oxidase B	Homo sapiens	172-177
18951902-6	2008	A molecule of l-proline was observed near the FAD, and this ligand superimposed well with isatin, a reversible inhibitor of MAO-B, when the structures of MAO-N proline and MAO-B-isatin were overlaid.	mao-n proline	154-167	monoamine oxidase B	Homo sapiens	124-129
18989091-0	2008	Rasagiline ethanedisulfonate: an inhibitor for monoamine oxygenase B (MAO(B)).	rasagiline ethanedisulfonate	0-28	monoamine oxidase B	Homo sapiens	47-68
18989091-0	2008	Rasagiline ethanedisulfonate: an inhibitor for monoamine oxygenase B (MAO(B)).	rasagiline ethanedisulfonate	0-28	monoamine oxidase B	Homo sapiens	70-76
18751929-2	2009	Ladostigil combines neuroprotective effects with monoamine oxidase (MAO)-A and MAO-B and cholinesterase (ChE) inhibitory activities in a single molecule, as a potential treatment for Alzheimer"s disease (AD) and Lewy body disease.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	0-10	monoamine oxidase B	Homo sapiens	79-84
19064321-2	2009	The 2-imidazoline ability to inhibit the activity of the A and B isoforms of monoamine oxidase (MAO) was investigated and some of them showed potent and selective MAO inhibitory activity especially for the MAO-B isoform and could become promising candidates for future development.	2-imidazoline	4-17	monoamine oxidase B	Homo sapiens	206-211
19053775-0	2008	Structural and mechanistic studies of mofegiline inhibition of recombinant human monoamine oxidase B.	mofegiline	38-48	monoamine oxidase B	Homo sapiens	81-100
19053775-1	2008	Mechanistic and structural studies have been carried out to investigate the molecular basis for the irreversible inhibition of human MAO-B by mofegiline.	mofegiline	142-152	monoamine oxidase B	Homo sapiens	133-138
19053775-4	2008	The absorption spectral properties of mofegiline inhibited MAO-B show features (lambda(max) approximately 450 nm) unlike those of traditional flavin N(5) or C(4a) adducts.	mofegiline	38-48	monoamine oxidase B	Homo sapiens	59-64
19053775-5	2008	Visible and near-UV circular dichroism spectra of the mofegiline-MAO-B adduct shows a negative peak at 340 nm with an intensity similar to that of N(5) flavocyanine adducts.	mofegiline	54-64	monoamine oxidase B	Homo sapiens	65-70
19053775-5	2008	Visible and near-UV circular dichroism spectra of the mofegiline-MAO-B adduct shows a negative peak at 340 nm with an intensity similar to that of N(5) flavocyanine adducts.	n(5) flavocyanine	147-164	monoamine oxidase B	Homo sapiens	65-70
19053775-6	2008	The X-ray crystal structure of the mofegiline-MAO-B adduct shows a covalent bond between the flavin cofactor N(5) with the distal allylamine carbon atom as well as the absence of the fluorine atom.	mofegiline	35-45	monoamine oxidase B	Homo sapiens	46-51
19053775-6	2008	The X-ray crystal structure of the mofegiline-MAO-B adduct shows a covalent bond between the flavin cofactor N(5) with the distal allylamine carbon atom as well as the absence of the fluorine atom.	4,6-dinitro-o-cresol	93-99	monoamine oxidase B	Homo sapiens	46-51
19053775-6	2008	The X-ray crystal structure of the mofegiline-MAO-B adduct shows a covalent bond between the flavin cofactor N(5) with the distal allylamine carbon atom as well as the absence of the fluorine atom.	Allylamine	130-140	monoamine oxidase B	Homo sapiens	46-51
19053775-6	2008	The X-ray crystal structure of the mofegiline-MAO-B adduct shows a covalent bond between the flavin cofactor N(5) with the distal allylamine carbon atom as well as the absence of the fluorine atom.	Carbon	141-147	monoamine oxidase B	Homo sapiens	46-51
18840519-3	2008	Furthermore, the accumulated evidence suggests that MPP(+), conversed by monoamine oxidase type B (MAO-B) in astrocytes principally, is the active metabolite of MPTP and the major cause to PD associated with mitochondrial dysfunction.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	161-165	monoamine oxidase B	Homo sapiens	73-97
18840519-3	2008	Furthermore, the accumulated evidence suggests that MPP(+), conversed by monoamine oxidase type B (MAO-B) in astrocytes principally, is the active metabolite of MPTP and the major cause to PD associated with mitochondrial dysfunction.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	161-165	monoamine oxidase B	Homo sapiens	99-104
18840519-5	2008	Our results showed that pre-treatment with catalpol (0.5mM) for 1h prior to MPTP treatment attenuated mitochondrial dysfunction not only by reversing the activity of mitochondrial complex I, mitochondrial membrane potential (MMP), intracellular Ca(2+) level, and ROS accumulation as well as mitochondrial permeability transition (MPT) pore opening in mesencephalic neuron-astrocyte cultures, but also inhibiting MAO-B activity to protect neurons from more MPP(+) toxicity produced in astrocytes.	catalpol	43-51	monoamine oxidase B	Homo sapiens	412-417
18952510-1	2008	Rasagiline is a highly potent, selective and irreversible second-generation monoamine oxidase inhibitor with selectivity for type B of the enzyme (MAO-B).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	147-152
18937611-1	2008	BACKGROUND: The role of monoamine oxidase type B inhibitors in the treatment of Parkinson"s disease has expanded with the new monoamine oxidase B inhibitor rasagiline and a new formulation, selegiline oral disintegrating tablets.	Selegiline	190-200	monoamine oxidase B	Homo sapiens	24-48
18937611-2	2008	As primary therapy in early disease monoamine oxidase B inhibitors reduce motor disability and delay the need for levodopa.	Levodopa	114-122	monoamine oxidase B	Homo sapiens	36-55
18937611-3	2008	In more advanced disease requiring levodopa, adjunctive monoamine oxidase B inhibitors reduce "off" time and may improve gait and freezing.	Levodopa	35-43	monoamine oxidase B	Homo sapiens	56-75
18937611-8	2008	CONCLUSION: Accumulating data support the use of monoamine oxidase B inhibitors as monotherapy for early and mild Parkinson"s disease and as adjunctive therapy for more advanced Parkinson"s disease with levodopa-associated motor fluctuations.	Levodopa	203-211	monoamine oxidase B	Homo sapiens	49-68
18937611-9	2008	The recently released monoamine oxidase B inhibitor rasagiline and a new formulation, selegiline oral disintegrating tablets, have potential advantages over conventional oral selegiline.	rasagiline	52-62	monoamine oxidase B	Homo sapiens	22-41
18937611-9	2008	The recently released monoamine oxidase B inhibitor rasagiline and a new formulation, selegiline oral disintegrating tablets, have potential advantages over conventional oral selegiline.	Selegiline	175-185	monoamine oxidase B	Homo sapiens	22-41
18937619-1	2008	The selective monoamine oxidase type B inhibitor selegiline is commonly administered as medical treatment to patients suffering from Parkinson"s disease.	Selegiline	49-59	monoamine oxidase B	Homo sapiens	14-38
19067259-2	2008	Although platelet monoamine oxidase activity (MAO-B) has been proposed as an index of cerebral serotonin activity, studies in patients with AN are scarce.	Serotonin	95-104	monoamine oxidase B	Homo sapiens	46-51
18678871-5	2008	In addition, based on a structural model of PuO(Rh) that was built using the crystal structure of human monoamine oxidase B (MAO-B), we constructed an active mutant enzyme, PuO(Rh) A394C, that contains covalently bound FAD.	puo	44-47	monoamine oxidase B	Homo sapiens	104-123
18678871-5	2008	In addition, based on a structural model of PuO(Rh) that was built using the crystal structure of human monoamine oxidase B (MAO-B), we constructed an active mutant enzyme, PuO(Rh) A394C, that contains covalently bound FAD.	puo	44-47	monoamine oxidase B	Homo sapiens	125-130
18678871-5	2008	In addition, based on a structural model of PuO(Rh) that was built using the crystal structure of human monoamine oxidase B (MAO-B), we constructed an active mutant enzyme, PuO(Rh) A394C, that contains covalently bound FAD.	Rhodium	48-50	monoamine oxidase B	Homo sapiens	104-123
18678871-5	2008	In addition, based on a structural model of PuO(Rh) that was built using the crystal structure of human monoamine oxidase B (MAO-B), we constructed an active mutant enzyme, PuO(Rh) A394C, that contains covalently bound FAD.	Rhodium	48-50	monoamine oxidase B	Homo sapiens	125-130
19946577-3	2008	We previously reported that ethanol exposure lowered cell proliferation and increased cell apoptosis in all cell types, but affects brain cell lines the most, while ethanol and the anti-depressant drug deprenyl, an monoamine oxidase B (MAO B) inhibitor, exposure in unison increases cell viability.	Ethanol	28-35	monoamine oxidase B	Homo sapiens	215-234
19946577-3	2008	We previously reported that ethanol exposure lowered cell proliferation and increased cell apoptosis in all cell types, but affects brain cell lines the most, while ethanol and the anti-depressant drug deprenyl, an monoamine oxidase B (MAO B) inhibitor, exposure in unison increases cell viability.	Ethanol	28-35	monoamine oxidase B	Homo sapiens	236-241
19946577-3	2008	We previously reported that ethanol exposure lowered cell proliferation and increased cell apoptosis in all cell types, but affects brain cell lines the most, while ethanol and the anti-depressant drug deprenyl, an monoamine oxidase B (MAO B) inhibitor, exposure in unison increases cell viability.	Selegiline	202-210	monoamine oxidase B	Homo sapiens	215-234
19946577-3	2008	We previously reported that ethanol exposure lowered cell proliferation and increased cell apoptosis in all cell types, but affects brain cell lines the most, while ethanol and the anti-depressant drug deprenyl, an monoamine oxidase B (MAO B) inhibitor, exposure in unison increases cell viability.	Selegiline	202-210	monoamine oxidase B	Homo sapiens	236-241
19946577-8	2008	We have found that ethanol exposure increases the levels of mRNA and protein/catalytic activity for both TIEG2 and MAO B, while ethanol and deprenyl exposure in unison reduce the expression of both TIEG2 and MAO B, however it increases cell viability.	Ethanol	19-26	monoamine oxidase B	Homo sapiens	115-120
19946577-8	2008	We have found that ethanol exposure increases the levels of mRNA and protein/catalytic activity for both TIEG2 and MAO B, while ethanol and deprenyl exposure in unison reduce the expression of both TIEG2 and MAO B, however it increases cell viability.	Ethanol	19-26	monoamine oxidase B	Homo sapiens	208-213
19946577-8	2008	We have found that ethanol exposure increases the levels of mRNA and protein/catalytic activity for both TIEG2 and MAO B, while ethanol and deprenyl exposure in unison reduce the expression of both TIEG2 and MAO B, however it increases cell viability.	Ethanol	128-135	monoamine oxidase B	Homo sapiens	208-213
19946577-11	2008	The inhibition of the TIEG2-MAO B pathway may be one of the mechanisms for the neuroprotective effect of deprenyl.	Selegiline	105-113	monoamine oxidase B	Homo sapiens	28-33
18408241-4	2008	CONCLUSIONS: Results suggested platelet MAO B as a trait marker also to type I alcohol-dependent patients and the two observed associations between platelet MAO B activity with neurocognitive measures of executive functions (nonverbal reasoning) and psychopathological dimension such as hostility may support the notion about the effect of platelet MAO B activity in the further development of an impulsive cognitive style.	Alcohols	79-86	monoamine oxidase B	Homo sapiens	40-45
18281126-1	2008	A series of N1-propanoyl-3,5-diphenyl-4,5-dihydro-(1H)-pyrazole derivatives were synthesized and assayed as inhibitors of MAO-A and MAO-B isoforms.	n1-propanoyl-3,5-diphenyl-4,5-dihydro-(1h)-pyrazole	12-63	monoamine oxidase B	Homo sapiens	132-137
18457821-2	2008	This also provided information about the rate of formation of the leaving group, 6-OH-(R)-3-prop-2-ynylamino-indan, designed as an MAO-B inhibitor with neuroprotective activity.	6-oh-(r)-3-prop-2-ynylamino-indan	81-114	monoamine oxidase B	Homo sapiens	131-136
18457821-10	2008	Only the N-ethyl and N-propyl derivatives showed AChE and BuChE inhibitory activity in vivo of a suitably slow onset and long duration, together with MAO-B inhibition.	n-ethyl and n-propyl	9-29	monoamine oxidase B	Homo sapiens	150-155
18713667-5	2008	The behavior of the tert-butoxyl radical mediated oxidation of MPTP contrasts with this reaction as catalyzed by monoamine oxidase B (MAO-B) that occurs selectively at the allylic alpha-carbon.	tert-butoxyl radical	20-40	monoamine oxidase B	Homo sapiens	113-132
18713667-5	2008	The behavior of the tert-butoxyl radical mediated oxidation of MPTP contrasts with this reaction as catalyzed by monoamine oxidase B (MAO-B) that occurs selectively at the allylic alpha-carbon.	tert-butoxyl radical	20-40	monoamine oxidase B	Homo sapiens	134-139
18713667-5	2008	The behavior of the tert-butoxyl radical mediated oxidation of MPTP contrasts with this reaction as catalyzed by monoamine oxidase B (MAO-B) that occurs selectively at the allylic alpha-carbon.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	63-67	monoamine oxidase B	Homo sapiens	113-132
18713667-5	2008	The behavior of the tert-butoxyl radical mediated oxidation of MPTP contrasts with this reaction as catalyzed by monoamine oxidase B (MAO-B) that occurs selectively at the allylic alpha-carbon.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	63-67	monoamine oxidase B	Homo sapiens	134-139
18713667-5	2008	The behavior of the tert-butoxyl radical mediated oxidation of MPTP contrasts with this reaction as catalyzed by monoamine oxidase B (MAO-B) that occurs selectively at the allylic alpha-carbon.	Carbon	186-192	monoamine oxidase B	Homo sapiens	113-132
18713667-5	2008	The behavior of the tert-butoxyl radical mediated oxidation of MPTP contrasts with this reaction as catalyzed by monoamine oxidase B (MAO-B) that occurs selectively at the allylic alpha-carbon.	Carbon	186-192	monoamine oxidase B	Homo sapiens	134-139
18678789-0	2008	Transtelephonic home blood pressure to assess the monoamine oxidase-B inhibitor rasagiline in Parkinson disease.	rasagiline	80-90	monoamine oxidase B	Homo sapiens	50-69
18678789-2	2008	Rasagiline mesylate is a novel irreversible selective monoamine oxidase type B inhibitor for Parkinson disease that may have a low risk of interaction with dietary tyramine because of its selectivity.	Rasagiline mesylate	0-19	monoamine oxidase B	Homo sapiens	54-78
18678789-2	2008	Rasagiline mesylate is a novel irreversible selective monoamine oxidase type B inhibitor for Parkinson disease that may have a low risk of interaction with dietary tyramine because of its selectivity.	Tyramine	164-172	monoamine oxidase B	Homo sapiens	54-78
18420288-1	2008	Selegiline, an irreversible inhibitor of monoamine oxidase B used in the treatment of Parkinson"s disease, has been demonstrated to have a potential cognition-improving effect in patients with Alzheimer"s disease (AD) undergoing treatment with an acetylcholinesterase inhibitor donepezil.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	41-60
18833504-2	2008	Rasagiline (Azilect) is a potent, highly selective and irreversible inhibitor of monoamine oxidase type B of the second generation.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	81-105
18833504-2	2008	Rasagiline (Azilect) is a potent, highly selective and irreversible inhibitor of monoamine oxidase type B of the second generation.	rasagiline	12-19	monoamine oxidase B	Homo sapiens	81-105
18598687-1	2008	The multifunctional, anti-Alzheimer drug, ladostigil (TV3326) [(N-propargyl-(3R) aminoindan-5yl)-ethyl methyl carbamate] combines the neuroprotective effects of the anti-Parkinson drug, rasagiline, a selective monoamine oxidase (MAO)-B inhibitor, with the cholinesterase (ChE) inhibitory activity of rivastigmine in a single molecule.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	42-52	monoamine oxidase B	Homo sapiens	210-235
18598687-1	2008	The multifunctional, anti-Alzheimer drug, ladostigil (TV3326) [(N-propargyl-(3R) aminoindan-5yl)-ethyl methyl carbamate] combines the neuroprotective effects of the anti-Parkinson drug, rasagiline, a selective monoamine oxidase (MAO)-B inhibitor, with the cholinesterase (ChE) inhibitory activity of rivastigmine in a single molecule.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	54-60	monoamine oxidase B	Homo sapiens	210-235
18598687-1	2008	The multifunctional, anti-Alzheimer drug, ladostigil (TV3326) [(N-propargyl-(3R) aminoindan-5yl)-ethyl methyl carbamate] combines the neuroprotective effects of the anti-Parkinson drug, rasagiline, a selective monoamine oxidase (MAO)-B inhibitor, with the cholinesterase (ChE) inhibitory activity of rivastigmine in a single molecule.	(n-propargyl-(3r) aminoindan-5yl	63-95	monoamine oxidase B	Homo sapiens	210-235
18723354-3	2008	We have reported recently that several members of the (E)-8-styrylcaffeine class of A(2A) antagonists also are potent inhibitors of monoamine oxidase B (MAO-B).	(e)-8-styrylcaffeine	54-74	monoamine oxidase B	Homo sapiens	132-151
18723354-3	2008	We have reported recently that several members of the (E)-8-styrylcaffeine class of A(2A) antagonists also are potent inhibitors of monoamine oxidase B (MAO-B).	(e)-8-styrylcaffeine	54-74	monoamine oxidase B	Homo sapiens	153-158
18666768-0	2008	Synthesis, stereochemical identification, and selective inhibitory activity against human monoamine oxidase-B of 2-methylcyclohexylidene-(4-arylthiazol-2-yl)hydrazones.	2-methylcyclohexylidene-(4-arylthiazol-2-yl)hydrazones	113-167	monoamine oxidase B	Homo sapiens	90-109
18774444-7	2008	In this article, the mechanism of action of MAO-B inhibitors, their potential neuroprotective effects, interactions such as the cheese reaction, and serotonin syndrome are discussed.	Serotonin	149-158	monoamine oxidase B	Homo sapiens	44-49
18423830-0	2008	The effect of lamotrigine on platelet monoamine oxidase type B activity in patients with bipolar depression.	Lamotrigine	14-25	monoamine oxidase B	Homo sapiens	38-62
18423830-3	2008	The aim of the study was to determine the effects of 6-weeks lamotrigine treatment on platelet MAO type B (MAO-B) activity in patient with bipolar depression.	Lamotrigine	61-72	monoamine oxidase B	Homo sapiens	95-105
18423830-3	2008	The aim of the study was to determine the effects of 6-weeks lamotrigine treatment on platelet MAO type B (MAO-B) activity in patient with bipolar depression.	Lamotrigine	61-72	monoamine oxidase B	Homo sapiens	107-112
18423830-5	2008	Platelet MAO-B activity was determined spectrofluorimetrically before and after 6 weeks of the treatment with a relatively low dose of lamotrigine (100 mg/day).	Lamotrigine	135-146	monoamine oxidase B	Homo sapiens	9-14
18423830-6	2008	Six weeks of treatment with lamotrigine significantly decreased platelet MAO-B activity in bipolar depressed patients.	Lamotrigine	28-39	monoamine oxidase B	Homo sapiens	73-78
18423830-9	2008	These findings provide in vivo insight of lamotrigine effect on platelet MAO-B activity in patients with bipolar depression.	Lamotrigine	42-53	monoamine oxidase B	Homo sapiens	73-78
18505360-8	2008	This COMT inhibitor should be applied together with an oxidative stress reducing monoamine oxidase-B inhibitor, in order to force central dopamine metabolism further down via the methylation path.	Dopamine	138-146	monoamine oxidase B	Homo sapiens	81-100
18307054-1	2008	Rasagiline is a selective and irreversible monoamine oxidase-B inhibitor.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	43-62
18426226-3	2008	Benzylhydrazine is bound more tightly to MAO B than to MAO A, and phenylhydrazine is bound weakly by either enzyme.	benzylhydrazine	0-15	monoamine oxidase B	Homo sapiens	41-46
18426226-4	2008	Phenylethylhydrazine stoichiometrically reduces the covalent FAD moieties of MAO A and of MAO B.	Phenelzine	0-20	monoamine oxidase B	Homo sapiens	90-95
18426226-5	2008	Molecular oxygen is required for the inhibition reactions, and the level of O2 consumption for phenylethylhydrazine is 6-7-fold higher with either MAO A or MAO B than for the corresponding reactions with benzylhydrazine or phenylhydrazine.	Oxygen	10-16	monoamine oxidase B	Homo sapiens	156-161
18426226-5	2008	Molecular oxygen is required for the inhibition reactions, and the level of O2 consumption for phenylethylhydrazine is 6-7-fold higher with either MAO A or MAO B than for the corresponding reactions with benzylhydrazine or phenylhydrazine.	Oxygen	76-78	monoamine oxidase B	Homo sapiens	156-161
18426226-5	2008	Molecular oxygen is required for the inhibition reactions, and the level of O2 consumption for phenylethylhydrazine is 6-7-fold higher with either MAO A or MAO B than for the corresponding reactions with benzylhydrazine or phenylhydrazine.	Phenelzine	95-115	monoamine oxidase B	Homo sapiens	156-161
18426226-8	2008	The three-dimensional (2.3 A) structures of phenylethylhydrazine- and benzylhydrazine-inhibited MAO B show that alkylation occurs at the N(5) position on the re face of the covalent flavin with loss of the hydrazyl nitrogens.	Phenelzine	44-64	monoamine oxidase B	Homo sapiens	96-101
18426226-8	2008	The three-dimensional (2.3 A) structures of phenylethylhydrazine- and benzylhydrazine-inhibited MAO B show that alkylation occurs at the N(5) position on the re face of the covalent flavin with loss of the hydrazyl nitrogens.	benzylhydrazine	70-85	monoamine oxidase B	Homo sapiens	96-101
18426226-8	2008	The three-dimensional (2.3 A) structures of phenylethylhydrazine- and benzylhydrazine-inhibited MAO B show that alkylation occurs at the N(5) position on the re face of the covalent flavin with loss of the hydrazyl nitrogens.	4,6-dinitro-o-cresol	182-188	monoamine oxidase B	Homo sapiens	96-101
18426226-8	2008	The three-dimensional (2.3 A) structures of phenylethylhydrazine- and benzylhydrazine-inhibited MAO B show that alkylation occurs at the N(5) position on the re face of the covalent flavin with loss of the hydrazyl nitrogens.	Nitrogen	215-224	monoamine oxidase B	Homo sapiens	96-101
18508693-1	2008	The neuroprotective action of a set of new hydroxypyridinone-based (3,4-HP) compounds (A, B and C), which are iron chelators extra-functionalized with a propargylamino group for potential MAO-B inhibition, was evaluated after cell treatment with MPP+ (an in vivo inducer of parkinsonism) and Abeta(1-40) and/or Abeta(1-42) peptides.	1-hydroxy-2(1H)-pyridinone	43-60	monoamine oxidase B	Homo sapiens	188-193
18237459-1	2008	Long-term administration of the monoamine oxidase (MAO)-B inhibitor selegiline may reduce neuronal death based on preclinical findings and reduce progression of chronic neurodegeneration due to outcomes of long-term clinical trials in patients with Parkinson"s disease.	Selegiline	68-78	monoamine oxidase B	Homo sapiens	32-57
18331475-0	2008	Anti-apoptotic effect of Mao-B inhibitor PF9601N [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine] is mediated by p53 pathway inhibition in MPP+-treated SH-SY5Y human dopaminergic cells.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	41-48	monoamine oxidase B	Homo sapiens	25-30
18331475-0	2008	Anti-apoptotic effect of Mao-B inhibitor PF9601N [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine] is mediated by p53 pathway inhibition in MPP+-treated SH-SY5Y human dopaminergic cells.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	50-100	monoamine oxidase B	Homo sapiens	25-30
18331475-0	2008	Anti-apoptotic effect of Mao-B inhibitor PF9601N [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine] is mediated by p53 pathway inhibition in MPP+-treated SH-SY5Y human dopaminergic cells.	mangion-purified polysaccharide (Candida albicans)	143-147	monoamine oxidase B	Homo sapiens	25-30
18331475-1	2008	PF9601N [N-(2-propynyl) 2-(5-benzyloxyindol) methylamine] is a non-amphetamine type MAO-B inhibitor that has shown neuroprotective properties in vivo using different experimental models of Parkinson"s disease.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	0-7	monoamine oxidase B	Homo sapiens	84-89
18331475-1	2008	PF9601N [N-(2-propynyl) 2-(5-benzyloxyindol) methylamine] is a non-amphetamine type MAO-B inhibitor that has shown neuroprotective properties in vivo using different experimental models of Parkinson"s disease.	n-(2-propynyl) 2-(5-benzyloxyindol) methylamine	9-56	monoamine oxidase B	Homo sapiens	84-89
20641420-2	2004	MAO-A preferentially oxidizes serotonin and noradrenaline, whereas MAO-B preferentially oxidizes phenethylamine.	phenethylamine	97-111	monoamine oxidase B	Homo sapiens	67-72
18426226-1	2008	The structure and mechanism of human monoamine oxidase B (MAO B) inhibition by hydrazines are investigated and compared with data on human monoamine oxidase A (MAO A).	Hydrazines	79-89	monoamine oxidase B	Homo sapiens	37-56
18426226-1	2008	The structure and mechanism of human monoamine oxidase B (MAO B) inhibition by hydrazines are investigated and compared with data on human monoamine oxidase A (MAO A).	Hydrazines	79-89	monoamine oxidase B	Homo sapiens	58-63
18391214-6	2008	The results confirm that the inhibitor selectivity of MAOA and MAOB is caused by the structural differences arising from Ile-335 in MAOA vs. Tyr-326 in MAOB.	Isoleucine	121-124	monoamine oxidase B	Homo sapiens	63-67
18391214-6	2008	The results confirm that the inhibitor selectivity of MAOA and MAOB is caused by the structural differences arising from Ile-335 in MAOA vs. Tyr-326 in MAOB.	Isoleucine	121-124	monoamine oxidase B	Homo sapiens	152-156
18391214-6	2008	The results confirm that the inhibitor selectivity of MAOA and MAOB is caused by the structural differences arising from Ile-335 in MAOA vs. Tyr-326 in MAOB.	Tyrosine	141-144	monoamine oxidase B	Homo sapiens	63-67
18391214-6	2008	The results confirm that the inhibitor selectivity of MAOA and MAOB is caused by the structural differences arising from Ile-335 in MAOA vs. Tyr-326 in MAOB.	Tyrosine	141-144	monoamine oxidase B	Homo sapiens	152-156
17918234-3	2008	The gene encoding monoamine oxidase B (MAOB), the main enzyme degrading dopamine in the human brain, is located in this region.	Dopamine	72-80	monoamine oxidase B	Homo sapiens	18-37
17918234-3	2008	The gene encoding monoamine oxidase B (MAOB), the main enzyme degrading dopamine in the human brain, is located in this region.	Dopamine	72-80	monoamine oxidase B	Homo sapiens	39-43
18205889-1	2008	The fibroblast growth factor 20 (FGF20) and monoamine oxidase B (MAOB) genes are associated with Parkinson Disease (PD) risk and both are in the dopamine bio-pathway.	Dopamine	145-153	monoamine oxidase B	Homo sapiens	44-63
18313306-0	2008	Stereochemical studies on the novel monoamine oxidase B substrates (1R,6S)- and (1S,6R)-3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane.	1r,6s)	68-74	monoamine oxidase B	Homo sapiens	36-55
18313306-0	2008	Stereochemical studies on the novel monoamine oxidase B substrates (1R,6S)- and (1S,6R)-3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane.	(1s,6r)-3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane	80-133	monoamine oxidase B	Homo sapiens	36-55
18313306-1	2008	Previous studies have established the unexpected monoamine oxidase-B (MAO-B) substrate properties of racemic 3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane, the 3,4-cyclopropyl analog of the achiral proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	3-methyl-6-phenyl-3-aza-bicyclo(4.1.0)heptane	109-154	monoamine oxidase B	Homo sapiens	49-68
18313306-1	2008	Previous studies have established the unexpected monoamine oxidase-B (MAO-B) substrate properties of racemic 3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane, the 3,4-cyclopropyl analog of the achiral proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	3-methyl-6-phenyl-3-aza-bicyclo(4.1.0)heptane	109-154	monoamine oxidase B	Homo sapiens	70-75
18313306-1	2008	Previous studies have established the unexpected monoamine oxidase-B (MAO-B) substrate properties of racemic 3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane, the 3,4-cyclopropyl analog of the achiral proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	3,4-cyclopropyl analog	160-182	monoamine oxidase B	Homo sapiens	49-68
18313306-1	2008	Previous studies have established the unexpected monoamine oxidase-B (MAO-B) substrate properties of racemic 3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane, the 3,4-cyclopropyl analog of the achiral proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	3,4-cyclopropyl analog	160-182	monoamine oxidase B	Homo sapiens	70-75
18313306-1	2008	Previous studies have established the unexpected monoamine oxidase-B (MAO-B) substrate properties of racemic 3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane, the 3,4-cyclopropyl analog of the achiral proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine	198-256	monoamine oxidase B	Homo sapiens	49-68
18313306-1	2008	Previous studies have established the unexpected monoamine oxidase-B (MAO-B) substrate properties of racemic 3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane, the 3,4-cyclopropyl analog of the achiral proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine	198-256	monoamine oxidase B	Homo sapiens	70-75
18313306-1	2008	Previous studies have established the unexpected monoamine oxidase-B (MAO-B) substrate properties of racemic 3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane, the 3,4-cyclopropyl analog of the achiral proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	258-262	monoamine oxidase B	Homo sapiens	49-68
18313306-1	2008	Previous studies have established the unexpected monoamine oxidase-B (MAO-B) substrate properties of racemic 3-methyl-6-phenyl-3-aza-bicyclo[4.1.0]heptane, the 3,4-cyclopropyl analog of the achiral proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	258-262	monoamine oxidase B	Homo sapiens	70-75
18313306-2	2008	The two stereocenters present in this compound provide an opportunity to examine the enantioselectivity and diastereoselectivity of the MAO-B-catalyzed ring alpha-carbon oxidation of cyclic tertiary amines to give the corresponding conjugated iminiumyl metabolites.	Carbon	163-169	monoamine oxidase B	Homo sapiens	136-141
18313306-2	2008	The two stereocenters present in this compound provide an opportunity to examine the enantioselectivity and diastereoselectivity of the MAO-B-catalyzed ring alpha-carbon oxidation of cyclic tertiary amines to give the corresponding conjugated iminiumyl metabolites.	Amines	199-205	monoamine oxidase B	Homo sapiens	136-141
18180269-7	2008	N-Dealkylation of 1, the principal metabolic route observed in vivo, was found to be predominately monoamine oxidase-B-mediated with the resulting putative aldehyde intermediate undergoing subsequent oxidation to 2 or reduction to 3.	Nitrogen	0-1	monoamine oxidase B	Homo sapiens	99-118
18180269-7	2008	N-Dealkylation of 1, the principal metabolic route observed in vivo, was found to be predominately monoamine oxidase-B-mediated with the resulting putative aldehyde intermediate undergoing subsequent oxidation to 2 or reduction to 3.	Aldehydes	156-164	monoamine oxidase B	Homo sapiens	99-118
18205889-1	2008	The fibroblast growth factor 20 (FGF20) and monoamine oxidase B (MAOB) genes are associated with Parkinson Disease (PD) risk and both are in the dopamine bio-pathway.	Dopamine	145-153	monoamine oxidase B	Homo sapiens	65-69
18065227-0	2008	Structure-activity relationships in the inhibition of monoamine oxidase B by 1-methyl-3-phenylpyrroles.	1-methyl-3-phenylpyrroles	77-102	monoamine oxidase B	Homo sapiens	54-73
18065227-1	2008	1-Methyl-3-phenyl-3-pyrrolines are structural analogues of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and like MPTP are selective substrates of monoamine oxidase B (MAO-B).	1-methyl-3-phenyl-3-pyrrolines	0-30	monoamine oxidase B	Homo sapiens	168-187
18065227-1	2008	1-Methyl-3-phenyl-3-pyrrolines are structural analogues of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and like MPTP are selective substrates of monoamine oxidase B (MAO-B).	1-methyl-3-phenyl-3-pyrrolines	0-30	monoamine oxidase B	Homo sapiens	189-194
18065227-1	2008	1-Methyl-3-phenyl-3-pyrrolines are structural analogues of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and like MPTP are selective substrates of monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	74-118	monoamine oxidase B	Homo sapiens	168-187
18065227-1	2008	1-Methyl-3-phenyl-3-pyrrolines are structural analogues of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and like MPTP are selective substrates of monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	74-118	monoamine oxidase B	Homo sapiens	189-194
18065227-1	2008	1-Methyl-3-phenyl-3-pyrrolines are structural analogues of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and like MPTP are selective substrates of monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	120-124	monoamine oxidase B	Homo sapiens	168-187
18065227-1	2008	1-Methyl-3-phenyl-3-pyrrolines are structural analogues of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and like MPTP are selective substrates of monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	120-124	monoamine oxidase B	Homo sapiens	189-194
18065227-1	2008	1-Methyl-3-phenyl-3-pyrrolines are structural analogues of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and like MPTP are selective substrates of monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	135-139	monoamine oxidase B	Homo sapiens	168-187
18065227-1	2008	1-Methyl-3-phenyl-3-pyrrolines are structural analogues of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and like MPTP are selective substrates of monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	135-139	monoamine oxidase B	Homo sapiens	189-194
18065227-2	2008	As part of an ongoing investigation into the substrate properties of various 1-methyl-3-phenyl-3-pyrrolinyl derivatives, it is shown in the present study that their respective MAO-B catalyzed oxidation products act as reversible competitive inhibitors of the enzyme.	1-methyl-3-phenyl-3-pyrrolinyl	77-107	monoamine oxidase B	Homo sapiens	176-181
18728767-6	2008	We propose that future guidelines include a trial with tolcapone in all PD patients who continue to complain about motor fluctuations despite treatment with entacapone and/or MAO-B inhibitors.	Tolcapone	55-64	monoamine oxidase B	Homo sapiens	175-180
18067186-3	2008	Treatment with the new irreversible monoamine oxidase B inhibitor rasagiline at standard doses resulted in a rapid, dramatic, and sustained improvement of the frequency and duration of FOG episodes.	rasagiline	66-76	monoamine oxidase B	Homo sapiens	36-55
18219438-1	2008	Our aim was to study fracture risk in users of various antidepressants (tricyclic antidepressants, selective serotonin reuptake inhibitors, and the group of other antidepressants including monoamine oxidase B inhibitors and drugs with effect on the norepinephrine system) and its relationship with effects on inhibition of the cholinergic and serotonin transporter system.	Norepinephrine	249-263	monoamine oxidase B	Homo sapiens	189-208
18322402-1	2008	BACKGROUND: A significant percentage of patients with Parkinson"s disease (PD) continue to experience motor fluctuations and dyskinesias despite the association of dopamine agonists and levodopa with COMT or MAO-B inhibitors.	Levodopa	186-194	monoamine oxidase B	Homo sapiens	208-213
18072817-1	2008	Rasagiline (Azilect) is a novel, selective, irreversible second-generation inhibitor of monoamine oxidase type B (MAO-B).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	88-112
18072817-1	2008	Rasagiline (Azilect) is a novel, selective, irreversible second-generation inhibitor of monoamine oxidase type B (MAO-B).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	114-119
18072817-1	2008	Rasagiline (Azilect) is a novel, selective, irreversible second-generation inhibitor of monoamine oxidase type B (MAO-B).	rasagiline	12-19	monoamine oxidase B	Homo sapiens	88-112
18072817-1	2008	Rasagiline (Azilect) is a novel, selective, irreversible second-generation inhibitor of monoamine oxidase type B (MAO-B).	rasagiline	12-19	monoamine oxidase B	Homo sapiens	114-119
18668620-8	2008	MAO-B inhibitors (selegiline and rasagiline) can decrease FOG frequency or severity, but its clinical significance is still unknown.	Selegiline	18-28	monoamine oxidase B	Homo sapiens	0-5
18668620-8	2008	MAO-B inhibitors (selegiline and rasagiline) can decrease FOG frequency or severity, but its clinical significance is still unknown.	rasagiline	33-43	monoamine oxidase B	Homo sapiens	0-5
18029114-0	2008	The MAO-A gene, platelet MAO-B activity and psychosocial environment in adolescent female alcohol-related problem behaviour.	Alcohols	90-97	monoamine oxidase B	Homo sapiens	25-30
18029114-7	2008	Furthermore, females with low platelet MAO-B activity showed an increased risk of alcohol-related problem behaviour in an unfavourable environment.	Alcohols	82-89	monoamine oxidase B	Homo sapiens	39-44
18029114-8	2008	CONCLUSIONS: Poor psychosocial environment interacts with the high activity MAO-A genotype and low platelet MAO-B enzyme activity to increase vulnerability for female adolescent alcohol-related problem behaviour.	Alcohols	178-185	monoamine oxidase B	Homo sapiens	108-113
17570647-0	2008	Specific binding of [3H]Ro 19-6327 (lazabemide) to monoamine oxidase B is increased in frontal cortex of suicide victims after controlling for age at death.	Tritium	21-23	monoamine oxidase B	Homo sapiens	51-70
17570647-0	2008	Specific binding of [3H]Ro 19-6327 (lazabemide) to monoamine oxidase B is increased in frontal cortex of suicide victims after controlling for age at death.	lazabemide	36-46	monoamine oxidase B	Homo sapiens	51-70
17570647-3	2008	We have evaluated the association of MAO-B density (assessed by [3H]Ro 19-6327 - lazabemide - binding) with type of death (suicide victims vs non-suicide controls) after controlling for age at death.	Tritium	65-67	monoamine oxidase B	Homo sapiens	37-42
17570647-3	2008	We have evaluated the association of MAO-B density (assessed by [3H]Ro 19-6327 - lazabemide - binding) with type of death (suicide victims vs non-suicide controls) after controlling for age at death.	lazabemide	81-91	monoamine oxidase B	Homo sapiens	37-42
18044898-6	2007	In contrast, an earlier study of MAO B only found evidence for an anionic flavin radical (DeRose, V. J.; et al.	flavin radical	74-88	monoamine oxidase B	Homo sapiens	33-38
18832861-1	2008	BACKGROUND: Monoamine oxidase B (MAO-B) enzyme is involved in the oxidative metabolism of dopamine.	Dopamine	90-98	monoamine oxidase B	Homo sapiens	12-31
18832861-1	2008	BACKGROUND: Monoamine oxidase B (MAO-B) enzyme is involved in the oxidative metabolism of dopamine.	Dopamine	90-98	monoamine oxidase B	Homo sapiens	33-38
19004128-0	2008	[The use of a new MAO B inhibitor rasagiline in the treatment of motor fluctuations in Parkinson"s disease].	rasagiline	34-44	monoamine oxidase B	Homo sapiens	18-23
17915852-0	2007	Structures of human monoamine oxidase B complexes with selective noncovalent inhibitors: safinamide and coumarin analogs.	safinamide	89-99	monoamine oxidase B	Homo sapiens	20-39
17881661-8	2007	This reaction was almost completely inhibited in human hepatic microsomes and mitochondria by the monoamine oxidase (MAO)-B-specific inhibitor selegiline.	Selegiline	143-153	monoamine oxidase B	Homo sapiens	98-123
17881661-11	2007	Overall, the data indicate that the primary enzymes responsible for the primary metabolism of bicifadine in humans are MAO-B and CYP2D6.	bicifadine	94-104	monoamine oxidase B	Homo sapiens	119-124
18041937-3	2007	The two available MAO-B inhibitors approved for use in the United States, rasagiline and selegiline, each provide symptomatic relief as monotherapy and as adjunctive therapy, and have shown potential disease-modifying effects in experimental models and clinical studies.	rasagiline	74-84	monoamine oxidase B	Homo sapiens	18-23
18041937-3	2007	The two available MAO-B inhibitors approved for use in the United States, rasagiline and selegiline, each provide symptomatic relief as monotherapy and as adjunctive therapy, and have shown potential disease-modifying effects in experimental models and clinical studies.	Selegiline	89-99	monoamine oxidase B	Homo sapiens	18-23
18041937-9	2007	A third agent with MAO-B inhibition properties, safinamide, is in phase III development.	safinamide	48-58	monoamine oxidase B	Homo sapiens	19-24
18041937-10	2007	Although not yet approved, safinamide may offer the added advantage of combined MAO-B and dopamine reuptake inhibition.	safinamide	27-37	monoamine oxidase B	Homo sapiens	80-85
17915852-0	2007	Structures of human monoamine oxidase B complexes with selective noncovalent inhibitors: safinamide and coumarin analogs.	coumarin	104-112	monoamine oxidase B	Homo sapiens	20-39
17915852-1	2007	Structures of human monoamine oxidase B (MAO B) in complex with safinamide and two coumarin derivatives, all sharing a common benzyloxy substituent, were determined by X-ray crystallography.	safinamide	64-74	monoamine oxidase B	Homo sapiens	20-39
17915852-1	2007	Structures of human monoamine oxidase B (MAO B) in complex with safinamide and two coumarin derivatives, all sharing a common benzyloxy substituent, were determined by X-ray crystallography.	safinamide	64-74	monoamine oxidase B	Homo sapiens	41-46
17915852-1	2007	Structures of human monoamine oxidase B (MAO B) in complex with safinamide and two coumarin derivatives, all sharing a common benzyloxy substituent, were determined by X-ray crystallography.	coumarin	83-91	monoamine oxidase B	Homo sapiens	20-39
17915852-1	2007	Structures of human monoamine oxidase B (MAO B) in complex with safinamide and two coumarin derivatives, all sharing a common benzyloxy substituent, were determined by X-ray crystallography.	coumarin	83-91	monoamine oxidase B	Homo sapiens	41-46
17635668-1	2007	The anti-Parkinson, selective irreversible monoamine oxidase B inhibitor drug, rasagiline (Azilect), recently approved by the US Food and Drug Administration, has been shown to possess neuroprotective-neurorescue activities in in vitro and in vivo models.	rasagiline	79-89	monoamine oxidase B	Homo sapiens	43-62
18042509-1	2007	OBJECTIVE: To assess the long-term safety (primary aim) and efficacy (secondary aim) of the MAO-B inhibitor Selegiline Transdermal System (STS) for the treatment of HIV-associated cognitive impairment.	Selegiline	108-118	monoamine oxidase B	Homo sapiens	92-97
17824599-1	2007	Safinamide, (S)-N2-{4-[(3-fluorobenzyl)oxy]benzyl}alaninamide methanesulfonate, which is in phase III clinical trials as an anti-Parkinson drug, and a library of alkanamidic analogues were prepared through an expeditious solid-phase synthesis and evaluated for their monoamine oxidase B (MAO-B) and monoamine oxidase A (MAO-A) inhibitory activity and selectivity.	safinamide	0-10	monoamine oxidase B	Homo sapiens	267-286
17824599-1	2007	Safinamide, (S)-N2-{4-[(3-fluorobenzyl)oxy]benzyl}alaninamide methanesulfonate, which is in phase III clinical trials as an anti-Parkinson drug, and a library of alkanamidic analogues were prepared through an expeditious solid-phase synthesis and evaluated for their monoamine oxidase B (MAO-B) and monoamine oxidase A (MAO-A) inhibitory activity and selectivity.	safinamide	0-10	monoamine oxidase B	Homo sapiens	288-293
17824599-2	2007	(S)-3-Chlorobenzyloxyalaninamide (8) and (S)-3-chlorobenzyloxyserinamide (13) derivatives proved to be more potent MAO-B inhibitors than safinamide (IC50 = 33 and 43 nM, respectively, vs 98 nM) but with a lower MAO-B selectivity (SI = 3455 and 1967, respectively, vs 5918).	(s)-3-chlorobenzyloxyalaninamide	0-32	monoamine oxidase B	Homo sapiens	115-120
17824599-2	2007	(S)-3-Chlorobenzyloxyalaninamide (8) and (S)-3-chlorobenzyloxyserinamide (13) derivatives proved to be more potent MAO-B inhibitors than safinamide (IC50 = 33 and 43 nM, respectively, vs 98 nM) but with a lower MAO-B selectivity (SI = 3455 and 1967, respectively, vs 5918).	(s)-3-chlorobenzyloxyalaninamide	0-32	monoamine oxidase B	Homo sapiens	211-216
17824599-2	2007	(S)-3-Chlorobenzyloxyalaninamide (8) and (S)-3-chlorobenzyloxyserinamide (13) derivatives proved to be more potent MAO-B inhibitors than safinamide (IC50 = 33 and 43 nM, respectively, vs 98 nM) but with a lower MAO-B selectivity (SI = 3455 and 1967, respectively, vs 5918).	(s)-3-chlorobenzyloxyserinamide	41-72	monoamine oxidase B	Homo sapiens	115-120
17824599-3	2007	The highest MAO-B inhibitory potency (IC50 = 17 nM) and a good selectivity (SI = 2941) were displayed by (R)-21, a tetrahydroisoquinoline analogue of safinamide.	dichlorofluoromethane	105-111	monoamine oxidase B	Homo sapiens	12-17
17824599-3	2007	The highest MAO-B inhibitory potency (IC50 = 17 nM) and a good selectivity (SI = 2941) were displayed by (R)-21, a tetrahydroisoquinoline analogue of safinamide.	1,2,3,4-tetrahydroisoquinoline	115-137	monoamine oxidase B	Homo sapiens	12-17
17824599-3	2007	The highest MAO-B inhibitory potency (IC50 = 17 nM) and a good selectivity (SI = 2941) were displayed by (R)-21, a tetrahydroisoquinoline analogue of safinamide.	safinamide	150-160	monoamine oxidase B	Homo sapiens	12-17
17824599-5	2007	The significantly diverse MAO-B affinities of a number of R and S alpha-aminoamide enantiomers, including the two rigid analogues (21) of safinamide, indicated likely enantioselective interactions at the enzymatic binding sites.	safinamide	138-148	monoamine oxidase B	Homo sapiens	26-31
17965517-7	2007	The involvement of CYP1A2, CYP3A4, and MAO-B was demonstrated in the pathways leading to 5-trifluoromethoxysalicylic acid.	5-trifluoromethoxysalicylic acid	89-121	monoamine oxidase B	Homo sapiens	39-44
17849100-2	2007	Previously we reported real-time monitoring of dopamine release from nerve model cells by enzyme-catalyzed luminescence measurement with tyramine oxidase and peroxidase.	Dopamine	47-55	monoamine oxidase B	Homo sapiens	137-153
17849100-3	2007	In the present study, the system was modified with glutamate oxidase instead of tyramine oxidase to detect L-glutamate sensitively ( approximately 10 nM) and rapidly with high temporal resolution (&lt;1 s).	Glutamic Acid	107-118	monoamine oxidase B	Homo sapiens	80-96
17910428-2	2007	Most of them showed higher inhibition potency toward MAO-B, the most effective one being 3-(3-nitrophenyl)-9H-indeno[1,2-e] [1,2,4]triazin-9-one (4c), which displayed an IC50 value of 80 nM and proved to be 10-fold more potent than its [2,1-e] fusion isomer 5.	3-(3-nitrophenyl)-9H-indeno(1,2-e)(1,2,4)triazin-9-one	89-144	monoamine oxidase B	Homo sapiens	53-58
17910428-3	2007	Replacing the 3-phenyl group of the known indeno[1,2-c]pyridazin-5-one MAO-B inhibitors with a flexible phenoxymethyl group enhanced the inhibitory potency.	indeno[1,2-c]pyridazin-5-one	42-70	monoamine oxidase B	Homo sapiens	71-76
17883257-8	2007	beta-Carbolines were isolated from raisins and acted as good competitive inhibitors of MAO-A (harman) and MAO-B (norharman) isozymes.	Carbolines	0-15	monoamine oxidase B	Homo sapiens	106-111
17635668-1	2007	The anti-Parkinson, selective irreversible monoamine oxidase B inhibitor drug, rasagiline (Azilect), recently approved by the US Food and Drug Administration, has been shown to possess neuroprotective-neurorescue activities in in vitro and in vivo models.	rasagiline	91-98	monoamine oxidase B	Homo sapiens	43-62
17885625-1	2007	OBJECTIVE: The genes of catalytic enzymes of dopamine, including monoamine oxidase (MAOA and MAOB) and catechol-O-methyltransferase (COMT), have been major candidates for genes that affect smoking behavior.	Dopamine	45-53	monoamine oxidase B	Homo sapiens	93-97
17931095-1	2007	Selegiline, a selective monoamine oxidase-B inhibitor, has been used for decades in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	24-43
17652642-2	2007	Selegiline is an MAO-B inhibitor with antioxidant and neurotrophic properties.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	17-22
17640790-9	2007	Our data provide first suggestive evidence that the MAOB A644G SNP is involved in the outcome of treatment with mirtazapine or paroxetine in females with major depression.	Mirtazapine	112-123	monoamine oxidase B	Homo sapiens	52-56
17640790-9	2007	Our data provide first suggestive evidence that the MAOB A644G SNP is involved in the outcome of treatment with mirtazapine or paroxetine in females with major depression.	Paroxetine	127-137	monoamine oxidase B	Homo sapiens	52-56
17909308-1	2007	BACKGROUND: Selegiline orally disintegrating tablet (ODT; Zelapar) is a selective monoamine oxidase B inhibitor developed as an adjunct to levodopa (LD) for Parkinson disease.	Selegiline	12-22	monoamine oxidase B	Homo sapiens	82-101
18035186-1	2007	BACKGROUND: Inhibitors of monoamine oxidase (MAO) with selectivity and specificity for MAO type B (MAO-B) prolong the duration of action of both endogenously and exogenously derived dopamine.	Dopamine	182-190	monoamine oxidase B	Homo sapiens	87-97
17909308-1	2007	BACKGROUND: Selegiline orally disintegrating tablet (ODT; Zelapar) is a selective monoamine oxidase B inhibitor developed as an adjunct to levodopa (LD) for Parkinson disease.	Selegiline	58-65	monoamine oxidase B	Homo sapiens	82-101
18035186-1	2007	BACKGROUND: Inhibitors of monoamine oxidase (MAO) with selectivity and specificity for MAO type B (MAO-B) prolong the duration of action of both endogenously and exogenously derived dopamine.	Dopamine	182-190	monoamine oxidase B	Homo sapiens	99-104
18035186-2	2007	Rasagiline [N-propargyl-l(R)-aminoindan] is a second-generation propargylamine pharmacophore that selectively and irreversibly inhibits brain MAO-B and is specifically designed for the treatment of Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	142-147
17367163-7	2007	2-PCPA shows limited selectivity for human MAOs versus LSD1, with kinact/KI values only 16-fold and 2.4-fold higher for MAO B and MAO A, respectively.	Tranylcypromine	0-6	monoamine oxidase B	Homo sapiens	120-125
18035186-2	2007	Rasagiline [N-propargyl-l(R)-aminoindan] is a second-generation propargylamine pharmacophore that selectively and irreversibly inhibits brain MAO-B and is specifically designed for the treatment of Parkinson"s disease (PD).	n-propargyl-l(r)-aminoindan	12-39	monoamine oxidase B	Homo sapiens	142-147
18035186-2	2007	Rasagiline [N-propargyl-l(R)-aminoindan] is a second-generation propargylamine pharmacophore that selectively and irreversibly inhibits brain MAO-B and is specifically designed for the treatment of Parkinson"s disease (PD).	propargylamine	64-78	monoamine oxidase B	Homo sapiens	142-147
18035186-8	2007	Based on the results from those studies, we concluded that rasagiline PO QD, at the therapeutic dosage range of 0.5 to 1 rag/d, is effective and well tolerated and completely, selectively, and specifically inhibited MAO-B.	rasagiline	59-69	monoamine oxidase B	Homo sapiens	216-221
17597580-1	2007	Monoamine oxidase B (MAO-B) functions in the deamination of monoamines, including dopamine and norepinephrine.	monoamines	60-70	monoamine oxidase B	Homo sapiens	0-19
17597580-1	2007	Monoamine oxidase B (MAO-B) functions in the deamination of monoamines, including dopamine and norepinephrine.	monoamines	60-70	monoamine oxidase B	Homo sapiens	21-26
17597580-1	2007	Monoamine oxidase B (MAO-B) functions in the deamination of monoamines, including dopamine and norepinephrine.	Dopamine	82-90	monoamine oxidase B	Homo sapiens	0-19
17597580-1	2007	Monoamine oxidase B (MAO-B) functions in the deamination of monoamines, including dopamine and norepinephrine.	Dopamine	82-90	monoamine oxidase B	Homo sapiens	21-26
17597580-1	2007	Monoamine oxidase B (MAO-B) functions in the deamination of monoamines, including dopamine and norepinephrine.	Norepinephrine	95-109	monoamine oxidase B	Homo sapiens	0-19
17597580-1	2007	Monoamine oxidase B (MAO-B) functions in the deamination of monoamines, including dopamine and norepinephrine.	Norepinephrine	95-109	monoamine oxidase B	Homo sapiens	21-26
17573034-1	2007	Due to their pharmacological importance in the oxidation of amine neurotransmitters, the membrane-bound flavoenzymes monoamine oxidase A and monoamine oxidase B have attracted numerous investigations and, as a result, two different mechanisms; the single electron transfer and the polar nucleophilic mechanisms, have been proposed to describe their catalytic mechanisms.	Amines	60-65	monoamine oxidase B	Homo sapiens	141-160
17347320-2	2007	It was postulated that certain carbamate esters would inhibit AChE and BChE with the concomitant release in the brain of the OH-derivatives of rasagiline or selegiline that can serve as inhibitors of MAO-B and as antioxidants.	carbamate esters	31-47	monoamine oxidase B	Homo sapiens	200-205
17347320-2	2007	It was postulated that certain carbamate esters would inhibit AChE and BChE with the concomitant release in the brain of the OH-derivatives of rasagiline or selegiline that can serve as inhibitors of MAO-B and as antioxidants.	rasagiline	143-153	monoamine oxidase B	Homo sapiens	200-205
17347320-2	2007	It was postulated that certain carbamate esters would inhibit AChE and BChE with the concomitant release in the brain of the OH-derivatives of rasagiline or selegiline that can serve as inhibitors of MAO-B and as antioxidants.	Selegiline	157-167	monoamine oxidase B	Homo sapiens	200-205
17347320-8	2007	The data show how the degree of enzyme inhibition can be manipulated by structural changes in the N-methyl, N-alkyl carbamates and the corresponding leaving group to achieve therapeutic levels of brain AChE, BChE, and MAO-B inhibition.	n-methyl, n-alkyl carbamates	98-126	monoamine oxidase B	Homo sapiens	218-223
17545750-1	2007	Monoamine oxidase type B (MAO-B) is the predominant isoform responsible for the metabolic breakdown of dopamine in the brain.	Dopamine	103-111	monoamine oxidase B	Homo sapiens	0-24
17545750-1	2007	Monoamine oxidase type B (MAO-B) is the predominant isoform responsible for the metabolic breakdown of dopamine in the brain.	Dopamine	103-111	monoamine oxidase B	Homo sapiens	26-31
17545750-2	2007	Selective inhibition of brain MAO-B results in elevation of synaptosomal dopamine concentrations.	Dopamine	73-81	monoamine oxidase B	Homo sapiens	30-35
17545750-3	2007	Data have been reported regarding the selective MAO-B inhibitors, rasagiline and selegiline, for the symptomatic treatment of Parkinson disease (PD).	rasagiline	66-76	monoamine oxidase B	Homo sapiens	48-53
17545750-3	2007	Data have been reported regarding the selective MAO-B inhibitors, rasagiline and selegiline, for the symptomatic treatment of Parkinson disease (PD).	Selegiline	81-91	monoamine oxidase B	Homo sapiens	48-53
17545750-7	2007	Rasagiline is a selective, second-generation, irreversible MAO-B inhibitor, with at least 5 times the potency of selegiline in vitro and in animal models.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	59-64
17659477-1	2007	Merck Serono SA (formerly Serono), under license from Newron Pharmaceuticals SpA (following its acquisition of the rights from Pharmacia and Upjohn AB [now Pfizer Inc]), is developing the oral alpha-aminoamide derivative of milacemide, safinamide, a monoamine oxidase-B and glutamate release inhibitor, for the potential treatment of Parkinson"s disease, epilepsy and restless legs syndrome.	serono	6-12	monoamine oxidase B	Homo sapiens	250-269
17659477-1	2007	Merck Serono SA (formerly Serono), under license from Newron Pharmaceuticals SpA (following its acquisition of the rights from Pharmacia and Upjohn AB [now Pfizer Inc]), is developing the oral alpha-aminoamide derivative of milacemide, safinamide, a monoamine oxidase-B and glutamate release inhibitor, for the potential treatment of Parkinson"s disease, epilepsy and restless legs syndrome.	alpha-aminoamide	193-209	monoamine oxidase B	Homo sapiens	250-269
17416530-0	2007	Inhibition of monoamine oxidase B by selected benzimidazole and caffeine analogues.	benzimidazole	46-59	monoamine oxidase B	Homo sapiens	14-33
17416530-0	2007	Inhibition of monoamine oxidase B by selected benzimidazole and caffeine analogues.	Caffeine	64-72	monoamine oxidase B	Homo sapiens	14-33
17416530-1	2007	We have recently reported that a series of (E)-8-styrylcaffeines and (E)-2-styrylbenzimidazoles are moderate to very potent competitive inhibitors of monoamine oxidase B (MAO-B).	(e)-8-styrylcaffeines	43-64	monoamine oxidase B	Homo sapiens	150-169
17416530-1	2007	We have recently reported that a series of (E)-8-styrylcaffeines and (E)-2-styrylbenzimidazoles are moderate to very potent competitive inhibitors of monoamine oxidase B (MAO-B).	(e)-8-styrylcaffeines	43-64	monoamine oxidase B	Homo sapiens	171-176
17416530-3	2007	In the present study, we have prepared additional caffeine and benzimidazole analogues in an attempt to identify compounds with improved MAO-B inhibition potency while still acting reversibly.	Caffeine	50-58	monoamine oxidase B	Homo sapiens	137-142
17416530-3	2007	In the present study, we have prepared additional caffeine and benzimidazole analogues in an attempt to identify compounds with improved MAO-B inhibition potency while still acting reversibly.	benzimidazole	63-76	monoamine oxidase B	Homo sapiens	137-142
18488080-0	2007	Rasagiline - a novel MAO B inhibitor in Parkinson"s disease therapy.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	21-26
18488080-3	2007	Recently, a novel selective and irreversible MAO B propargylamine inhibitor rasagiline (N-propargyl-1-R-aminoindan, Azilect((R))) was approved for PD therapy.	propargylamine	51-65	monoamine oxidase B	Homo sapiens	45-50
18488080-3	2007	Recently, a novel selective and irreversible MAO B propargylamine inhibitor rasagiline (N-propargyl-1-R-aminoindan, Azilect((R))) was approved for PD therapy.	rasagiline	76-86	monoamine oxidase B	Homo sapiens	45-50
18488080-3	2007	Recently, a novel selective and irreversible MAO B propargylamine inhibitor rasagiline (N-propargyl-1-R-aminoindan, Azilect((R))) was approved for PD therapy.	n-propargyl-1-r-aminoindan	88-114	monoamine oxidase B	Homo sapiens	45-50
18488080-3	2007	Recently, a novel selective and irreversible MAO B propargylamine inhibitor rasagiline (N-propargyl-1-R-aminoindan, Azilect((R))) was approved for PD therapy.	rasagiline	116-123	monoamine oxidase B	Homo sapiens	45-50
17495756-4	2007	Although no medication has been proven to slow the progression of Parkinson disease, preclinical studies have demonstrated neuroprotective effects of MAO-B inhibitors, and a recent study of rasagiline found that PD patients treated with rasagiline for 12 months experienced less progression of symptoms than patients treated with placebo for 6 months followed by rasagiline for 6 months.	rasagiline	237-247	monoamine oxidase B	Homo sapiens	150-155
17495756-4	2007	Although no medication has been proven to slow the progression of Parkinson disease, preclinical studies have demonstrated neuroprotective effects of MAO-B inhibitors, and a recent study of rasagiline found that PD patients treated with rasagiline for 12 months experienced less progression of symptoms than patients treated with placebo for 6 months followed by rasagiline for 6 months.	rasagiline	237-247	monoamine oxidase B	Homo sapiens	150-155
17495756-7	2007	CONCLUSION: Treatment of early PD with an MAO-B inhibitor, dopamine agonist, or amantadine, may provide useful alternatives to treatment with levodopa.	Levodopa	142-150	monoamine oxidase B	Homo sapiens	42-47
17346749-3	2007	L-deprenyl binds to MAO-B and autoradiography with 3H-L-deprenyl has been used to map astrocytosis in vitro.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	20-25
17489352-1	2007	1-Methyl-2-undecyl-4(1H)-quinolone (1) was previously isolated as a selective MAO-B inhibitor from the Evodiae Fructus.	1-methyl-2-undecyl-4(1H)-quinolone	0-34	monoamine oxidase B	Homo sapiens	78-83
17480205-1	2007	The two forms of monoamine oxidase, monoamine oxidase A and monoamine oxidase B, have been associated with imidazoline-binding sites (type 2).	Imidazolines	107-118	monoamine oxidase B	Homo sapiens	60-79
17256833-2	2007	N-Methyl,N-(benzyl),N-(pyrrol-2-ylmethyl)amine (7) and N-(2-benzyl),N-(1-methylpyrrol-2-ylmethyl)amine (18) were the most selective MAO-B (7, SI = 0.0057) and MAO-A (18, SI = 12500) inhibitors, respectively.	N-methyl,N-(benzyl),N-(pyrrol-2-ylmethyl)amine	0-46	monoamine oxidase B	Homo sapiens	132-137
17256833-2	2007	N-Methyl,N-(benzyl),N-(pyrrol-2-ylmethyl)amine (7) and N-(2-benzyl),N-(1-methylpyrrol-2-ylmethyl)amine (18) were the most selective MAO-B (7, SI = 0.0057) and MAO-A (18, SI = 12500) inhibitors, respectively.	N-(2-benzyl),N-(1-methylpyrrol-2-ylmethyl)amine	55-102	monoamine oxidase B	Homo sapiens	132-137
17256833-7	2007	The slightly different binding pose of 18 into the MAO-B active site seems to be forced by a bulkier Tyr residue, which replaces a smaller Ile residue present in MAO-A.	Tyrosine	101-104	monoamine oxidase B	Homo sapiens	51-56
17256833-7	2007	The slightly different binding pose of 18 into the MAO-B active site seems to be forced by a bulkier Tyr residue, which replaces a smaller Ile residue present in MAO-A.	Isoleucine	139-142	monoamine oxidase B	Homo sapiens	51-56
17311421-2	2007	We examine and compare how two monotopic proteins, monoamine oxidase B (MAO-B) and cyclooxygenase-2 (COX-2), interact with a phospholipid bilayer using molecular dynamics simulations.	Phospholipids	125-137	monoamine oxidase B	Homo sapiens	51-70
17311421-2	2007	We examine and compare how two monotopic proteins, monoamine oxidase B (MAO-B) and cyclooxygenase-2 (COX-2), interact with a phospholipid bilayer using molecular dynamics simulations.	Phospholipids	125-137	monoamine oxidase B	Homo sapiens	72-77
17401535-2	2007	The pH dependence of the kinetic parameters for kynuramine oxidation by purified human MAO-A and for phenylethylamine oxidation by MAO-B in granulocytes at pH values from 5 to 10 was consistent with the protonated amine being used.	Phenethylamines	101-117	monoamine oxidase B	Homo sapiens	131-136
17266193-1	2007	A series of 3,5-diaryl pyrazoles were prepared and assayed for their ability to inhibit reversibly monoamine oxidase-A (MAO-A) and monoamine oxidase B (MAO-B).	3,5-diaryl pyrazoles	12-32	monoamine oxidase B	Homo sapiens	131-150
17266193-1	2007	A series of 3,5-diaryl pyrazoles were prepared and assayed for their ability to inhibit reversibly monoamine oxidase-A (MAO-A) and monoamine oxidase B (MAO-B).	3,5-diaryl pyrazoles	12-32	monoamine oxidase B	Homo sapiens	152-157
17630819-5	2007	Agents that block MAO-B, such as rasagiline and selegiline, are used as both initial and adjunctive therapy in patients with Parkinson"s disease.	rasagiline	33-43	monoamine oxidase B	Homo sapiens	18-23
17630819-5	2007	Agents that block MAO-B, such as rasagiline and selegiline, are used as both initial and adjunctive therapy in patients with Parkinson"s disease.	Selegiline	48-58	monoamine oxidase B	Homo sapiens	18-23
17630819-8	2007	MAO-B inhibition may elicit drug-drug interactions if administered with TCAs, SSRIs or SNRIs.	Trichloroacetic Acid	72-76	monoamine oxidase B	Homo sapiens	0-5
17683172-1	2007	Rasagiline (Azilect) is a novel, selective, irreversible second-generation inhibitor of monoamine oxidase type B (MAO-B).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	88-112
17683172-1	2007	Rasagiline (Azilect) is a novel, selective, irreversible second-generation inhibitor of monoamine oxidase type B (MAO-B).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	114-119
17683172-1	2007	Rasagiline (Azilect) is a novel, selective, irreversible second-generation inhibitor of monoamine oxidase type B (MAO-B).	rasagiline	12-19	monoamine oxidase B	Homo sapiens	88-112
17683172-1	2007	Rasagiline (Azilect) is a novel, selective, irreversible second-generation inhibitor of monoamine oxidase type B (MAO-B).	rasagiline	12-19	monoamine oxidase B	Homo sapiens	114-119
17702535-10	2007	Rasagiline is a new, selective, second-generation MAO-B inhibitor that is chemically and metabolically distinct from selegiline.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	50-55
17417741-1	2007	Dopamine behaves mainly as a MAO-A substrate in rodent brain, but selective inhibition of MAO-B results in an increased turning activity following L-DOPA administration in hemi-Parkinsonian rodents.	Levodopa	147-153	monoamine oxidase B	Homo sapiens	90-95
17284087-1	2007	The monamine oxidase (MAO) inhibitor selegiline is selective for MAO-B at the low oral dosages used in the treatment of Parkinson"s disease.	Selegiline	37-47	monoamine oxidase B	Homo sapiens	65-70
17348765-3	2007	The first-generation MAOIs such as phenelzine and isocarboxazid were largely nonselective inhibitors of both subtypes of MAO, MAO(A) and MAO(B).	Phenelzine	35-45	monoamine oxidase B	Homo sapiens	137-143
17348765-3	2007	The first-generation MAOIs such as phenelzine and isocarboxazid were largely nonselective inhibitors of both subtypes of MAO, MAO(A) and MAO(B).	Isocarboxazid	50-63	monoamine oxidase B	Homo sapiens	137-143
17348765-5	2007	The second-generation MAOI selegiline is selective for MAO(B) at oral doses of up to 10 mg/day.	Selegiline	27-37	monoamine oxidase B	Homo sapiens	55-61
17348765-6	2007	At higher doses, selegiline loses selectivity and inhibits both MAO(A) and MAO(B).	Selegiline	17-27	monoamine oxidase B	Homo sapiens	75-81
17417741-4	2007	MAO-B as well as MAO-A may contribute to deamination of dopamine produced from L-DOPA.	Dopamine	56-64	monoamine oxidase B	Homo sapiens	0-5
17417741-4	2007	MAO-B as well as MAO-A may contribute to deamination of dopamine produced from L-DOPA.	Levodopa	79-85	monoamine oxidase B	Homo sapiens	0-5
17401536-0	2007	The aromatic cage in the active site of monoamine oxidase B: effect on the structural and electronic properties of bound benzylamine and p-nitrobenzylamine.	benzylamine	121-132	monoamine oxidase B	Homo sapiens	40-59
17401536-0	2007	The aromatic cage in the active site of monoamine oxidase B: effect on the structural and electronic properties of bound benzylamine and p-nitrobenzylamine.	4-nitrobenzylamine	137-155	monoamine oxidase B	Homo sapiens	40-59
17401536-1	2007	Computational studies using the ONIOM methods have been performed to probe the catalytic roles of tyrosine residues 398 and 435 which constitute the "aromatic cage" in the active site of MAO-B.	Tyrosine	98-106	monoamine oxidase B	Homo sapiens	187-192
17401536-2	2007	The results presented here provide additional new insights into the interactions that take place on activation of the amine substrate by the aromatic cage residues in MAO-B catalysis and have relevance to the MAO-A catalytic mechanism.	Amines	118-123	monoamine oxidase B	Homo sapiens	167-172
17296539-1	2006	OBJECTIVE: This article reviews the chemistry, pharmacodynamics, pharmacokinetics, clinical efficacy, tolerability, drug-interaction potential, indications, dosing, and potential role of rasagiline mesylate, a new selective monoamine oxidase (MAO) type B (MAO-B) inhibitor, in the treatment of Parkinson"s disease.	Rasagiline mesylate	187-206	monoamine oxidase B	Homo sapiens	224-254
18261369-1	2007	PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine.	Selegiline	62-72	monoamine oxidase B	Homo sapiens	23-42
18261369-1	2007	PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine.	Selegiline	62-72	monoamine oxidase B	Homo sapiens	44-49
18261369-1	2007	PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine.	Amphetamine	183-196	monoamine oxidase B	Homo sapiens	23-42
18261369-1	2007	PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine.	Amphetamine	183-196	monoamine oxidase B	Homo sapiens	44-49
18261369-1	2007	PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine.	Methamphetamine	201-218	monoamine oxidase B	Homo sapiens	23-42
18261369-1	2007	PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine.	Methamphetamine	201-218	monoamine oxidase B	Homo sapiens	44-49
17055733-1	2007	The anti-Parkinson monoamine oxidase (MAO)-B inhibitor rasagiline (Azilect) was shown to possess neuroprotective activities, involving the induction of brain-derived- and glial cell line-derived neurotrophic factors (BDNF, GDNF).	rasagiline	55-65	monoamine oxidase B	Homo sapiens	19-44
17055733-1	2007	The anti-Parkinson monoamine oxidase (MAO)-B inhibitor rasagiline (Azilect) was shown to possess neuroprotective activities, involving the induction of brain-derived- and glial cell line-derived neurotrophic factors (BDNF, GDNF).	rasagiline	67-74	monoamine oxidase B	Homo sapiens	19-44
18267281-5	2007	MAO-B inhibitors rasagiline or selegiline can be also added.	rasagiline	17-27	monoamine oxidase B	Homo sapiens	0-5
17186710-6	2006	After levodopa-related motor complications develop in advanced Parkinson"s disease, it is beneficial to initiate adjuvant therapy with dopamine agonists, catechol O-methyltransferase inhibitors, or monoamine oxidase-B inhibitors.	Levodopa	6-14	monoamine oxidase B	Homo sapiens	198-217
18259087-8	2007	In conclusion, it seems that both, alcohol and tobacco consumption, may contribute to the lowering of overall platelet MAO-B activity.	Alcohols	35-42	monoamine oxidase B	Homo sapiens	119-124
17056035-0	2006	The imidazoline I2-site ligands BU 224 and 2-BFI inhibit MAO-A and MAO-B activities, hydrogen peroxide production, and lipolysis in rodent and human adipocytes.	Imidazolines	4-15	monoamine oxidase B	Homo sapiens	67-72
17056035-0	2006	The imidazoline I2-site ligands BU 224 and 2-BFI inhibit MAO-A and MAO-B activities, hydrogen peroxide production, and lipolysis in rodent and human adipocytes.	2-(2-benzofuranyl)-2-imidazoline	43-48	monoamine oxidase B	Homo sapiens	67-72
17296539-1	2006	OBJECTIVE: This article reviews the chemistry, pharmacodynamics, pharmacokinetics, clinical efficacy, tolerability, drug-interaction potential, indications, dosing, and potential role of rasagiline mesylate, a new selective monoamine oxidase (MAO) type B (MAO-B) inhibitor, in the treatment of Parkinson"s disease.	Rasagiline mesylate	187-206	monoamine oxidase B	Homo sapiens	256-261
17296539-5	2006	RESULTS: Rasagiline mesylate was developed with the goal of producing a selective MAO-B inhibitor that is not metabolized to (presumed) toxic metabolites (eg, amphetamine and methamphetamine, which are byproducts of the metabolism of selegiline, another selective MAO-B inhibitor).	Rasagiline mesylate	9-28	monoamine oxidase B	Homo sapiens	82-87
17296539-5	2006	RESULTS: Rasagiline mesylate was developed with the goal of producing a selective MAO-B inhibitor that is not metabolized to (presumed) toxic metabolites (eg, amphetamine and methamphetamine, which are byproducts of the metabolism of selegiline, another selective MAO-B inhibitor).	Rasagiline mesylate	9-28	monoamine oxidase B	Homo sapiens	264-269
17296539-18	2006	In addition, bifunctional molecules combining selective MAO-B inhibition (based on the active moiety of rasagiline) with acetylcholinesterase inhibition or iron chelation may eventually be useful in Alzheimer"s disease.	rasagiline	104-114	monoamine oxidase B	Homo sapiens	56-61
17168653-1	2006	The therapeutic use of enzyme inhibitors in treatment of neurodegenerative diseases has its origin in the anti Parkinson action of the selective monoamine oxidase (MAO) B inhibitor, l-deprenyl (selegiline ), a failed anti depressant in 1975.	Selegiline	182-192	monoamine oxidase B	Homo sapiens	145-170
17168653-1	2006	The therapeutic use of enzyme inhibitors in treatment of neurodegenerative diseases has its origin in the anti Parkinson action of the selective monoamine oxidase (MAO) B inhibitor, l-deprenyl (selegiline ), a failed anti depressant in 1975.	Selegiline	194-204	monoamine oxidase B	Homo sapiens	145-170
16730924-2	2006	Selegiline is an irreversible selective inhibitor of monoamine oxidase type B (MAO-B) which may affect cocaine addiction through several potential mechanisms.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	53-77
16730924-2	2006	Selegiline is an irreversible selective inhibitor of monoamine oxidase type B (MAO-B) which may affect cocaine addiction through several potential mechanisms.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	79-84
16730924-2	2006	Selegiline is an irreversible selective inhibitor of monoamine oxidase type B (MAO-B) which may affect cocaine addiction through several potential mechanisms.	Cocaine	103-110	monoamine oxidase B	Homo sapiens	53-77
16730924-2	2006	Selegiline is an irreversible selective inhibitor of monoamine oxidase type B (MAO-B) which may affect cocaine addiction through several potential mechanisms.	Cocaine	103-110	monoamine oxidase B	Homo sapiens	79-84
16870220-2	2006	This research has studied the oxidation of MPTP by human CYP2D6 (CYP2D6*1 and CYP2D6*10 allelic variants) as well as by a mixture of cytochrome P450s-resembling HLM, and the products generated compared with those afforded by human monoamine oxidase (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	43-47	monoamine oxidase B	Homo sapiens	250-255
17100591-1	2006	Selegiline inhibits the activity of monoamine oxidase B, enhances the release of dopamine, blocks the uptake of dopamine, acts as a calmodulin antagonist, and enhances the level of cyclic AMP, which in turn protects dopaminergic neurons.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	36-55
16985099-2	2006	For instance, the oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to the neurotoxic pyridinium ion metabolite 1-methyl-4-phenylpyridinium by monoamine oxidase (MAO) B in the brain has been of interest to a number of investigators.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	31-75	monoamine oxidase B	Homo sapiens	151-176
16985099-2	2006	For instance, the oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to the neurotoxic pyridinium ion metabolite 1-methyl-4-phenylpyridinium by monoamine oxidase (MAO) B in the brain has been of interest to a number of investigators.	pyridine	94-104	monoamine oxidase B	Homo sapiens	151-176
16985099-2	2006	For instance, the oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to the neurotoxic pyridinium ion metabolite 1-methyl-4-phenylpyridinium by monoamine oxidase (MAO) B in the brain has been of interest to a number of investigators.	1-Methyl-4-phenylpyridinium	120-147	monoamine oxidase B	Homo sapiens	151-176
16985099-3	2006	It has also been reported that although the aromatization of N-methyl-tetrahydroisoquinoline occurs with MAO B, the metabolism does not proceed for its isomer, N-methyl-tetrahydroquinoline, by the same enzyme.	n-methyl-tetrahydroisoquinoline	61-92	monoamine oxidase B	Homo sapiens	105-110
17197368-2	2006	These include ladostigil (TV3326) [(N-propargyl-(3R) aminoindan-5yl)-ethyl methyl carbamate], which combines the pharmacophore-neuroprotective effects of rasagiline, a selective monoamine oxidase (MAO)-B inhibitor, with the cholinesterase (ChE) inhibitory activity of rivastigmine or iron chelating moiety such as M30.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	14-24	monoamine oxidase B	Homo sapiens	178-203
17197368-2	2006	These include ladostigil (TV3326) [(N-propargyl-(3R) aminoindan-5yl)-ethyl methyl carbamate], which combines the pharmacophore-neuroprotective effects of rasagiline, a selective monoamine oxidase (MAO)-B inhibitor, with the cholinesterase (ChE) inhibitory activity of rivastigmine or iron chelating moiety such as M30.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	26-32	monoamine oxidase B	Homo sapiens	178-203
17197368-2	2006	These include ladostigil (TV3326) [(N-propargyl-(3R) aminoindan-5yl)-ethyl methyl carbamate], which combines the pharmacophore-neuroprotective effects of rasagiline, a selective monoamine oxidase (MAO)-B inhibitor, with the cholinesterase (ChE) inhibitory activity of rivastigmine or iron chelating moiety such as M30.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	35-91	monoamine oxidase B	Homo sapiens	178-203
16870220-5	2006	CYP2D6 competed with MAO-B for the oxidation of MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	48-52	monoamine oxidase B	Homo sapiens	21-26
16870220-6	2006	MPTP oxidation by MAO-B to MPDP+ and MPP+ toxins (bioactivation) was up to 3-fold higher than CYP2D6 detoxification to PTP and MPTP-OH.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	18-23
17034132-6	2006	Moreover, the influence of substituents on the in vitro inhibition of human MAO B was markedly different between homogeneous series of coumarin and 5H-indeno[1,2-c]pyridazin-5-one derivatives, suggesting different binding modes, a hypothesis clearly supported by molecular docking simulations of inhibitors into the active site of human MAO B.	coumarin	135-143	monoamine oxidase B	Homo sapiens	76-81
17034132-6	2006	Moreover, the influence of substituents on the in vitro inhibition of human MAO B was markedly different between homogeneous series of coumarin and 5H-indeno[1,2-c]pyridazin-5-one derivatives, suggesting different binding modes, a hypothesis clearly supported by molecular docking simulations of inhibitors into the active site of human MAO B.	5h-indeno[1,2-c]pyridazin-5-one	148-179	monoamine oxidase B	Homo sapiens	76-81
17034132-6	2006	Moreover, the influence of substituents on the in vitro inhibition of human MAO B was markedly different between homogeneous series of coumarin and 5H-indeno[1,2-c]pyridazin-5-one derivatives, suggesting different binding modes, a hypothesis clearly supported by molecular docking simulations of inhibitors into the active site of human MAO B.	5h-indeno[1,2-c]pyridazin-5-one	148-179	monoamine oxidase B	Homo sapiens	337-342
17030737-0	2006	Symptom relief in Parkinson disease by safinamide: Biochemical and clinical evidence of efficacy beyond MAO-B inhibition.	safinamide	39-49	monoamine oxidase B	Homo sapiens	104-109
17030739-8	2006	Analogous MAO-B-specific inhibitors that bind in a manner traversing both cavities include trans-trans farnesol and chlorostyrylcaffeine.	chlorostyrylcaffeine	116-136	monoamine oxidase B	Homo sapiens	10-15
17030739-2	2006	The 3A resolution structure of recombinant human MAO-B originally determined was of the enzyme complexed with pargyline, an irreversible inhibitor covalently bound to the N5 atom of the flavin coenzyme.	Pargyline	110-119	monoamine oxidase B	Homo sapiens	49-54
16828804-2	2006	Rasagiline (N-propargyl-1(R)-aminoindan) mesylate is a novel, second-generation, selective, irreversible monoamine oxidase type B inhibitor, demonstrated in monotherapy and adjunctive trials to be effective for PD with excellent tolerability.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	105-129
17030739-2	2006	The 3A resolution structure of recombinant human MAO-B originally determined was of the enzyme complexed with pargyline, an irreversible inhibitor covalently bound to the N5 atom of the flavin coenzyme.	4,6-dinitro-o-cresol	186-192	monoamine oxidase B	Homo sapiens	49-54
17030739-7	2006	A novel specific reversible MAO-B inhibitor, which is found as a contaminant in polystyrene plastics (1,4-diphenyl-2-butene), binds in both the entrance and the substrate cavity.	Polystyrenes	80-91	monoamine oxidase B	Homo sapiens	28-33
16828804-2	2006	Rasagiline (N-propargyl-1(R)-aminoindan) mesylate is a novel, second-generation, selective, irreversible monoamine oxidase type B inhibitor, demonstrated in monotherapy and adjunctive trials to be effective for PD with excellent tolerability.	n-propargyl-1(r)-aminoindan) mesylate	12-49	monoamine oxidase B	Homo sapiens	105-129
17030739-7	2006	A novel specific reversible MAO-B inhibitor, which is found as a contaminant in polystyrene plastics (1,4-diphenyl-2-butene), binds in both the entrance and the substrate cavity.	1,4-diphenyl-2-butene	102-123	monoamine oxidase B	Homo sapiens	28-33
17030739-8	2006	Analogous MAO-B-specific inhibitors that bind in a manner traversing both cavities include trans-trans farnesol and chlorostyrylcaffeine.	trans-trans farnesol	91-111	monoamine oxidase B	Homo sapiens	10-15
16935943-2	2006	Ladostigil combines the neuroprotective effects of the antiparkinson drug rasagiline, a selective monoamine oxidase (MAO)-B inhibitor, with the cholinesterase (ChE) inhibitory activity of rivastigmine in a single molecule, as a potential treatment for Alzheimer"s disease (AD) and Lewy Body disease.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	0-10	monoamine oxidase B	Homo sapiens	98-123
16935943-2	2006	Ladostigil combines the neuroprotective effects of the antiparkinson drug rasagiline, a selective monoamine oxidase (MAO)-B inhibitor, with the cholinesterase (ChE) inhibitory activity of rivastigmine in a single molecule, as a potential treatment for Alzheimer"s disease (AD) and Lewy Body disease.	rasagiline	74-84	monoamine oxidase B	Homo sapiens	98-123
16806814-8	2006	Adjustment for heavy smoking weakened the association between MAO-B and CCI in the worst eye (P=0.140), but did not alter this association for both eyes (P=0.006).	CCI	72-75	monoamine oxidase B	Homo sapiens	62-67
16884303-1	2006	A new series of 3-, 4-, 7-polysubstituted coumarins have been designed and evaluated for their monoamine oxidase A and monoamine oxidase B (MAO-A and MAO-B) inhibitory potency.	3-, 4-, 7-polysubstituted coumarins	16-51	monoamine oxidase B	Homo sapiens	119-138
16884303-1	2006	A new series of 3-, 4-, 7-polysubstituted coumarins have been designed and evaluated for their monoamine oxidase A and monoamine oxidase B (MAO-A and MAO-B) inhibitory potency.	3-, 4-, 7-polysubstituted coumarins	16-51	monoamine oxidase B	Homo sapiens	150-155
16856145-0	2006	Effects of tyramine administration in Parkinson"s disease patients treated with selective MAO-B inhibitor rasagiline.	rasagiline	106-116	monoamine oxidase B	Homo sapiens	90-95
16856145-1	2006	Rasagiline is a novel, potent, and selective MAO-B inhibitor shown to be effective for Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	45-50
16927880-1	2006	(-)-Deprenyl, the irreversible inhibitor of monoamine oxidase B, has been used for decades in the therapy of Parkinson"s disease.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	44-63
16927880-4	2006	Recently, (-)-deprenyl has been demonstrated to exert antiapoptotic, neuroprotective effects on a number of in vitro and in vivo models in a dose significantly lower than required for monoamine oxidase B inhibition.	Selegiline	10-22	monoamine oxidase B	Homo sapiens	184-203
16767355-1	2006	PF9601N, N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine, an monoamine oxidase (MAO) B inhibitor, has shown neuroprotective properties against dopaminergic toxins.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	0-7	monoamine oxidase B	Homo sapiens	64-89
16723097-5	2006	The K(m) value of serotonin to MAO-A was 1.66 micromol/L, while that of benzylamine to MAO-B was 0.80 micromol/L.	benzylamine	72-83	monoamine oxidase B	Homo sapiens	87-92
16723097-6	2006	The IC(50) value of clorgyline to MAO-A was 2.99 nmol/L, and that of deprenyl to MAO-B was 7.04 nmol/L, matching those obtained from traditional spectrometric assays.	Selegiline	69-77	monoamine oxidase B	Homo sapiens	81-86
16631124-5	2006	On the other hand, both c-RESV and t-RESV (5-200 microM) concentration-dependently inhibited the enzymatic activity of commercial (human recombinant) MAO isoform (MAO-A and MAO-B) activity, c-RESV being slightly less effective than t-RESV.	c-resv	24-30	monoamine oxidase B	Homo sapiens	173-178
16631124-5	2006	On the other hand, both c-RESV and t-RESV (5-200 microM) concentration-dependently inhibited the enzymatic activity of commercial (human recombinant) MAO isoform (MAO-A and MAO-B) activity, c-RESV being slightly less effective than t-RESV.	Resveratrol	26-30	monoamine oxidase B	Homo sapiens	173-178
16767355-1	2006	PF9601N, N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine, an monoamine oxidase (MAO) B inhibitor, has shown neuroprotective properties against dopaminergic toxins.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	9-59	monoamine oxidase B	Homo sapiens	64-89
16717254-5	2006	Selegiline is a monamine oxidase type B (MAO-B) inhibitor that incorporates a propargyl ring within its molecular structure.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	16-39
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	Dopamine	83-91	monoamine oxidase B	Homo sapiens	16-35
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	Dopamine	83-91	monoamine oxidase B	Homo sapiens	37-42
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	benzylamine	93-104	monoamine oxidase B	Homo sapiens	16-35
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	benzylamine	93-104	monoamine oxidase B	Homo sapiens	37-42
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	Phenethylamines	106-122	monoamine oxidase B	Homo sapiens	16-35
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	Phenethylamines	106-122	monoamine oxidase B	Homo sapiens	37-42
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	Tyramine	124-132	monoamine oxidase B	Homo sapiens	16-35
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	Tyramine	124-132	monoamine oxidase B	Homo sapiens	37-42
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	tryptamine	137-147	monoamine oxidase B	Homo sapiens	16-35
16807522-1	2006	OBJECTIVES: The monoamine oxidase B (MAO-B) is an enzyme involved in metabolism of dopamine, benzylamine, phenylethylamine, tyramine and tryptamine.	tryptamine	137-147	monoamine oxidase B	Homo sapiens	37-42
16427095-1	2006	Monoamine oxidase (MAO), a mitochondrial flavine containing enzyme, exists in two isoenzymes, MAO-A and MAO-B.	3,6-DIAMINO-10-METHYLACRIDINIUM CHLORIDE	41-48	monoamine oxidase B	Homo sapiens	104-109
16717254-5	2006	Selegiline is a monamine oxidase type B (MAO-B) inhibitor that incorporates a propargyl ring within its molecular structure.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	41-46
16717254-7	2006	Rasagiline is another MAO-B inhibitor that contains a propargyl ring and has protective effects in laboratory models.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	22-27
16717255-1	2006	Rasagiline (N-propargyl-1 (R)-aminoindan) is a selective, potent irreversible inhibitor of MAO-B that possesses neuroprotective and anti-apoptotic properties in a variety of in vitro and in vivo animal models relevant to Parkinson"s disease (PD).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	91-96
16717255-1	2006	Rasagiline (N-propargyl-1 (R)-aminoindan) is a selective, potent irreversible inhibitor of MAO-B that possesses neuroprotective and anti-apoptotic properties in a variety of in vitro and in vivo animal models relevant to Parkinson"s disease (PD).	n-propargyl-1 (r)-aminoindan	12-40	monoamine oxidase B	Homo sapiens	91-96
16674552-2	2006	Dopamine availability is controlled largely by three enzymes: COMT, MAOA and MAOB, and by the dopamine transporter SLC6A3, and each gene has a well-characterized functional variant.	Dopamine	0-8	monoamine oxidase B	Homo sapiens	77-81
16442801-0	2006	Inhibition of monoamine oxidase B by analogues of the adenosine A2A receptor antagonist (E)-8-(3-chlorostyryl)caffeine (CSC).	(E)-8-(3-chlorostyryl)caffeine	88-118	monoamine oxidase B	Homo sapiens	14-33
16442801-0	2006	Inhibition of monoamine oxidase B by analogues of the adenosine A2A receptor antagonist (E)-8-(3-chlorostyryl)caffeine (CSC).	8-(3-Chlorostyryl)caffeine	120-123	monoamine oxidase B	Homo sapiens	14-33
16442801-7	2006	The results of a SAR study established that the potency of MAO-B inhibition by (E)-8-styrylcaffeinyl analogues depends upon the van der Waals volume (V(w)), lipophilicity (pi), and the Hammett constant (sigma(m)) of the substituents attached to C-3 of the phenyl ring of the styryl moiety.	(e)-8-styrylcaffeinyl	79-100	monoamine oxidase B	Homo sapiens	59-64
20104716-4	2006	For young patients, dopamine-agonists and, indeed, once again increasingly MAO-B inhibitors, such as rasagiline, are mainly used for therapy.	rasagiline	101-111	monoamine oxidase B	Homo sapiens	75-80
16675649-0	2006	Rasagiline: A second-generation monoamine oxidase type-B inhibitor for the treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	32-56
16675649-2	2006	SUMMARY: Rasagiline is a novel, investigational propargylamine that irreversibly and selectively inhibits monoamine oxidase type B (MAO-B).	rasagiline	9-19	monoamine oxidase B	Homo sapiens	106-130
16675649-2	2006	SUMMARY: Rasagiline is a novel, investigational propargylamine that irreversibly and selectively inhibits monoamine oxidase type B (MAO-B).	rasagiline	9-19	monoamine oxidase B	Homo sapiens	132-137
16675649-2	2006	SUMMARY: Rasagiline is a novel, investigational propargylamine that irreversibly and selectively inhibits monoamine oxidase type B (MAO-B).	propargylamine	48-62	monoamine oxidase B	Homo sapiens	106-130
16675649-2	2006	SUMMARY: Rasagiline is a novel, investigational propargylamine that irreversibly and selectively inhibits monoamine oxidase type B (MAO-B).	propargylamine	48-62	monoamine oxidase B	Homo sapiens	132-137
16675649-3	2006	Rasagiline demonstrates complete and selective inhibition of MAO-B and is at least five times more potent than selegiline.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	61-66
16675649-12	2006	CONCLUSION: Rasagiline is an investigational selective and irreversible inhibitor of MAO-B that has demonstrated efficacy and safety for the treatment of PD.	rasagiline	12-22	monoamine oxidase B	Homo sapiens	85-90
16252076-0	2006	The antioxidant anethole dithiolethione inhibits monoamine oxidase-B but not monoamine oxidase A activity in extracts of cultured astrocytes.	anethole dithiolethione	16-39	monoamine oxidase B	Homo sapiens	49-68
16641841-4	2006	Selegiline, a selective monoamine oxidase B inhibitor, has been approved for the adjunctive treatment of Parkinson"s disease at low doses.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	24-43
16252076-2	2006	Here, using extracts from cultured astrocytes, containing both monoamine oxidase (MAO) A and B activity, we demonstrate that ADT concentration-dependently inhibits MAO-B activity in a clinically relevant concentration range (0.03-30 microM, IC-50 = 0.5 microM) without affecting MAO A activity.	adt	125-128	monoamine oxidase B	Homo sapiens	164-169
16252076-3	2006	Considering the alleged contribution of MAO activity in general, and MAO-B in particular, to oxidative stress and neurodegeneration in PD, our data further support the neuroprotective potential of ADT.	adt	197-200	monoamine oxidase B	Homo sapiens	69-74
16450340-2	2006	Rasagiline, a potent, second-generation, irreversible, selective monoamine oxidase B inhibitor improves PD symptoms in patients with early PD.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	65-84
16494947-0	2006	Relationship between platelet monoamine oxidase-B (MAO-B) activity and mercury exposure in fish consumers from the Lake St. Pierre region of Que., Canada.	Mercury	71-78	monoamine oxidase B	Homo sapiens	51-56
16605246-1	2006	Current structural results of several flavin-dependent amine oxidizing enzymes including human monoamine oxidases A and B (MAO A and MAO B) show aromatic amino acid residues oriented approximately perpendicular to the flavin ring, suggesting a functional role in catalysis.	flavin-dependent amine	38-60	monoamine oxidase B	Homo sapiens	133-138
17704848-3	2006	Receptor I2, displaying high similarity of sequence with monoamine oxidase-B (MAO-B), is structurally related to MAO-B, but the I2 imidazoline binding site (I2BS) with ligand is distinct from the catalytic site of MAO-B.	Imidazolines	131-142	monoamine oxidase B	Homo sapiens	78-83
16605246-1	2006	Current structural results of several flavin-dependent amine oxidizing enzymes including human monoamine oxidases A and B (MAO A and MAO B) show aromatic amino acid residues oriented approximately perpendicular to the flavin ring, suggesting a functional role in catalysis.	Amino Acids, Aromatic	145-164	monoamine oxidase B	Homo sapiens	133-138
16605246-1	2006	Current structural results of several flavin-dependent amine oxidizing enzymes including human monoamine oxidases A and B (MAO A and MAO B) show aromatic amino acid residues oriented approximately perpendicular to the flavin ring, suggesting a functional role in catalysis.	4,6-dinitro-o-cresol	38-44	monoamine oxidase B	Homo sapiens	133-138
16605246-2	2006	In the case of human MAO B, two tyrosyl residues (Y398 and Y435) are found in the substrate binding site on the re face of the covalent flavin ring [Binda et al.	cyclo(tyrosyl-tyrosyl)	32-39	monoamine oxidase B	Homo sapiens	21-26
16605246-2	2006	In the case of human MAO B, two tyrosyl residues (Y398 and Y435) are found in the substrate binding site on the re face of the covalent flavin ring [Binda et al.	4,6-dinitro-o-cresol	136-142	monoamine oxidase B	Homo sapiens	21-26
16605246-6	2006	To probe the functional significance of this structure, Tyr435 in MAO B was mutated with the amino acids Phe, His, Leu, or Trp, the mutant proteins expressed in Pichia pastoris, and purified to homogeneity.	Tryptophan	123-126	monoamine oxidase B	Homo sapiens	66-71
16605246-11	2006	p-Nitrobenzylamine is found to be a poor substrate while p-nitrophenethylamine is found to be a good substrate for all WT and mutant forms of MAO B.	4-nitrobenzylamine	0-18	monoamine oxidase B	Homo sapiens	142-147
16605246-11	2006	p-Nitrobenzylamine is found to be a poor substrate while p-nitrophenethylamine is found to be a good substrate for all WT and mutant forms of MAO B.	2-(4-nitrophenyl)ethanamine	57-78	monoamine oxidase B	Homo sapiens	142-147
16343694-4	2006	Actually, the beneficial effect of selegiline, a MAO-B inhibitor, in AD has been noted in several clinical studies.	Selegiline	35-45	monoamine oxidase B	Homo sapiens	49-54
16451296-4	2006	Rasagiline is a novel, second-generation, irreversible, selective monoamine oxidase type B inhibitor that is indicated for the treatment of idiopathic PD, either as initial monotherapy or as adjunct therapy (with levodopa) for patients experiencing end-of-dose motor fluctuations.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	66-90
16425668-4	2006	The methyl-esterified form of L-DOPA (melevodopa) and the monoamine oxidase type B inhibitor rasagiline have both been launched.	rasagiline	93-103	monoamine oxidase B	Homo sapiens	58-82
16289465-1	2006	The present study shows that deprenyl, a known inhibitor of monoamine oxidase B (MAO B), may generate changes in mitochondrial function.	Selegiline	29-37	monoamine oxidase B	Homo sapiens	60-79
16289465-1	2006	The present study shows that deprenyl, a known inhibitor of monoamine oxidase B (MAO B), may generate changes in mitochondrial function.	Selegiline	29-37	monoamine oxidase B	Homo sapiens	81-86
16485914-18	2006	Buccal administration of the monoamine oxidase-B inhibitor selegiline (deprenyl) provides better absorption and less formation of metabolites compared with standard tablets.	Selegiline	59-69	monoamine oxidase B	Homo sapiens	29-48
16485914-18	2006	Buccal administration of the monoamine oxidase-B inhibitor selegiline (deprenyl) provides better absorption and less formation of metabolites compared with standard tablets.	Selegiline	71-79	monoamine oxidase B	Homo sapiens	29-48
16139309-5	2006	Subsequently, the pyrido-indole (beta-carboline) alkaloids, norharman and harman, were identified and isolated from MAO-inhibiting coffee, and were good inhibitors on MAO A (harman and norharman) and MAO B (norharman) isozymes.	pyrido-indole (beta-carboline) alkaloids	18-58	monoamine oxidase B	Homo sapiens	200-205
16139309-5	2006	Subsequently, the pyrido-indole (beta-carboline) alkaloids, norharman and harman, were identified and isolated from MAO-inhibiting coffee, and were good inhibitors on MAO A (harman and norharman) and MAO B (norharman) isozymes.	norharman	60-69	monoamine oxidase B	Homo sapiens	200-205
17447416-3	2006	MAO B also oxidizes the xenobiotic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to a parkinsonism-producing neurotoxin, 1-methyl-4-phenyl-pyridinium (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	35-79	monoamine oxidase B	Homo sapiens	0-5
16719786-8	2006	The molecular modeling work was carried out combining the Glide docking approach with CoMFA with the aim to rationalize the structure-activity relationships of each pyrazoline inhibitor toward MAO-A and MAO-B isoforms and to derive a suitable selectivity model.	pyrazoline	165-175	monoamine oxidase B	Homo sapiens	203-208
15959855-0	2006	Platelet monoamine oxidase B (MAO-B) activity and its relationship to DL-fenfluramine-induced prolactin response in healthy men.	Fenfluramine	70-85	monoamine oxidase B	Homo sapiens	9-28
15959855-0	2006	Platelet monoamine oxidase B (MAO-B) activity and its relationship to DL-fenfluramine-induced prolactin response in healthy men.	Fenfluramine	70-85	monoamine oxidase B	Homo sapiens	30-35
15959855-3	2006	The aim of the present study was therefore to investigate if platelet MAO-B activity could be related to hormonal and temperature responses to the serotonin active drug DL-fenfluramine in healthy men.	Serotonin	147-156	monoamine oxidase B	Homo sapiens	70-75
15959855-3	2006	The aim of the present study was therefore to investigate if platelet MAO-B activity could be related to hormonal and temperature responses to the serotonin active drug DL-fenfluramine in healthy men.	Fenfluramine	169-184	monoamine oxidase B	Homo sapiens	70-75
15959855-11	2006	The results support the notion that the peripheral marker platelet MAO-B activity is related to the function of the central serotonergic neurotransmitter system as assessed by the prolactin response to 60 mg DL-fenfluramin.	dl-fenfluramin	208-222	monoamine oxidase B	Homo sapiens	67-72
17447417-9	2006	MAO-B oxidized dopamine with production of hydrogen peroxide, whereas in control cells expressing only MAO-A, dopamine autoxidation produced superoxide and dopamine-quinone, and induced mitochondrial permeability transition and apoptosis.	Dopamine	15-23	monoamine oxidase B	Homo sapiens	0-5
17017567-3	2006	Iron chelators (desferal, Vk-28 and clioquinol) but not copper chelators have been shown to be neuroprotective in the 6-hydroxydoapmine and MPTP models of Parkinson"s disease (PD), as are monoamine oxidase B inhibitors such as selegiline and rasagiline.	Iron	0-4	monoamine oxidase B	Homo sapiens	188-207
17017568-1	2006	Our recent studies aimed to elucidate the molecular and biochemical mechanism of actions of the novel anti-Parkinson"s drug, rasagiline, an irreversible and selective monoamine oxidase (MAO)-B inhibitor and its propargyl moiety, propargylamine.	rasagiline	125-135	monoamine oxidase B	Homo sapiens	167-192
17017568-1	2006	Our recent studies aimed to elucidate the molecular and biochemical mechanism of actions of the novel anti-Parkinson"s drug, rasagiline, an irreversible and selective monoamine oxidase (MAO)-B inhibitor and its propargyl moiety, propargylamine.	propargylamine	229-243	monoamine oxidase B	Homo sapiens	167-192
17447417-9	2006	MAO-B oxidized dopamine with production of hydrogen peroxide, whereas in control cells expressing only MAO-A, dopamine autoxidation produced superoxide and dopamine-quinone, and induced mitochondrial permeability transition and apoptosis.	Hydrogen Peroxide	43-60	monoamine oxidase B	Homo sapiens	0-5
17447416-3	2006	MAO B also oxidizes the xenobiotic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to a parkinsonism-producing neurotoxin, 1-methyl-4-phenyl-pyridinium (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	81-85	monoamine oxidase B	Homo sapiens	0-5
17447416-3	2006	MAO B also oxidizes the xenobiotic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to a parkinsonism-producing neurotoxin, 1-methyl-4-phenyl-pyridinium (MPP+).	1-Methyl-4-phenylpyridinium	127-155	monoamine oxidase B	Homo sapiens	0-5
17447416-3	2006	MAO B also oxidizes the xenobiotic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to a parkinsonism-producing neurotoxin, 1-methyl-4-phenyl-pyridinium (MPP+).	mangion-purified polysaccharide (Candida albicans)	157-161	monoamine oxidase B	Homo sapiens	0-5
17447416-4	2006	MAO B may be closely related to the pathogenesis of Parkinson"s disease (PD), in which neuromelanin-containing DA neurons in the substantia nigra projecting to the striatum in the brain selectively degenerate.	neuromelanin	87-99	monoamine oxidase B	Homo sapiens	0-5
17447416-4	2006	MAO B may be closely related to the pathogenesis of Parkinson"s disease (PD), in which neuromelanin-containing DA neurons in the substantia nigra projecting to the striatum in the brain selectively degenerate.	Dopamine	111-113	monoamine oxidase B	Homo sapiens	0-5
17447416-5	2006	MAO B degrades the neurotransmitter DA that is deficient in the nigro-striatal region in PD, and forms H2O2 and toxic aldehyde metabolites of DA.	Dopamine	36-38	monoamine oxidase B	Homo sapiens	0-5
17447416-5	2006	MAO B degrades the neurotransmitter DA that is deficient in the nigro-striatal region in PD, and forms H2O2 and toxic aldehyde metabolites of DA.	Hydrogen Peroxide	103-107	monoamine oxidase B	Homo sapiens	0-5
17447416-5	2006	MAO B degrades the neurotransmitter DA that is deficient in the nigro-striatal region in PD, and forms H2O2 and toxic aldehyde metabolites of DA.	Aldehydes	118-126	monoamine oxidase B	Homo sapiens	0-5
17447416-5	2006	MAO B degrades the neurotransmitter DA that is deficient in the nigro-striatal region in PD, and forms H2O2 and toxic aldehyde metabolites of DA.	Dopamine	142-144	monoamine oxidase B	Homo sapiens	0-5
17447416-7	2006	MAO B inhibitors such as L-(-)-deprenyl (selegiline) and rasagiline are effective for the treatment of PD.	Selegiline	25-39	monoamine oxidase B	Homo sapiens	0-5
17447416-7	2006	MAO B inhibitors such as L-(-)-deprenyl (selegiline) and rasagiline are effective for the treatment of PD.	Selegiline	41-51	monoamine oxidase B	Homo sapiens	0-5
17447416-7	2006	MAO B inhibitors such as L-(-)-deprenyl (selegiline) and rasagiline are effective for the treatment of PD.	rasagiline	57-67	monoamine oxidase B	Homo sapiens	0-5
17447416-8	2006	Concerning the mechanism of the clinical efficacy of MAO B inhibitors in PD, the inhibition of DA degradation (a symptomatic effect) and also the prevention of the formation of neurotoxic DA metabolites, i.e., ROS and dopamine derived aldehydes have been speculated.	Dopamine	95-97	monoamine oxidase B	Homo sapiens	53-58
17447416-8	2006	Concerning the mechanism of the clinical efficacy of MAO B inhibitors in PD, the inhibition of DA degradation (a symptomatic effect) and also the prevention of the formation of neurotoxic DA metabolites, i.e., ROS and dopamine derived aldehydes have been speculated.	Dopamine	188-190	monoamine oxidase B	Homo sapiens	53-58
17447416-8	2006	Concerning the mechanism of the clinical efficacy of MAO B inhibitors in PD, the inhibition of DA degradation (a symptomatic effect) and also the prevention of the formation of neurotoxic DA metabolites, i.e., ROS and dopamine derived aldehydes have been speculated.	Reactive Oxygen Species	210-213	monoamine oxidase B	Homo sapiens	53-58
17447416-8	2006	Concerning the mechanism of the clinical efficacy of MAO B inhibitors in PD, the inhibition of DA degradation (a symptomatic effect) and also the prevention of the formation of neurotoxic DA metabolites, i.e., ROS and dopamine derived aldehydes have been speculated.	Dopamine	218-226	monoamine oxidase B	Homo sapiens	53-58
17447416-8	2006	Concerning the mechanism of the clinical efficacy of MAO B inhibitors in PD, the inhibition of DA degradation (a symptomatic effect) and also the prevention of the formation of neurotoxic DA metabolites, i.e., ROS and dopamine derived aldehydes have been speculated.	Aldehydes	235-244	monoamine oxidase B	Homo sapiens	53-58
17447416-9	2006	As another mechanism of clinical efficacy, MAO B inhibitors such as selegiline are speculated to have neuroprotective effects to prevent progress of PD.	Selegiline	68-78	monoamine oxidase B	Homo sapiens	43-48
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	Selegiline	60-72	monoamine oxidase B	Homo sapiens	26-50
16366596-2	2005	Rasagiline is an irreversible, MAO B-selective inhibitor that has been approved as a novel anti-Parkinson"s drug.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	31-36
16366596-3	2005	In this study, we investigate the inhibition of recombinant human MAO A and MAO B by several rasagiline analogues.	rasagiline	93-103	monoamine oxidase B	Homo sapiens	76-81
16366596-6	2005	The 1.7 A crystal structure of MAO B in complex with 4-(N-methyl-N-ethyl-carbamoyloxy)-N-methyl-N-propargyl-1(R)-aminoindan shows that the binding mode is similar to that of rasagiline with the carbamate moiety occupying the entrance cavity space.	R-M4CPAI	53-123	monoamine oxidase B	Homo sapiens	31-36
16366596-6	2005	The 1.7 A crystal structure of MAO B in complex with 4-(N-methyl-N-ethyl-carbamoyloxy)-N-methyl-N-propargyl-1(R)-aminoindan shows that the binding mode is similar to that of rasagiline with the carbamate moiety occupying the entrance cavity space.	rasagiline	174-184	monoamine oxidase B	Homo sapiens	31-36
16366596-6	2005	The 1.7 A crystal structure of MAO B in complex with 4-(N-methyl-N-ethyl-carbamoyloxy)-N-methyl-N-propargyl-1(R)-aminoindan shows that the binding mode is similar to that of rasagiline with the carbamate moiety occupying the entrance cavity space.	Carbamates	194-203	monoamine oxidase B	Homo sapiens	31-36
16366596-7	2005	1(R)-Aminoindan, the major metabolic product of rasagiline, and its analogues reversibly inhibit both MAO A and MAO B.	(r)-aminoindan	1-15	monoamine oxidase B	Homo sapiens	112-117
16366596-7	2005	1(R)-Aminoindan, the major metabolic product of rasagiline, and its analogues reversibly inhibit both MAO A and MAO B.	rasagiline	48-58	monoamine oxidase B	Homo sapiens	112-117
16366596-8	2005	The crystal structure of N-methyl-1(R)-aminoindan bound to MAO B shows that its aminoindan ring adopts a different orientation compared to that of rasagiline.	N-METHYL-1(R)-AMINOINDAN	25-49	monoamine oxidase B	Homo sapiens	59-64
16366596-8	2005	The crystal structure of N-methyl-1(R)-aminoindan bound to MAO B shows that its aminoindan ring adopts a different orientation compared to that of rasagiline.	1-aminoindan	39-49	monoamine oxidase B	Homo sapiens	59-64
16366596-8	2005	The crystal structure of N-methyl-1(R)-aminoindan bound to MAO B shows that its aminoindan ring adopts a different orientation compared to that of rasagiline.	rasagiline	147-157	monoamine oxidase B	Homo sapiens	59-64
16413604-1	2005	Selegiline (L-deprenyl) is a selective irreversible monoamine oxidase B inhibitor shown to be effective in the treatment of Parkinson"s and Alzheimer"s diseases.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	52-71
16413604-1	2005	Selegiline (L-deprenyl) is a selective irreversible monoamine oxidase B inhibitor shown to be effective in the treatment of Parkinson"s and Alzheimer"s diseases.	Selegiline	12-22	monoamine oxidase B	Homo sapiens	52-71
16054369-3	2005	Comparison of inhibition potencies (pIC50 values) determined with human cloned and human platelet MAO B for the two series of MAO B inhibitors, coumarin and 5H-indeno[1,2-c]pyridazin-5-one derivatives, showed that the difference between pIC50 values obtained with the two enzyme sources was not significant (P&gt;0.05, Student"s t-test).	5h-indeno[1,2-c]pyridazin-5-one	157-188	monoamine oxidase B	Homo sapiens	98-103
16054369-3	2005	Comparison of inhibition potencies (pIC50 values) determined with human cloned and human platelet MAO B for the two series of MAO B inhibitors, coumarin and 5H-indeno[1,2-c]pyridazin-5-one derivatives, showed that the difference between pIC50 values obtained with the two enzyme sources was not significant (P&gt;0.05, Student"s t-test).	5h-indeno[1,2-c]pyridazin-5-one	157-188	monoamine oxidase B	Homo sapiens	126-131
16274328-1	2005	Selegiline orally disintegrating tablet is a potent, selective and irreversible inhibitor of monoamine oxidase type B.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	93-117
16274338-2	2005	Selegiline is currently the most widely used monoamine oxidase-B inhibitor for Parkinson"s disease, but has a low and variable bioavailability, and is metabolized to L-methamphetamine and L-amphetamine that carry a risk for potential neurotoxicity.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	45-64
16274338-8	2005	Clinical data suggest, in addition, a disease-modifying effect of rasagiline that may correlate with neuroprotective activity of monoamine oxidase-B inhibitors in animal models of Parkinson"s disease.	rasagiline	66-76	monoamine oxidase B	Homo sapiens	129-148
16296809-4	2005	Preventing the breakdown of dopamine has also been achieved by monoamine oxidase-B inhibition; this approach now having been formulated for sublingual use (Zelapar, Valeant Pharmaceuticals).	Selegiline	156-163	monoamine oxidase B	Homo sapiens	63-82
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	159-163	monoamine oxidase B	Homo sapiens	52-57
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	1-Methyl-4-phenylpyridinium	189-216	monoamine oxidase B	Homo sapiens	26-50
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	1-Methyl-4-phenylpyridinium	189-216	monoamine oxidase B	Homo sapiens	52-57
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	mangion-purified polysaccharide (Candida albicans)	222-226	monoamine oxidase B	Homo sapiens	26-50
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	mangion-purified polysaccharide (Candida albicans)	222-226	monoamine oxidase B	Homo sapiens	52-57
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	Selegiline	60-72	monoamine oxidase B	Homo sapiens	52-57
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	Selegiline	74-84	monoamine oxidase B	Homo sapiens	26-50
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	Selegiline	74-84	monoamine oxidase B	Homo sapiens	52-57
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	113-157	monoamine oxidase B	Homo sapiens	26-50
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	113-157	monoamine oxidase B	Homo sapiens	52-57
16099847-1	2005	Through the inhibition of monoamine oxidase type B (MAO-B), (-)-deprenyl (selegiline) prevents the conversion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the toxic metabolite 1-methyl-4-phenylpyridinium ion (MPP+) and also prevents the neurotoxicity in the dopaminergic neurons in animal models.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	159-163	monoamine oxidase B	Homo sapiens	26-50
16204711-0	2005	In vivo measurement of brain monoamine oxidase B occupancy by rasagiline, using (11)C-l-deprenyl and PET.	rasagiline	62-72	monoamine oxidase B	Homo sapiens	29-48
16139174-1	2005	Although selegiline, a monoamine oxidase (MAO)-B inhibitor, is reported to exert antidepressant effects in depressant patients, evidence in rodents for effects of selegiline is quite limited.	Selegiline	9-19	monoamine oxidase B	Homo sapiens	23-48
16139174-5	2005	But nortriptyline repeatedly given 24, 5 and 1 h before behavioral tests significantly decreased an immobility time in FST without effects in motor activities, and showed weak brain MAO-B inhibition.	Nortriptyline	4-17	monoamine oxidase B	Homo sapiens	182-187
16139174-8	2005	Selegiline at 1 and 3 mg/kg, which failed to decrease immobility time, markedly inhibited brain total-MAO and MAO-B activities.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	110-115
16197359-2	2005	Rasagiline is a monoamine oxidase-B inhibitor that has demonstrated efficacy against the cardinal symptoms of Parkinson"s disease when used as monotherapy in early Parkinson"s disease, and as an adjunct to levodopa in advanced disease stages.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	16-35
16204711-6	2005	The areas of high uptake were absent from scan 2, on which activity throughout the brain was comparable to that in white matter, presumably because of blocking of MAO-B binding sites by rasagiline.	rasagiline	186-196	monoamine oxidase B	Homo sapiens	163-168
16204711-8	2005	CONCLUSION: (11)C-l-deprenyl PET showed binding of rasagiline to MAO-B, confirming blocking of MAO-B sites after 10 d of treatment with 1 mg of rasagiline per day, with immediate post-rasagiline treatment tracer uptake and metabolism in the basal ganglia compatible only with nonspecific binding.	rasagiline	51-61	monoamine oxidase B	Homo sapiens	65-70
16204711-8	2005	CONCLUSION: (11)C-l-deprenyl PET showed binding of rasagiline to MAO-B, confirming blocking of MAO-B sites after 10 d of treatment with 1 mg of rasagiline per day, with immediate post-rasagiline treatment tracer uptake and metabolism in the basal ganglia compatible only with nonspecific binding.	rasagiline	144-154	monoamine oxidase B	Homo sapiens	95-100
16204711-8	2005	CONCLUSION: (11)C-l-deprenyl PET showed binding of rasagiline to MAO-B, confirming blocking of MAO-B sites after 10 d of treatment with 1 mg of rasagiline per day, with immediate post-rasagiline treatment tracer uptake and metabolism in the basal ganglia compatible only with nonspecific binding.	rasagiline	144-154	monoamine oxidase B	Homo sapiens	95-100
16204711-10	2005	This finding is compatible with the known rate of de novo synthesis of MAO-B, confirming the irreversible binding of rasagiline.	rasagiline	117-127	monoamine oxidase B	Homo sapiens	71-76
16204711-0	2005	In vivo measurement of brain monoamine oxidase B occupancy by rasagiline, using (11)C-l-deprenyl and PET.	c-l-deprenyl	84-96	monoamine oxidase B	Homo sapiens	29-48
16204711-2	2005	(11)C-l-deprenyl PET has been used by others to characterize MAO-B ligands in terms of their in vivo potency toward MAO-B and duration of action.	c-l-deprenyl	4-16	monoamine oxidase B	Homo sapiens	61-66
16204711-2	2005	(11)C-l-deprenyl PET has been used by others to characterize MAO-B ligands in terms of their in vivo potency toward MAO-B and duration of action.	c-l-deprenyl	4-16	monoamine oxidase B	Homo sapiens	116-121
16204711-3	2005	In this study, we used (11)C-l-deprenyl PET to demonstrate the specific binding characteristics of the new irreversible selective MAO-B inhibitor rasagiline in 3 healthy volunteers.	rasagiline	146-156	monoamine oxidase B	Homo sapiens	130-135
15925113-0	2005	1-N-Substituted thiocarbamoyl-3-phenyl-5-thienyl-2-pyrazolines: a novel cholinesterase and selective monoamine oxidase B inhibitors for the treatment of Parkinson"s and Alzheimer"s diseases.	1-n-substituted thiocarbamoyl-3-phenyl-5-thienyl-2-pyrazolines	0-62	monoamine oxidase B	Homo sapiens	101-120
16143772-0	2005	(E)-8-(3-Chlorostyryl)-1,3,7-trimethylxanthine, a caffeine derivative acting both as antagonist of adenosine A2A receptors and as inhibitor of MAO-B.	8-(3-Chlorostyryl)caffeine	0-46	monoamine oxidase B	Homo sapiens	143-148
16143772-0	2005	(E)-8-(3-Chlorostyryl)-1,3,7-trimethylxanthine, a caffeine derivative acting both as antagonist of adenosine A2A receptors and as inhibitor of MAO-B.	Caffeine	50-58	monoamine oxidase B	Homo sapiens	143-148
16027398-1	2005	Rasagiline is a novel second-generation propargylamine that irreversibly and selectively inhibits monoamine oxidase type B (MAO-B).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	98-122
16027398-1	2005	Rasagiline is a novel second-generation propargylamine that irreversibly and selectively inhibits monoamine oxidase type B (MAO-B).	rasagiline	0-10	monoamine oxidase B	Homo sapiens	124-129
16027398-1	2005	Rasagiline is a novel second-generation propargylamine that irreversibly and selectively inhibits monoamine oxidase type B (MAO-B).	propargylamine	40-54	monoamine oxidase B	Homo sapiens	98-122
16027398-1	2005	Rasagiline is a novel second-generation propargylamine that irreversibly and selectively inhibits monoamine oxidase type B (MAO-B).	propargylamine	40-54	monoamine oxidase B	Homo sapiens	124-129
16027398-3	2005	Rasagiline completely and selectively inhibits MAO-B with a potency 5 to 10 times greater than selegiline.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	47-52
16034956-15	2005	There was a marked levodopa-sparing effect with MAO-B inhibitors which was associated with a significant reduction in motor fluctuations (OR 0.75; 95% CI 0.59 to 0.94) but not dyskinesia (OR 0.97; 95% CI 0.76 to 1.25).	Levodopa	19-27	monoamine oxidase B	Homo sapiens	48-53
15925113-2	2005	Compounds 3i-3l of newly synthesized N-substituted pyrazolines, which were presented as selective and irreversible MAO-B inhibitors in our previous report, were found to inhibit human erythrocyte and plasma AChE activities selectively and non-competitively suggesting that these compounds may interact with a region close to the peripheral site of the enzyme molecule which could shift the proper positioning of the catalytic center.	n-substituted pyrazolines	37-62	monoamine oxidase B	Homo sapiens	115-120
15925113-5	2005	These data suggested that newly synthesized N-substituted pyrazoline derivatives can be evaluated as both MAO-B and cholinesterase inhibitors which may have promising features in the treatment of Alzheimer"s and Parkinson"s diseases.	n-substituted pyrazoline	44-68	monoamine oxidase B	Homo sapiens	106-111
16062100-0	2005	Remarkable effect of selegiline (L-deprenyl), a selective monoamine oxidase type-B inhibitor, in a patient with severe refractory depression: a case report.	Selegiline	33-43	monoamine oxidase B	Homo sapiens	58-82
16062100-3	2005	Switching from amoxapine 150 mg/day to selegiline 7.5 mg/day, a selective monoamine oxidase type-B inhibitor, produced a dramatic reduction in hypobulia and lassitude, leading to a complete remission of all depressive symptoms.	Amoxapine	15-24	monoamine oxidase B	Homo sapiens	74-98
16062100-0	2005	Remarkable effect of selegiline (L-deprenyl), a selective monoamine oxidase type-B inhibitor, in a patient with severe refractory depression: a case report.	Selegiline	21-31	monoamine oxidase B	Homo sapiens	58-82
16062100-3	2005	Switching from amoxapine 150 mg/day to selegiline 7.5 mg/day, a selective monoamine oxidase type-B inhibitor, produced a dramatic reduction in hypobulia and lassitude, leading to a complete remission of all depressive symptoms.	Selegiline	39-49	monoamine oxidase B	Homo sapiens	74-98
15582589-8	2005	Norharman was an inhibitor of MAO-A (K(i)=1.2+/-0.18 microM) and MAO-B (K(i)=1.12+/-0.19 microM), and harman of MAO-A (K(i)=55.54+/-5.3nM).	norharman	0-9	monoamine oxidase B	Homo sapiens	65-70
15974574-1	2005	Pyrrolylethanoneamines 1-12, 18-23 and related amino alcohols 13-15, 24-27 were synthesized and tested against monoamine oxidases A and B (MAO-A and MAO-B) enzymes.	pyrrolylethanoneamines	0-22	monoamine oxidase B	Homo sapiens	149-154
15974574-4	2005	Interestingly, amino alcohol 25 selectively inhibited MAO-B enzyme and could be a lead compound for designing more potent and selective MAO-B inhibitors.	Amino Alcohols	15-28	monoamine oxidase B	Homo sapiens	54-59
15974574-4	2005	Interestingly, amino alcohol 25 selectively inhibited MAO-B enzyme and could be a lead compound for designing more potent and selective MAO-B inhibitors.	Amino Alcohols	15-28	monoamine oxidase B	Homo sapiens	136-141
15848762-10	2005	These results are compared with previous work on the equivalent residue in MAO B, namely, cysteine 365.	Cysteine	90-98	monoamine oxidase B	Homo sapiens	75-80
15710600-0	2005	Demonstration of isoleucine 199 as a structural determinant for the selective inhibition of human monoamine oxidase B by specific reversible inhibitors.	Isoleucine	17-27	monoamine oxidase B	Homo sapiens	98-117
15755651-3	2005	Unlike the parent 1-phenylcyclopropylamine, which is a selective inhibitor of MAO B, both (E)- and (Z)-diastereomers of derivatives having fluorine at the 2-position of the cyclopropane ring were potent and selective irreversible inhibitors of MAO A.	cyclopropane	173-185	monoamine oxidase B	Homo sapiens	78-83
15755651-6	2005	Surprisingly, (1S,2R)-2-fluoro-1-phenylcyclopropylamine and the (1R,2S)-enantiomer were essential equally potent as inhibitors of MAO A and MAO B.	(1s,2r)-2-fluoro-1-phenylcyclopropylamine	14-55	monoamine oxidase B	Homo sapiens	140-145
15850677-3	2005	Rasagiline (N-propargyl-1R-aminoindan) is a novel, highly potent irreversible monoamine oxidase (MAO) B inhibitor, anti-Parkinson drug.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	78-103
15850677-3	2005	Rasagiline (N-propargyl-1R-aminoindan) is a novel, highly potent irreversible monoamine oxidase (MAO) B inhibitor, anti-Parkinson drug.	n-propargyl-1r-aminoindan	12-37	monoamine oxidase B	Homo sapiens	78-103
15710852-1	2005	BACKGROUND: Rasagiline (n-propargyl-1[R]-aminoindan) mesylate is a novel irreversible selective monoamine oxidase type B inhibitor, previously demonstrated to improve symptoms in early Parkinson disease (PD).	rasagiline	12-22	monoamine oxidase B	Homo sapiens	96-120
15710852-1	2005	BACKGROUND: Rasagiline (n-propargyl-1[R]-aminoindan) mesylate is a novel irreversible selective monoamine oxidase type B inhibitor, previously demonstrated to improve symptoms in early Parkinson disease (PD).	n-propargyl-1[r]-aminoindan) mesylate	24-61	monoamine oxidase B	Homo sapiens	96-120
16007239-2	2005	The search for pharmacological treatments able to counteract the nigrostriatal degeneration, possibly by interfering with these phenomena, has recently raised considerable interest in rasagiline [R(+)-N-propargyl-1-aminoindan], a potent, selective, and irreversible inhibitor of monoamine oxidase B (MAO-B).	rasagiline	184-194	monoamine oxidase B	Homo sapiens	279-298
16007239-2	2005	The search for pharmacological treatments able to counteract the nigrostriatal degeneration, possibly by interfering with these phenomena, has recently raised considerable interest in rasagiline [R(+)-N-propargyl-1-aminoindan], a potent, selective, and irreversible inhibitor of monoamine oxidase B (MAO-B).	rasagiline	184-194	monoamine oxidase B	Homo sapiens	300-305
16007239-2	2005	The search for pharmacological treatments able to counteract the nigrostriatal degeneration, possibly by interfering with these phenomena, has recently raised considerable interest in rasagiline [R(+)-N-propargyl-1-aminoindan], a potent, selective, and irreversible inhibitor of monoamine oxidase B (MAO-B).	r(+)-n-propargyl-1-aminoindan	196-225	monoamine oxidase B	Homo sapiens	279-298
16110345-0	2005	Neuropharmacological, neuroprotective and amyloid precursor processing properties of selective MAO-B inhibitor antiparkinsonian drug, rasagiline.	rasagiline	134-144	monoamine oxidase B	Homo sapiens	95-100
16110345-1	2005	Rasagiline (N-propargyl-1R-aminoindan) is a novel, highly potent, irreversible monoamine oxidase (MAO)-B inhibitor designed for use as an antiparkinsonian drug.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	79-104
16110345-1	2005	Rasagiline (N-propargyl-1R-aminoindan) is a novel, highly potent, irreversible monoamine oxidase (MAO)-B inhibitor designed for use as an antiparkinsonian drug.	n-propargyl-1r-aminoindan	12-37	monoamine oxidase B	Homo sapiens	79-104
15710600-3	2005	In contrast, the reversible competitive inhibitor isatin binds to all known MAO B and MAO A with similar affinities.	Isatin	50-56	monoamine oxidase B	Homo sapiens	76-81
15710600-4	2005	Sequence alignments and the crystal structures of human MAO B in complex with 1,4-diphenyl-2-butene or with trans,trans-farnesol provide molecular insights into these specificities.	1,4-diphenyl-2-butene	78-99	monoamine oxidase B	Homo sapiens	56-61
15710600-4	2005	Sequence alignments and the crystal structures of human MAO B in complex with 1,4-diphenyl-2-butene or with trans,trans-farnesol provide molecular insights into these specificities.	Farnesol	108-128	monoamine oxidase B	Homo sapiens	56-61
15710600-8	2005	The human MAO B I199F mutant protein of MAO B binds to isatin (K(i) = 3 microM) but not to the three inhibitors listed above.	Isatin	55-61	monoamine oxidase B	Homo sapiens	10-15
15710600-8	2005	The human MAO B I199F mutant protein of MAO B binds to isatin (K(i) = 3 microM) but not to the three inhibitors listed above.	Isatin	55-61	monoamine oxidase B	Homo sapiens	40-45
15717295-2	2005	Monoamine oxidases A and B (MAO-A and MAO-B) degrade biogenic amines such as dopamine and serotonin and thereby control the levels of these neurotransmitters in the central nervous system.	Amines	62-68	monoamine oxidase B	Homo sapiens	38-43
15717295-2	2005	Monoamine oxidases A and B (MAO-A and MAO-B) degrade biogenic amines such as dopamine and serotonin and thereby control the levels of these neurotransmitters in the central nervous system.	Dopamine	77-85	monoamine oxidase B	Homo sapiens	38-43
15717295-2	2005	Monoamine oxidases A and B (MAO-A and MAO-B) degrade biogenic amines such as dopamine and serotonin and thereby control the levels of these neurotransmitters in the central nervous system.	Serotonin	90-99	monoamine oxidase B	Homo sapiens	38-43
15755651-3	2005	Unlike the parent 1-phenylcyclopropylamine, which is a selective inhibitor of MAO B, both (E)- and (Z)-diastereomers of derivatives having fluorine at the 2-position of the cyclopropane ring were potent and selective irreversible inhibitors of MAO A.	1-phenylcyclopropylamine	18-42	monoamine oxidase B	Homo sapiens	78-83
15766996-1	2005	BACKGROUND: Rasagiline mesylate is a novel drug for Parkinson"s disease with selective, irreversible monoamine oxidase B (MAO-B) inhibitor activity, and is effective as monotherapy in early disease.	Rasagiline mesylate	12-31	monoamine oxidase B	Homo sapiens	101-120
15766996-1	2005	BACKGROUND: Rasagiline mesylate is a novel drug for Parkinson"s disease with selective, irreversible monoamine oxidase B (MAO-B) inhibitor activity, and is effective as monotherapy in early disease.	Rasagiline mesylate	12-31	monoamine oxidase B	Homo sapiens	122-127
15694196-6	2005	The platelet MAO-B activity was determined fluorimetrically using kynuramine as a substrate.	Kynuramine	66-76	monoamine oxidase B	Homo sapiens	13-18
15621213-0	2005	Bifunctional drug derivatives of MAO-B inhibitor rasagiline and iron chelator VK-28 as a more effective approach to treatment of brain ageing and ageing neurodegenerative diseases.	rasagiline	49-59	monoamine oxidase B	Homo sapiens	33-38
15621213-7	2005	We have therefore prepared a series of novel bifunctional drugs from the neuroprotective-antiapoptotic antiparkinson monoamine oxidase B inhibitor, rasagiline, by introducing a carbamate cholinesterase (ChE) inhibitory moiety into it.	rasagiline	148-158	monoamine oxidase B	Homo sapiens	117-136
15621213-7	2005	We have therefore prepared a series of novel bifunctional drugs from the neuroprotective-antiapoptotic antiparkinson monoamine oxidase B inhibitor, rasagiline, by introducing a carbamate cholinesterase (ChE) inhibitory moiety into it.	Carbamates	177-186	monoamine oxidase B	Homo sapiens	117-136
15621213-10	2005	Ladostigil like MAO-B inhibitor it prevents MPTP Parkinsonism in mice model and retains the in vitro and in vivo neuroprotective activity of rasagiline.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	0-10	monoamine oxidase B	Homo sapiens	16-21
15589121-2	2004	As phenylethylamine, a very toxic metabolite of phenylalanine, is rapidly degraded by monoamine oxydase type B, an enzyme that has a very low activity in neonates, these results are consistent with those of the hypothesis of MAO-B acting as a modifying gene in phenylketonuria.	Phenethylamines	3-19	monoamine oxidase B	Homo sapiens	225-230
15663351-1	2005	Rasagiline is a second-generation potent, irreversible and selective inhibitor of monoamine-oxidase type B (MAO-B), which has been evaluated for the treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	82-106
15663351-1	2005	Rasagiline is a second-generation potent, irreversible and selective inhibitor of monoamine-oxidase type B (MAO-B), which has been evaluated for the treatment of Parkinson"s disease.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	108-113
15573406-3	2005	Rasagiline (N-propargyl-1R-aminoindan) is a novel, highly potent irreversible monoamine oxidase (MAO) B inhibitor anti-Parkinson drug.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	78-103
15573406-3	2005	Rasagiline (N-propargyl-1R-aminoindan) is a novel, highly potent irreversible monoamine oxidase (MAO) B inhibitor anti-Parkinson drug.	n-propargyl-1r-aminoindan	12-37	monoamine oxidase B	Homo sapiens	78-103
15567979-1	2004	BACKGROUND: The neuroprotective effect of N-(2-propynyl)2-(5-benzyloxy-indol)methylamine (PF 9601N), a novel MAO B inhibitor, and its metabolite FA 72 on the human neuroblastoma SHSY5Y cell line lesioned with (300 microM) dopamine was assessed and compared with that of 1-deprenyl assayed at identical experimental conditions.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	90-98	monoamine oxidase B	Homo sapiens	109-114
16156677-7	2005	Selective monoamine oxidase type B (MAO-B) inhibitors, used as monotherapy, delay the need for the introduction of levodopa by about 9 months.	Levodopa	115-123	monoamine oxidase B	Homo sapiens	10-34
16156677-7	2005	Selective monoamine oxidase type B (MAO-B) inhibitors, used as monotherapy, delay the need for the introduction of levodopa by about 9 months.	Levodopa	115-123	monoamine oxidase B	Homo sapiens	36-41
16156677-9	2005	Concern has been expressed about the potential of the MAO-B inhibitor selegiline (deprenyl) to induce cardiovascular adverse effects (orthostatic hypotension), either directly or through its amphetamine catabolites.	Selegiline	70-80	monoamine oxidase B	Homo sapiens	54-59
16156677-9	2005	Concern has been expressed about the potential of the MAO-B inhibitor selegiline (deprenyl) to induce cardiovascular adverse effects (orthostatic hypotension), either directly or through its amphetamine catabolites.	Selegiline	82-90	monoamine oxidase B	Homo sapiens	54-59
16156677-9	2005	Concern has been expressed about the potential of the MAO-B inhibitor selegiline (deprenyl) to induce cardiovascular adverse effects (orthostatic hypotension), either directly or through its amphetamine catabolites.	Amphetamine	191-202	monoamine oxidase B	Homo sapiens	54-59
16156677-10	2005	Rasagiline is a new MAO-B inhibitor that is not broken down to amphetamine derivatives and is indicated as both monotherapy in early PD and as adjunctive therapy in PD patients with motor fluctuations.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	20-25
15569272-3	2004	Metabolism of 2-phenylethylamine to phenylacetaldehyde is catalysed by monoamine oxidase B but the oxidation to its acid is usually ascribed to aldehyde dehydrogenase and the contribution of aldehyde oxidase and xanthine oxidase, if any, is ignored.	phenethylamine	14-32	monoamine oxidase B	Homo sapiens	71-90
15569272-3	2004	Metabolism of 2-phenylethylamine to phenylacetaldehyde is catalysed by monoamine oxidase B but the oxidation to its acid is usually ascribed to aldehyde dehydrogenase and the contribution of aldehyde oxidase and xanthine oxidase, if any, is ignored.	phenylacetaldehyde	36-54	monoamine oxidase B	Homo sapiens	71-90
15589121-2	2004	As phenylethylamine, a very toxic metabolite of phenylalanine, is rapidly degraded by monoamine oxydase type B, an enzyme that has a very low activity in neonates, these results are consistent with those of the hypothesis of MAO-B acting as a modifying gene in phenylketonuria.	Phenylalanine	48-61	monoamine oxidase B	Homo sapiens	225-230
15355491-3	2004	The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations.	Levodopa	113-121	monoamine oxidase B	Homo sapiens	51-55
15571301-1	2004	In the group of medication acting on the dopaminergic system the transdermal application of a dopamine agonist (Rotigotine) and a new MAO B inhibitor (Rasigiline) are receiving most attention.	Dopamine	41-49	monoamine oxidase B	Homo sapiens	134-139
15571301-1	2004	In the group of medication acting on the dopaminergic system the transdermal application of a dopamine agonist (Rotigotine) and a new MAO B inhibitor (Rasigiline) are receiving most attention.	rasigiline	151-161	monoamine oxidase B	Homo sapiens	134-139
15199371-1	2004	In the monkey dorsal raphe, we reported that 1-month (mo) of estrogen replacement, with or without progesterone supplementation for 14 days, significantly increased tryptophan hydroxylase-1 (TPH-1) mRNA; decreased serotonin reuptake transporter (SERT) mRNA and decreased monoamine oxidase (MAO)-A mRNA, but had no effect on MAO-B mRNA.	Progesterone	99-111	monoamine oxidase B	Homo sapiens	324-329
15199371-14	2004	However, the addition of progesterone significantly increased MAO-B.	Progesterone	25-37	monoamine oxidase B	Homo sapiens	62-67
15355491-10	2004	MAOB and COMT AG-HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG-LL haplotype in the group of females treated with low daily doses of levodopa (<500 mg/24 h).	Levodopa	100-108	monoamine oxidase B	Homo sapiens	0-4
15355491-11	2004	CONCLUSION: The results of the study suggest that patients with COMT(L/L) genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy.	Levodopa	154-162	monoamine oxidase B	Homo sapiens	96-100
15628826-13	2004	CONCLUSION: Rasagiline is well tolerated at doses up to 20 mg once/day and is a potent inhibitor of platelet MAO-B in humans.	rasagiline	12-22	monoamine oxidase B	Homo sapiens	109-114
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenethylamines	73-89	monoamine oxidase B	Homo sapiens	21-45
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenethylamines	73-89	monoamine oxidase B	Homo sapiens	47-51
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenethylamines	73-89	monoamine oxidase B	Homo sapiens	201-205
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenylalanine	118-131	monoamine oxidase B	Homo sapiens	21-45
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenylalanine	118-131	monoamine oxidase B	Homo sapiens	47-51
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenylalanine	118-131	monoamine oxidase B	Homo sapiens	201-205
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenylalanine	235-248	monoamine oxidase B	Homo sapiens	21-45
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenylalanine	235-248	monoamine oxidase B	Homo sapiens	47-51
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenylalanine	235-248	monoamine oxidase B	Homo sapiens	201-205
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenethylamines	282-298	monoamine oxidase B	Homo sapiens	21-45
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenethylamines	282-298	monoamine oxidase B	Homo sapiens	47-51
15461973-4	2004	We suggest here that monoamine oxidase type B, MAOB, an enzyme degrading phenylethylamine, a very toxic metabolite of phenylalanine, could act as a modifying gene since a variant enzymatic activity of MAOB in PKU patients with similar phenylalanine levels would result in different phenylethylamine levels and different clinical outcomes.	Phenethylamines	282-298	monoamine oxidase B	Homo sapiens	201-205
15461973-5	2004	Finally the report of low MAOB, and consequently expectedly high phenylethylamine levels in neonates is consistent with a phenylethylamine-mediated brain injury possibly causing irreversible damages in PKU newborns prior to onset of the low protein diet.	Phenethylamines	122-138	monoamine oxidase B	Homo sapiens	26-30
15628826-0	2004	Tolerability, safety, pharmacodynamics, and pharmacokinetics of rasagiline: a potent, selective, and irreversible monoamine oxidase type B inhibitor.	rasagiline	64-74	monoamine oxidase B	Homo sapiens	114-138
15628826-12	2004	In the repeated-dose study, all doses of rasagiline were well tolerated; almost full inhibition of platelet MAO-B activity was achieved with each rasagiline dose.	rasagiline	41-51	monoamine oxidase B	Homo sapiens	108-113
15308297-2	2004	Several studies have suggested that dopamine (DA) uptake into serotonin (5-HT) terminals by the 5-HT reuptake transporter (SERT) and subsequent deamination by monoamine oxidase-B (MAO-B) leads to the formation of hydrogen peroxide and may be major contributors to this serotonergic toxicity.	Dopamine	36-44	monoamine oxidase B	Homo sapiens	159-178
15308297-0	2004	3,4-methylenedioxymethamphetamine (MDMA, ecstasy)-mediated production of hydrogen peroxide in an in vitro model: the role of dopamine, the serotonin-reuptake transporter, and monoamine oxidase-B.	N-Methyl-3,4-methylenedioxyamphetamine	0-33	monoamine oxidase B	Homo sapiens	175-194
15308297-2	2004	Several studies have suggested that dopamine (DA) uptake into serotonin (5-HT) terminals by the 5-HT reuptake transporter (SERT) and subsequent deamination by monoamine oxidase-B (MAO-B) leads to the formation of hydrogen peroxide and may be major contributors to this serotonergic toxicity.	Dopamine	36-44	monoamine oxidase B	Homo sapiens	180-185
15308297-2	2004	Several studies have suggested that dopamine (DA) uptake into serotonin (5-HT) terminals by the 5-HT reuptake transporter (SERT) and subsequent deamination by monoamine oxidase-B (MAO-B) leads to the formation of hydrogen peroxide and may be major contributors to this serotonergic toxicity.	Dopamine	46-48	monoamine oxidase B	Homo sapiens	159-178
15308297-2	2004	Several studies have suggested that dopamine (DA) uptake into serotonin (5-HT) terminals by the 5-HT reuptake transporter (SERT) and subsequent deamination by monoamine oxidase-B (MAO-B) leads to the formation of hydrogen peroxide and may be major contributors to this serotonergic toxicity.	Dopamine	46-48	monoamine oxidase B	Homo sapiens	180-185
15308297-2	2004	Several studies have suggested that dopamine (DA) uptake into serotonin (5-HT) terminals by the 5-HT reuptake transporter (SERT) and subsequent deamination by monoamine oxidase-B (MAO-B) leads to the formation of hydrogen peroxide and may be major contributors to this serotonergic toxicity.	Serotonin	62-71	monoamine oxidase B	Homo sapiens	180-185
15308297-2	2004	Several studies have suggested that dopamine (DA) uptake into serotonin (5-HT) terminals by the 5-HT reuptake transporter (SERT) and subsequent deamination by monoamine oxidase-B (MAO-B) leads to the formation of hydrogen peroxide and may be major contributors to this serotonergic toxicity.	Hydrogen Peroxide	213-230	monoamine oxidase B	Homo sapiens	159-178
15308297-2	2004	Several studies have suggested that dopamine (DA) uptake into serotonin (5-HT) terminals by the 5-HT reuptake transporter (SERT) and subsequent deamination by monoamine oxidase-B (MAO-B) leads to the formation of hydrogen peroxide and may be major contributors to this serotonergic toxicity.	Hydrogen Peroxide	213-230	monoamine oxidase B	Homo sapiens	180-185
15308297-5	2004	Incubation of MDMA treated cells with the SERT inhibitor, fluoxetine (500 nM) or the MAO-B inhibitor, L-deprenyl (0.1 mM) for 30 min prior to DA, significantly blocked free radical production and cell death.	N-Methyl-3,4-methylenedioxyamphetamine	14-18	monoamine oxidase B	Homo sapiens	85-90
15308297-5	2004	Incubation of MDMA treated cells with the SERT inhibitor, fluoxetine (500 nM) or the MAO-B inhibitor, L-deprenyl (0.1 mM) for 30 min prior to DA, significantly blocked free radical production and cell death.	Selegiline	102-112	monoamine oxidase B	Homo sapiens	85-90
15308297-6	2004	These findings support the hypothesis that the deamination of DA by MAO-B within the serotonergic cell can lead to hydrogen peroxide formation and ultimately cell death.	Dopamine	62-64	monoamine oxidase B	Homo sapiens	68-73
15308297-6	2004	These findings support the hypothesis that the deamination of DA by MAO-B within the serotonergic cell can lead to hydrogen peroxide formation and ultimately cell death.	Hydrogen Peroxide	115-132	monoamine oxidase B	Homo sapiens	68-73
15279562-1	2004	Monoamine oxidases A and B (MAO A and MAO B) are mitochondrial outer membrane-bound flavoproteins that catalyze the oxidative deamination of neurotransmitters and biogenic amines.	Amines	172-178	monoamine oxidase B	Homo sapiens	38-43
15246083-2	2004	The oxo derivatives ("cathinones") were in general less active as MAO-A inhibitors than the corresponding arylisopropylamines, but exhibited an interesting MAO-B inhibiting activity, which was absent in the hydroxy, methoxy, and beta-unsubstituted analogues.	cathinone	22-32	monoamine oxidase B	Homo sapiens	156-161
15279563-9	2004	MAO B, but not MAO A gene, could be activated by PMA (phorbol 12-myristate 13-acetate) by protein kinase C, MAPkinase signal transduction pathway involves cJun and Egr-1.	Tetradecanoylphorbol Acetate	54-85	monoamine oxidase B	Homo sapiens	0-5
15279565-1	2004	Deprenyl, the selective irreversible inhibitor of monoamine oxidase-B (MAO-B), has been synthesised as a potential antidepressant, however, due to its dopamine potentiating capacity, became a registered drug in the treatment of Parkinson"s disease.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	50-69
15279562-4	2004	The recent development of high level expression systems for producing recombinant human liver MAO A and MAO B in Pichia pastoris has facilitated the determination of the three dimensional crystal structures of MAO B (up to 1.7 angstroms resolution) in complex with different reversible (isatin, 1,4-diphenyl-2-butene) and irreversible inhibitors (pargyline, N-(2-aminoethyl)-p-chlorobenzamide, and trans-2-phenylcyclopropylamine).	Isatin	287-293	monoamine oxidase B	Homo sapiens	210-215
15279565-1	2004	Deprenyl, the selective irreversible inhibitor of monoamine oxidase-B (MAO-B), has been synthesised as a potential antidepressant, however, due to its dopamine potentiating capacity, became a registered drug in the treatment of Parkinson"s disease.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	71-76
15279565-1	2004	Deprenyl, the selective irreversible inhibitor of monoamine oxidase-B (MAO-B), has been synthesised as a potential antidepressant, however, due to its dopamine potentiating capacity, became a registered drug in the treatment of Parkinson"s disease.	Dopamine	151-159	monoamine oxidase B	Homo sapiens	71-76
15279562-4	2004	The recent development of high level expression systems for producing recombinant human liver MAO A and MAO B in Pichia pastoris has facilitated the determination of the three dimensional crystal structures of MAO B (up to 1.7 angstroms resolution) in complex with different reversible (isatin, 1,4-diphenyl-2-butene) and irreversible inhibitors (pargyline, N-(2-aminoethyl)-p-chlorobenzamide, and trans-2-phenylcyclopropylamine).	1,4-diphenyl-2-butene	295-316	monoamine oxidase B	Homo sapiens	210-215
15279562-4	2004	The recent development of high level expression systems for producing recombinant human liver MAO A and MAO B in Pichia pastoris has facilitated the determination of the three dimensional crystal structures of MAO B (up to 1.7 angstroms resolution) in complex with different reversible (isatin, 1,4-diphenyl-2-butene) and irreversible inhibitors (pargyline, N-(2-aminoethyl)-p-chlorobenzamide, and trans-2-phenylcyclopropylamine).	Pargyline	347-356	monoamine oxidase B	Homo sapiens	210-215
15279562-4	2004	The recent development of high level expression systems for producing recombinant human liver MAO A and MAO B in Pichia pastoris has facilitated the determination of the three dimensional crystal structures of MAO B (up to 1.7 angstroms resolution) in complex with different reversible (isatin, 1,4-diphenyl-2-butene) and irreversible inhibitors (pargyline, N-(2-aminoethyl)-p-chlorobenzamide, and trans-2-phenylcyclopropylamine).	4-CHLORO-N-(2-HYDROXYETHYL)BENZAMIDE	358-392	monoamine oxidase B	Homo sapiens	210-215
15279562-4	2004	The recent development of high level expression systems for producing recombinant human liver MAO A and MAO B in Pichia pastoris has facilitated the determination of the three dimensional crystal structures of MAO B (up to 1.7 angstroms resolution) in complex with different reversible (isatin, 1,4-diphenyl-2-butene) and irreversible inhibitors (pargyline, N-(2-aminoethyl)-p-chlorobenzamide, and trans-2-phenylcyclopropylamine).	Tranylcypromine	398-428	monoamine oxidase B	Homo sapiens	210-215
15279563-9	2004	MAO B, but not MAO A gene, could be activated by PMA (phorbol 12-myristate 13-acetate) by protein kinase C, MAPkinase signal transduction pathway involves cJun and Egr-1.	Tetradecanoylphorbol Acetate	49-52	monoamine oxidase B	Homo sapiens	0-5
15203146-2	2004	The coumarin-3-carboxylic acids, 2a-e, proved to be reversible and selective inhibitors of the MAO-B isoform, displaying pIC(50) values of particular interest: 2a shows pIC(50) 7.76 and a selectivity index (pS.I.)	coumarin-3-carboxylic acid	4-31	monoamine oxidase B	Homo sapiens	95-100
15247489-1	2004	The catecholamine-oxidizing enzyme monoamine oxidase-B (MAO-B) has been hypothesized to be an important determining factor in the etiology of both normal aging and age-related neurological disorders such as Parkinson"s disease (PD).	Catecholamines	4-17	monoamine oxidase B	Homo sapiens	35-54
15247489-1	2004	The catecholamine-oxidizing enzyme monoamine oxidase-B (MAO-B) has been hypothesized to be an important determining factor in the etiology of both normal aging and age-related neurological disorders such as Parkinson"s disease (PD).	Catecholamines	4-17	monoamine oxidase B	Homo sapiens	56-61
15300656-1	2004	Rasagiline (N-propargyl-1(R)-aminoindan) mesylate is a potent, selective, and irreversible monoamine oxidase-B inhibitor.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	91-110
15300656-1	2004	Rasagiline (N-propargyl-1(R)-aminoindan) mesylate is a potent, selective, and irreversible monoamine oxidase-B inhibitor.	n-propargyl-1(r)-aminoindan) mesylate	12-49	monoamine oxidase B	Homo sapiens	91-110
15203146-5	2004	The coumarin-3-acyl chlorides 3a-e showed high pIC(50) values against both MAO-A and MAO-B isoforms, 3d being the highest against MAO-B with a pIC(50) value of 8.00.	coumarin-3-acyl chlorides	4-29	monoamine oxidase B	Homo sapiens	85-90
15203146-5	2004	The coumarin-3-acyl chlorides 3a-e showed high pIC(50) values against both MAO-A and MAO-B isoforms, 3d being the highest against MAO-B with a pIC(50) value of 8.00.	coumarin-3-acyl chlorides	4-29	monoamine oxidase B	Homo sapiens	130-135
15082228-8	2004	Although, the MAO-mediated metabolism of DA increases MAO-B activity, the presence of iron inhibits both MAO-A and MAO-B activities.	amsonic acid	41-43	monoamine oxidase B	Homo sapiens	54-59
15082228-8	2004	Although, the MAO-mediated metabolism of DA increases MAO-B activity, the presence of iron inhibits both MAO-A and MAO-B activities.	Iron	86-90	monoamine oxidase B	Homo sapiens	115-120
15082032-1	2004	OBJECTIVE: This paper describes the pharmacokinetics and the pharmacodynamics, in terms of monoamino oxidase type B (MAO-B) inhibition, in male healthy volunteers of orally administered safinamide, a new neuroprotectant that in experimental models has demonstrated strong anticonvulsant and antiparkinson activities.	safinamide	186-196	monoamine oxidase B	Homo sapiens	91-115
15082032-1	2004	OBJECTIVE: This paper describes the pharmacokinetics and the pharmacodynamics, in terms of monoamino oxidase type B (MAO-B) inhibition, in male healthy volunteers of orally administered safinamide, a new neuroprotectant that in experimental models has demonstrated strong anticonvulsant and antiparkinson activities.	safinamide	186-196	monoamine oxidase B	Homo sapiens	117-122
15082032-8	2004	Monoamine oxidase activity of both types A and B (MAO-A and MAO-B) was determined in plasma at different times (MAO-B) and correlated to safinamide levels, or in urine (MAO-A).	safinamide	137-147	monoamine oxidase B	Homo sapiens	60-65
15082032-12	2004	The drug was cleared with a t(1/2) of about 22 h. Safinamide reversibly inhibited MAO-B enzyme.	safinamide	50-60	monoamine oxidase B	Homo sapiens	82-87
15082032-17	2004	The MAO-B inhibitory activity, without affecting MAO-A, is useful to prevent a dopamine bioinactivation in patients suffering from Parkinson"s disease.	Dopamine	79-87	monoamine oxidase B	Homo sapiens	4-9
15110846-6	2004	Interestingly, fluorination at the 2-position of 1-phenycyclopropylamine, which is known as a selective inhibitor of MAO B relative to MAO A, reversed the selectivity and resulted in a potent inhibitor selective for MAO A.	1-phenycyclopropylamine	49-72	monoamine oxidase B	Homo sapiens	117-122
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	rasagiline	112-122	monoamine oxidase B	Homo sapiens	68-87
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	rasagiline	112-122	monoamine oxidase B	Homo sapiens	89-94
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	N-propargyl	124-135	monoamine oxidase B	Homo sapiens	68-87
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	N-propargyl	124-135	monoamine oxidase B	Homo sapiens	89-94
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	1R	137-139	monoamine oxidase B	Homo sapiens	68-87
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	1R	137-139	monoamine oxidase B	Homo sapiens	89-94
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	1-aminoindan	141-151	monoamine oxidase B	Homo sapiens	68-87
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	199-205	monoamine oxidase B	Homo sapiens	68-87
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	199-205	monoamine oxidase B	Homo sapiens	89-94
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	(N-propargyl-(3R) and (3S) aminoindan-5-yl)-ethyl methyl carbamate	210-216	monoamine oxidase B	Homo sapiens	68-87
15147504-1	2004	We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan], and its cholinesterase inhibitor derivatives TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism in SH-SY5Y neuroblastoma and PC12 cells.	(N-propargyl-(3R) and (3S) aminoindan-5-yl)-ethyl methyl carbamate	210-216	monoamine oxidase B	Homo sapiens	89-94
15110758-4	2004	FAST is tethered to mitochondria by a lysine/arginine-rich domain at its carboxyl terminus that is structurally similar to the mitochondrial tethering motifs of monoamine oxidase B and cytochrome b5.	Lysine	38-44	monoamine oxidase B	Homo sapiens	161-180
15056494-1	2004	The structure of monoamine oxidase B revealed three aromatic amino acid residues within contact distance of the flavin cofactor and a large number of aromatic residues in the substrate binding site.	Amino Acids, Aromatic	52-71	monoamine oxidase B	Homo sapiens	17-36
15111100-1	2004	Monoamine oxidase B (MAO B) is an outer mitochondrial membrane protein that oxidizes arylalkylamine neurotransmitters and has been a valuable drug target for many neurological disorders.	arylalkylamine	85-99	monoamine oxidase B	Homo sapiens	0-19
15111100-1	2004	Monoamine oxidase B (MAO B) is an outer mitochondrial membrane protein that oxidizes arylalkylamine neurotransmitters and has been a valuable drug target for many neurological disorders.	arylalkylamine	85-99	monoamine oxidase B	Homo sapiens	21-26
15056494-1	2004	The structure of monoamine oxidase B revealed three aromatic amino acid residues within contact distance of the flavin cofactor and a large number of aromatic residues in the substrate binding site.	4,6-dinitro-o-cresol	112-118	monoamine oxidase B	Homo sapiens	17-36
15027867-4	2004	Rasagiline has the highest specificity for MAO B, as demonstrated by a 100-fold higher inhibition potency (k(inact)/K(i)) compared to MAO A, with the remaining compounds exhibiting lower isozyme specificities.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	43-48
15096406-1	2004	BACKGROUND: Treatment with rasagiline mesylate, an irreversible monoamine oxidase type B inhibitor, improves symptoms of early Parkinson disease (PD).	Rasagiline mesylate	27-46	monoamine oxidase B	Homo sapiens	64-88
15027867-5	2004	MAO B and MAO A are more selective for the R-enantiomer (rasagiline) compared to the S-enantiomer (S-PAI) by 2500-fold and 17-fold, respectively.	rasagiline	57-67	monoamine oxidase B	Homo sapiens	0-5
15027867-6	2004	Differences in UV/vis and CD spectral data of the complexes of the studied compounds with both MAO A and MAO B are interpreted in light of crystallographic data of complexes of MAO B with rasagiline and its analogues (Binda, C.; et al.	rasagiline	188-198	monoamine oxidase B	Homo sapiens	105-110
15027867-6	2004	Differences in UV/vis and CD spectral data of the complexes of the studied compounds with both MAO A and MAO B are interpreted in light of crystallographic data of complexes of MAO B with rasagiline and its analogues (Binda, C.; et al.	rasagiline	188-198	monoamine oxidase B	Homo sapiens	177-182
15027868-0	2004	Crystal structures of monoamine oxidase B in complex with four inhibitors of the N-propargylaminoindan class.	n-propargylaminoindan	81-102	monoamine oxidase B	Homo sapiens	22-41
15027868-1	2004	Monoamine oxidase B (MAO B) is an outer mitochondrial membrane enzyme that catalyzes the oxidation of arylalkylamine neurotransmitters.	arylalkylamine	102-116	monoamine oxidase B	Homo sapiens	0-19
15027868-1	2004	Monoamine oxidase B (MAO B) is an outer mitochondrial membrane enzyme that catalyzes the oxidation of arylalkylamine neurotransmitters.	arylalkylamine	102-116	monoamine oxidase B	Homo sapiens	21-26
15027872-2	2004	Synthesis and effect of fluorine substitution at the cyclopropane ring on inhibition of microbial tyramine oxidase.	Fluorine	24-32	monoamine oxidase B	Homo sapiens	98-114
15027872-2	2004	Synthesis and effect of fluorine substitution at the cyclopropane ring on inhibition of microbial tyramine oxidase.	cyclopropane	53-65	monoamine oxidase B	Homo sapiens	98-114
15027872-5	2004	Characterization of tyramine oxidase, carried out prior to the inhibition experiments, confirmed earlier suggestions that this enzyme is a semicarbazide-sensitive copper-containing monoamine oxidase.	carbamylhydrazine	139-152	monoamine oxidase B	Homo sapiens	20-36
15027872-7	2004	2-Fluoro-1-phenylcyclopropylmethylamine was found to be a weak noncompetitive inhibitor of tyramine oxidase.	2-fluoro-1-phenylcyclopropylmethylamine	0-39	monoamine oxidase B	Homo sapiens	91-107
15027872-8	2004	The presence of a free amino group, directly bonded to the cyclopropane ring, and a fluorine atom in a relationship cis to the amino group were structural features that increased tyramine oxidase inhibition.	cyclopropane	59-71	monoamine oxidase B	Homo sapiens	179-195
15027872-8	2004	The presence of a free amino group, directly bonded to the cyclopropane ring, and a fluorine atom in a relationship cis to the amino group were structural features that increased tyramine oxidase inhibition.	Fluorine	84-92	monoamine oxidase B	Homo sapiens	179-195
15108383-1	2004	Dependence of the activity of monoamine oxidase-B (MAO-B) in different human bone marrow (BM) sections on death-coming prescription (DCP) and on age was investigated.	dcp	133-136	monoamine oxidase B	Homo sapiens	30-49
14962063-1	2004	1-Methyl-4-phenylpyridinium (MPP(+)) ion, a toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, is produced by monoamine oxidase B in astrocytes.	1-Methyl-4-phenylpyridinium	0-27	monoamine oxidase B	Homo sapiens	125-144
14962063-1	2004	1-Methyl-4-phenylpyridinium (MPP(+)) ion, a toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, is produced by monoamine oxidase B in astrocytes.	mangion-purified polysaccharide (Candida albicans)	29-35	monoamine oxidase B	Homo sapiens	125-144
14962063-1	2004	1-Methyl-4-phenylpyridinium (MPP(+)) ion, a toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, is produced by monoamine oxidase B in astrocytes.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	64-108	monoamine oxidase B	Homo sapiens	125-144
15108383-1	2004	Dependence of the activity of monoamine oxidase-B (MAO-B) in different human bone marrow (BM) sections on death-coming prescription (DCP) and on age was investigated.	dcp	133-136	monoamine oxidase B	Homo sapiens	51-56
15108383-2	2004	It was established that the activity of MAO-B in BM cervical intumescence is an objective DCP marker (within a time span of 12 hours).	dcp	90-93	monoamine oxidase B	Homo sapiens	40-45
15233592-12	2004	Disulfiram and selegiline increase brain dopamine concentrations by inhibition of dopamine-catabolising enzymes (dopamine-beta-hydroxylase and monoamine oxidase B, respectively).	Disulfiram	0-10	monoamine oxidase B	Homo sapiens	143-162
14697793-1	2004	A new molecule, the 4-methyl-thio-phenyl-propylamine (PrNH(2)) was synthesized and its biological interaction with different amine oxidases such as semicarbazide sensitive amine oxidase (SSAO) [E.C.1.4.3.6], and monoamine oxidase [E.C.1.4.3.4] under its two isoforms, MAO A and MAO B, has been assessed.	prnh(2)	54-61	monoamine oxidase B	Homo sapiens	278-283
14965331-12	2004	Therefore, it is suggested that the activation of dopamine synthesis and the moderate level of MAOB inhibition are main mechanisms of ZNS effects on PD.	Zonisamide	134-137	monoamine oxidase B	Homo sapiens	95-99
14605792-2	2004	Selegiline, a selective monoamine oxidase B inhibitor, indirectly modulates dopamine levels, and research suggests selegiline may modify subjective effects of cocaine.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	24-43
14696044-3	2004	Selegiline is a selective and irreversible propargylamine type B monoamine oxidase (MAO-B) inhibitor.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	84-89
14696044-3	2004	Selegiline is a selective and irreversible propargylamine type B monoamine oxidase (MAO-B) inhibitor.	propargylamine	43-57	monoamine oxidase B	Homo sapiens	84-89
14696044-6	2004	To circumvent this obstacle, a novel MAO-B inhibitor, rasagiline, was developed.	rasagiline	54-64	monoamine oxidase B	Homo sapiens	37-42
14696044-8	2004	Recent investigations into the neuroprotective mechanism of propargylamines indicate that glyceraldehyde-3-phosphate dehydrogenase (GAPDH), MAO-B and/or other unknown proteins may represent pivotal proteins in the survival of the injured neurons.	propargylamine	60-75	monoamine oxidase B	Homo sapiens	140-145
15563241-11	2004	Safinamide combines sodium and calcium channel modulatory activity with monoamine oxidase B inhibition.	safinamide	0-10	monoamine oxidase B	Homo sapiens	72-91
15233592-12	2004	Disulfiram and selegiline increase brain dopamine concentrations by inhibition of dopamine-catabolising enzymes (dopamine-beta-hydroxylase and monoamine oxidase B, respectively).	Selegiline	15-25	monoamine oxidase B	Homo sapiens	143-162
15233592-12	2004	Disulfiram and selegiline increase brain dopamine concentrations by inhibition of dopamine-catabolising enzymes (dopamine-beta-hydroxylase and monoamine oxidase B, respectively).	Dopamine	41-49	monoamine oxidase B	Homo sapiens	143-162
15233592-12	2004	Disulfiram and selegiline increase brain dopamine concentrations by inhibition of dopamine-catabolising enzymes (dopamine-beta-hydroxylase and monoamine oxidase B, respectively).	Dopamine	82-90	monoamine oxidase B	Homo sapiens	143-162
14697876-3	2004	MAO-A is inhibited by clorgyline; and MAO-B, by deprenyl.	Selegiline	48-56	monoamine oxidase B	Homo sapiens	38-43
15262334-3	2004	Utilizing [3H]BC, we have identified several proteins to which BC binds with high affinity (e.g. the chaperone member glucose regulated protein 78, the enzyme carboxylesterase, the cytochrome P450 2E1, the enzyme monoamine oxidase B and a small G-protein of the Rho subfamily).	Tritium	11-13	monoamine oxidase B	Homo sapiens	213-232
14697876-10	2004	MAO-A oxidizes noradrenaline and serotonin; and MAO-B, mainly beta-phenylethylamine.	phenethylamine	62-83	monoamine oxidase B	Homo sapiens	48-53
14697880-1	2004	The recently published crystal structure of monoamine oxidase (MAO) B was a major breakthrough for structural and functional understanding of flavin containing amine oxidases: it opens a new era of research and provides new opportunities to those interested in the biochemistry and pharmacology of those important drug targets.	4,6-dinitro-o-cresol	142-148	monoamine oxidase B	Homo sapiens	44-69
14697881-1	2004	The structural details of the interactions of the covalent 8alpha-S-cysteinyl-FAD with the protein moiety in monoamine oxidase B (MAO B) based on the MAO B crystal structure are described.	8alpha-s-cysteinyl-fad	59-81	monoamine oxidase B	Homo sapiens	109-128
14697881-1	2004	The structural details of the interactions of the covalent 8alpha-S-cysteinyl-FAD with the protein moiety in monoamine oxidase B (MAO B) based on the MAO B crystal structure are described.	8alpha-s-cysteinyl-fad	59-81	monoamine oxidase B	Homo sapiens	130-135
14697881-1	2004	The structural details of the interactions of the covalent 8alpha-S-cysteinyl-FAD with the protein moiety in monoamine oxidase B (MAO B) based on the MAO B crystal structure are described.	8alpha-s-cysteinyl-fad	59-81	monoamine oxidase B	Homo sapiens	150-155
14697881-3	2004	Since those amino acids interacting with the FAD are conserved in monoamine oxidase A (MAO A), it is proposed that the FAD binding site in MAO A is quite similar to that in MAO B.	Flavin-Adenine Dinucleotide	45-48	monoamine oxidase B	Homo sapiens	173-178
14697881-3	2004	Since those amino acids interacting with the FAD are conserved in monoamine oxidase A (MAO A), it is proposed that the FAD binding site in MAO A is quite similar to that in MAO B.	Flavin-Adenine Dinucleotide	119-122	monoamine oxidase B	Homo sapiens	173-178
14697881-6	2004	The normally flat oxidized flavin ring is in a bent, puckered conformation in the MAO B binding site which is suggested to contribute to its reactivity in catalysis.	4,6-dinitro-o-cresol	27-33	monoamine oxidase B	Homo sapiens	82-87
14697881-7	2004	This structural information is then used to explain previous studies on flavin analog incorporation into either MAO B or into MAO A.	4,6-dinitro-o-cresol	72-78	monoamine oxidase B	Homo sapiens	112-117
14697882-11	2004	65 (2001) 129], we have identified three amino acids residues (Phe 423, Glu 427, and Thr 428) that appear to play a role in generating catalytically active MAO B.	Phenylalanine	63-66	monoamine oxidase B	Homo sapiens	156-161
14697882-11	2004	65 (2001) 129], we have identified three amino acids residues (Phe 423, Glu 427, and Thr 428) that appear to play a role in generating catalytically active MAO B.	Glutamic Acid	72-75	monoamine oxidase B	Homo sapiens	156-161
14697882-11	2004	65 (2001) 129], we have identified three amino acids residues (Phe 423, Glu 427, and Thr 428) that appear to play a role in generating catalytically active MAO B.	Threonine	85-88	monoamine oxidase B	Homo sapiens	156-161
14697882-13	2004	Thus, it appears that Phe 423, Glu 427 and Thr 428 do not directly affect the active site, but they could modulate activity through an independent function such as non-covalent binding of FAD during synthesis of the MAO B polypeptide chain.	Phenylalanine	22-25	monoamine oxidase B	Homo sapiens	216-221
14697882-13	2004	Thus, it appears that Phe 423, Glu 427 and Thr 428 do not directly affect the active site, but they could modulate activity through an independent function such as non-covalent binding of FAD during synthesis of the MAO B polypeptide chain.	Glutamic Acid	31-34	monoamine oxidase B	Homo sapiens	216-221
14697882-13	2004	Thus, it appears that Phe 423, Glu 427 and Thr 428 do not directly affect the active site, but they could modulate activity through an independent function such as non-covalent binding of FAD during synthesis of the MAO B polypeptide chain.	Threonine	43-46	monoamine oxidase B	Homo sapiens	216-221
14697895-2	2004	Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	45-50
14697895-2	2004	Selegiline [(-)-deprenil] was developed as a MAO-B inhibitor more than 30 years ago and widely used in the treatment of Parkinson"s disease.	Selegiline	12-24	monoamine oxidase B	Homo sapiens	45-50
14697896-3	2004	The selective monoamine oxidase-B inhibitor selegiline and the selective and reversible inhibitor of monoamine oxidase-A (RIMA) moclobemide are free from the hypertensive crisis, the so-called "cheese effect."	Selegiline	44-54	monoamine oxidase B	Homo sapiens	14-33
14697898-0	2004	(-)-Deprenyl, a selective MAO-B inhibitor, with apoptotic and anti-apoptotic properties.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	26-31
14697898-1	2004	(-)-Deprenyl (selegiline) is an irreversible inhibitor of monoamine oxidase (MAO) B, which was discovered in 1962 and become the "golden standard" of MAO research.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	58-83
14697898-1	2004	(-)-Deprenyl (selegiline) is an irreversible inhibitor of monoamine oxidase (MAO) B, which was discovered in 1962 and become the "golden standard" of MAO research.	Selegiline	14-24	monoamine oxidase B	Homo sapiens	58-83
14697898-6	2004	(-)-Deprenyl in much lower concentrations needed to induce MAO-B inhibition (10(-9) to 10(-13) M) potently inhibits MPTP or serum withdrawal induced apoptosis in tissue cultures of neuro-ectodermal origin (PC12, M1, M2058).	Selegiline	0-12	monoamine oxidase B	Homo sapiens	59-64
14697898-6	2004	(-)-Deprenyl in much lower concentrations needed to induce MAO-B inhibition (10(-9) to 10(-13) M) potently inhibits MPTP or serum withdrawal induced apoptosis in tissue cultures of neuro-ectodermal origin (PC12, M1, M2058).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	116-120	monoamine oxidase B	Homo sapiens	59-64
14697899-4	2004	However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction of L-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms.	Selegiline	162-172	monoamine oxidase B	Homo sapiens	84-89
14697899-4	2004	However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction of L-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms.	Selegiline	174-184	monoamine oxidase B	Homo sapiens	84-89
14697899-4	2004	However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction of L-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms.	Dopamine	219-227	monoamine oxidase B	Homo sapiens	84-89
14697899-8	2004	This was not possible until recently, with the development of the novel cholinesterase-brain selective MAO-AB inhibitor, TV3326 (N-propargyl-(3R)-aminoidnan-5-yl-ethyl methylcarbamate hemitartiate), a carbamate derivative of the irreversible MAO-B inhibitor anti-Parkinson drug, rasagiline.	(N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate	121-127	monoamine oxidase B	Homo sapiens	242-247
14697899-8	2004	This was not possible until recently, with the development of the novel cholinesterase-brain selective MAO-AB inhibitor, TV3326 (N-propargyl-(3R)-aminoidnan-5-yl-ethyl methylcarbamate hemitartiate), a carbamate derivative of the irreversible MAO-B inhibitor anti-Parkinson drug, rasagiline.	n-propargyl-(3r)-aminoidnan-5-yl-ethyl methylcarbamate hemitartiate	129-196	monoamine oxidase B	Homo sapiens	242-247
14697904-7	2004	In comparison with milacemide, N,N-bis(carbamoylmethyl)-N-pentylamine was the best and exclusive substrate for MAO-B.	milacemide	19-29	monoamine oxidase B	Homo sapiens	111-116
14697904-7	2004	In comparison with milacemide, N,N-bis(carbamoylmethyl)-N-pentylamine was the best and exclusive substrate for MAO-B.	n,n-bis(carbamoylmethyl)-n-pentylamine	31-69	monoamine oxidase B	Homo sapiens	111-116
14697904-8	2004	2-N-(phenylethylamino)-acetoamide was the good substrate for MAO-A and MAO-B same as milacemide.	2-n-(phenylethylamino)-acetoamide	0-33	monoamine oxidase B	Homo sapiens	71-76
14697904-8	2004	2-N-(phenylethylamino)-acetoamide was the good substrate for MAO-A and MAO-B same as milacemide.	milacemide	85-95	monoamine oxidase B	Homo sapiens	71-76
15262334-3	2004	Utilizing [3H]BC, we have identified several proteins to which BC binds with high affinity (e.g. the chaperone member glucose regulated protein 78, the enzyme carboxylesterase, the cytochrome P450 2E1, the enzyme monoamine oxidase B and a small G-protein of the Rho subfamily).	Carbolines	14-16	monoamine oxidase B	Homo sapiens	213-232
14636968-1	2003	Selegiline is a specific MAO-B inhibitor.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	25-30
15028609-0	2003	Association between I(2) binding sites and monoamine oxidase-B activity in platelets.	Iodine	20-24	monoamine oxidase B	Homo sapiens	43-62
15028609-1	2003	An I(2) imidazoline binding site on monoamine oxidase-B (MAO-B) is known to be encoded by a noncatalytic part of the enzyme, different from that which recognizes mechanism-based inhibitors.	Imidazolines	8-19	monoamine oxidase B	Homo sapiens	36-55
15028609-1	2003	An I(2) imidazoline binding site on monoamine oxidase-B (MAO-B) is known to be encoded by a noncatalytic part of the enzyme, different from that which recognizes mechanism-based inhibitors.	Imidazolines	8-19	monoamine oxidase B	Homo sapiens	57-62
15028609-2	2003	Herein, the relationship between I(2)-imidazoline binding sites and MAO-B activity has been assessed using a semi-purified source of MAO-B: platelet mitochondrial membranes.	i(2)-imidazoline	33-49	monoamine oxidase B	Homo sapiens	68-73
15028609-2	2003	Herein, the relationship between I(2)-imidazoline binding sites and MAO-B activity has been assessed using a semi-purified source of MAO-B: platelet mitochondrial membranes.	i(2)-imidazoline	33-49	monoamine oxidase B	Homo sapiens	133-138
14636968-2	2003	As MAO-B has been shown to be significantly involved in the metabolism of dopamine in certain regions of the primate brain, selegiline has been proposed for use in the treatment of drug addiction.	Dopamine	74-82	monoamine oxidase B	Homo sapiens	3-8
14636968-2	2003	As MAO-B has been shown to be significantly involved in the metabolism of dopamine in certain regions of the primate brain, selegiline has been proposed for use in the treatment of drug addiction.	Selegiline	124-134	monoamine oxidase B	Homo sapiens	3-8
14604687-0	2003	Synthesis and in vitro biological evaluation of fluoro-substituted-4-phenyl-1,2,3,6-tetrahydropyridines as monoamine oxidase B substrates.	fluoro-substituted-4-phenyl-1,2,3,6-tetrahydropyridines	48-103	monoamine oxidase B	Homo sapiens	107-126
14604687-1	2003	The substrate properties of three beta-fluoro-4-phenyl-1,2,3,6-tetrahydropyridines related to the proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine have been examined in an effort to evaluate the contribution of electronic parameters to the MAO-B catalyzed allylic-alpha-carbon oxidation of the tetrahydropyridinyl system.	proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-156	monoamine oxidase B	Homo sapiens	250-255
14651728-7	2003	The oxidative deaminase activities of RIZ were inhibited completely by the nanomolar-order concentration of clorgyline and Ro 41-1049 (MAO-A selective inhibitors), but not by that of Ro 16-6491 (MAO-B selective inhibitor).	Clorgyline	108-118	monoamine oxidase B	Homo sapiens	195-200
14612913-1	2003	l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	59-78
14612913-1	2003	l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	80-85
14612913-1	2003	l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults.	r-(-)-deprenyl	12-26	monoamine oxidase B	Homo sapiens	59-78
14612913-1	2003	l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults.	r-(-)-deprenyl	12-26	monoamine oxidase B	Homo sapiens	80-85
14612913-1	2003	l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults.	Selegiline	28-38	monoamine oxidase B	Homo sapiens	59-78
14612913-1	2003	l-Deprenyl (R-(-)-deprenyl, selegiline) is an inhibitor of monoamine oxidase-B (MAO-B) that is known to protect nerve cells from a variety of chemical and physical insults.	Selegiline	28-38	monoamine oxidase B	Homo sapiens	80-85
14563485-1	2003	L-Deprenyl, an inhibitor of mitochondrial monoamine oxidase B (MAO B), inhibits the swelling of liver mitochondria induced by the pro-oxidant 2-methyl-1,4-naphtoquinone with a K(i) dependent on quinone concentration.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	42-61
14563485-1	2003	L-Deprenyl, an inhibitor of mitochondrial monoamine oxidase B (MAO B), inhibits the swelling of liver mitochondria induced by the pro-oxidant 2-methyl-1,4-naphtoquinone with a K(i) dependent on quinone concentration.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	63-68
14563485-1	2003	L-Deprenyl, an inhibitor of mitochondrial monoamine oxidase B (MAO B), inhibits the swelling of liver mitochondria induced by the pro-oxidant 2-methyl-1,4-naphtoquinone with a K(i) dependent on quinone concentration.	2-methyl-1,4-naphtoquinone	142-168	monoamine oxidase B	Homo sapiens	42-61
14563485-1	2003	L-Deprenyl, an inhibitor of mitochondrial monoamine oxidase B (MAO B), inhibits the swelling of liver mitochondria induced by the pro-oxidant 2-methyl-1,4-naphtoquinone with a K(i) dependent on quinone concentration.	2-methyl-1,4-naphtoquinone	142-168	monoamine oxidase B	Homo sapiens	63-68
14563485-1	2003	L-Deprenyl, an inhibitor of mitochondrial monoamine oxidase B (MAO B), inhibits the swelling of liver mitochondria induced by the pro-oxidant 2-methyl-1,4-naphtoquinone with a K(i) dependent on quinone concentration.	quinone	161-168	monoamine oxidase B	Homo sapiens	42-61
14563485-1	2003	L-Deprenyl, an inhibitor of mitochondrial monoamine oxidase B (MAO B), inhibits the swelling of liver mitochondria induced by the pro-oxidant 2-methyl-1,4-naphtoquinone with a K(i) dependent on quinone concentration.	quinone	161-168	monoamine oxidase B	Homo sapiens	63-68
14563485-6	2003	These results indicate a more generalized protective effect of L-deprenyl on mitochondrial functions, involving the inhibition of membrane permeability transition induced not only by the oxidation of substrates of MAO B, but also by pro-oxidant agents such as 2-methyl-1,4-naphtoquinone, which does not involve MAO B activity.	Selegiline	63-73	monoamine oxidase B	Homo sapiens	214-219
14563485-6	2003	These results indicate a more generalized protective effect of L-deprenyl on mitochondrial functions, involving the inhibition of membrane permeability transition induced not only by the oxidation of substrates of MAO B, but also by pro-oxidant agents such as 2-methyl-1,4-naphtoquinone, which does not involve MAO B activity.	Selegiline	63-73	monoamine oxidase B	Homo sapiens	311-316
14563485-6	2003	These results indicate a more generalized protective effect of L-deprenyl on mitochondrial functions, involving the inhibition of membrane permeability transition induced not only by the oxidation of substrates of MAO B, but also by pro-oxidant agents such as 2-methyl-1,4-naphtoquinone, which does not involve MAO B activity.	2-methyl-1,4-naphtoquinone	260-286	monoamine oxidase B	Homo sapiens	311-316
19810877-3	2003	One such agent is the anti-Parkinson drug, rasagiline, a novel neuroprotective-antiapoptotic second-generation potent irreversible selective inhibitor of monoamine oxidase B.	rasagiline	43-53	monoamine oxidase B	Homo sapiens	154-173
12958079-14	2003	This 4.96 Mb region contains, among others, the genes for monoamine oxidase A (MAOA) and B (MAOB), which are involved in the oxidative deamination of several neurotransmitters, including dopamine and serotonin.	Dopamine	187-195	monoamine oxidase B	Homo sapiens	92-96
12958079-14	2003	This 4.96 Mb region contains, among others, the genes for monoamine oxidase A (MAOA) and B (MAOB), which are involved in the oxidative deamination of several neurotransmitters, including dopamine and serotonin.	Serotonin	200-209	monoamine oxidase B	Homo sapiens	92-96
14628189-19	2003	Thus, the lower but equally MAO-B inhibitory dose of selegiline in Zydis Selegiline 1.25 mg, which is associated with lower concentrations of potentially harmful metabolites, could offer a safer and more predictable treatment in the management of patients with Parkinson"s disease.	Selegiline	53-63	monoamine oxidase B	Homo sapiens	28-33
14628189-0	2003	A new formulation of selegiline: improved bioavailability and selectivity for MAO-B inhibition.	Selegiline	21-31	monoamine oxidase B	Homo sapiens	78-83
14628190-0	2003	A new low-dose formulation of selegiline: clinical efficacy, patient preference and selectivity for MAO-B inhibition.	Selegiline	30-40	monoamine oxidase B	Homo sapiens	100-105
14628189-4	2003	Inhibition of monoamine-oxidase type B (MAO-B) and monoamine oxidase type A (MAO-A) activity was determined by measurement of as beta-phenylethylamine (PEA) by GCMS and 5-hydroxyindoleacetic acid (5-HIAA) by High Performance Liquid Chromatography (HPLC) assays.	phenethylamine	129-150	monoamine oxidase B	Homo sapiens	14-38
14628189-4	2003	Inhibition of monoamine-oxidase type B (MAO-B) and monoamine oxidase type A (MAO-A) activity was determined by measurement of as beta-phenylethylamine (PEA) by GCMS and 5-hydroxyindoleacetic acid (5-HIAA) by High Performance Liquid Chromatography (HPLC) assays.	phenethylamine	152-155	monoamine oxidase B	Homo sapiens	14-38
14628190-24	2003	Furthermore, Zydis Selegiline was well tolerated and, unlike conventional selegiline tablets, appeared to retain specificity for inhibition of monoamine oxidase type B (MAO-B), since it did not potentiate the pressor response to tyramine.	Selegiline hydrochloride	13-29	monoamine oxidase B	Homo sapiens	143-167
14628189-4	2003	Inhibition of monoamine-oxidase type B (MAO-B) and monoamine oxidase type A (MAO-A) activity was determined by measurement of as beta-phenylethylamine (PEA) by GCMS and 5-hydroxyindoleacetic acid (5-HIAA) by High Performance Liquid Chromatography (HPLC) assays.	phenethylamine	152-155	monoamine oxidase B	Homo sapiens	40-45
14628190-24	2003	Furthermore, Zydis Selegiline was well tolerated and, unlike conventional selegiline tablets, appeared to retain specificity for inhibition of monoamine oxidase type B (MAO-B), since it did not potentiate the pressor response to tyramine.	Selegiline hydrochloride	13-29	monoamine oxidase B	Homo sapiens	169-174
14628189-4	2003	Inhibition of monoamine-oxidase type B (MAO-B) and monoamine oxidase type A (MAO-A) activity was determined by measurement of as beta-phenylethylamine (PEA) by GCMS and 5-hydroxyindoleacetic acid (5-HIAA) by High Performance Liquid Chromatography (HPLC) assays.	Hydroxyindoleacetic Acid	169-195	monoamine oxidase B	Homo sapiens	14-38
14555244-1	2003	The anti-Parkinson drug, rasagiline, a irreversible propargyl possessing monoamine oxidase B inhibitor can protect neurons in vitro and in vivo from a variety of neurotoxic insults including SIN-1, glutamate, the parkinsonism inducing neurotoxin, N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, N-methyl-(R)-salsolinol and including beta amyloid protein.	rasagiline	25-35	monoamine oxidase B	Homo sapiens	73-92
14628189-4	2003	Inhibition of monoamine-oxidase type B (MAO-B) and monoamine oxidase type A (MAO-A) activity was determined by measurement of as beta-phenylethylamine (PEA) by GCMS and 5-hydroxyindoleacetic acid (5-HIAA) by High Performance Liquid Chromatography (HPLC) assays.	Hydroxyindoleacetic Acid	197-203	monoamine oxidase B	Homo sapiens	14-38
14628189-12	2003	A significant (r=0.0001) correlation between daily PEA excretion (a measure of brain MAO-B inhibition) and the log-transformed AUC((0-t)) for selegiline was demonstrated.	Selegiline	142-152	monoamine oxidase B	Homo sapiens	85-90
14501143-0	2003	Polystyrene microbridges used in sitting-drop crystallization release 1,4-diphenyl-2-butene, a novel inhibitor of human MAO B.	Polystyrenes	0-11	monoamine oxidase B	Homo sapiens	120-125
14501143-0	2003	Polystyrene microbridges used in sitting-drop crystallization release 1,4-diphenyl-2-butene, a novel inhibitor of human MAO B.	1,4-diphenyl-2-butene	70-91	monoamine oxidase B	Homo sapiens	120-125
14501143-3	2003	This compound is present at a level of approximately 0.3 mg ( approximately 1.5 micro mol) per microbridge and functions as a competitive inhibitor of MAO B with a K(i) of 35 micro M. The presence of detergents in the crystallization solutions facilitates the extraction of this compound from the polymer medium.	Polymers	297-304	monoamine oxidase B	Homo sapiens	151-156
13129579-0	2003	Inactivation of mitochondrial monoamine oxidase B by methylthio-substituted benzylamines.	methylthio-substituted benzylamines	53-88	monoamine oxidase B	Homo sapiens	30-49
14521485-12	2003	Monoamine oxidase-B inhibitors, specifically selegiline, may provide symptomatic improvement; the question as to whether a neuroprotective benefit is present remains unanswered.	Selegiline	45-55	monoamine oxidase B	Homo sapiens	0-19
12849931-0	2003	Serotonin transporter and MAO-B levels in monoamine nuclei of the human brainstem are normal in major depression.	monoamine	42-51	monoamine oxidase B	Homo sapiens	26-31
12855685-6	2003	In vitro methylation of MAO B promoter with 5-aza-2"-deoxycytidine, a DNA methyltransferase inhibitor, up-regulated MAO B gene expression in both HeLa and Caco-2 cells.	Decitabine	44-66	monoamine oxidase B	Homo sapiens	24-29
12855685-6	2003	In vitro methylation of MAO B promoter with 5-aza-2"-deoxycytidine, a DNA methyltransferase inhibitor, up-regulated MAO B gene expression in both HeLa and Caco-2 cells.	Decitabine	44-66	monoamine oxidase B	Homo sapiens	116-121
14606950-3	2003	However, only two of them, NO donors (7-nitro-benzotetrazine-1,3-dioxide (7-NBTDO) and benzodifuroxan), caused nonselective inhibition of MAO A and MAO B with IC(50) values of 1.3-1.6 and 6.8-6.3 microM, respectively.	7-nitro-benzotetrazine-1,3-dioxide	38-72	monoamine oxidase B	Homo sapiens	148-153
14606950-3	2003	However, only two of them, NO donors (7-nitro-benzotetrazine-1,3-dioxide (7-NBTDO) and benzodifuroxan), caused nonselective inhibition of MAO A and MAO B with IC(50) values of 1.3-1.6 and 6.8-6.3 microM, respectively.	7-nitro-benzotetrazine-1,3-dioxide	74-81	monoamine oxidase B	Homo sapiens	148-153
14606950-3	2003	However, only two of them, NO donors (7-nitro-benzotetrazine-1,3-dioxide (7-NBTDO) and benzodifuroxan), caused nonselective inhibition of MAO A and MAO B with IC(50) values of 1.3-1.6 and 6.8-6.3 microM, respectively.	benzo(1,2-c:3,4-c')bis(1,2,5)oxadiazole-1,6-dioxide	87-101	monoamine oxidase B	Homo sapiens	148-153
14606950-7	2003	The data suggest that nonselective inhibition of MAO A and MAO B by benzodifuroxan and 7-NBTDO can be attributed to the properties of the chemical structures of these compounds.	benzo(1,2-c:3,4-c')bis(1,2,5)oxadiazole-1,6-dioxide	68-82	monoamine oxidase B	Homo sapiens	59-64
14606950-7	2003	The data suggest that nonselective inhibition of MAO A and MAO B by benzodifuroxan and 7-NBTDO can be attributed to the properties of the chemical structures of these compounds.	7-nitro-benzotetrazine-1,3-dioxide	87-94	monoamine oxidase B	Homo sapiens	59-64
12849931-5	2003	The binding of [(3)H]paroxetine to SERT and [(3)H]lazabemide to MAO-B were higher in the raphe nuclei than in the LC.	[(3)h]paroxetine	15-31	monoamine oxidase B	Homo sapiens	64-69
12849931-5	2003	The binding of [(3)H]paroxetine to SERT and [(3)H]lazabemide to MAO-B were higher in the raphe nuclei than in the LC.	[(3)h]lazabemide	44-60	monoamine oxidase B	Homo sapiens	64-69
12467619-4	2003	These requirements were applied in the design and synthesis of a novel reversible and selective MAO-B inhibitor, 3-methyl-8-(4,4,4-trifluoro-butoxy)indeno[1,2-c]pyridazin-5-one, that is ca.	3-methyl-8-(4,4,4-trifluoro-butoxy)indeno[1,2-c]pyridazin-5-one	113-176	monoamine oxidase B	Homo sapiens	96-101
12633131-2	2003	A selegiline transdermal system (STS) has been developed with unique pharmacokinetic and pharmacodynamic properties that allow inhibition of central nervous system MAO-A and MAO-B enzymes while substantially avoiding inhibition of intestinal and liver MAO-A enzyme.	Selegiline	2-12	monoamine oxidase B	Homo sapiens	174-179
12427476-1	2003	Monoamine oxidase isoform B (MAO-B) is involved in Parkinson"s disease (PD) induced by the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxin (MPTP) in human and non-human-primate.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	91-135	monoamine oxidase B	Homo sapiens	0-27
12427476-1	2003	Monoamine oxidase isoform B (MAO-B) is involved in Parkinson"s disease (PD) induced by the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxin (MPTP) in human and non-human-primate.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	91-135	monoamine oxidase B	Homo sapiens	29-34
12547469-1	2003	BACKGROUND: Since dopaminergic mechanisms appear to be involved in nicotine dependence, we studied the safety and efficacy of the monoamine oxidase B inhibitor selegiline hydrochloride compared with placebo for smoking cessation in nicotine-dependent cigarette smokers.	Selegiline	160-184	monoamine oxidase B	Homo sapiens	130-149
12913124-1	2003	Monoamine oxidase B (MAO-B) is an outer mitochondrial membrane-bound enzyme that catalyzes the oxidative deamination of arylalkylamine neurotransmitters and has been a target for a number of clinically used drug inhibitors.	arylalkylamine	120-134	monoamine oxidase B	Homo sapiens	0-19
12913124-1	2003	Monoamine oxidase B (MAO-B) is an outer mitochondrial membrane-bound enzyme that catalyzes the oxidative deamination of arylalkylamine neurotransmitters and has been a target for a number of clinically used drug inhibitors.	arylalkylamine	120-134	monoamine oxidase B	Homo sapiens	21-26
12913124-3	2003	1,4-Diphenyl-2-butene is found to be a reversible MAO-B inhibitor, which occupies both the entrance and substrate cavity space in the enzyme.	1,4-diphenyl-2-butene	0-21	monoamine oxidase B	Homo sapiens	50-55
12913124-7	2003	Inhibition of MAO-B with the clinically used trans-2-phenylcyclopropylamine results in the formation of a covalent C(4a) flavin adduct with an opened cyclopropyl ring and the phenyl ring in a parallel orientation to the flavin.	Tranylcypromine	45-75	monoamine oxidase B	Homo sapiens	14-19
12913124-7	2003	Inhibition of MAO-B with the clinically used trans-2-phenylcyclopropylamine results in the formation of a covalent C(4a) flavin adduct with an opened cyclopropyl ring and the phenyl ring in a parallel orientation to the flavin.	4,6-dinitro-o-cresol	121-127	monoamine oxidase B	Homo sapiens	14-19
12913124-7	2003	Inhibition of MAO-B with the clinically used trans-2-phenylcyclopropylamine results in the formation of a covalent C(4a) flavin adduct with an opened cyclopropyl ring and the phenyl ring in a parallel orientation to the flavin.	4,6-dinitro-o-cresol	220-226	monoamine oxidase B	Homo sapiens	14-19
12777388-3	2003	Human MAO A and MAO B each contain 9 cysteine residues (7 in conserved sequence locations).	Cysteine	37-45	monoamine oxidase B	Homo sapiens	16-21
12777388-7	2003	Cys5 and Cys266 were identified as the only residues modified by biotin-derivatized NEM in clorgyline-inactivated MAO A and pargyline-inactivated MAO B, respectively.	Biotin	65-71	monoamine oxidase B	Homo sapiens	146-151
12777388-7	2003	Cys5 and Cys266 were identified as the only residues modified by biotin-derivatized NEM in clorgyline-inactivated MAO A and pargyline-inactivated MAO B, respectively.	Clorgyline	91-101	monoamine oxidase B	Homo sapiens	146-151
12777388-7	2003	Cys5 and Cys266 were identified as the only residues modified by biotin-derivatized NEM in clorgyline-inactivated MAO A and pargyline-inactivated MAO B, respectively.	Pargyline	124-133	monoamine oxidase B	Homo sapiens	146-151
12777388-14	2003	These thiol residues are also modified by biotin-derivatized NEM in the mitochondrial membrane-bound MAO A and MAO B.	Sulfhydryl Compounds	6-11	monoamine oxidase B	Homo sapiens	111-116
12777388-14	2003	These thiol residues are also modified by biotin-derivatized NEM in the mitochondrial membrane-bound MAO A and MAO B.	Biotin	42-48	monoamine oxidase B	Homo sapiens	111-116
12777388-15	2003	This study shows that the MAO A structure is "more flexible" than that of MAO B and that clorgyline and pargyline inactivation of MAO A and B, respectively, increases the structural stability of both enzymes.	Clorgyline	89-99	monoamine oxidase B	Homo sapiens	74-79
12777388-15	2003	This study shows that the MAO A structure is "more flexible" than that of MAO B and that clorgyline and pargyline inactivation of MAO A and B, respectively, increases the structural stability of both enzymes.	Pargyline	104-113	monoamine oxidase B	Homo sapiens	74-79
12897643-0	2003	Pressor response to intravenous tyramine in healthy subjects after safinamide, a novel neuroprotectant with selective, reversible monoamine oxidase B inhibition.	Tyramine	32-40	monoamine oxidase B	Homo sapiens	130-149
12897643-0	2003	Pressor response to intravenous tyramine in healthy subjects after safinamide, a novel neuroprotectant with selective, reversible monoamine oxidase B inhibition.	safinamide	67-77	monoamine oxidase B	Homo sapiens	130-149
12897643-1	2003	Safinamide is a novel neuroprotectant combining sodium and calcium channel blocking properties with selective, reversible monoamine oxidase type B (MAO B) inhibition.	safinamide	0-10	monoamine oxidase B	Homo sapiens	122-146
12897643-1	2003	Safinamide is a novel neuroprotectant combining sodium and calcium channel blocking properties with selective, reversible monoamine oxidase type B (MAO B) inhibition.	safinamide	0-10	monoamine oxidase B	Homo sapiens	148-153
12620419-2	2003	Among selective MAOIs, MAO-A inhibitors (e.g. clorgyline) are used as antidepressant and antianxiety drugs and are claimed to protect neuronal cells against apoptosis, and selective MAO-B inhibitors (e.g. L-deprenyl) can be used in the treatment of Parkinson"s disease either alone or in combination with L-DOPA.	Clorgyline	46-56	monoamine oxidase B	Homo sapiens	182-187
12504917-3	2002	Reserpine-induced ptosis was reversed by rasagiline at doses above 2 mg x kg(-1) i.p., which inhibit MAO-A as well as MAO-B, but not at MAO-B-selective doses.	Reserpine	0-9	monoamine oxidase B	Homo sapiens	118-123
12483414-3	2003	The examinations were performed in one session starting with oxygen-15 labelled water scan to measure regional cerebral blood flow, followed by imaging with the monoamine oxidase B inhibitor N-[(11)C-methyl]- L-deuterodeprenyl (DED) to assess astrocytosis in the brain and finally imaging with fluor-18 2-fluorodeoxyglucose (FDG) to assess regional cerebral glucose metabolism (rCMR(glu)) [corrected].	n-[(11)c-methyl]- l-deuterodeprenyl	191-226	monoamine oxidase B	Homo sapiens	161-180
15035819-1	2003	In Parkinson"s disease and other neurodegenerative diseases, (-)deprenyl, an inhibitor of type B monoamine oxidase (MAO-B), has been proposed to protect or rescue declining neurons.	Selegiline	64-72	monoamine oxidase B	Homo sapiens	116-121
15035819-3	2003	This paper describes the activities of propargylamine MAO-B inhibitors against apoptosis induced by an endogenous selective dopaminergic neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells.	salsoline	149-170	monoamine oxidase B	Homo sapiens	54-59
12470183-2	2002	OBJECTIVE: To evaluate the safety and efficacy of the selective monoamine oxidase type B inhibitor rasagiline.	rasagiline	99-109	monoamine oxidase B	Homo sapiens	64-88
12873156-7	2003	Although the negative studies obtained with the MAO-B inhibitor selegiline (deprenyl) and the antioxidant tocopherol (vitamin E) may have resulted from an inappropriate choice of drug (selegiline) or an inadequate dose (tocopherol), the niggling problem that still remains is why these drugs, and others, do work in animals while they fail in the clinic.	Selegiline	64-74	monoamine oxidase B	Homo sapiens	48-53
12946055-2	2003	This hypothesis is, for many clinicians, the rationale for postponing the employment of and reducing the applied dosage of L-DOPA and for beginning therapy with dopamine receptor agonists or the monoamine oxidase type B (MAO-B) inhibitor selegiline.	Selegiline	238-248	monoamine oxidase B	Homo sapiens	195-219
12946055-2	2003	This hypothesis is, for many clinicians, the rationale for postponing the employment of and reducing the applied dosage of L-DOPA and for beginning therapy with dopamine receptor agonists or the monoamine oxidase type B (MAO-B) inhibitor selegiline.	Selegiline	238-248	monoamine oxidase B	Homo sapiens	221-226
12443774-0	2002	Natural and synthetic geiparvarins are strong and selective MAO-B inhibitors.	geiparvarin	22-34	monoamine oxidase B	Homo sapiens	60-65
12443774-3	2002	The desmethyl congener 6 of geiparvarin, proved potent and selective MAO-B inhibitor (pIC(50)=7.55 vs 4.62).	geiparvarin	28-39	monoamine oxidase B	Homo sapiens	69-74
12504917-3	2002	Reserpine-induced ptosis was reversed by rasagiline at doses above 2 mg x kg(-1) i.p., which inhibit MAO-A as well as MAO-B, but not at MAO-B-selective doses.	rasagiline	41-51	monoamine oxidase B	Homo sapiens	118-123
12504917-8	2002	), did not induce the behavioural hyperactivity syndrome which is seen following inhibition of both MAO-A and MAO-B by tranylcypromine together with the monoamine precursors.	Tranylcypromine	119-134	monoamine oxidase B	Homo sapiens	110-115
12414548-8	2002	CONCLUSIONS: MAO-B can be regarded as a state marker of alcohol consumption.	Alcohols	56-63	monoamine oxidase B	Homo sapiens	13-18
12414550-0	2002	Platelet monoamine oxidase B in family history positive and family history negative type 1 alcohol-dependent subjects.	Alcohols	91-98	monoamine oxidase B	Homo sapiens	9-28
12414550-1	2002	AIMS AND METHODS: In the present study platelet monoamine oxidase B (MAO-B) activity was investigated in 76 male type 1 alcohol-dependent subjects with and without a family history of alcoholism.	Alcohols	120-127	monoamine oxidase B	Homo sapiens	48-67
12414550-1	2002	AIMS AND METHODS: In the present study platelet monoamine oxidase B (MAO-B) activity was investigated in 76 male type 1 alcohol-dependent subjects with and without a family history of alcoholism.	Alcohols	120-127	monoamine oxidase B	Homo sapiens	69-74
12414550-4	2002	It should, however, be noted that platelet MAO-B activity was lower in alcohol-dependent subjects with three or four alcohol-dependent first-degree relatives.	Alcohols	71-78	monoamine oxidase B	Homo sapiens	43-48
12414550-4	2002	It should, however, be noted that platelet MAO-B activity was lower in alcohol-dependent subjects with three or four alcohol-dependent first-degree relatives.	Alcohols	117-124	monoamine oxidase B	Homo sapiens	43-48
12414550-5	2002	CONCLUSIONS: Although this latter finding should be interpreted with caution due to the small number of subjects, it cannot be excluded that FHP alcohol-dependent subjects with a large number of alcohol-dependent first-degree relatives may have lower platelet MAO-B activity.	Alcohols	145-152	monoamine oxidase B	Homo sapiens	260-265
12825788-2	2002	A set of 130 reversible and selective inhibitors of MAO-B (including tetrazole, oxadiazolone, and oxadiazinone derivatives) were taken from the literature and subjected to a three-dimensional quantitative structure-activity relationship (3D-QSAR) study, using CoMFA and GOLPE procedures.	1H-tetrazole	69-78	monoamine oxidase B	Homo sapiens	52-57
12825788-2	2002	A set of 130 reversible and selective inhibitors of MAO-B (including tetrazole, oxadiazolone, and oxadiazinone derivatives) were taken from the literature and subjected to a three-dimensional quantitative structure-activity relationship (3D-QSAR) study, using CoMFA and GOLPE procedures.	oxadiazolone	80-92	monoamine oxidase B	Homo sapiens	52-57
12825788-2	2002	A set of 130 reversible and selective inhibitors of MAO-B (including tetrazole, oxadiazolone, and oxadiazinone derivatives) were taken from the literature and subjected to a three-dimensional quantitative structure-activity relationship (3D-QSAR) study, using CoMFA and GOLPE procedures.	oxadiazinone	98-110	monoamine oxidase B	Homo sapiens	52-57
12202968-3	2002	OBJECTIVES: To examine the effects of the selective MAO-B inhibitor selegiline on withdrawal symptoms, smoking behavior and smoking satisfaction ratings.	Selegiline	68-78	monoamine oxidase B	Homo sapiens	52-57
12866710-3	2002	1-Methyl-4-phenyl- 1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of MAOB-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-45	monoamine oxidase B	Homo sapiens	159-163
12866710-3	2002	1-Methyl-4-phenyl- 1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of MAOB-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	47-51	monoamine oxidase B	Homo sapiens	159-163
12866710-3	2002	1-Methyl-4-phenyl- 1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of MAOB-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	1-Methyl-4-phenylpyridinium	198-230	monoamine oxidase B	Homo sapiens	159-163
12866710-3	2002	1-Methyl-4-phenyl- 1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of MAOB-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	mangion-purified polysaccharide (Candida albicans)	232-236	monoamine oxidase B	Homo sapiens	159-163
12200198-2	2002	An inhibitor of type B monoamine oxidase (MAO-B), (-)deprenyl (selegiline), was reported to have neuroprotective activity, but clinical trials failed to confirm it.	Selegiline	53-61	monoamine oxidase B	Homo sapiens	42-47
12200198-2	2002	An inhibitor of type B monoamine oxidase (MAO-B), (-)deprenyl (selegiline), was reported to have neuroprotective activity, but clinical trials failed to confirm it.	Selegiline	63-73	monoamine oxidase B	Homo sapiens	42-47
12359039-0	2002	Lazabemide, a selective, reversible monoamine oxidase B inhibitor, as an aid to smoking cessation.	lazabemide	0-10	monoamine oxidase B	Homo sapiens	36-55
12359039-5	2002	AIMS: To assess whether lazabemide, a reversible selective MAOB inhibitor, promotes smoking cessation.	lazabemide	24-34	monoamine oxidase B	Homo sapiens	59-63
12359039-20	2002	Further studies may associate MAOB inhibitors with nicotine replacement therapies to increase therapeutic efficacy.	Nicotine	51-59	monoamine oxidase B	Homo sapiens	30-34
12368371-15	2002	This study indicates that 11C-L-deprenyl-D2 will be useful for measuring the effects of different variables, including tobacco smoke exposure on MAO B activity in peripheral organs in humans.	L-deprenyl-D2 C-11	26-43	monoamine oxidase B	Homo sapiens	145-150
12214665-2	2002	The initial step in the overall reaction is the two-electron ring alpha-carbon oxidation to give the 1-methyl-4-phenyl-2,3-dihydropyridinium species, a reaction that is catalyzed by monoamine oxidase B.	Carbon	72-78	monoamine oxidase B	Homo sapiens	182-201
12214665-2	2002	The initial step in the overall reaction is the two-electron ring alpha-carbon oxidation to give the 1-methyl-4-phenyl-2,3-dihydropyridinium species, a reaction that is catalyzed by monoamine oxidase B.	4-phenyl-2,3-dihydropyridinium	110-140	monoamine oxidase B	Homo sapiens	182-201
12107035-0	2002	Platelet monoamine oxidase-B activity in type 1 alcohol-dependent subjects in sustained full remission.	Alcohols	48-55	monoamine oxidase B	Homo sapiens	9-28
12136372-1	2002	OBJECTIVE: The aim of this study was to investigate the effect of hormone-replacement therapy (HRT) on the pharmacokinetics of the selective monoamine oxidase B inhibitor selegiline and its primary metabolites desmethylselegiline and l-metamphetamine.	Selegiline	171-181	monoamine oxidase B	Homo sapiens	141-160
12107035-2	2002	METHODS: MAO-B activity was examined in 16 alcohol-dependent subjects, characterized as type 1 alcoholics, with an abstinence period of 6 +/- 7 years (mean +/- SD) and in 12 healthy controls.	Alcohols	43-50	monoamine oxidase B	Homo sapiens	9-14
12107035-4	2002	CONCLUSIONS: Type 1 male alcohol-dependent subjects appear to have normal platelet MAO-B activity.	Alcohols	25-32	monoamine oxidase B	Homo sapiens	83-88
12045467-1	2002	BACKGROUND: Monoamine oxidase B (MAO-B) degrades catecholamines in presynaptic nerve endings and is also active in platelets.	Catecholamines	49-63	monoamine oxidase B	Homo sapiens	12-31
11956220-3	2002	In this study, we have shown that phorbol 12-myristate 13-acetate (PMA) increases human MAO B, but not MAO A, gene expression.	Tetradecanoylphorbol Acetate	34-65	monoamine oxidase B	Homo sapiens	88-93
11956220-3	2002	In this study, we have shown that phorbol 12-myristate 13-acetate (PMA) increases human MAO B, but not MAO A, gene expression.	Tetradecanoylphorbol Acetate	67-70	monoamine oxidase B	Homo sapiens	88-93
11956220-9	2002	Furthermore, protein kinase C inhibitor blocks the PMA-dependent activation of MAO B.	Tetradecanoylphorbol Acetate	51-54	monoamine oxidase B	Homo sapiens	79-84
11956220-10	2002	Co-transfection of the MAO B promoter with dominant negative forms of Ras, Raf-1, MEKK1, MEK1, MEK3, MEK7, ERK2, JNK1, and p38/RK inhibit the PMA-dependent activation of the MAO B promoter.	Tetradecanoylphorbol Acetate	142-145	monoamine oxidase B	Homo sapiens	23-28
11861643-3	2002	We have recently generated 14 site-directed mutants of human MAO A and B, and we found that four key amino acids, Lys-305, Trp-397, Tyr-407, and Tyr-444, in MAO A and their corresponding amino acids in MAO B, Lys-296, Trp-388, Tyr-398, and Tyr-435, play important roles in MAO catalytic activity.	Lysine	114-117	monoamine oxidase B	Homo sapiens	202-207
12473970-4	2002	Selegiline, a selective inhibitor of MAO-B has been shown to be effective in the treatment of depression at higher oral doses where selectivity for MAO-B is lost.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	37-42
12473970-4	2002	Selegiline, a selective inhibitor of MAO-B has been shown to be effective in the treatment of depression at higher oral doses where selectivity for MAO-B is lost.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	148-153
12044541-2	2002	Although MPTP produces a parkinsonian syndrome after its conversion to 1-methyl-4-phenylpyridine (MPP(+)) by type B monoamine oxidase (MAO-B) in the brain, the etiology of this disease remains obscure.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	9-13	monoamine oxidase B	Homo sapiens	135-140
12044541-2	2002	Although MPTP produces a parkinsonian syndrome after its conversion to 1-methyl-4-phenylpyridine (MPP(+)) by type B monoamine oxidase (MAO-B) in the brain, the etiology of this disease remains obscure.	1-Methyl-4-phenylpyridinium	71-96	monoamine oxidase B	Homo sapiens	135-140
12044541-2	2002	Although MPTP produces a parkinsonian syndrome after its conversion to 1-methyl-4-phenylpyridine (MPP(+)) by type B monoamine oxidase (MAO-B) in the brain, the etiology of this disease remains obscure.	mangion-purified polysaccharide (Candida albicans)	98-101	monoamine oxidase B	Homo sapiens	135-140
11861643-3	2002	We have recently generated 14 site-directed mutants of human MAO A and B, and we found that four key amino acids, Lys-305, Trp-397, Tyr-407, and Tyr-444, in MAO A and their corresponding amino acids in MAO B, Lys-296, Trp-388, Tyr-398, and Tyr-435, play important roles in MAO catalytic activity.	Tryptophan	123-126	monoamine oxidase B	Homo sapiens	202-207
11861643-3	2002	We have recently generated 14 site-directed mutants of human MAO A and B, and we found that four key amino acids, Lys-305, Trp-397, Tyr-407, and Tyr-444, in MAO A and their corresponding amino acids in MAO B, Lys-296, Trp-388, Tyr-398, and Tyr-435, play important roles in MAO catalytic activity.	Tyrosine	145-148	monoamine oxidase B	Homo sapiens	202-207
11861643-3	2002	We have recently generated 14 site-directed mutants of human MAO A and B, and we found that four key amino acids, Lys-305, Trp-397, Tyr-407, and Tyr-444, in MAO A and their corresponding amino acids in MAO B, Lys-296, Trp-388, Tyr-398, and Tyr-435, play important roles in MAO catalytic activity.	Tyrosine	145-148	monoamine oxidase B	Homo sapiens	202-207
11861643-3	2002	We have recently generated 14 site-directed mutants of human MAO A and B, and we found that four key amino acids, Lys-305, Trp-397, Tyr-407, and Tyr-444, in MAO A and their corresponding amino acids in MAO B, Lys-296, Trp-388, Tyr-398, and Tyr-435, play important roles in MAO catalytic activity.	Tyrosine	145-148	monoamine oxidase B	Homo sapiens	202-207
11861643-4	2002	Based on the polyamine oxidase three-dimensional crystal structure, it is suggested that Lys-305, Trp-397, and Tyr-407 in MAO A and Lys-296, Trp-388, and Tyr-398 in MAO B may be involved in the non-covalent binding to FAD.	Lysine	89-92	monoamine oxidase B	Homo sapiens	165-170
11861643-4	2002	Based on the polyamine oxidase three-dimensional crystal structure, it is suggested that Lys-305, Trp-397, and Tyr-407 in MAO A and Lys-296, Trp-388, and Tyr-398 in MAO B may be involved in the non-covalent binding to FAD.	Tyrosine	111-114	monoamine oxidase B	Homo sapiens	165-170
11861643-4	2002	Based on the polyamine oxidase three-dimensional crystal structure, it is suggested that Lys-305, Trp-397, and Tyr-407 in MAO A and Lys-296, Trp-388, and Tyr-398 in MAO B may be involved in the non-covalent binding to FAD.	Lysine	132-135	monoamine oxidase B	Homo sapiens	165-170
11861643-5	2002	Tyr-407 and Tyr-444 in MAO A (Tyr-398 and Tyr-435 in MAO B) may form an aromatic sandwich that stabilizes the substrate binding.	Tyrosine	0-3	monoamine oxidase B	Homo sapiens	53-58
11861643-5	2002	Tyr-407 and Tyr-444 in MAO A (Tyr-398 and Tyr-435 in MAO B) may form an aromatic sandwich that stabilizes the substrate binding.	Tyrosine	12-15	monoamine oxidase B	Homo sapiens	53-58
11861643-5	2002	Tyr-407 and Tyr-444 in MAO A (Tyr-398 and Tyr-435 in MAO B) may form an aromatic sandwich that stabilizes the substrate binding.	Tyrosine	12-15	monoamine oxidase B	Homo sapiens	53-58
11861643-5	2002	Tyr-407 and Tyr-444 in MAO A (Tyr-398 and Tyr-435 in MAO B) may form an aromatic sandwich that stabilizes the substrate binding.	Tyrosine	12-15	monoamine oxidase B	Homo sapiens	53-58
11861643-6	2002	Asp-132 in MAO A (Asp-123 in MAO B) located at the entrance of the U-shaped substrate-binding site has no effect on MAO A nor MAO B catalytic activity.	Aspartic Acid	0-3	monoamine oxidase B	Homo sapiens	29-34
11861643-6	2002	Asp-132 in MAO A (Asp-123 in MAO B) located at the entrance of the U-shaped substrate-binding site has no effect on MAO A nor MAO B catalytic activity.	Aspartic Acid	18-21	monoamine oxidase B	Homo sapiens	29-34
12003917-0	2002	Monoamine oxidase-B activity in alcohol withdrawal of smokers: is there any relationship with aggressiveness?	Alcohols	32-39	monoamine oxidase B	Homo sapiens	0-19
12003917-3	2002	We assayed platelet MAO-B levels spectrophotometrically in 22 male inpatients with alcohol dependence in their first and fourth weeks of withdrawal and in 20 healthy controls.	Alcohols	83-90	monoamine oxidase B	Homo sapiens	20-25
12003917-5	2002	Our data revealed that the significantly lower platelet MAO-B activity observed during the first week of alcohol withdrawal in patients, compared to controls, did not continue in the fourth week, and that there was no relationship between aggressiveness and MAO activity.	Alcohols	105-112	monoamine oxidase B	Homo sapiens	56-61
12045467-1	2002	BACKGROUND: Monoamine oxidase B (MAO-B) degrades catecholamines in presynaptic nerve endings and is also active in platelets.	Catecholamines	49-63	monoamine oxidase B	Homo sapiens	33-38
12036014-0	2002	Synthesis and characterization of radioiodinated MD-230254: a new ligand for potential imaging of monoamine oxidase B activity by single photon emission computed tomography.	5-(4-(benzyloxy)phenyl)-3-(2-cyanoethyl)-1,3,4-oxadiazol-2(3H)-one	49-58	monoamine oxidase B	Homo sapiens	98-117
12036014-4	2002	The new radioligand for MAO-B, [125I]2-IBPO was conveniently synthesized from a tributylstannyl precursor by an iododestannylation reaction using sodium [125I]iodide and hydrogen peroxide with high radiochemical yield.	2-ibpo	37-43	monoamine oxidase B	Homo sapiens	24-29
12036014-1	2002	A series of iodinated analogues of MD-230254 was synthesized and evaluated for inhibitory potency and selectivity toward monoamine oxidase B (MAO-B).	5-(4-(benzyloxy)phenyl)-3-(2-cyanoethyl)-1,3,4-oxadiazol-2(3H)-one	35-44	monoamine oxidase B	Homo sapiens	121-140
12036014-1	2002	A series of iodinated analogues of MD-230254 was synthesized and evaluated for inhibitory potency and selectivity toward monoamine oxidase B (MAO-B).	5-(4-(benzyloxy)phenyl)-3-(2-cyanoethyl)-1,3,4-oxadiazol-2(3H)-one	35-44	monoamine oxidase B	Homo sapiens	142-147
12036014-4	2002	The new radioligand for MAO-B, [125I]2-IBPO was conveniently synthesized from a tributylstannyl precursor by an iododestannylation reaction using sodium [125I]iodide and hydrogen peroxide with high radiochemical yield.	tributylstannyl	80-95	monoamine oxidase B	Homo sapiens	24-29
12036014-2	2002	Among them, 5-[4-(2-iodobenzyloxy)phenyl]-3-(cyanoethyl)-1,3,4-oxadiazole-2(3H)one (2-IBPO) was found to have high inhibitory potency and selectivity toward MAO-B (IC50=2.0 nM, MAO-A/MAO-B &gt;50000).	5-[4-(2-iodobenzyloxy)phenyl]-3-(cyanoethyl)-1,3,4-oxadiazole-2(3h)one	12-82	monoamine oxidase B	Homo sapiens	157-162
12036014-4	2002	The new radioligand for MAO-B, [125I]2-IBPO was conveniently synthesized from a tributylstannyl precursor by an iododestannylation reaction using sodium [125I]iodide and hydrogen peroxide with high radiochemical yield.	sodium [125i]iodide	146-165	monoamine oxidase B	Homo sapiens	24-29
12036014-2	2002	Among them, 5-[4-(2-iodobenzyloxy)phenyl]-3-(cyanoethyl)-1,3,4-oxadiazole-2(3H)one (2-IBPO) was found to have high inhibitory potency and selectivity toward MAO-B (IC50=2.0 nM, MAO-A/MAO-B &gt;50000).	5-[4-(2-iodobenzyloxy)phenyl]-3-(cyanoethyl)-1,3,4-oxadiazole-2(3h)one	12-82	monoamine oxidase B	Homo sapiens	183-188
12036014-4	2002	The new radioligand for MAO-B, [125I]2-IBPO was conveniently synthesized from a tributylstannyl precursor by an iododestannylation reaction using sodium [125I]iodide and hydrogen peroxide with high radiochemical yield.	Hydrogen Peroxide	170-187	monoamine oxidase B	Homo sapiens	24-29
12036014-6	2002	A selective interaction of [125I]2-IBPO with MAO-B was confirmed by the pretreatment experiment with well known MAO specific inhibitors, l-deprenyl, Ro-16-6491, clorgyline, and Ro-41-1049.	[125i]2-ibpo	27-39	monoamine oxidase B	Homo sapiens	45-50
12036014-2	2002	Among them, 5-[4-(2-iodobenzyloxy)phenyl]-3-(cyanoethyl)-1,3,4-oxadiazole-2(3H)one (2-IBPO) was found to have high inhibitory potency and selectivity toward MAO-B (IC50=2.0 nM, MAO-A/MAO-B &gt;50000).	2-ibpo	84-90	monoamine oxidase B	Homo sapiens	157-162
12036014-6	2002	A selective interaction of [125I]2-IBPO with MAO-B was confirmed by the pretreatment experiment with well known MAO specific inhibitors, l-deprenyl, Ro-16-6491, clorgyline, and Ro-41-1049.	Selegiline	137-147	monoamine oxidase B	Homo sapiens	45-50
12036014-2	2002	Among them, 5-[4-(2-iodobenzyloxy)phenyl]-3-(cyanoethyl)-1,3,4-oxadiazole-2(3H)one (2-IBPO) was found to have high inhibitory potency and selectivity toward MAO-B (IC50=2.0 nM, MAO-A/MAO-B &gt;50000).	2-ibpo	84-90	monoamine oxidase B	Homo sapiens	183-188
12036014-6	2002	A selective interaction of [125I]2-IBPO with MAO-B was confirmed by the pretreatment experiment with well known MAO specific inhibitors, l-deprenyl, Ro-16-6491, clorgyline, and Ro-41-1049.	ro-16	149-154	monoamine oxidase B	Homo sapiens	45-50
12036014-3	2002	Analysis of the inhibition kinetics indicated that 2-IBPO acts in a two-step mechanism as a competitive, slow, and tight-binding inhibitor of MAO-B with a Ki value of 2.4 nM and an overall Ki* value at an equilibrium of 3.8 nM.	2-ibpo	51-57	monoamine oxidase B	Homo sapiens	142-147
12036014-6	2002	A selective interaction of [125I]2-IBPO with MAO-B was confirmed by the pretreatment experiment with well known MAO specific inhibitors, l-deprenyl, Ro-16-6491, clorgyline, and Ro-41-1049.	RO-41	177-182	monoamine oxidase B	Homo sapiens	45-50
11911838-2	2002	Since there are known differences between rats and humans in substrate and inhibitor specificities of MAOs, the interactions of phentermine with recombinant human purified preparations of MAO A and MAO B were determined.	Phentermine	128-139	monoamine oxidase B	Homo sapiens	198-203
12036014-7	2002	These very desirable characteristics of [125I]2-IBPO suggested that a 123I-labeled counterpart, [123I]2-IBPO, would have great potential in in vivo studies of MAO-B in the human brain with single photon emission computed tomography (SPECT).	2-ibpo	46-52	monoamine oxidase B	Homo sapiens	159-164
12036014-7	2002	These very desirable characteristics of [125I]2-IBPO suggested that a 123I-labeled counterpart, [123I]2-IBPO, would have great potential in in vivo studies of MAO-B in the human brain with single photon emission computed tomography (SPECT).	Iodine-123	70-74	monoamine oxidase B	Homo sapiens	159-164
12036014-7	2002	These very desirable characteristics of [125I]2-IBPO suggested that a 123I-labeled counterpart, [123I]2-IBPO, would have great potential in in vivo studies of MAO-B in the human brain with single photon emission computed tomography (SPECT).	2-ibpo	102-108	monoamine oxidase B	Homo sapiens	159-164
12044957-1	2002	A number of studies have shown that the selective monoamine oxidase (MAO)-B inhibitor l-selegiline has neuroprotective activities in several cell culture systems and in vivo.	Selegiline	86-98	monoamine oxidase B	Homo sapiens	50-75
12044957-3	2002	We have therefore developed a number of novel drugs based on rasagiline (N-propargyl-1R-(+)-aminoindan), a potent anti-Parkinson-propargyl-containing MAO-B inhibitor drug with structural resemblance to selegiline, for the treatment of Alzheimer"s disease.	rasagiline	61-71	monoamine oxidase B	Homo sapiens	150-155
12044957-3	2002	We have therefore developed a number of novel drugs based on rasagiline (N-propargyl-1R-(+)-aminoindan), a potent anti-Parkinson-propargyl-containing MAO-B inhibitor drug with structural resemblance to selegiline, for the treatment of Alzheimer"s disease.	n-propargyl-1r-(+)-aminoindan	73-102	monoamine oxidase B	Homo sapiens	150-155
12090555-2	2002	Rasagiline is a selective and potent irreversible MAO(B) inhibitor which is under development by Teva for the treatment of neurological diseases.	rasagiline	0-10	monoamine oxidase B	Homo sapiens	50-56
12090555-2	2002	Rasagiline is a selective and potent irreversible MAO(B) inhibitor which is under development by Teva for the treatment of neurological diseases.	teva	97-101	monoamine oxidase B	Homo sapiens	50-56
12111451-6	2002	7NI alone caused some increase in levels of dopamine and a decrease in the metabolite DOPAC, which is consistent with it also acting as an inhibitor of monoamine oxidase-B.	7-nitroindazole	0-3	monoamine oxidase B	Homo sapiens	152-171
12111469-1	2002	Deprenyl, an irreversible MAO-B inhibitor, is known to have a symptomatic effect in de novo patients with Parkinson"s disease (PD).	Selegiline	0-8	monoamine oxidase B	Homo sapiens	26-31
11911838-4	2002	Phentermine was also observed to be a competitive inhibitor of recombinant human liver MAO B with a K(I) value of 375+/-42 microM, a value similar to that observed with the rat enzyme (310-416 microM).	Phentermine	0-11	monoamine oxidase B	Homo sapiens	87-92
11911838-6	2002	Difference absorption spectral studies showed similar perturbations of the covalent FAD moieties of both human MAO A and MAO B, which suggests a similar mode of binding in both enzymes.	Flavin-Adenine Dinucleotide	84-87	monoamine oxidase B	Homo sapiens	121-126
11911838-7	2002	These data suggest that phentermine inhibition of human MAO A (or of MAO B) is too weak to be of pharmacological relevance.	Phentermine	24-35	monoamine oxidase B	Homo sapiens	69-74
11877901-3	2002	The reported association between vascular dysfunction and neurodegenerative diseases prompted us to investigate the effect of l-deprenyl, a MAO-B inhibitor, on low density lipoprotein (LDL) oxidation.	Selegiline	126-136	monoamine oxidase B	Homo sapiens	140-145
11978145-2	2002	Drugs that have been used for symptomatic therapy are levodopa, usually combined with a peripheral decarboxylase inhibitor, synthetic dopamine receptor agonists, centrally-acting antimuscarinic drugs, amantadine, monoamine oxidase-B (MAO-B) inhibitors and catechol-O-methyltransferase (COMT) inhibitors.	Levodopa	54-62	monoamine oxidase B	Homo sapiens	234-239
11813232-1	2002	Selegiline, a selective inhibitor of monoamine oxidase-B (MAO-B), was one of the first adjunct therapies in clinical neurology.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	37-56
11813232-1	2002	Selegiline, a selective inhibitor of monoamine oxidase-B (MAO-B), was one of the first adjunct therapies in clinical neurology.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	58-63
11813232-3	2002	The mechanism of action of selegiline is complex and cannot be explained solely by its MAO-B inhibitory action.	Selegiline	27-37	monoamine oxidase B	Homo sapiens	87-92
11813232-9	2002	Most of the aforementioned properties occur independently of selegiline"s efficacy to inhibit MAO-B.	Selegiline	61-71	monoamine oxidase B	Homo sapiens	94-99
11889496-5	2002	OBJECTIVES: We questioned the effect of ovarian steroid hormones on MAO-A and MAO-B mRNA expression in the dorsal raphe nucleus and hypothalamus using in situ hybridization in non-human primates.	Steroids	48-55	monoamine oxidase B	Homo sapiens	78-83
11978145-3	2002	Drugs for which there is at least some evidence for neuroprotective effect are certain dopamine agonists, amantadine and MAO-B inhibitors (selegiline).	Selegiline	139-149	monoamine oxidase B	Homo sapiens	121-126
11978145-18	2002	The MAO-B inhibitor selegiline may have a dual effect: reducing the catabolism of dopamine and limiting the formation of neurotoxic free radicals.	Selegiline	20-30	monoamine oxidase B	Homo sapiens	4-9
11978145-18	2002	The MAO-B inhibitor selegiline may have a dual effect: reducing the catabolism of dopamine and limiting the formation of neurotoxic free radicals.	Dopamine	82-90	monoamine oxidase B	Homo sapiens	4-9
11793163-8	2002	CONCLUSION: The elevation of DOPAC and the decrease of HVA and HVA / DOPAC reflect a shift of the levodopa metabolism towards the MAO-B dependent oxidative pathway.	3,4-Dihydroxyphenylacetic Acid	29-34	monoamine oxidase B	Homo sapiens	130-135
11793163-8	2002	CONCLUSION: The elevation of DOPAC and the decrease of HVA and HVA / DOPAC reflect a shift of the levodopa metabolism towards the MAO-B dependent oxidative pathway.	Homovanillic Acid	55-58	monoamine oxidase B	Homo sapiens	130-135
11793163-8	2002	CONCLUSION: The elevation of DOPAC and the decrease of HVA and HVA / DOPAC reflect a shift of the levodopa metabolism towards the MAO-B dependent oxidative pathway.	3,4-Dihydroxyphenylacetic Acid	69-74	monoamine oxidase B	Homo sapiens	130-135
11793163-8	2002	CONCLUSION: The elevation of DOPAC and the decrease of HVA and HVA / DOPAC reflect a shift of the levodopa metabolism towards the MAO-B dependent oxidative pathway.	Levodopa	98-106	monoamine oxidase B	Homo sapiens	130-135
11371556-10	2001	In contrast to crude homogenate, the water-soluble C481 mutant was rapidly inactivated at 4 degrees C and 37 degrees C, which indicates that the membrane environment is required for the stability of MAO B.	Water	37-42	monoamine oxidase B	Homo sapiens	199-204
11840311-7	2002	Apparent Km and Vmax of S-citalopram biotransformation in human frontal cortex by monoamine oxidase B were found to be 266 microM and 6.0 pmol min(-1) mg(-1) protein and by monoamine oxidase A 856 microM and 6.4 pmol min(-1) mg(-1) protein, respectively.	Citalopram	24-36	monoamine oxidase B	Homo sapiens	82-101
11753429-4	2002	The electron density shows that pargyline, an analog of the clinically used MAO B inhibitor, deprenyl, binds covalently to the flavin N5 atom.	Pargyline	32-41	monoamine oxidase B	Homo sapiens	76-81
11753429-4	2002	The electron density shows that pargyline, an analog of the clinically used MAO B inhibitor, deprenyl, binds covalently to the flavin N5 atom.	Selegiline	93-101	monoamine oxidase B	Homo sapiens	76-81
11753429-4	2002	The electron density shows that pargyline, an analog of the clinically used MAO B inhibitor, deprenyl, binds covalently to the flavin N5 atom.	flavin n5	127-136	monoamine oxidase B	Homo sapiens	76-81
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	phenethylamine	52-73	monoamine oxidase B	Homo sapiens	131-155
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	phenethylamine	52-73	monoamine oxidase B	Homo sapiens	157-162
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	phenethylamine	75-83	monoamine oxidase B	Homo sapiens	131-155
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	phenethylamine	75-83	monoamine oxidase B	Homo sapiens	157-162
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	Amines	68-73	monoamine oxidase B	Homo sapiens	131-155
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	Amines	68-73	monoamine oxidase B	Homo sapiens	157-162
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	Cocaine	208-215	monoamine oxidase B	Homo sapiens	131-155
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	Cocaine	208-215	monoamine oxidase B	Homo sapiens	157-162
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	Methamphetamine	219-234	monoamine oxidase B	Homo sapiens	131-155
11797065-1	2001	RATIONALE AND OBJECTIVE: Sufficiently high doses of beta-phenylethylamine (beta-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA).	Methamphetamine	219-234	monoamine oxidase B	Homo sapiens	157-162
11797065-2	2001	The present experiments were conducted to study how the discriminative-stimulus (S(D)) and reinforcing-stimulus (S(R)) effects of beta-PEA in monkeys are modified by treatment with inhibitors of MAO-B [R-(-)-deprenyl and MDL 72974].	Selegiline	204-216	monoamine oxidase B	Homo sapiens	195-200
11797065-7	2001	MAO-B inhibition by R-(-)-deprenyl or MDL 72974 enhanced the S(R) effects of beta-PEA in all monkeys and, under the FR schedule, induced a 30-fold or greater leftward shift in the dose-response function for its i.v.	r-(-)-deprenyl	20-34	monoamine oxidase B	Homo sapiens	0-5
11572661-1	2001	Safinamide (formerly PNU-151774E), a sodium and calcium channel modulator that also inhibits monoamine oxidase B (MAOB), is under development by Newron Pharmaceuticals for the potential treatment of epilepsy, Parkinson"s disease (PD), pain and stroke [345222], [348351].	safinamide	0-10	monoamine oxidase B	Homo sapiens	93-112
11430877-5	2001	In contrast, rat, monkey and human brain MAO-B activities were inhibited by thioperamide, with respective K(i) values of 174.6, 8.2 and 10.8 microM, more potently than MAO-A activity.	thioperamide	76-88	monoamine oxidase B	Homo sapiens	41-46
11430877-6	2001	These results indicate that thioperamide, which elicits a strong activation of histamine release and turnover to N-tele-methylhistamine from histamine, competitively inhibits the conversion of N-tele-methylhistamine to N-tele-methylimidazoleacetic acid in human and monkey brains where MAO-B predominates.	thioperamide	28-40	monoamine oxidase B	Homo sapiens	286-291
11430877-6	2001	These results indicate that thioperamide, which elicits a strong activation of histamine release and turnover to N-tele-methylhistamine from histamine, competitively inhibits the conversion of N-tele-methylhistamine to N-tele-methylimidazoleacetic acid in human and monkey brains where MAO-B predominates.	Histamine	79-88	monoamine oxidase B	Homo sapiens	286-291
11430877-6	2001	These results indicate that thioperamide, which elicits a strong activation of histamine release and turnover to N-tele-methylhistamine from histamine, competitively inhibits the conversion of N-tele-methylhistamine to N-tele-methylimidazoleacetic acid in human and monkey brains where MAO-B predominates.	tele-methylhistamine	113-135	monoamine oxidase B	Homo sapiens	286-291
11430877-6	2001	These results indicate that thioperamide, which elicits a strong activation of histamine release and turnover to N-tele-methylhistamine from histamine, competitively inhibits the conversion of N-tele-methylhistamine to N-tele-methylimidazoleacetic acid in human and monkey brains where MAO-B predominates.	Histamine	126-135	monoamine oxidase B	Homo sapiens	286-291
11430877-6	2001	These results indicate that thioperamide, which elicits a strong activation of histamine release and turnover to N-tele-methylhistamine from histamine, competitively inhibits the conversion of N-tele-methylhistamine to N-tele-methylimidazoleacetic acid in human and monkey brains where MAO-B predominates.	tele-methylhistamine	193-215	monoamine oxidase B	Homo sapiens	286-291
11430877-6	2001	These results indicate that thioperamide, which elicits a strong activation of histamine release and turnover to N-tele-methylhistamine from histamine, competitively inhibits the conversion of N-tele-methylhistamine to N-tele-methylimidazoleacetic acid in human and monkey brains where MAO-B predominates.	n-tele-methylimidazoleacetic acid	219-252	monoamine oxidase B	Homo sapiens	286-291
11572661-1	2001	Safinamide (formerly PNU-151774E), a sodium and calcium channel modulator that also inhibits monoamine oxidase B (MAOB), is under development by Newron Pharmaceuticals for the potential treatment of epilepsy, Parkinson"s disease (PD), pain and stroke [345222], [348351].	safinamide	0-10	monoamine oxidase B	Homo sapiens	114-118
11572661-1	2001	Safinamide (formerly PNU-151774E), a sodium and calcium channel modulator that also inhibits monoamine oxidase B (MAOB), is under development by Newron Pharmaceuticals for the potential treatment of epilepsy, Parkinson"s disease (PD), pain and stroke [345222], [348351].	N-neopentyl-N-nitrosourea	21-24	monoamine oxidase B	Homo sapiens	93-112
11572661-1	2001	Safinamide (formerly PNU-151774E), a sodium and calcium channel modulator that also inhibits monoamine oxidase B (MAOB), is under development by Newron Pharmaceuticals for the potential treatment of epilepsy, Parkinson"s disease (PD), pain and stroke [345222], [348351].	N-neopentyl-N-nitrosourea	21-24	monoamine oxidase B	Homo sapiens	114-118
11160474-1	2001	OBJECTIVE: To evaluate the correlation between changes in platelet monoamine oxidase type B (MAO-B) activity and plasma beta-phenylethylamine (PEA) concentrations in patients with Parkinson"s disease and controls.	phenethylamine	120-141	monoamine oxidase B	Homo sapiens	67-91
11331009-1	2001	The spectral properties of the covalent adduct formed between the flavin cofactor of MAO N and 1-PCPA are similar to those reported for the irreversible inactivation product formed with 1-PCPA and mammalian mitochondrial monoamine oxidase B [Silverman, R. B., and Zieske, P. A.	4,6-dinitro-o-cresol	66-72	monoamine oxidase B	Homo sapiens	221-240
11331009-1	2001	The spectral properties of the covalent adduct formed between the flavin cofactor of MAO N and 1-PCPA are similar to those reported for the irreversible inactivation product formed with 1-PCPA and mammalian mitochondrial monoamine oxidase B [Silverman, R. B., and Zieske, P. A.	mao n	85-90	monoamine oxidase B	Homo sapiens	221-240
11331009-1	2001	The spectral properties of the covalent adduct formed between the flavin cofactor of MAO N and 1-PCPA are similar to those reported for the irreversible inactivation product formed with 1-PCPA and mammalian mitochondrial monoamine oxidase B [Silverman, R. B., and Zieske, P. A.	1-phenylcyclopropylamine	95-101	monoamine oxidase B	Homo sapiens	221-240
11331009-4	2001	Use of the fungal enzyme, MAO N, which lacks the covalent attachment to the flavin adenine dinucleotide (FAD) cofactor present in the mammalian forms MAO A and MAO B, has allowed for the isolation and further structural identification of the flavin-inactivator adduct.	Flavin-Adenine Dinucleotide	105-108	monoamine oxidase B	Homo sapiens	160-165
11481866-8	2001	In vivo microdialysis studies showed that the irreversible monoamine oxidase A inhibitor clorgyline and the irreversible monoamine oxidase B inhibitor selegiline induced a mild increase and no increase in extracellular serotonin, respectively.	Selegiline	151-161	monoamine oxidase B	Homo sapiens	121-140
11259630-1	2001	The human monoamine oxidase (MAO) B plays a major role in the degradation of biogenic and dietary amines such as phenylethylamine, benzylamine, dopamine, and tyramine.	Amines	98-104	monoamine oxidase B	Homo sapiens	10-35
11259630-1	2001	The human monoamine oxidase (MAO) B plays a major role in the degradation of biogenic and dietary amines such as phenylethylamine, benzylamine, dopamine, and tyramine.	Phenethylamines	113-129	monoamine oxidase B	Homo sapiens	10-35
11259630-1	2001	The human monoamine oxidase (MAO) B plays a major role in the degradation of biogenic and dietary amines such as phenylethylamine, benzylamine, dopamine, and tyramine.	benzylamine	131-142	monoamine oxidase B	Homo sapiens	10-35
11259630-1	2001	The human monoamine oxidase (MAO) B plays a major role in the degradation of biogenic and dietary amines such as phenylethylamine, benzylamine, dopamine, and tyramine.	Dopamine	144-152	monoamine oxidase B	Homo sapiens	10-35
11259630-1	2001	The human monoamine oxidase (MAO) B plays a major role in the degradation of biogenic and dietary amines such as phenylethylamine, benzylamine, dopamine, and tyramine.	Tyramine	158-166	monoamine oxidase B	Homo sapiens	10-35
11134050-5	2001	Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-phenylethylamine than for the MAO A preferred substrate serotonin (5-hydroxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor).	phenethylamine	77-98	monoamine oxidase B	Homo sapiens	31-36
11134050-5	2001	Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-phenylethylamine than for the MAO A preferred substrate serotonin (5-hydroxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor).	Serotonin	138-147	monoamine oxidase B	Homo sapiens	31-36
11171904-8	2001	CONCLUSIONS: These results suggest that, in Taiwanese, PD risk is associated with MAOB G intron 13 polymorphism, and this association is augmented in the presence of the COMT(L) genotype, indicating an interaction of these two dopamine-metabolizing enzymes in the pathogenesis of sporadic PD.	Dopamine	227-235	monoamine oxidase B	Homo sapiens	82-86
11226815-0	2001	In vitro metabolism of citalopram by monoamine oxidase B in human blood.	Citalopram	23-33	monoamine oxidase B	Homo sapiens	37-56
11226815-1	2001	The metabolism of the antidepressant citalopram (CIT) by monoamine oxidase B (MAO-B) was studied in vitro.	Citalopram	37-47	monoamine oxidase B	Homo sapiens	57-76
11226815-1	2001	The metabolism of the antidepressant citalopram (CIT) by monoamine oxidase B (MAO-B) was studied in vitro.	Citalopram	37-47	monoamine oxidase B	Homo sapiens	78-83
11226815-1	2001	The metabolism of the antidepressant citalopram (CIT) by monoamine oxidase B (MAO-B) was studied in vitro.	Citalopram	49-52	monoamine oxidase B	Homo sapiens	57-76
11226815-1	2001	The metabolism of the antidepressant citalopram (CIT) by monoamine oxidase B (MAO-B) was studied in vitro.	Citalopram	49-52	monoamine oxidase B	Homo sapiens	78-83
11226815-3	2001	S-CITPROP production was 5.6 times higher than R-CITPROP production and in incubations containing the MAO-B inhibitor deprenyl, racemic CITPROP production was diminished to 9.1%.	s-citprop	0-9	monoamine oxidase B	Homo sapiens	102-107
11226815-3	2001	S-CITPROP production was 5.6 times higher than R-CITPROP production and in incubations containing the MAO-B inhibitor deprenyl, racemic CITPROP production was diminished to 9.1%.	r-citprop	47-56	monoamine oxidase B	Homo sapiens	102-107
11226815-3	2001	S-CITPROP production was 5.6 times higher than R-CITPROP production and in incubations containing the MAO-B inhibitor deprenyl, racemic CITPROP production was diminished to 9.1%.	Selegiline	118-126	monoamine oxidase B	Homo sapiens	102-107
11226815-3	2001	S-CITPROP production was 5.6 times higher than R-CITPROP production and in incubations containing the MAO-B inhibitor deprenyl, racemic CITPROP production was diminished to 9.1%.	citprop	2-9	monoamine oxidase B	Homo sapiens	102-107
11442353-7	2001	l-Dopa and apomorphine (dopaminergic agonists), ropinirole (selective D2 agonist), and selegiline (an monoamino-oxidase B [MAO-B] inhibitor) improve their clinical status.	Levodopa	0-6	monoamine oxidase B	Homo sapiens	102-121
11442353-7	2001	l-Dopa and apomorphine (dopaminergic agonists), ropinirole (selective D2 agonist), and selegiline (an monoamino-oxidase B [MAO-B] inhibitor) improve their clinical status.	Selegiline	87-97	monoamine oxidase B	Homo sapiens	102-121
11400918-1	2001	In this study, we investigated whether treatment with L-deprenyl, a selective monoamine oxidase B (MAO B) inhibitor, also inhibits MAO A or the dopamine transporter in the human brain.	Selegiline	54-64	monoamine oxidase B	Homo sapiens	78-97
11400918-1	2001	In this study, we investigated whether treatment with L-deprenyl, a selective monoamine oxidase B (MAO B) inhibitor, also inhibits MAO A or the dopamine transporter in the human brain.	Selegiline	54-64	monoamine oxidase B	Homo sapiens	99-104
11400918-8	2001	These results confirm that L-deprenyl after one week of treatment at doses typically used clinically is selective for MAO B and that it does not produce a measurable affect on the dopamine transporter, suggesting that MAO A inhibition and dopamine transporter blockade do not contribute to its pharmacological effects.	Selegiline	27-37	monoamine oxidase B	Homo sapiens	118-123
11134050-5	2001	Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-phenylethylamine than for the MAO A preferred substrate serotonin (5-hydroxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor).	Serotonin	149-168	monoamine oxidase B	Homo sapiens	31-36
11134050-5	2001	Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-phenylethylamine than for the MAO A preferred substrate serotonin (5-hydroxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor).	Selegiline	200-208	monoamine oxidase B	Homo sapiens	31-36
11134050-5	2001	Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-phenylethylamine than for the MAO A preferred substrate serotonin (5-hydroxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor).	Clorgyline	244-254	monoamine oxidase B	Homo sapiens	31-36
11134050-6	2001	The reciprocal mutant MAO B-Y326I exhibited an increased preference for 5-hydroxytryptamine, a decreased preference for beta-phenylethylamine, and, similar to MAO A, was more sensitive to clorgyline than to deprenyl.	Serotonin	72-91	monoamine oxidase B	Homo sapiens	22-27
11134050-6	2001	The reciprocal mutant MAO B-Y326I exhibited an increased preference for 5-hydroxytryptamine, a decreased preference for beta-phenylethylamine, and, similar to MAO A, was more sensitive to clorgyline than to deprenyl.	phenethylamine	120-141	monoamine oxidase B	Homo sapiens	22-27
11134050-6	2001	The reciprocal mutant MAO B-Y326I exhibited an increased preference for 5-hydroxytryptamine, a decreased preference for beta-phenylethylamine, and, similar to MAO A, was more sensitive to clorgyline than to deprenyl.	Clorgyline	188-198	monoamine oxidase B	Homo sapiens	22-27
11134050-6	2001	The reciprocal mutant MAO B-Y326I exhibited an increased preference for 5-hydroxytryptamine, a decreased preference for beta-phenylethylamine, and, similar to MAO A, was more sensitive to clorgyline than to deprenyl.	Selegiline	207-215	monoamine oxidase B	Homo sapiens	22-27
11134050-9	2001	Our results indicate that Ile-335 in MAO A and Tyr-326 in MAO B play a critical role in determining substrate and inhibitor specificities in human MAO A and B.	Isoleucine	26-29	monoamine oxidase B	Homo sapiens	58-63
11134050-9	2001	Our results indicate that Ile-335 in MAO A and Tyr-326 in MAO B play a critical role in determining substrate and inhibitor specificities in human MAO A and B.	Tyrosine	47-50	monoamine oxidase B	Homo sapiens	58-63
11245920-9	2001	Our data are consistent with clinical studies that demonstrate pretreatment with the MAO-B selective inhibitor, selegeline, fails to alter cocaine-induced subjective effects in human drug users.	selegeline	112-122	monoamine oxidase B	Homo sapiens	85-90
11172770-5	2001	MPTP is converted by monoamine oxidase-B (MAO-B) to its neurotoxic metabolite 1-methyl-4-phenyl-pyridinium (MPP+), which is then taken up into the dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	21-40
11172770-5	2001	MPTP is converted by monoamine oxidase-B (MAO-B) to its neurotoxic metabolite 1-methyl-4-phenyl-pyridinium (MPP+), which is then taken up into the dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	42-47
11172770-5	2001	MPTP is converted by monoamine oxidase-B (MAO-B) to its neurotoxic metabolite 1-methyl-4-phenyl-pyridinium (MPP+), which is then taken up into the dopaminergic neurons.	1-Methyl-4-phenylpyridinium	78-106	monoamine oxidase B	Homo sapiens	21-40
11172770-5	2001	MPTP is converted by monoamine oxidase-B (MAO-B) to its neurotoxic metabolite 1-methyl-4-phenyl-pyridinium (MPP+), which is then taken up into the dopaminergic neurons.	1-Methyl-4-phenylpyridinium	78-106	monoamine oxidase B	Homo sapiens	42-47
11172770-5	2001	MPTP is converted by monoamine oxidase-B (MAO-B) to its neurotoxic metabolite 1-methyl-4-phenyl-pyridinium (MPP+), which is then taken up into the dopaminergic neurons.	mangion-purified polysaccharide (Candida albicans)	108-112	monoamine oxidase B	Homo sapiens	21-40
11172770-5	2001	MPTP is converted by monoamine oxidase-B (MAO-B) to its neurotoxic metabolite 1-methyl-4-phenyl-pyridinium (MPP+), which is then taken up into the dopaminergic neurons.	mangion-purified polysaccharide (Candida albicans)	108-112	monoamine oxidase B	Homo sapiens	42-47
11160474-1	2001	OBJECTIVE: To evaluate the correlation between changes in platelet monoamine oxidase type B (MAO-B) activity and plasma beta-phenylethylamine (PEA) concentrations in patients with Parkinson"s disease and controls.	phenethylamine	120-141	monoamine oxidase B	Homo sapiens	93-98
11160474-1	2001	OBJECTIVE: To evaluate the correlation between changes in platelet monoamine oxidase type B (MAO-B) activity and plasma beta-phenylethylamine (PEA) concentrations in patients with Parkinson"s disease and controls.	phenethylamine	143-146	monoamine oxidase B	Homo sapiens	67-91
11160474-1	2001	OBJECTIVE: To evaluate the correlation between changes in platelet monoamine oxidase type B (MAO-B) activity and plasma beta-phenylethylamine (PEA) concentrations in patients with Parkinson"s disease and controls.	phenethylamine	143-146	monoamine oxidase B	Homo sapiens	93-98
11160474-7	2001	CONCLUSIONS: The increase in platelet MAO-B activity and decrease in plasma PEA concentrations in patients with Parkinson"s disease may be involved in the pathophysiological processes of the disease, and these changes are reversed by treatment with selegiline.	Selegiline	249-259	monoamine oxidase B	Homo sapiens	38-43
11233301-2	2001	Although MPTP produces a parkinsonian syndrome after its conversion to 1-methyl-4-phenylpyridine (MPP+) by type B monoamine oxidase (MAO-B) in the brain, the etiology of this disease remains obscure.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	9-13	monoamine oxidase B	Homo sapiens	133-138
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	Dopamine	26-34	monoamine oxidase B	Homo sapiens	153-158
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	Dopamine	26-34	monoamine oxidase B	Homo sapiens	160-194
11233301-2	2001	Although MPTP produces a parkinsonian syndrome after its conversion to 1-methyl-4-phenylpyridine (MPP+) by type B monoamine oxidase (MAO-B) in the brain, the etiology of this disease remains obscure.	1-Methyl-4-phenylpyridinium	71-96	monoamine oxidase B	Homo sapiens	133-138
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	Levodopa	91-99	monoamine oxidase B	Homo sapiens	153-158
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	Dopamine	103-111	monoamine oxidase B	Homo sapiens	153-158
11233301-2	2001	Although MPTP produces a parkinsonian syndrome after its conversion to 1-methyl-4-phenylpyridine (MPP+) by type B monoamine oxidase (MAO-B) in the brain, the etiology of this disease remains obscure.	mangion-purified polysaccharide (Candida albicans)	98-102	monoamine oxidase B	Homo sapiens	133-138
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	Dihydroxyphenylalanine	26-30	monoamine oxidase B	Homo sapiens	153-158
11008487-10	2001	A deleterious role played by MAO B is the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a proneurotoxin that can cause a parkinsonian syndrome in mammals.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	56-100	monoamine oxidase B	Homo sapiens	29-34
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	Dihydroxyphenylalanine	26-30	monoamine oxidase B	Homo sapiens	160-194
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	Dopamine	103-111	monoamine oxidase B	Homo sapiens	153-158
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	Dopamine	103-111	monoamine oxidase B	Homo sapiens	153-158
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	N-Methylaspartate	352-372	monoamine oxidase B	Homo sapiens	153-158
11233302-7	2001	At present, supplement of dopamine by levodopa administration, retarding the metabolism of levodopa or dopamine by a dopa decarboxylase inhibitor (DCI), MAO-B (monoamine oxidase inhibitor type B) inhibitor or catechol-O-methyltransferase (COMT) inhibitor, dopamine receptor agonists, anticholinergic agents, dopamine release enhancer/uptake inhibitor, N-methyl-D-aspartate (NMDA) receptor antagonists are applied for the treatment of Parkinson"s disease.	N-Methylaspartate	374-378	monoamine oxidase B	Homo sapiens	153-158
11697041-1	2001	A molecular modelling study was performed using the CATALYST software package on a dataset of 100 thiosemicarbazide and thiazole derivatives acting as MAO-B irreversible inhibitors in order to, (i) better elucidate the possible role of the ligand features which are significant for binding and (ii) generate chemical features based pharmacophore models which were subsequently used as 3D queries for database searching.	thiosemicarbazide	98-115	monoamine oxidase B	Homo sapiens	151-156
11697041-1	2001	A molecular modelling study was performed using the CATALYST software package on a dataset of 100 thiosemicarbazide and thiazole derivatives acting as MAO-B irreversible inhibitors in order to, (i) better elucidate the possible role of the ligand features which are significant for binding and (ii) generate chemical features based pharmacophore models which were subsequently used as 3D queries for database searching.	Thiazoles	120-128	monoamine oxidase B	Homo sapiens	151-156
11314774-2	2001	Following a two-months of placebo-controlled withdrawal, the MAO-B inhibitor selegiline was found to maintain a long term significant mild to moderate symptomatic effect on bradykinesia and tremor at rest in nine patients with Parkinson"s disease (stage II and III of H&Y), whose functional impairment had also required a dopaminergic therapy with low-dose bromocriptine.	Selegiline	77-87	monoamine oxidase B	Homo sapiens	61-66
11361012-4	2001	Regardless of preincubation, 2-BEA could not appreciably inhibit MAO-A and MAO-B activity, but 3-BPA at relatively high concentrations inhibited only MAO-B activity.	3-bromopropylamine	95-100	monoamine oxidase B	Homo sapiens	150-155
11944739-1	2001	OBJECTIVE: Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease.	Selegiline	11-21	monoamine oxidase B	Homo sapiens	50-69
11944739-1	2001	OBJECTIVE: Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease.	Selegiline	11-21	monoamine oxidase B	Homo sapiens	71-76
11944739-1	2001	OBJECTIVE: Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease.	Selegiline	23-33	monoamine oxidase B	Homo sapiens	50-69
11944739-1	2001	OBJECTIVE: Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease.	Selegiline	23-33	monoamine oxidase B	Homo sapiens	71-76
11008487-10	2001	A deleterious role played by MAO B is the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a proneurotoxin that can cause a parkinsonian syndrome in mammals.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	102-106	monoamine oxidase B	Homo sapiens	29-34
11008487-11	2001	Deprenyl, an inhibitor of MAO B, has been used for the treatment of early-stage Parkinson"s disease and provides protection of neurons from age-related decay.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	26-31
11085911-1	2000	R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease.	r-(-)-deprenyl	0-14	monoamine oxidase B	Homo sapiens	41-60
11123983-2	2000	Most of the compounds acted preferentially on MAO-B with IC(50) values in the micromolar to low-nanomolar range; high inhibitory activities toward MAO-A were also measured for sulfonic acid esters.	sulfonic acid esters	176-196	monoamine oxidase B	Homo sapiens	46-51
11085911-1	2000	R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease.	r-(-)-deprenyl	0-14	monoamine oxidase B	Homo sapiens	62-67
11085911-1	2000	R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease.	Selegiline	16-24	monoamine oxidase B	Homo sapiens	41-60
11085911-1	2000	R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease.	Selegiline	16-24	monoamine oxidase B	Homo sapiens	62-67
11085911-1	2000	R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease.	Selegiline	26-36	monoamine oxidase B	Homo sapiens	41-60
11085911-1	2000	R-(-)-Deprenyl (deprenyl, selegiline), a monoamine oxidase B (MAO-B) inhibitor, delays progression of Parkinson"s disease.	Selegiline	26-36	monoamine oxidase B	Homo sapiens	62-67
11575866-1	2000	Rasagiline mesylate (TVP-1012) is a potent, selective, non-reversible MAO-B inhibitor, without the tyramine-potentiating effect and with neuroprotective activities.	Rasagiline mesylate	21-29	monoamine oxidase B	Homo sapiens	70-75
11090954-0	2000	Cell death induced by MPTP, a substrate for monoamine oxidase B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	22-26	monoamine oxidase B	Homo sapiens	44-63
11090954-2	2000	In order to exert its neurotoxicity MPTP must be converted by monoamine oxidase B into MPP(+) which is the true toxic agent.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	36-40	monoamine oxidase B	Homo sapiens	62-81
11575866-0	2000	Rasagiline mesylate, a new MAO-B inhibitor for the treatment of Parkinson"s disease: a double-blind study as adjunctive therapy to levodopa.	Rasagiline mesylate	0-19	monoamine oxidase B	Homo sapiens	27-32
11575866-1	2000	Rasagiline mesylate (TVP-1012) is a potent, selective, non-reversible MAO-B inhibitor, without the tyramine-potentiating effect and with neuroprotective activities.	Rasagiline mesylate	0-19	monoamine oxidase B	Homo sapiens	70-75
11575866-8	2000	Almost complete platelet MAO-B inhibition was obtained at all rasagiline doses.	rasagiline	62-72	monoamine oxidase B	Homo sapiens	25-30
11049757-9	2000	One mole of covalent FAD per mole of MAO B is present in the purified enzyme and is bound by an 8alpha-S-cysteinyl(397) linkage, as identified by electrospray mass spectrometry of the isolated tryptic/chymotryptic flavin peptide.	Flavin-Adenine Dinucleotide	21-24	monoamine oxidase B	Homo sapiens	37-42
11049757-9	2000	One mole of covalent FAD per mole of MAO B is present in the purified enzyme and is bound by an 8alpha-S-cysteinyl(397) linkage, as identified by electrospray mass spectrometry of the isolated tryptic/chymotryptic flavin peptide.	8alpha-s-cysteinyl	96-114	monoamine oxidase B	Homo sapiens	37-42
11049757-9	2000	One mole of covalent FAD per mole of MAO B is present in the purified enzyme and is bound by an 8alpha-S-cysteinyl(397) linkage, as identified by electrospray mass spectrometry of the isolated tryptic/chymotryptic flavin peptide.	flavin peptide	214-228	monoamine oxidase B	Homo sapiens	37-42
11049757-10	2000	Recombinant human liver MAO B and bovine liver MAO B are shown to be acetylated at the seryl residues at their respective amino termini.	seryl	87-92	monoamine oxidase B	Homo sapiens	24-29
11049757-13	2000	Recombinant MAO B exhibits a (D)k(cat) = 4.7, a (D)[k(cat)/K(m)(benzylamine)] = 4.5, and a (D)[k(cat)/K(m)(O(2))] = 1.0.	benzylamine	64-75	monoamine oxidase B	Homo sapiens	12-17
10900396-1	2000	Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders.	Levodopa	127-133	monoamine oxidase B	Homo sapiens	74-93
11068448-15	2000	Monoamine oxidase B inhibitor, Selegiline, is useful as an economizer effect to levodopa.	Selegiline	31-41	monoamine oxidase B	Homo sapiens	0-19
11068448-15	2000	Monoamine oxidase B inhibitor, Selegiline, is useful as an economizer effect to levodopa.	Levodopa	80-88	monoamine oxidase B	Homo sapiens	0-19
10900396-1	2000	Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders.	Levodopa	127-133	monoamine oxidase B	Homo sapiens	95-100
10900396-1	2000	Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders.	Selegiline	112-122	monoamine oxidase B	Homo sapiens	74-93
10900396-1	2000	Both the catechol-O-methyltransferase (COMT) inhibitor entacapone and the monoamine oxidase B (MAO-B) inhibitor selegiline are L-dopa extenders.	Selegiline	112-122	monoamine oxidase B	Homo sapiens	95-100
11154095-1	2000	The present pharmacoepidemiologic study was performed to characterize the profile of adverse drug reactions (ADRs) reported with selegiline, a monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease and previously reported to induce an excess of mortality.	Selegiline	129-139	monoamine oxidase B	Homo sapiens	143-162
11022024-2	2000	In the present study, the relationship between these two markers was investigated in a group of socially stable Caucasian middle-aged men with a mean (+/-SD) daily ethanol consumption of 85 +/- 57 g. The platelet MAO-B activity was significantly lower in individuals with the DRD2 A1 allele (n = 8), compared to those without it (n = 29).	Ethanol	164-171	monoamine oxidase B	Homo sapiens	213-218
10927030-0	2000	Antioxidant activity of the monoamine oxidase B inhibitor lazabemide.	lazabemide	58-68	monoamine oxidase B	Homo sapiens	28-47
10927030-3	2000	In this study, the intrinsic antioxidant activity of lazabemide, a potent and reversible inhibitor of monoamine oxidase B (MAO-B), was tested in a membrane-based model of oxidative stress.	lazabemide	53-63	monoamine oxidase B	Homo sapiens	102-121
10927030-3	2000	In this study, the intrinsic antioxidant activity of lazabemide, a potent and reversible inhibitor of monoamine oxidase B (MAO-B), was tested in a membrane-based model of oxidative stress.	lazabemide	53-63	monoamine oxidase B	Homo sapiens	123-128
10927030-6	2000	The antioxidant activity of lazabemide was significantly more effective than that of either vitamin E or the MAO-B inhibitor, selegiline.	Selegiline	126-136	monoamine oxidase B	Homo sapiens	109-114
11154095-1	2000	The present pharmacoepidemiologic study was performed to characterize the profile of adverse drug reactions (ADRs) reported with selegiline, a monoamine oxidase B (MAO-B) inhibitor used in the treatment of Parkinson"s disease and previously reported to induce an excess of mortality.	Selegiline	129-139	monoamine oxidase B	Homo sapiens	164-169
10936214-3	2000	When compared with MAO A, MAO A-F208I showed a sixfold decrease in the specificity constant k(cat)/K(m) for both the MAO A- and the MAO B-preferring substrates 5-hydroxytryptamine and beta-phenylethylamine, respectively.	Serotonin	160-179	monoamine oxidase B	Homo sapiens	132-137
10936214-3	2000	When compared with MAO A, MAO A-F208I showed a sixfold decrease in the specificity constant k(cat)/K(m) for both the MAO A- and the MAO B-preferring substrates 5-hydroxytryptamine and beta-phenylethylamine, respectively.	phenethylamine	184-205	monoamine oxidase B	Homo sapiens	132-137
10981823-2	2000	Inhibitors of monoamine oxidase B (MAO-B) have been used in the treatment of PD and at least one of them, i.e., deprenyl, also displays antioxidant activity.	Selegiline	112-120	monoamine oxidase B	Homo sapiens	14-33
10981823-2	2000	Inhibitors of monoamine oxidase B (MAO-B) have been used in the treatment of PD and at least one of them, i.e., deprenyl, also displays antioxidant activity.	Selegiline	112-120	monoamine oxidase B	Homo sapiens	35-40
10943729-6	2000	Inhibition of progression of the disease (neuroprotective effect) and improvements of symptoms (MAO-B inhibition) may occur at the same dose level using PFS, while these doses are separated in case of selegiline.	1-(3-(pentafluorosulfanyl)phenyl)propan-2-amine	153-156	monoamine oxidase B	Homo sapiens	96-101
10794685-1	2000	A series of indolylmethylamine derivatives were assayed toward MAO-A and MAO-B inhibition.	indolylmethylamine	12-30	monoamine oxidase B	Homo sapiens	73-78
11082824-4	2000	Platelet MAO-B activity has been found to be correlated with plasma thiocyanate concentration.	thiocyanate	68-79	monoamine oxidase B	Homo sapiens	9-14
11082824-5	2000	The aim of this study was to investigate in smokers whether platelet MAO-B activity is related to plasma cotinine concentration, an indirect index of use of smoked tobacco.	Cotinine	105-113	monoamine oxidase B	Homo sapiens	69-74
11082824-8	2000	Platelet MAO-B activity correlated positively with age (r = 0.26, p = 0.01) and inversely with plasma cotinine concentration (r = -0.32, p = 0.002) but not with number of cigarettes smoked or with Fagerstrom Tolerance Questionnaire score.	Cotinine	102-110	monoamine oxidase B	Homo sapiens	9-14
11082824-9	2000	Multiple linear regression analysis showed that 49% of the age-adjusted variance in platelet MAO-B activity (R2 = 0.489, p &lt; 0.0001) was explained by plasma cotinine concentration (p &lt; 0.001) and gender (p = 0.037).	Cotinine	160-168	monoamine oxidase B	Homo sapiens	93-98
11082824-10	2000	It was concluded that platelet MAO-B activity in smokers is inversely associated with plasma cotinine level, an index of smoked tobacco use.	Cotinine	93-101	monoamine oxidase B	Homo sapiens	31-36
10906004-3	2000	We therefore assessed platelet MAO-B activity repeatedly in 13 male alcohol-dependent patients over the 2 months after the end of a period of heavy alcohol intake.	Alcohols	68-75	monoamine oxidase B	Homo sapiens	31-36
10906004-5	2000	In the alcohol-dependent patients, platelet MAO-B activity was transiently increased from 2 to 6 weeks after the end of alcohol intake and the values during this time period were not different from those of controls.	Alcohols	7-14	monoamine oxidase B	Homo sapiens	44-49
10906004-5	2000	In the alcohol-dependent patients, platelet MAO-B activity was transiently increased from 2 to 6 weeks after the end of alcohol intake and the values during this time period were not different from those of controls.	Alcohols	120-127	monoamine oxidase B	Homo sapiens	44-49
10906004-6	2000	Platelet MAO-B activity was, however, significantly lower in the alcohol-dependent patients at 1 week and at 2 months after the end of alcohol intake, in comparison to controls.	Alcohols	65-72	monoamine oxidase B	Homo sapiens	9-14
10906004-6	2000	Platelet MAO-B activity was, however, significantly lower in the alcohol-dependent patients at 1 week and at 2 months after the end of alcohol intake, in comparison to controls.	Alcohols	135-142	monoamine oxidase B	Homo sapiens	9-14
10906004-7	2000	It is concluded that the transient increase in platelet MAO-B activity after the end of alcohol intake in alcohol-dependent patients may conceal a difference from a control group.	Alcohols	88-95	monoamine oxidase B	Homo sapiens	56-61
10906004-7	2000	It is concluded that the transient increase in platelet MAO-B activity after the end of alcohol intake in alcohol-dependent patients may conceal a difference from a control group.	Alcohols	106-113	monoamine oxidase B	Homo sapiens	56-61
10794685-4	2000	Comparison of MAO-A and MAO-B CoMFA models showed that both the steric and electrostatic properties at the 5 position of the indole ring are determinant for MAO selectivity.	indole	125-131	monoamine oxidase B	Homo sapiens	24-29
10794685-5	2000	Computational simulations of the complex between this part of the ligand and Phe-208 of MAO-A or Ile-199 of MAO-B, experimentally identified as responsible for substrate selectivity, allowed us to further characterize the nature of these enzyme-inhibitor interactions.	Phenylalanine	77-80	monoamine oxidase B	Homo sapiens	108-113
10794685-5	2000	Computational simulations of the complex between this part of the ligand and Phe-208 of MAO-A or Ile-199 of MAO-B, experimentally identified as responsible for substrate selectivity, allowed us to further characterize the nature of these enzyme-inhibitor interactions.	Isoleucine	97-100	monoamine oxidase B	Homo sapiens	108-113
10777699-0	2000	Monoamine oxidase B induces ERK-dependent cell mitogenesis by hydrogen peroxide generation.	Hydrogen Peroxide	62-79	monoamine oxidase B	Homo sapiens	0-19
10777699-2	2000	In the present study, we used human embryonic kidney 293 (HEK 293) cells stably transfected with human MAO-B cDNA to investigate the potential role of hydrogen peroxide (H(2)O(2)) produced by MAO-B isoform as an intracellular messenger involved in regulation of cell signaling and function.	Hydrogen Peroxide	151-168	monoamine oxidase B	Homo sapiens	192-197
10777699-3	2000	The MAO substrate tyramine induced tyrosine phosphorylation of Shc, ERK activation, and an increase in DNA synthesis in HEK 293 expressing MAO-B, but not in wild type HEK 293 cells, which do not express MAO.	Tyramine	18-26	monoamine oxidase B	Homo sapiens	139-144
10787399-0	2000	Alcohol-dependent patients with neuroendocrine evidence for reduced dopamine d(2) receptor function have decreased platelet monoamine oxidase-B activity.	Alcohols	0-7	monoamine oxidase B	Homo sapiens	124-143
10777699-5	2000	These results show that MAO-B induces MAPK/ERK activation and cell mitogenesis through H(2)O(2) production.	Hydrogen Peroxide	87-95	monoamine oxidase B	Homo sapiens	24-29
10727736-4	2000	This result is not due to poor crossing of the placental and blood-brain barriers, since deprenyl caused a dose-dependent inhibition of brain MAO-B activity in pups at birth.	Selegiline	89-97	monoamine oxidase B	Homo sapiens	142-147
10753262-2	2000	L-dopa therapy was unsuccessful, whereas a combination with selegiline, a selective monoamine oxidase-beta inhibitor, with low-dose L-dopa markedly improved the severe clinical picture.	Selegiline	60-70	monoamine oxidase B	Homo sapiens	84-106
10706994-1	2000	In the course of investigating the mechanisms underlying the beneficial effect of fluvoxamine augmentation on negative symptoms of schizophrenia, the authors found a reduction in human platelet monoamine oxidase-B activity after 5 weeks of treatment.	Fluvoxamine	82-93	monoamine oxidase B	Homo sapiens	194-213
10867219-1	2000	The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease, with a concomitant extension of life span.	Selegiline	42-52	monoamine oxidase B	Homo sapiens	4-23
10688633-0	2000	Imidazoline-binding domains on monoamine oxidase B and subpopulations of enzyme.	Imidazolines	0-11	monoamine oxidase B	Homo sapiens	31-50
10688633-1	2000	A series of phenoxy-substituted methylimidazoline derivatives were synthesized and used to define the ligand recognition properties of the imidazoline-binding domain (IBD) on monoamine oxidase (MAO)-B and its role in substrate processing.	phenoxy-substituted methylimidazoline	12-49	monoamine oxidase B	Homo sapiens	175-200
10688633-1	2000	A series of phenoxy-substituted methylimidazoline derivatives were synthesized and used to define the ligand recognition properties of the imidazoline-binding domain (IBD) on monoamine oxidase (MAO)-B and its role in substrate processing.	Imidazolines	38-49	monoamine oxidase B	Homo sapiens	175-200
10688633-3	2000	IC(50) values for inhibition of MAO-B activity by imidazoline/guanidinium ligands were one to two orders of magnitude greater than ligand concentrations that probably saturate the IBD, but were equal to the K(d) values of these ligands in competitive binding assays with the reversible MAO-B inhibitor [(3)H]Ro 19-6327.	Imidazolines	50-61	monoamine oxidase B	Homo sapiens	32-37
10688633-3	2000	IC(50) values for inhibition of MAO-B activity by imidazoline/guanidinium ligands were one to two orders of magnitude greater than ligand concentrations that probably saturate the IBD, but were equal to the K(d) values of these ligands in competitive binding assays with the reversible MAO-B inhibitor [(3)H]Ro 19-6327.	Imidazolines	50-61	monoamine oxidase B	Homo sapiens	286-291
10688633-3	2000	IC(50) values for inhibition of MAO-B activity by imidazoline/guanidinium ligands were one to two orders of magnitude greater than ligand concentrations that probably saturate the IBD, but were equal to the K(d) values of these ligands in competitive binding assays with the reversible MAO-B inhibitor [(3)H]Ro 19-6327.	Guanidine	62-73	monoamine oxidase B	Homo sapiens	32-37
10688633-3	2000	IC(50) values for inhibition of MAO-B activity by imidazoline/guanidinium ligands were one to two orders of magnitude greater than ligand concentrations that probably saturate the IBD, but were equal to the K(d) values of these ligands in competitive binding assays with the reversible MAO-B inhibitor [(3)H]Ro 19-6327.	Guanidine	62-73	monoamine oxidase B	Homo sapiens	286-291
10688633-5	2000	These data suggested that the inhibitory effect of these compounds on MAO-B activity involved a secondary interaction with the enzyme domain recognizing the inhibitor Ro 19-6327 and does not involve interaction with the IBD.	lazabemide	167-177	monoamine oxidase B	Homo sapiens	70-75
10867219-1	2000	The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease, with a concomitant extension of life span.	Selegiline	42-52	monoamine oxidase B	Homo sapiens	25-30
10867219-1	2000	The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease, with a concomitant extension of life span.	Selegiline	54-64	monoamine oxidase B	Homo sapiens	4-23
10867219-1	2000	The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease, with a concomitant extension of life span.	Selegiline	54-64	monoamine oxidase B	Homo sapiens	25-30
10867219-2	2000	It has been suggested that the therapeutic efficacy of L-deprenyl may involve actions other than the inhibition of the enzyme MAO-B.	Selegiline	55-65	monoamine oxidase B	Homo sapiens	126-131
10682227-9	2000	We suggest that the most likely explanation for the apparent accumulation of selegiline and desmethylselegiline was the saturation of the MAO-B binding sites in tissues, although decreased first-pass metabolism of selegiline cannot be ruled out.	Selegiline	77-87	monoamine oxidase B	Homo sapiens	138-143
10643794-2	2000	The A form of monoamine oxidase (MAO-A) shares with MAO-B many characteristics that could be relevant to PD, especially proneuroxicant bioactivation and dopamine metabolism.	Dopamine	153-161	monoamine oxidase B	Homo sapiens	52-57
10863544-0	2000	Effect of MAO-B inhibitors on MPP+ toxicity in Vivo.	mangion-purified polysaccharide (Candida albicans)	30-34	monoamine oxidase B	Homo sapiens	10-15
10863544-2	2000	Recently, it is proposed as a putative neuroprotective agent in delaying the progression of cell death based on its capability of reducing the oxidative stress derived from the MAO-B dependent metabolism of dopamine, and blocking the development of MPTP-parkinsonism.	Dopamine	207-215	monoamine oxidase B	Homo sapiens	177-182
10863544-6	2000	Our data show that non of these MAO-B inhibitors changes the dopamine loss in the striatum induced by intranigral injection of MPP+.	Dopamine	61-69	monoamine oxidase B	Homo sapiens	32-37
10863544-6	2000	Our data show that non of these MAO-B inhibitors changes the dopamine loss in the striatum induced by intranigral injection of MPP+.	mangion-purified polysaccharide (Candida albicans)	127-131	monoamine oxidase B	Homo sapiens	32-37
10606764-2	2000	Using a rib5 disrupted strain of Saccharomyces cerevisiae which is auxotrophic for riboflavin, MAO A and MAO B were expressed separately under control of a galactose inducible GAL10/CYC1 promoter in the presence of N(10)-omega-hydroxypentyl-isoalloxazine as the only available riboflavin analogue.	Galactose	156-165	monoamine oxidase B	Homo sapiens	105-110
10606764-8	2000	This is in contrast to the suggestion based on mutagenesis studies that an interaction between the 3"-hydroxyl group of the flavin and the beta-carbonyl of Asp(227) is required for the covalent flavinylation reaction of MAO B (Zhou et al., J. Biol.	4,6-dinitro-o-cresol	124-130	monoamine oxidase B	Homo sapiens	220-225
10606764-8	2000	This is in contrast to the suggestion based on mutagenesis studies that an interaction between the 3"-hydroxyl group of the flavin and the beta-carbonyl of Asp(227) is required for the covalent flavinylation reaction of MAO B (Zhou et al., J. Biol.	Aspartic Acid	156-159	monoamine oxidase B	Homo sapiens	220-225
10649964-4	2000	The isolation procedure was guided by estimating the inhibitory properties of tobacco leaf extracts on the liver mitochondrial MAO-B-catalyzed oxidation of 1-methyl-4-(1-methylpyrrol-2-yl)-1,2,3, 6-tetrahydropyridine to the corresponding dihydropyridinium metabolite.	1-methyl-4-(1-methylpyrrol-2-yl)-1,2,3, 6-tetrahydropyridine	156-216	monoamine oxidase B	Homo sapiens	127-132
10649964-4	2000	The isolation procedure was guided by estimating the inhibitory properties of tobacco leaf extracts on the liver mitochondrial MAO-B-catalyzed oxidation of 1-methyl-4-(1-methylpyrrol-2-yl)-1,2,3, 6-tetrahydropyridine to the corresponding dihydropyridinium metabolite.	dihydropyridinium	238-255	monoamine oxidase B	Homo sapiens	127-132
10649964-5	2000	Fractionation of extracts from flue-cured tobacco leaves led to the isolation of a competitive inhibitor of human MAO-A (K(i) = 3 microM) and MAO-B (K(i) = 6 microM), the structure of which could be assigned by classical spectroscopic analysis and confirmed by synthesis.	flue	31-35	monoamine oxidase B	Homo sapiens	142-147
10682227-9	2000	We suggest that the most likely explanation for the apparent accumulation of selegiline and desmethylselegiline was the saturation of the MAO-B binding sites in tissues, although decreased first-pass metabolism of selegiline cannot be ruled out.	desmethylselegiline	92-111	monoamine oxidase B	Homo sapiens	138-143
10682227-9	2000	We suggest that the most likely explanation for the apparent accumulation of selegiline and desmethylselegiline was the saturation of the MAO-B binding sites in tissues, although decreased first-pass metabolism of selegiline cannot be ruled out.	Selegiline	101-111	monoamine oxidase B	Homo sapiens	138-143
10850952-0	2000	Selective inhibition of monoamine oxidase B by aminoethyl substituted benzyl ethers.	aminoethyl substituted benzyl ethers	47-83	monoamine oxidase B	Homo sapiens	24-43
11200788-12	2000	L-deprenyl, a MAO-B inhibitor, is significantly more effective in reducing prolactin levels in migraineurs than in controls.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	14-19
10701898-1	2000	Monoamine oxidase B (MAOB) metabolises dopamine and activates neurotoxins known to induce parkinsonism in humans and primates.	Dopamine	39-47	monoamine oxidase B	Homo sapiens	0-19
11005543-1	2000	(-)Deprenyl (selegeline) is a monoamine oxidase B (MAO-B) inhibitor, but it also exerts several effects independent of MAO-B inhibition.	Selegiline	0-11	monoamine oxidase B	Homo sapiens	30-49
11005543-1	2000	(-)Deprenyl (selegeline) is a monoamine oxidase B (MAO-B) inhibitor, but it also exerts several effects independent of MAO-B inhibition.	Selegiline	0-11	monoamine oxidase B	Homo sapiens	51-56
11005543-1	2000	(-)Deprenyl (selegeline) is a monoamine oxidase B (MAO-B) inhibitor, but it also exerts several effects independent of MAO-B inhibition.	selegeline	13-23	monoamine oxidase B	Homo sapiens	30-49
11005543-1	2000	(-)Deprenyl (selegeline) is a monoamine oxidase B (MAO-B) inhibitor, but it also exerts several effects independent of MAO-B inhibition.	selegeline	13-23	monoamine oxidase B	Homo sapiens	51-56
10701898-1	2000	Monoamine oxidase B (MAOB) metabolises dopamine and activates neurotoxins known to induce parkinsonism in humans and primates.	Dopamine	39-47	monoamine oxidase B	Homo sapiens	21-25
16787846-9	2000	Similar to selegiline, 7-nitroindazole is a MAO-B inhibitor, which blocks the bio-activation of MPTP and oxidative stress.	Selegiline	11-21	monoamine oxidase B	Homo sapiens	44-49
11061215-3	2000	Among various isatin analogues with nearllanar structure selective MAO B inhibitors fit to 3D box of 8.5x5.1x1.8 A, whereas 3D box of 14.2x5.6x1.8 A accommodates selective MAO A inhibitors.	Isatin	14-20	monoamine oxidase B	Homo sapiens	67-72
16787846-9	2000	Similar to selegiline, 7-nitroindazole is a MAO-B inhibitor, which blocks the bio-activation of MPTP and oxidative stress.	7-nitroindazole	23-38	monoamine oxidase B	Homo sapiens	44-49
10755644-1	2000	The purpose of this study was to assess the reproducibility of repeated positron emission tomography (PET) measures of brain monoamine oxidase B (MAO B) using deuterium-substituted [11C]L-deprenyl ([11C]L-deprenyl-D2) in normal subjects and to validate the method used for estimating the kinetic constants from the irreversible 3-compartment model applied to the tracer binding.	Deuterium	159-168	monoamine oxidase B	Homo sapiens	146-151
16787846-9	2000	Similar to selegiline, 7-nitroindazole is a MAO-B inhibitor, which blocks the bio-activation of MPTP and oxidative stress.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	96-100	monoamine oxidase B	Homo sapiens	44-49
10658587-0	1999	Synthesis and monoamine oxidase B substrate properties of 1-methyl-4-heteroaryl-1,2,3,6-tetrahydropyridines.	1-methyl-4-heteroaryl-1,2,3,6-tetrahydropyridines	58-107	monoamine oxidase B	Homo sapiens	14-33
10658587-1	1999	Six analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine [MPTP, (1)] bearing various heteroaryl groups at C-4 were synthesized and examined for their monoamine oxidase B substrate properties.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	17-61	monoamine oxidase B	Homo sapiens	155-174
10658587-3	1999	The results provide information concerning steric and polar interactions between the C-4 substituent and the active site of MAO-B that are transmitted to the position of oxidation at C-6 of the tetrahydropyridinyl moiety.	tetrahydropyridinyl	194-213	monoamine oxidase B	Homo sapiens	124-129
10641793-2	1999	Clorgyline and deprenyl in fact represent archetypal MAO-A and MAO-B inhibitors respectively.	Clorgyline	0-10	monoamine oxidase B	Homo sapiens	63-68
10641793-2	1999	Clorgyline and deprenyl in fact represent archetypal MAO-A and MAO-B inhibitors respectively.	Selegiline	15-23	monoamine oxidase B	Homo sapiens	63-68
10626094-0	1999	Safety study of lazabemide (Ro19-6327), a new MAO-B inhibitor, on cardiac arrhythmias and blood pressure of patients with Parkinson"s disease.	lazabemide	16-26	monoamine oxidase B	Homo sapiens	46-51
10641793-3	1999	In the present study several ring-substituted deprenyl structural analogues were synthesized and alterations of selectivity and potency towards MAO-A and MAO-B activities were found.	Selegiline	46-54	monoamine oxidase B	Homo sapiens	154-159
10641793-5	1999	i.e. by attaching either an extra propargyl or a methyl group to the nitrogen atom, the potency of inhibition of MAO-B activity was drastically reduced and inhibition of MAO-A activity substantially increased.	Nitrogen	69-77	monoamine oxidase B	Homo sapiens	113-118
10619718-1	1999	An active role of monoamine oxidase B (MAO-B) in the pathogenesis of neurodegenerative disorders such as Parkinson"s disease has been proposed as the enzyme is known to be a generator of free radicals which seem to be responsible for neuron oxidative damage.	Free Radicals	187-200	monoamine oxidase B	Homo sapiens	18-37
10619718-1	1999	An active role of monoamine oxidase B (MAO-B) in the pathogenesis of neurodegenerative disorders such as Parkinson"s disease has been proposed as the enzyme is known to be a generator of free radicals which seem to be responsible for neuron oxidative damage.	Free Radicals	187-200	monoamine oxidase B	Homo sapiens	39-44
10761214-0	1999	[Ethanol inhibits platelet monoamine oxidase type B activity in patients with alcoholism].	Ethanol	1-8	monoamine oxidase B	Homo sapiens	27-51
10938531-0	1999	Selective Inhibition of Monoamine Oxidase B by Aminoethyl Substituted Benzyl Ethers.	aminoethyl substituted benzyl ethers	47-83	monoamine oxidase B	Homo sapiens	24-43
10656537-2	1999	The parent family--the aliphatic N-methylpropargylamines are potent, specific, irreversible MAO-B inhibitors, like R-deprenyl; but devoid of R-deprenyl"s toxicity and amphetaminergic effects.	n-methylpropargylamines	33-56	monoamine oxidase B	Homo sapiens	92-97
10656537-2	1999	The parent family--the aliphatic N-methylpropargylamines are potent, specific, irreversible MAO-B inhibitors, like R-deprenyl; but devoid of R-deprenyl"s toxicity and amphetaminergic effects.	r-deprenyl	115-125	monoamine oxidase B	Homo sapiens	92-97
10761214-1	1999	The influence of 400 mM ethanol on the activity of monoamine oxidase type B (MAO-B) of blood platelets has been studied in vitro in 30 alcoholic patients and 30 healthy volunteers.	Ethanol	24-31	monoamine oxidase B	Homo sapiens	51-75
10761214-1	1999	The influence of 400 mM ethanol on the activity of monoamine oxidase type B (MAO-B) of blood platelets has been studied in vitro in 30 alcoholic patients and 30 healthy volunteers.	Ethanol	24-31	monoamine oxidase B	Homo sapiens	77-82
10761214-2	1999	Benzylamine was used as a substrate for MAO-B.	benzylamine	0-11	monoamine oxidase B	Homo sapiens	40-45
10761214-3	1999	MAO-B inhibition by ethanol was higher in alcoholics compared to healthy volunteers.	Ethanol	20-27	monoamine oxidase B	Homo sapiens	0-5
10761214-4	1999	The higher vulnerability of MAO-B of alcoholics inhibiting action to of ethanol may be one of the mechanisms underlying some symptoms of alcoholism.	Ethanol	72-79	monoamine oxidase B	Homo sapiens	28-33
11281991-4	1999	Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson"s disease may conceivably favour recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine.	Selegiline	129-137	monoamine oxidase B	Homo sapiens	245-264
10579543-1	1999	We studied the effects of selegiline, a monoamine oxidase B inhibitor, on the subjective effects of experimentally administered cocaine in chronically cocaine-dependent subjects.	Selegiline	26-36	monoamine oxidase B	Homo sapiens	40-59
11281991-2	1999	Phenylethylamine, however, is not stored in intra-neuronal vesicles and is rapidly degraded by monoamine oxidase-B.	Phenethylamines	0-16	monoamine oxidase B	Homo sapiens	95-114
10438531-6	1999	The selectivities of MAO A and MAO B for flavin analogue incorporation are found to be similar, although 8alpha-methylation of the flavin resulted in a higher level of catalytic activity for MAO B than for MAO A.	4,6-dinitro-o-cresol	41-47	monoamine oxidase B	Homo sapiens	31-36
11281991-4	1999	Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson"s disease may conceivably favour recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine.	Selegiline	117-127	monoamine oxidase B	Homo sapiens	245-264
10438531-6	1999	The selectivities of MAO A and MAO B for flavin analogue incorporation are found to be similar, although 8alpha-methylation of the flavin resulted in a higher level of catalytic activity for MAO B than for MAO A.	4,6-dinitro-o-cresol	131-137	monoamine oxidase B	Homo sapiens	191-196
10346935-0	1999	Studies on the monoamine oxidase-B-catalyzed biotransformation of 4-azaaryl-1-methyl-1,2,3,6-tetrahydropyridine derivatives.	4-azaaryl-1-methyl-1,2,3,6-tetrahydropyridine	66-111	monoamine oxidase B	Homo sapiens	15-34
10415893-0	1999	Imidazoline binding domains on MAO-B.	Imidazolines	0-11	monoamine oxidase B	Homo sapiens	31-36
10778622-1	1999	BACKGROUND: Selegiline hydrochloride, a selective MAO-B inhibitor is known to improve motor functions in Parkinson"s disease (PD).	Selegiline	12-36	monoamine oxidase B	Homo sapiens	50-55
10433493-0	1999	Relevance of benzyloxy group in 2-indolyl methylamines in the selective MAO-B inhibition.	2-indolyl methylamines	32-54	monoamine oxidase B	Homo sapiens	72-77
10433493-6	1999	Amongst all of these benzyloxy-indolyl methylamines, N-(2-propynyl)-2-(5-benzyloxyindol)methylamine FA-73 was the most potent MAO-B "suicide" inhibitor studied.	benzyloxy-indolyl methylamines	21-51	monoamine oxidase B	Homo sapiens	126-131
10433493-6	1999	Amongst all of these benzyloxy-indolyl methylamines, N-(2-propynyl)-2-(5-benzyloxyindol)methylamine FA-73 was the most potent MAO-B "suicide" inhibitor studied.	n-(2-propynyl)-2-(5-benzyloxyindol)methylamine	53-99	monoamine oxidase B	Homo sapiens	126-131
10433493-9	1999	These data represent a selectivity value of 1066 for MAO-B, being 48 times more selective than L-deprenyl (Ki values of 376+/-0.032 and 16.8+/-0.1 nM for MAO A and MAO-B, respectively).	Selegiline	95-105	monoamine oxidase B	Homo sapiens	164-169
10433493-13	1999	These novel molecules should provide a better understanding of the active site of monoamine oxidase and could be the starting point for the design of further selective, non-amphetamine-like MAO-B inhibitors with therapeutic potential for the treatment of neurological disorders.	Amphetamine	173-184	monoamine oxidase B	Homo sapiens	190-195
10367991-1	1999	The I2-imidazoline receptor is expressed in brain and platelets and could represent a new binding domain on MAO-B enzyme.	Imidazolines	7-18	monoamine oxidase B	Homo sapiens	108-113
10408736-10	1999	Free radical scavengers/antioxidants such as idebenone, and selective prevention MAO-B inhibitors such as lazabemide are well tolerated, but require additional studies in order to demonstrate preventative effects.	lazabemide	106-116	monoamine oxidase B	Homo sapiens	81-86
10367991-6	1999	MAO-B activity was quantified by [14C]PEA oxidation.	Carbon-14	34-37	monoamine oxidase B	Homo sapiens	0-5
10367991-10	1999	Significant correlations between I2-imidazoline receptors and MAO-B activity were observed.	Imidazolines	36-47	monoamine oxidase B	Homo sapiens	62-67
10367991-13	1999	The dissociation between I2-imidazoline receptors and MAO-B in platelets suggests that the enzyme contributes to but not exclusively represents the I2-imidazoline receptor.	Imidazolines	151-162	monoamine oxidase B	Homo sapiens	54-59
10498294-5	1999	Our results showed that cell incubation with tyramine (50 micromol/l) led to a time-dependent H2O2 generation which was fully inhibited by MAO A (clorgyline and RO 41-1049) and MAO B (selegiline and RO 19-6327) inhibitors.	Tyramine	45-53	monoamine oxidase B	Homo sapiens	177-182
10498294-5	1999	Our results showed that cell incubation with tyramine (50 micromol/l) led to a time-dependent H2O2 generation which was fully inhibited by MAO A (clorgyline and RO 41-1049) and MAO B (selegiline and RO 19-6327) inhibitors.	Hydrogen Peroxide	94-98	monoamine oxidase B	Homo sapiens	177-182
10091612-1	1999	The monoamine oxidase B gene (MAOB; Xp15.21-4) is a candidate gene for Parkinson"s disease (PD) given its role in dopamine metabolism and its possible role in the activation of neurotoxins.	Dopamine	114-122	monoamine oxidase B	Homo sapiens	4-23
10221302-7	1999	Other pharmacologic treatments include drugs that inhibit dopamine-metabolizing enzymes (monoamine oxidase-B and catechol O-methyltransferase).	Dopamine	58-66	monoamine oxidase B	Homo sapiens	89-108
10091612-1	1999	The monoamine oxidase B gene (MAOB; Xp15.21-4) is a candidate gene for Parkinson"s disease (PD) given its role in dopamine metabolism and its possible role in the activation of neurotoxins.	Dopamine	114-122	monoamine oxidase B	Homo sapiens	30-34
10218814-0	1999	Synthesis and MAO-B substrate properties of 1-methyl-4-heteroaryl-1,2,3,6-tetrahydropyridines.	1-methyl-4-heteroaryl-1,2,3,6-tetrahydropyridines	44-93	monoamine oxidase B	Homo sapiens	14-19
10218814-1	1999	The parkinsonian inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated in a reaction catalyzed by the flavoenzyme monoamine oxidase B (MAO-B) to form the corresponding dihydropyridinium and subsequently pyridinium metabolites.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	31-75	monoamine oxidase B	Homo sapiens	142-161
10218814-1	1999	The parkinsonian inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated in a reaction catalyzed by the flavoenzyme monoamine oxidase B (MAO-B) to form the corresponding dihydropyridinium and subsequently pyridinium metabolites.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	31-75	monoamine oxidase B	Homo sapiens	163-168
10218814-1	1999	The parkinsonian inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated in a reaction catalyzed by the flavoenzyme monoamine oxidase B (MAO-B) to form the corresponding dihydropyridinium and subsequently pyridinium metabolites.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	77-81	monoamine oxidase B	Homo sapiens	142-161
10218814-1	1999	The parkinsonian inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated in a reaction catalyzed by the flavoenzyme monoamine oxidase B (MAO-B) to form the corresponding dihydropyridinium and subsequently pyridinium metabolites.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	77-81	monoamine oxidase B	Homo sapiens	163-168
10218814-1	1999	The parkinsonian inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated in a reaction catalyzed by the flavoenzyme monoamine oxidase B (MAO-B) to form the corresponding dihydropyridinium and subsequently pyridinium metabolites.	dihydropyridinium	196-213	monoamine oxidase B	Homo sapiens	142-161
10218814-1	1999	The parkinsonian inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated in a reaction catalyzed by the flavoenzyme monoamine oxidase B (MAO-B) to form the corresponding dihydropyridinium and subsequently pyridinium metabolites.	dihydropyridinium	196-213	monoamine oxidase B	Homo sapiens	163-168
10218814-1	1999	The parkinsonian inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated in a reaction catalyzed by the flavoenzyme monoamine oxidase B (MAO-B) to form the corresponding dihydropyridinium and subsequently pyridinium metabolites.	pyridine	203-213	monoamine oxidase B	Homo sapiens	142-161
10218814-1	1999	The parkinsonian inducing drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated in a reaction catalyzed by the flavoenzyme monoamine oxidase B (MAO-B) to form the corresponding dihydropyridinium and subsequently pyridinium metabolites.	pyridine	203-213	monoamine oxidase B	Homo sapiens	163-168
9974121-4	1999	Using in vivo microdialysis, we investigated the pharmacological activity of selegiline, a selective irreversible inhibitor of MAO B, in the striatum of marmosets.	Selegiline	77-87	monoamine oxidase B	Homo sapiens	127-132
10599872-1	1999	This study examined the potential of L-Deprenyl, a selective monoamine oxidase-B (MAO-B) inhibitor, for the treatment of neuroleptic-induced parkinsonism (NIP).	Selegiline	37-47	monoamine oxidase B	Homo sapiens	82-87
11741212-1	1999	Benzazoles containing two or three nitrogen atoms were screened for their inhibitory activity toward monoamine oxidases MAO-A and MAO-B.	benzazoles	0-10	monoamine oxidase B	Homo sapiens	130-135
11741212-3	1999	The mode of binding of benzazoles to MAO-B appears different from that of previously investigated heterocycles.	benzazoles	23-33	monoamine oxidase B	Homo sapiens	37-42
10514872-2	1999	11C-Flumazenil binds to the central benzodiazepine receptor (cBZR)-gamma-aminobutyric acid (GABA) A receptor complex; 11C-diprenorphine, 18F-cyclofoxy, and 11C-carfentanil to opiate receptors; and 11C-Deprenyl to monoamine oxidase B.	Flumazenil C-11	0-14	monoamine oxidase B	Homo sapiens	213-232
10514872-2	1999	11C-Flumazenil binds to the central benzodiazepine receptor (cBZR)-gamma-aminobutyric acid (GABA) A receptor complex; 11C-diprenorphine, 18F-cyclofoxy, and 11C-carfentanil to opiate receptors; and 11C-Deprenyl to monoamine oxidase B.	Aminobutyrates	72-90	monoamine oxidase B	Homo sapiens	213-232
10514872-2	1999	11C-Flumazenil binds to the central benzodiazepine receptor (cBZR)-gamma-aminobutyric acid (GABA) A receptor complex; 11C-diprenorphine, 18F-cyclofoxy, and 11C-carfentanil to opiate receptors; and 11C-Deprenyl to monoamine oxidase B.	gamma-Aminobutyric Acid	92-96	monoamine oxidase B	Homo sapiens	213-232
10047935-3	1999	To assess the effect of deprenyl, a monoamine oxidase type B inhibitor, on VMC in the early stages of parkinsonism.	Selegiline	24-32	monoamine oxidase B	Homo sapiens	36-60
10370904-2	1999	1) The primary action of budipine is an indirect dopaminergic effect as shown by facilitation of dopamine (DA) release, inhibition of monoamine oxidase type B (MAO-B) and of DA (re) up-take and stimulation of aromatic L-amino acid decarboxylase (AADC), which in sum might be responsible for enhancing the endogenous dopaminergic activity.	budipine	25-33	monoamine oxidase B	Homo sapiens	134-158
10370904-2	1999	1) The primary action of budipine is an indirect dopaminergic effect as shown by facilitation of dopamine (DA) release, inhibition of monoamine oxidase type B (MAO-B) and of DA (re) up-take and stimulation of aromatic L-amino acid decarboxylase (AADC), which in sum might be responsible for enhancing the endogenous dopaminergic activity.	budipine	25-33	monoamine oxidase B	Homo sapiens	160-165
10591051-5	1999	SKF-525A pretreatment diminished the protective effect of selegiline against DSP-4, while phenobarbital pretreatment decreased its MAO-B inhibitory potency.	Phenobarbital	90-103	monoamine oxidase B	Homo sapiens	131-136
10597450-6	1999	Platelet monoamine oxidase B (MAOB) levels showed evidence of linkage to D4S1651.	d4s1651	73-80	monoamine oxidase B	Homo sapiens	9-28
10597450-6	1999	Platelet monoamine oxidase B (MAOB) levels showed evidence of linkage to D4S1651.	d4s1651	73-80	monoamine oxidase B	Homo sapiens	30-34
11672383-2	1998	(E)-2-(Iodoethenyl)benzylamine (3a) was shown to be a reversible inhibitor of MAO B, but the corresponding Z isomer (3b) was a good substrate.	(e)-2-(iodoethenyl)benzylamine	0-30	monoamine oxidase B	Homo sapiens	78-83
9829163-3	1998	While the classical, nonselective and nonreversible MAOIs, such as phenelzine and tranylcypromine, are characterised by the risk of inducing a hypertensive crisis when dietary tyramine is ingested, the selective monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl) and, even more so, the selective and reversible monoamine oxidase-A (MAO-A) inhibitor moclobemide, are free from this potential interaction.	Phenelzine	67-77	monoamine oxidase B	Homo sapiens	212-231
9829163-3	1998	While the classical, nonselective and nonreversible MAOIs, such as phenelzine and tranylcypromine, are characterised by the risk of inducing a hypertensive crisis when dietary tyramine is ingested, the selective monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl) and, even more so, the selective and reversible monoamine oxidase-A (MAO-A) inhibitor moclobemide, are free from this potential interaction.	Phenelzine	67-77	monoamine oxidase B	Homo sapiens	233-238
9829163-3	1998	While the classical, nonselective and nonreversible MAOIs, such as phenelzine and tranylcypromine, are characterised by the risk of inducing a hypertensive crisis when dietary tyramine is ingested, the selective monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl) and, even more so, the selective and reversible monoamine oxidase-A (MAO-A) inhibitor moclobemide, are free from this potential interaction.	Tranylcypromine	82-97	monoamine oxidase B	Homo sapiens	212-231
9829163-3	1998	While the classical, nonselective and nonreversible MAOIs, such as phenelzine and tranylcypromine, are characterised by the risk of inducing a hypertensive crisis when dietary tyramine is ingested, the selective monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl) and, even more so, the selective and reversible monoamine oxidase-A (MAO-A) inhibitor moclobemide, are free from this potential interaction.	Tranylcypromine	82-97	monoamine oxidase B	Homo sapiens	233-238
10370911-12	1999	Addition of dopamine agonists, MAO-B inhibitors, COMT inhibitors and controlled release levodopa preparations may be helpful in prolonging the duration of efficacy of each single levodopa dose.	Levodopa	179-187	monoamine oxidase B	Homo sapiens	31-36
9853994-3	1998	This study, based on monoamine oxidase-B (MAO-B) inhibition, investigates whether a reduction in selegiline dose can provide the same beneficial effects seen with a 10-mg dose.	Selegiline	97-107	monoamine oxidase B	Homo sapiens	21-40
9853994-3	1998	This study, based on monoamine oxidase-B (MAO-B) inhibition, investigates whether a reduction in selegiline dose can provide the same beneficial effects seen with a 10-mg dose.	Selegiline	97-107	monoamine oxidase B	Homo sapiens	42-47
9853994-4	1998	The inhibition of platelet MAO-B activity against multiple dosing of selegiline (2.5, 5, and 7.5 mg) was predicted from the data obtained from literature (0.5, 1.0, 1.5, and 10 mg).	Selegiline	69-79	monoamine oxidase B	Homo sapiens	27-32
9853994-6	1998	The data suggested that by 96 hours (four doses) the inhibition of platelet MAO-B activity is approximately 95% after a daily dose of 2.5 mg selegiline, whereas it takes only 48 hours (two doses) for doses of 5 mg and 7.5 mg to achieve this degree of inhibition.	Selegiline	141-151	monoamine oxidase B	Homo sapiens	76-81
9853994-8	1998	Based on the inhibition of MAO-B activity, a reduction in daily oral dose of selegiline appears possible without compromising the therapeutic effect.	Selegiline	77-87	monoamine oxidase B	Homo sapiens	27-32
9833630-1	1998	Selegiline is an irreversible inhibitor of monoamine oxidase B with trophic and neuroprotective effects.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	43-62
9808270-9	1998	CONCLUSIONS: PET with 11C-L-deuterium-deprenyl gives a good correlation between calculated in vivo binding and MAO-B activity.	11c-l-deuterium-deprenyl	22-46	monoamine oxidase B	Homo sapiens	111-116
9839014-0	1998	Inactivation of monoamine oxidase B by cis- and trans-5-aminomethyl-3-(4-methoxyphenyl)dihydrofuran-2(3H)-ones.	cis- and trans-5-aminomethyl-3-(4-methoxyphenyl)dihydrofuran-2(3h)-ones	39-110	monoamine oxidase B	Homo sapiens	16-35
9839014-1	1998	Monoamine oxidase B was previously shown to be inactivated by cis- (3) and trans-5-(aminomethyl)-3-(4-methoxyphenyl)dihydrofuran-2(3H)-one hydrochloride (4) in a time-dependent manner (Ding, Z.; Silverman, R. B. J. Med.	cis- (3) and trans-5-(aminomethyl)-3-(4-methoxyphenyl)dihydrofuran-2(3h)-one hydrochloride	62-152	monoamine oxidase B	Homo sapiens	0-19
9749568-6	1998	By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months.	Selegiline	53-61	monoamine oxidase B	Homo sapiens	13-38
9749568-6	1998	By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months.	Levodopa	118-126	monoamine oxidase B	Homo sapiens	13-38
9724550-9	1998	These results indicate that Arg-42 and Thr-45 form critical noncovalent interactions with FAD that are required for the subsequent activation of MAO B by covalent coupling of FAD.	Arginine	28-31	monoamine oxidase B	Homo sapiens	145-150
9724550-9	1998	These results indicate that Arg-42 and Thr-45 form critical noncovalent interactions with FAD that are required for the subsequent activation of MAO B by covalent coupling of FAD.	Threonine	39-42	monoamine oxidase B	Homo sapiens	145-150
9724550-9	1998	These results indicate that Arg-42 and Thr-45 form critical noncovalent interactions with FAD that are required for the subsequent activation of MAO B by covalent coupling of FAD.	Flavin-Adenine Dinucleotide	90-93	monoamine oxidase B	Homo sapiens	145-150
9724550-9	1998	These results indicate that Arg-42 and Thr-45 form critical noncovalent interactions with FAD that are required for the subsequent activation of MAO B by covalent coupling of FAD.	Flavin-Adenine Dinucleotide	175-178	monoamine oxidase B	Homo sapiens	145-150
9726430-8	1998	Together, these results suggest that both (-)-deprenyl and melatonin up-regulate GDNF gene expression at threshold doses lower than that needed for altering MAOB activity and/or the antioxidant enzyme systems, respectively.	Selegiline	42-54	monoamine oxidase B	Homo sapiens	157-161
9726430-8	1998	Together, these results suggest that both (-)-deprenyl and melatonin up-regulate GDNF gene expression at threshold doses lower than that needed for altering MAOB activity and/or the antioxidant enzyme systems, respectively.	Melatonin	59-68	monoamine oxidase B	Homo sapiens	157-161
9706728-0	1998	Platelet monoamine oxidase B activity in "de novo" and l-dopa treated parkinsonian patients and controls.	Levodopa	55-61	monoamine oxidase B	Homo sapiens	9-28
9748356-0	1998	Inhibition of monoamine oxidase-B by condensed pyridazines and pyrimidines: effects of lipophilicity and structure-activity relationships.	Pyridazines	47-58	monoamine oxidase B	Homo sapiens	14-33
9748356-0	1998	Inhibition of monoamine oxidase-B by condensed pyridazines and pyrimidines: effects of lipophilicity and structure-activity relationships.	Pyrimidines	63-74	monoamine oxidase B	Homo sapiens	14-33
9748356-5	1998	Thus, while most of the condensed pyridazines were reversible inhibitors of MAO-B with little or no MAO-A effects, the pyrimidine derivatives proved to be reversible and selective MAO-A inhibitors.	Pyridazines	34-45	monoamine oxidase B	Homo sapiens	76-81
9748356-7	1998	A QSAR analysis of X-substituted 3-X-phenyl-5H-indeno[1,2-c]pyridazin-5-ones showed lipophilicity to increase MAO-B and not MAO-A inhibitory activity.	x-substituted 3-x-phenyl-5h-indeno[1,2-c]pyridazin-5-ones	19-76	monoamine oxidase B	Homo sapiens	110-115
9724550-0	1998	Arginine-42 and threonine-45 are required for FAD incorporation and catalytic activity in human monoamine oxidase B.	Arginine	0-8	monoamine oxidase B	Homo sapiens	96-115
9724550-0	1998	Arginine-42 and threonine-45 are required for FAD incorporation and catalytic activity in human monoamine oxidase B.	Threonine	16-25	monoamine oxidase B	Homo sapiens	96-115
9724550-0	1998	Arginine-42 and threonine-45 are required for FAD incorporation and catalytic activity in human monoamine oxidase B.	Flavin-Adenine Dinucleotide	46-49	monoamine oxidase B	Homo sapiens	96-115
9724550-1	1998	Monoamine oxidase B (MAO B) is an integral protein of the outer mitochondrial membrane that is involved in the deamination of vasoactive and neuroactive amines.	Amines	153-159	monoamine oxidase B	Homo sapiens	0-19
9724550-1	1998	Monoamine oxidase B (MAO B) is an integral protein of the outer mitochondrial membrane that is involved in the deamination of vasoactive and neuroactive amines.	Amines	153-159	monoamine oxidase B	Homo sapiens	21-26
9724550-2	1998	The oxidation of these amine substrates requires the cofactor FAD, which is covalently bound to Cys-397 of human MAO B.	Amines	23-28	monoamine oxidase B	Homo sapiens	113-118
9724550-2	1998	The oxidation of these amine substrates requires the cofactor FAD, which is covalently bound to Cys-397 of human MAO B.	Flavin-Adenine Dinucleotide	62-65	monoamine oxidase B	Homo sapiens	113-118
9724550-2	1998	The oxidation of these amine substrates requires the cofactor FAD, which is covalently bound to Cys-397 of human MAO B.	Cysteine	96-99	monoamine oxidase B	Homo sapiens	113-118
9724550-3	1998	Previously, Glu-34 and Tyr-44 of MAO B have been identified as residues which engage in noncovalent interactions with FAD that are required for subsequent covalent FAD binding and generation of catalytic activity.	Glutamic Acid	12-15	monoamine oxidase B	Homo sapiens	33-38
9724550-3	1998	Previously, Glu-34 and Tyr-44 of MAO B have been identified as residues which engage in noncovalent interactions with FAD that are required for subsequent covalent FAD binding and generation of catalytic activity.	Tyrosine	23-26	monoamine oxidase B	Homo sapiens	33-38
9724550-3	1998	Previously, Glu-34 and Tyr-44 of MAO B have been identified as residues which engage in noncovalent interactions with FAD that are required for subsequent covalent FAD binding and generation of catalytic activity.	Flavin-Adenine Dinucleotide	118-121	monoamine oxidase B	Homo sapiens	33-38
9724550-3	1998	Previously, Glu-34 and Tyr-44 of MAO B have been identified as residues which engage in noncovalent interactions with FAD that are required for subsequent covalent FAD binding and generation of catalytic activity.	Flavin-Adenine Dinucleotide	164-167	monoamine oxidase B	Homo sapiens	33-38
9724550-8	1998	However, conservative substitutions of Arg-42 with lysine or Thr-45 with serine resulted in MAO B variants that retain both partial activity and partial FAD incorporation.	Serine	73-79	monoamine oxidase B	Homo sapiens	92-97
9724550-8	1998	However, conservative substitutions of Arg-42 with lysine or Thr-45 with serine resulted in MAO B variants that retain both partial activity and partial FAD incorporation.	Flavin-Adenine Dinucleotide	153-156	monoamine oxidase B	Homo sapiens	92-97
9826303-2	1998	MAO-B activity was significantly higher in the former group, suggesting monoamine dysfunction in Prader-Willi syndrome.	monoamine	72-81	monoamine oxidase B	Homo sapiens	0-5
9721939-1	1998	The monoamine oxidase-B inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease.	Selegiline	34-44	monoamine oxidase B	Homo sapiens	4-23
9721939-1	1998	The monoamine oxidase-B inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson"s disease and possibly Alzheimer"s disease.	Selegiline	46-56	monoamine oxidase B	Homo sapiens	4-23
9704592-8	1998	Our results suggest that DA is metabolized preferentially, if not exclusively by MAO-B in some regions of the monkey brain.	Dopamine	25-27	monoamine oxidase B	Homo sapiens	81-86
9698084-9	1998	Indeed, the irreversible monoamine oxidase type A inhibitor clorgyline and the irreversible monoamine oxidase type B inhibitor selegiline (both at 0.5 microM in the incubation mixture) inhibited CIT-PROP formation, depending on the substrate, up to 70% and 88%, respectively.	Selegiline	127-137	monoamine oxidase B	Homo sapiens	92-116
9698084-9	1998	Indeed, the irreversible monoamine oxidase type A inhibitor clorgyline and the irreversible monoamine oxidase type B inhibitor selegiline (both at 0.5 microM in the incubation mixture) inhibited CIT-PROP formation, depending on the substrate, up to 70% and 88%, respectively.	cit-prop	195-203	monoamine oxidase B	Homo sapiens	92-116
12671304-3	1998	In addition, selegiline in a dosage below the level that inhibits monoamine oxidase B (MAO-B), protects dopaminergic neurons in culture against toxic factor(s) present in the CSF of patients with PD, and the said effect is mediated via elaboration of brain-derived neurotrophic factor (BDNF).	Selegiline	13-23	monoamine oxidase B	Homo sapiens	66-85
9642149-1	1998	Monoamine oxidase (MAO), which exists in two forms (MAOA and MAOB), plays an important role in the oxidative metabolism of neurotransmitters such as dopamine, and has been implicated in the etiology of Parkinson"s disease (PD).	Dopamine	149-157	monoamine oxidase B	Homo sapiens	61-65
9673855-1	1998	Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	62-86
9673855-1	1998	Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	88-93
9673855-1	1998	Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson"s disease.	Selegiline	12-20	monoamine oxidase B	Homo sapiens	62-86
9673855-1	1998	Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson"s disease.	Selegiline	12-20	monoamine oxidase B	Homo sapiens	88-93
9614088-0	1998	Characterization of a highly conserved FAD-binding site in human monoamine oxidase B.	Flavin-Adenine Dinucleotide	39-42	monoamine oxidase B	Homo sapiens	65-84
9614088-1	1998	Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of biogenic and xenobiotic amines.	xenobiotic amines	80-97	monoamine oxidase B	Homo sapiens	0-19
9614088-1	1998	Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of biogenic and xenobiotic amines.	xenobiotic amines	80-97	monoamine oxidase B	Homo sapiens	21-26
9614088-3	1998	Our previous studies identified two noncovalent flavin-binding regions in MAO B (residues 6-34 and 39-46) (Kwan, S.-W., Lewis, D. A., Zhou, B. P., and Abell, C. W. (1995) Arch.	4,6-dinitro-o-cresol	48-54	monoamine oxidase B	Homo sapiens	74-79
9614088-8	1998	By comparing sequences with enzymes in the oxidoreductase family, we now have found an additional FAD-binding site in MAO B (residues 222-227), which is highly conserved across species (human, bovine, and rat).	Flavin-Adenine Dinucleotide	98-101	monoamine oxidase B	Homo sapiens	118-123
9614088-19	1998	Based on these collective results, we propose that the coupling of FAD to the MAO B apoenzyme is a multistep process.	Flavin-Adenine Dinucleotide	67-70	monoamine oxidase B	Homo sapiens	78-83
9603903-1	1998	Mitochondrial monoamine oxidases A and B (MAO A and MAO B) are ubiquitous homodimeric FAD-containing oxidases that catalyze the oxidation of biogenic amines.	Amines	150-156	monoamine oxidase B	Homo sapiens	52-57
9603903-4	1998	The experiments reported here show that both MAO A and MAO B contain a redox-active disulfide at the catalytic center.	Disulfides	84-93	monoamine oxidase B	Homo sapiens	55-60
9663810-24	1998	The effects of the two drugs on platelet MAO activity and plasma DHPG concentration are in agreement with previous reports and consistent with the relative selectivity of moclobemide for MAO-A and of selegiline for MAO-B.	Selegiline	200-210	monoamine oxidase B	Homo sapiens	215-220
9572675-3	1998	Platelet MAO-B activity was measured using [14C]tyramine as substrate.	Tyramine	48-56	monoamine oxidase B	Homo sapiens	9-14
9572675-7	1998	Platelet MAO-B activity was higher in the haloperidol treated group, compared with patients treated with anxyolitics.	Haloperidol	42-53	monoamine oxidase B	Homo sapiens	9-14
12671304-3	1998	In addition, selegiline in a dosage below the level that inhibits monoamine oxidase B (MAO-B), protects dopaminergic neurons in culture against toxic factor(s) present in the CSF of patients with PD, and the said effect is mediated via elaboration of brain-derived neurotrophic factor (BDNF).	Selegiline	13-23	monoamine oxidase B	Homo sapiens	87-92
9879512-0	1998	Effect of the locus of the oxygen atom in amino ethers on the inactivation of monoamine oxidase B.	Oxygen	27-33	monoamine oxidase B	Homo sapiens	78-97
9730267-0	1998	The role of MAO-A and MAO-B in the metabolic degradation of noradrenaline in human arteries.	Norepinephrine	60-73	monoamine oxidase B	Homo sapiens	22-27
9730267-9	1998	Both clorgyline (a selective MAO-A inhibitor) and selegiline (a selective MAO-B inhibitor) reduced the formation of dihydroxyphenylglycol (DOPEG), DOMA and O-methylated-deaminated metabolites (OMDA), and increased that of normetanephrine (NMN).	Clorgyline	5-15	monoamine oxidase B	Homo sapiens	74-79
9730267-9	1998	Both clorgyline (a selective MAO-A inhibitor) and selegiline (a selective MAO-B inhibitor) reduced the formation of dihydroxyphenylglycol (DOPEG), DOMA and O-methylated-deaminated metabolites (OMDA), and increased that of normetanephrine (NMN).	Selegiline	50-60	monoamine oxidase B	Homo sapiens	74-79
9730267-9	1998	Both clorgyline (a selective MAO-A inhibitor) and selegiline (a selective MAO-B inhibitor) reduced the formation of dihydroxyphenylglycol (DOPEG), DOMA and O-methylated-deaminated metabolites (OMDA), and increased that of normetanephrine (NMN).	dihydroxyphenylglycol	116-137	monoamine oxidase B	Homo sapiens	74-79
9730267-9	1998	Both clorgyline (a selective MAO-A inhibitor) and selegiline (a selective MAO-B inhibitor) reduced the formation of dihydroxyphenylglycol (DOPEG), DOMA and O-methylated-deaminated metabolites (OMDA), and increased that of normetanephrine (NMN).	3,4-dihydroxyphenylglycol	139-144	monoamine oxidase B	Homo sapiens	74-79
9568282-0	1998	Chemical model studies on the monoamine oxidase-B catalyzed oxidation of 4-substituted 1-cyclopropyl-1,2,3,6-tetrahydropyridines.	4-substituted 1-cyclopropyl-1,2,3,6-tetrahydropyridines	73-128	monoamine oxidase B	Homo sapiens	30-49
9568282-1	1998	Two catalytic pathways have been proposed for the flavoenzyme monoamine oxidase B (MAO-B)--one based on an initial single electron transfer (SET) step from the nitrogen lone pair and the second based on an initial alpha-carbon hydrogen atom transfer (HAT) step.	Nitrogen	160-168	monoamine oxidase B	Homo sapiens	62-81
9568282-1	1998	Two catalytic pathways have been proposed for the flavoenzyme monoamine oxidase B (MAO-B)--one based on an initial single electron transfer (SET) step from the nitrogen lone pair and the second based on an initial alpha-carbon hydrogen atom transfer (HAT) step.	Nitrogen	160-168	monoamine oxidase B	Homo sapiens	83-88
9568282-1	1998	Two catalytic pathways have been proposed for the flavoenzyme monoamine oxidase B (MAO-B)--one based on an initial single electron transfer (SET) step from the nitrogen lone pair and the second based on an initial alpha-carbon hydrogen atom transfer (HAT) step.	Carbon	220-226	monoamine oxidase B	Homo sapiens	62-81
9568282-1	1998	Two catalytic pathways have been proposed for the flavoenzyme monoamine oxidase B (MAO-B)--one based on an initial single electron transfer (SET) step from the nitrogen lone pair and the second based on an initial alpha-carbon hydrogen atom transfer (HAT) step.	Carbon	220-226	monoamine oxidase B	Homo sapiens	83-88
9568282-1	1998	Two catalytic pathways have been proposed for the flavoenzyme monoamine oxidase B (MAO-B)--one based on an initial single electron transfer (SET) step from the nitrogen lone pair and the second based on an initial alpha-carbon hydrogen atom transfer (HAT) step.	Hydrogen	227-235	monoamine oxidase B	Homo sapiens	62-81
9568282-1	1998	Two catalytic pathways have been proposed for the flavoenzyme monoamine oxidase B (MAO-B)--one based on an initial single electron transfer (SET) step from the nitrogen lone pair and the second based on an initial alpha-carbon hydrogen atom transfer (HAT) step.	Hydrogen	227-235	monoamine oxidase B	Homo sapiens	83-88
9568282-3	1998	The observation that MAO-B catalyzes the efficient oxidation of certain 1-cyclopropyl-4-substituted-1,2,3,6-tetrahydropyridines to the corresponding dihydropyridinium metabolites suggests that the catalytic pathway for these cyclic tertiary allylamines may not proceed via the putative SET generated aminyl radical cations.	1-cyclopropyl-4-substituted-1,2,3,6-tetrahydropyridines	72-127	monoamine oxidase B	Homo sapiens	21-26
9568282-3	1998	The observation that MAO-B catalyzes the efficient oxidation of certain 1-cyclopropyl-4-substituted-1,2,3,6-tetrahydropyridines to the corresponding dihydropyridinium metabolites suggests that the catalytic pathway for these cyclic tertiary allylamines may not proceed via the putative SET generated aminyl radical cations.	dihydropyridinium	149-166	monoamine oxidase B	Homo sapiens	21-26
9568282-3	1998	The observation that MAO-B catalyzes the efficient oxidation of certain 1-cyclopropyl-4-substituted-1,2,3,6-tetrahydropyridines to the corresponding dihydropyridinium metabolites suggests that the catalytic pathway for these cyclic tertiary allylamines may not proceed via the putative SET generated aminyl radical cations.	cyclic tertiary allylamines	225-252	monoamine oxidase B	Homo sapiens	21-26
9568282-3	1998	The observation that MAO-B catalyzes the efficient oxidation of certain 1-cyclopropyl-4-substituted-1,2,3,6-tetrahydropyridines to the corresponding dihydropyridinium metabolites suggests that the catalytic pathway for these cyclic tertiary allylamines may not proceed via the putative SET generated aminyl radical cations.	Ammonia	300-314	monoamine oxidase B	Homo sapiens	21-26
9547937-0	1998	1-Methyl-3-pyrrolines and 2-methylisoindolines: new classes of cyclic tertiary amine monoamine oxidase B substrates.	1-methyl-3-pyrrolines	0-21	monoamine oxidase B	Homo sapiens	85-104
9547937-0	1998	1-Methyl-3-pyrrolines and 2-methylisoindolines: new classes of cyclic tertiary amine monoamine oxidase B substrates.	2-methylisoindolines	26-46	monoamine oxidase B	Homo sapiens	85-104
9547937-1	1998	Both 1-methyl-3-pyrrolines and 2-methylisoindolines are substrates for MAO-B with Vmax/Km values ranging from 200 to 2000 min-1 mM-1 at 37 degrees C. These compounds represent new classes of cyclic tertiary amine substrates for this flavoenzyme.	1-methyl-3-pyrrolines	5-26	monoamine oxidase B	Homo sapiens	71-76
9547937-1	1998	Both 1-methyl-3-pyrrolines and 2-methylisoindolines are substrates for MAO-B with Vmax/Km values ranging from 200 to 2000 min-1 mM-1 at 37 degrees C. These compounds represent new classes of cyclic tertiary amine substrates for this flavoenzyme.	2-methylisoindolines	31-51	monoamine oxidase B	Homo sapiens	71-76
9547937-1	1998	Both 1-methyl-3-pyrrolines and 2-methylisoindolines are substrates for MAO-B with Vmax/Km values ranging from 200 to 2000 min-1 mM-1 at 37 degrees C. These compounds represent new classes of cyclic tertiary amine substrates for this flavoenzyme.	Amines	207-212	monoamine oxidase B	Homo sapiens	71-76
9547937-2	1998	The only other known cyclic amines that are MAO-B substrates are 1,4-disubstituted 1,2,3,6-tetrahydropyridinyl derivatives.	cyclic amines	21-34	monoamine oxidase B	Homo sapiens	44-49
9547937-2	1998	The only other known cyclic amines that are MAO-B substrates are 1,4-disubstituted 1,2,3,6-tetrahydropyridinyl derivatives.	1,4-disubstituted 1,2,3,6-tetrahydropyridinyl derivatives	65-122	monoamine oxidase B	Homo sapiens	44-49
9547937-3	1998	The presence of an allylic (benzylic) amino functionality in all of these compounds may be linked to their substrate properties since related piperidinyl and pyrrolidinyl analogs are stable in the presence of MAO-B.	pyrrolidinyl	158-170	monoamine oxidase B	Homo sapiens	209-214
9879512-0	1998	Effect of the locus of the oxygen atom in amino ethers on the inactivation of monoamine oxidase B.	amino ethers	42-54	monoamine oxidase B	Homo sapiens	78-97
9879512-5	1998	The analogues in which the oxygen atom is closest to the alpha-carbon (9 and 10) inactivate MAO B, but activity slowly returns with time.	Oxygen	27-33	monoamine oxidase B	Homo sapiens	92-97
9879512-5	1998	The analogues in which the oxygen atom is closest to the alpha-carbon (9 and 10) inactivate MAO B, but activity slowly returns with time.	Carbon	63-69	monoamine oxidase B	Homo sapiens	92-97
9489486-1	1998	Deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, has a wide range of pharmacological properties that are beneficial therapeutically in the treatment of human neurodegenerative diseases.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	12-31
9489486-1	1998	Deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, has a wide range of pharmacological properties that are beneficial therapeutically in the treatment of human neurodegenerative diseases.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	33-38
9327902-0	1998	Aliphatic N-methylpropargylamines: monoamine oxidase-B inhibitors and antiapoptotic drugs.	aliphatic n-methylpropargylamines	0-33	monoamine oxidase B	Homo sapiens	35-54
9564606-0	1998	Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B (selegiline and pargyline).	Amines	19-24	monoamine oxidase B	Homo sapiens	109-114
9564606-0	1998	Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B (selegiline and pargyline).	Selegiline	116-126	monoamine oxidase B	Homo sapiens	109-114
9564606-0	1998	Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B (selegiline and pargyline).	Pargyline	131-140	monoamine oxidase B	Homo sapiens	109-114
9564606-2	1998	In comparative studies with other, structurally similar acetylenic inhibitors of MAO, pargyline, an MAO-B &gt; MAO-A inhibitor used in doses of 90 mg/day for three or more weeks, produced elevations in these trace amines which were similar to those found with the highest dose of selegiline studied.	Pargyline	86-95	monoamine oxidase B	Homo sapiens	100-105
9443715-3	1998	Selegiline hydrochloride (Eldepryl) is a monoamine oxidase-B inhibitor with antioxidant properties.	Selegiline	0-24	monoamine oxidase B	Homo sapiens	41-60
9443715-3	1998	Selegiline hydrochloride (Eldepryl) is a monoamine oxidase-B inhibitor with antioxidant properties.	Selegiline	26-34	monoamine oxidase B	Homo sapiens	41-60
9564614-1	1998	The pharmacological effects of (-)-deprenyl is multi-fold in its nature (dopamine sparing activity, neuroprotective and neuronal rescue effects), which cannot be explained solely by the irreversible MAO-B inhibitory action of the substance.	Selegiline	35-43	monoamine oxidase B	Homo sapiens	199-204
9564616-1	1998	The rate of oxidation by monoamine oxidase (MAO) of a particular amine in a given cell depends on the levels of MAO-A and MAO-B expressed in the mitochondrial outer membranes, on the amine concentration and the oxygen concentration.	Amines	29-34	monoamine oxidase B	Homo sapiens	122-127
9564616-1	1998	The rate of oxidation by monoamine oxidase (MAO) of a particular amine in a given cell depends on the levels of MAO-A and MAO-B expressed in the mitochondrial outer membranes, on the amine concentration and the oxygen concentration.	Amines	65-70	monoamine oxidase B	Homo sapiens	122-127
9564616-5	1998	(b) It accelerates the reactivity of the covalently bound flavin with oxygen, effectively increasing the Vm (particularly for MAO-B).	4,6-dinitro-o-cresol	58-64	monoamine oxidase B	Homo sapiens	126-131
9564616-5	1998	(b) It accelerates the reactivity of the covalently bound flavin with oxygen, effectively increasing the Vm (particularly for MAO-B).	Oxygen	70-76	monoamine oxidase B	Homo sapiens	126-131
9564606-2	1998	In comparative studies with other, structurally similar acetylenic inhibitors of MAO, pargyline, an MAO-B &gt; MAO-A inhibitor used in doses of 90 mg/day for three or more weeks, produced elevations in these trace amines which were similar to those found with the highest dose of selegiline studied.	Amines	214-220	monoamine oxidase B	Homo sapiens	100-105
9564606-2	1998	In comparative studies with other, structurally similar acetylenic inhibitors of MAO, pargyline, an MAO-B &gt; MAO-A inhibitor used in doses of 90 mg/day for three or more weeks, produced elevations in these trace amines which were similar to those found with the highest dose of selegiline studied.	Selegiline	280-290	monoamine oxidase B	Homo sapiens	100-105
9564606-5	1998	Selegiline produced larger changes in trace amines--at least at the higher doses studied--than found in individuals lacking the gene for MAO-B, in agreement with other data suggesting a lesser selectivity for MAO-B inhibition when selegiline was given in doses higher than 10 mg/day.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	209-214
9564606-5	1998	Selegiline produced larger changes in trace amines--at least at the higher doses studied--than found in individuals lacking the gene for MAO-B, in agreement with other data suggesting a lesser selectivity for MAO-B inhibition when selegiline was given in doses higher than 10 mg/day.	Selegiline	231-241	monoamine oxidase B	Homo sapiens	137-142
9466361-0	1998	In vivo properties of N-(2-aminoethyl)-5-halogeno-2-pyridinecarboxamide 18F- and 123I-labelled reversible inhibitors of monoamine oxidase B.	n-(2-aminoethyl)-5-halogeno-2-pyridinecarboxamide	22-71	monoamine oxidase B	Homo sapiens	120-139
9564606-6	1998	Overall, trace amine elevations in individuals receiving the highest dose of deprenyl or receiving pargyline were approximately three to five-fold lower than the elevations observed in individuals lacking the genes for both MAO-A and MAO-B, suggesting that these drug doses yield incomplete inhibition of MAO-A and MAO-B.	Amines	15-20	monoamine oxidase B	Homo sapiens	315-320
9564606-6	1998	Overall, trace amine elevations in individuals receiving the highest dose of deprenyl or receiving pargyline were approximately three to five-fold lower than the elevations observed in individuals lacking the genes for both MAO-A and MAO-B, suggesting that these drug doses yield incomplete inhibition of MAO-A and MAO-B.	Selegiline	77-85	monoamine oxidase B	Homo sapiens	234-239
9564606-6	1998	Overall, trace amine elevations in individuals receiving the highest dose of deprenyl or receiving pargyline were approximately three to five-fold lower than the elevations observed in individuals lacking the genes for both MAO-A and MAO-B, suggesting that these drug doses yield incomplete inhibition of MAO-A and MAO-B.	Selegiline	77-85	monoamine oxidase B	Homo sapiens	315-320
9564608-1	1998	Deprenyl is a potent MAO-B inhibitor which is commonly prescribed for treatment of parkinsonism.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	21-26
9564630-0	1998	(R)(+)-N-propargyl-1-aminoindan (rasagiline) and derivatives: highly selective and potent inhibitors of monoamine oxidase B.	(r)(+)-n-propargyl-1-aminoindan	0-31	monoamine oxidase B	Homo sapiens	104-123
9564630-0	1998	(R)(+)-N-propargyl-1-aminoindan (rasagiline) and derivatives: highly selective and potent inhibitors of monoamine oxidase B.	rasagiline	33-43	monoamine oxidase B	Homo sapiens	104-123
9564631-9	1998	Isatin is an endogenous selective inhibitor of MAO-B (K1 approximately 3 microM).	Isatin	0-6	monoamine oxidase B	Homo sapiens	47-52
9564633-1	1998	In clinical studies the MAO-B inhibitor selegiline appears to slow the progression of neurological deficits in Parkinson"s disease (PD) and the cognitive decline in Alzheimer"s disease (AD).	Selegiline	40-50	monoamine oxidase B	Homo sapiens	24-29
9466361-0	1998	In vivo properties of N-(2-aminoethyl)-5-halogeno-2-pyridinecarboxamide 18F- and 123I-labelled reversible inhibitors of monoamine oxidase B.	Iodine-123	81-85	monoamine oxidase B	Homo sapiens	120-139
9466361-1	1998	The reversible and highly selective monoamine oxidase B (MAO-B) inhibitor Ro 19-6327, a picolinic acid derivative, was selected for the development of new radiopharmaceuticals, whereby in place of Cl either 123I or 18F was introduced.	lazabemide	74-84	monoamine oxidase B	Homo sapiens	36-55
9466361-1	1998	The reversible and highly selective monoamine oxidase B (MAO-B) inhibitor Ro 19-6327, a picolinic acid derivative, was selected for the development of new radiopharmaceuticals, whereby in place of Cl either 123I or 18F was introduced.	lazabemide	74-84	monoamine oxidase B	Homo sapiens	57-62
9466361-1	1998	The reversible and highly selective monoamine oxidase B (MAO-B) inhibitor Ro 19-6327, a picolinic acid derivative, was selected for the development of new radiopharmaceuticals, whereby in place of Cl either 123I or 18F was introduced.	picolinic acid	88-102	monoamine oxidase B	Homo sapiens	36-55
9466361-1	1998	The reversible and highly selective monoamine oxidase B (MAO-B) inhibitor Ro 19-6327, a picolinic acid derivative, was selected for the development of new radiopharmaceuticals, whereby in place of Cl either 123I or 18F was introduced.	picolinic acid	88-102	monoamine oxidase B	Homo sapiens	57-62
9466361-6	1998	First experiments with single photon emission tomography and positron emission tomography (PET) showed that the iodo compound can be used to investigate MAO-B in vivo while the fluoro compound is accumulated in the brain to such a low degree that no PET studies can be performed.	iodo	112-116	monoamine oxidase B	Homo sapiens	153-158
9372556-0	1997	Striatal 6-[18F]fluorodopa accumulation after combined inhibition of peripheral catechol-O-methyltransferase and monoamine oxidase type B: differing response in relation to presynaptic dopaminergic dysfunction.	6-[18f]fluorodopa	9-26	monoamine oxidase B	Homo sapiens	113-137
9372556-1	1997	The aim was to investigate the effects of inhibition of monoamine oxidase type B (MAO-B) with selegiline alone and the combined inhibition of peripheral catechol-O-methyltransferase (COMT) with entacapone and MAO-B with selegiline on striatal 6-[18F]fluorodopa (FDOPA) accumulation, and whether the effect of entacapone + selegiline on FDOPA uptake differed depending on the severity of the presynaptic dopaminergic dysfunction.	Selegiline	94-104	monoamine oxidase B	Homo sapiens	82-87
9406907-2	1997	Our results showed that the 5-hydroxytryptamine (5-HT) content in platelets was: (1) increased in the subgroup of anti-social alcoholics; (2) transiently and differently altered in alcoholics compared to opiate addicts; and (3) lowered in drinking alcoholics and normal in alcoholics who were drinking as well as smoking (that may occur via MAO-B inhibition by smoke).	Serotonin	28-47	monoamine oxidase B	Homo sapiens	341-346
9394121-2	1997	The density of MAO-B sites was quantified by the specific binding of the selective inhibitor [3H]Ro 19-6327 (lazabemide) (8 nM) to cortical membranes.	Tritium	94-96	monoamine oxidase B	Homo sapiens	15-20
9394121-2	1997	The density of MAO-B sites was quantified by the specific binding of the selective inhibitor [3H]Ro 19-6327 (lazabemide) (8 nM) to cortical membranes.	lazabemide	97-107	monoamine oxidase B	Homo sapiens	15-20
9394121-2	1997	The density of MAO-B sites was quantified by the specific binding of the selective inhibitor [3H]Ro 19-6327 (lazabemide) (8 nM) to cortical membranes.	lazabemide	109-119	monoamine oxidase B	Homo sapiens	15-20
9373724-1	1997	Selegiline is a selective, irreversible inhibitor of MAO-B, used in the treatment of Parkinson"s disease, either alone or as an adjunct to L-DOPA.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	53-58
9503561-4	1997	MAO-A preferentially deaminates serotonin (5HT) and is selectively inhibited by harmine and clorgyline, while MAO-B preferentially deaminates phenethylamine and benzylamine, and is selectively inhibited by (-)deprenyl as well as low concentrations of pargyline.	phenethylamine	142-156	monoamine oxidase B	Homo sapiens	110-115
9503561-4	1997	MAO-A preferentially deaminates serotonin (5HT) and is selectively inhibited by harmine and clorgyline, while MAO-B preferentially deaminates phenethylamine and benzylamine, and is selectively inhibited by (-)deprenyl as well as low concentrations of pargyline.	benzylamine	161-172	monoamine oxidase B	Homo sapiens	110-115
9503561-4	1997	MAO-A preferentially deaminates serotonin (5HT) and is selectively inhibited by harmine and clorgyline, while MAO-B preferentially deaminates phenethylamine and benzylamine, and is selectively inhibited by (-)deprenyl as well as low concentrations of pargyline.	Selegiline	206-217	monoamine oxidase B	Homo sapiens	110-115
9503561-4	1997	MAO-A preferentially deaminates serotonin (5HT) and is selectively inhibited by harmine and clorgyline, while MAO-B preferentially deaminates phenethylamine and benzylamine, and is selectively inhibited by (-)deprenyl as well as low concentrations of pargyline.	Pargyline	251-260	monoamine oxidase B	Homo sapiens	110-115
9503563-1	1997	MAO A and MAO B follow the same chemical mechanism to oxidise primary, secondary, and tertiary amines, but they are distinguished by differences in their substrate and inhibitor specificities and in their kinetic behaviour.	Amines	95-101	monoamine oxidase B	Homo sapiens	10-15
9503565-0	1997	[History of deprenyl--the first selective inhibitor of monoamine oxidase type B].	Selegiline	12-20	monoamine oxidase B	Homo sapiens	55-79
9503565-6	1997	(-)Deprenyl, the first selective inhibitor of MAO-B described in the literature, has become a universally used research tool for selectively blocking B-type MAO and is still the only selective MAO-B inhibitor in world wide clinical use.	Selegiline	3-11	monoamine oxidase B	Homo sapiens	46-51
9503565-6	1997	(-)Deprenyl, the first selective inhibitor of MAO-B described in the literature, has become a universally used research tool for selectively blocking B-type MAO and is still the only selective MAO-B inhibitor in world wide clinical use.	Selegiline	3-11	monoamine oxidase B	Homo sapiens	193-198
9503567-1	1997	The complexity of the pharmacological activity of selegiline cannot be considered only as a result of a simple MAO-B inhibition.	Selegiline	50-60	monoamine oxidase B	Homo sapiens	111-116
9503568-4	1997	In vitro, isatin selectively inhibits monoamine oxidase (MAO) B (IC50 3-8 microM, Ki approximately 20 microM) and, more potently, atrial natriuretic peptide(ANP) binding (IC50, 0.4 microM).	Isatin	10-16	monoamine oxidase B	Homo sapiens	38-63
9359458-2	1997	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of monoamine oxidase type B (MAO-B)-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-44	monoamine oxidase B	Homo sapiens	158-182
9330778-1	1997	Selegiline (SEL) is a selective, irreversible inhibitor of MAO-B, used in the treatment of Parkinson"s disease, either alone or as an adjunct to L-DOPA.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	59-64
9330778-1	1997	Selegiline (SEL) is a selective, irreversible inhibitor of MAO-B, used in the treatment of Parkinson"s disease, either alone or as an adjunct to L-DOPA.	Selegiline	12-15	monoamine oxidase B	Homo sapiens	59-64
9380016-0	1997	Localization of the imidazoline binding domain on monoamine oxidase B.	Imidazolines	20-31	monoamine oxidase B	Homo sapiens	50-69
9380016-1	1997	Monoamine oxidase B (MAO-B) was recently identified as a member of the family of imidazoline binding proteins.	Imidazolines	81-92	monoamine oxidase B	Homo sapiens	0-19
9380016-1	1997	Monoamine oxidase B (MAO-B) was recently identified as a member of the family of imidazoline binding proteins.	Imidazolines	81-92	monoamine oxidase B	Homo sapiens	21-26
9380016-3	1997	Based on species-specific fragmentation patterns and immunoprecipitation of labeled peptides, the imidazoline binding domain was localized to residues K149 to M222 of human MAO-B.	Imidazolines	98-109	monoamine oxidase B	Homo sapiens	173-178
9380016-6	1997	Identification of an imidazoline binding domain on MAO-B provides a new opportunity for the potential pharmacological development of imidazoline/guanidinium compounds and also presents additional avenues for structure/function analysis of the monoamine oxidase enzymes.	Imidazolines	21-32	monoamine oxidase B	Homo sapiens	51-56
9380016-6	1997	Identification of an imidazoline binding domain on MAO-B provides a new opportunity for the potential pharmacological development of imidazoline/guanidinium compounds and also presents additional avenues for structure/function analysis of the monoamine oxidase enzymes.	Imidazolines	133-144	monoamine oxidase B	Homo sapiens	51-56
9380016-6	1997	Identification of an imidazoline binding domain on MAO-B provides a new opportunity for the potential pharmacological development of imidazoline/guanidinium compounds and also presents additional avenues for structure/function analysis of the monoamine oxidase enzymes.	Guanidine	145-156	monoamine oxidase B	Homo sapiens	51-56
9331518-1	1997	We have evaluated the risk for pharmacokinetic and/or pharmacodynamic interactions of concomitantly administered selegiline, a selective monoamine oxidase type B inhibitor, and citalopram, a widely used selective serotonin uptake inhibitor antidepressant.	Selegiline	113-123	monoamine oxidase B	Homo sapiens	137-161
9359458-2	1997	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of monoamine oxidase type B (MAO-B)-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-44	monoamine oxidase B	Homo sapiens	184-189
9359458-2	1997	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of monoamine oxidase type B (MAO-B)-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	46-50	monoamine oxidase B	Homo sapiens	158-182
9359458-2	1997	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of monoamine oxidase type B (MAO-B)-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	46-50	monoamine oxidase B	Homo sapiens	184-189
9359458-2	1997	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of monoamine oxidase type B (MAO-B)-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	-phenyl-pyridinium	235-253	monoamine oxidase B	Homo sapiens	158-182
9359458-2	1997	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of monoamine oxidase type B (MAO-B)-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons.	mangion-purified polysaccharide (Candida albicans)	259-262	monoamine oxidase B	Homo sapiens	158-182
9313858-0	1997	Chemical model studies on the monoamine oxidase-B catalyzed oxidation of 4-substituted 1-methyl-1,2,3,6-tetrahydropyridines.	4-substituted 1-methyl-1,2,3,6-tetrahydropyridines	73-123	monoamine oxidase B	Homo sapiens	30-49
9305573-2	1997	The most dramatic illustration of this type of bioactivation process is the conversion of the parkinsonian-inducing neurotoxin MPTP (23) by brain MAO-B to the iminium (dihydropyridinium) metabolite 24 which is oxidized further to the pyridinium species MPP+ (25).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	127-131	monoamine oxidase B	Homo sapiens	146-151
9305573-2	1997	The most dramatic illustration of this type of bioactivation process is the conversion of the parkinsonian-inducing neurotoxin MPTP (23) by brain MAO-B to the iminium (dihydropyridinium) metabolite 24 which is oxidized further to the pyridinium species MPP+ (25).	iminium	159-166	monoamine oxidase B	Homo sapiens	146-151
9305573-2	1997	The most dramatic illustration of this type of bioactivation process is the conversion of the parkinsonian-inducing neurotoxin MPTP (23) by brain MAO-B to the iminium (dihydropyridinium) metabolite 24 which is oxidized further to the pyridinium species MPP+ (25).	dihydropyridinium	168-185	monoamine oxidase B	Homo sapiens	146-151
9305573-2	1997	The most dramatic illustration of this type of bioactivation process is the conversion of the parkinsonian-inducing neurotoxin MPTP (23) by brain MAO-B to the iminium (dihydropyridinium) metabolite 24 which is oxidized further to the pyridinium species MPP+ (25).	pyridine	175-185	monoamine oxidase B	Homo sapiens	146-151
9305573-2	1997	The most dramatic illustration of this type of bioactivation process is the conversion of the parkinsonian-inducing neurotoxin MPTP (23) by brain MAO-B to the iminium (dihydropyridinium) metabolite 24 which is oxidized further to the pyridinium species MPP+ (25).	mangion-purified polysaccharide (Candida albicans)	253-257	monoamine oxidase B	Homo sapiens	146-151
9313858-1	1997	The MAO-B catalyzed alpha-carbon oxidation of amines has been proposed to proceed via either a single electron transfer (SET) or hydrogen atom transfer (HAT) pathway.	Carbon	26-32	monoamine oxidase B	Homo sapiens	4-9
9313858-1	1997	The MAO-B catalyzed alpha-carbon oxidation of amines has been proposed to proceed via either a single electron transfer (SET) or hydrogen atom transfer (HAT) pathway.	Amines	46-52	monoamine oxidase B	Homo sapiens	4-9
9313858-1	1997	The MAO-B catalyzed alpha-carbon oxidation of amines has been proposed to proceed via either a single electron transfer (SET) or hydrogen atom transfer (HAT) pathway.	Hydrogen	129-137	monoamine oxidase B	Homo sapiens	4-9
9377092-1	1997	The monoamine oxidases A and B (MAO-A and MAO-B) catalyze the alpha-carbon oxidation of a variety of 4-substituted 1-methyl-1,2,3,6-tetrahydropyridine derivatives to yield the corresponding 2,3-dihydropyridinium species.	Carbon	68-74	monoamine oxidase B	Homo sapiens	42-47
9260033-2	1997	Selegiline is a selective inhibitor of monoamine oxidase-B (MAO-B) at a dose of 10 mg/day and is given to patients with Parkinson"s disease as an adjunct to levodopa therapy.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	39-58
9260033-2	1997	Selegiline is a selective inhibitor of monoamine oxidase-B (MAO-B) at a dose of 10 mg/day and is given to patients with Parkinson"s disease as an adjunct to levodopa therapy.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	60-65
9260033-3	1997	By inhibiting MAO-B, selegiline increases the dopamine levels in the substantia nigra.	Selegiline	21-31	monoamine oxidase B	Homo sapiens	14-19
9260033-3	1997	By inhibiting MAO-B, selegiline increases the dopamine levels in the substantia nigra.	Dopamine	46-54	monoamine oxidase B	Homo sapiens	14-19
9260033-15	1997	One of the metabolites of selegiline, desmethylselegiline, is believed to posses some MAO-B inhibitory property, though to a lesser extent than that of selegiline.	Selegiline	26-36	monoamine oxidase B	Homo sapiens	86-91
9260033-15	1997	One of the metabolites of selegiline, desmethylselegiline, is believed to posses some MAO-B inhibitory property, though to a lesser extent than that of selegiline.	desmethylselegiline	38-57	monoamine oxidase B	Homo sapiens	86-91
9260033-15	1997	One of the metabolites of selegiline, desmethylselegiline, is believed to posses some MAO-B inhibitory property, though to a lesser extent than that of selegiline.	Selegiline	47-57	monoamine oxidase B	Homo sapiens	86-91
9260033-16	1997	Within 2 to 4 hours of an oral dose of selegiline 10 mg, 86% of the platelet MAO-B activity was inhibited and it took almost 2 weeks for platelet MAO-B activity to return to the baseline values.	Selegiline	39-49	monoamine oxidase B	Homo sapiens	77-82
9260033-16	1997	Within 2 to 4 hours of an oral dose of selegiline 10 mg, 86% of the platelet MAO-B activity was inhibited and it took almost 2 weeks for platelet MAO-B activity to return to the baseline values.	Selegiline	39-49	monoamine oxidase B	Homo sapiens	146-151
9258314-3	1997	We describe an uneventful perioperative course in a parkinsonian patient who required urgent coronary artery bypass graft surgery while he was taking selegiline, a selective inhibitor of monoamine oxidase type B.	Selegiline	150-160	monoamine oxidase B	Homo sapiens	187-211
9280684-16	1997	Selegiline, a MAOB inhibitor with a possible neuroprotective effect, should also be considered as initial option for Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	14-18
9377092-1	1997	The monoamine oxidases A and B (MAO-A and MAO-B) catalyze the alpha-carbon oxidation of a variety of 4-substituted 1-methyl-1,2,3,6-tetrahydropyridine derivatives to yield the corresponding 2,3-dihydropyridinium species.	4-substituted 1-methyl-1,2,3,6-tetrahydropyridine	101-150	monoamine oxidase B	Homo sapiens	42-47
9377092-1	1997	The monoamine oxidases A and B (MAO-A and MAO-B) catalyze the alpha-carbon oxidation of a variety of 4-substituted 1-methyl-1,2,3,6-tetrahydropyridine derivatives to yield the corresponding 2,3-dihydropyridinium species.	2,3-dihydropyridinium	190-211	monoamine oxidase B	Homo sapiens	42-47
9377092-3	1997	In this paper we summarize our efforts to exploit this metabolic pathway to develop latent nitrogen mustard derivatives related to the oxazaphosphorine antitumor agent cyclophosphamide which may target MAO-A and/or MAO-B rich cells.	Nitrogen	91-99	monoamine oxidase B	Homo sapiens	215-220
9377092-3	1997	In this paper we summarize our efforts to exploit this metabolic pathway to develop latent nitrogen mustard derivatives related to the oxazaphosphorine antitumor agent cyclophosphamide which may target MAO-A and/or MAO-B rich cells.	oxazaphosphorine	135-151	monoamine oxidase B	Homo sapiens	215-220
9377092-3	1997	In this paper we summarize our efforts to exploit this metabolic pathway to develop latent nitrogen mustard derivatives related to the oxazaphosphorine antitumor agent cyclophosphamide which may target MAO-A and/or MAO-B rich cells.	Cyclophosphamide	168-184	monoamine oxidase B	Homo sapiens	215-220
9159721-6	1997	These results demonstrate that 20 mg weekly is the minimal dosage of selegiline able to induce a maximal and long-lasting inhibition of platelet MAO-B activity in patients with parkinsonism.	Selegiline	69-79	monoamine oxidase B	Homo sapiens	145-150
9432289-4	1997	The inhibition of MAO-A cause the rise of norepinephrine, dopamine and serotonin in the synaptic cleft, of MAO-B only of dopamine.	Norepinephrine	42-56	monoamine oxidase B	Homo sapiens	107-112
9432289-12	1997	of MAO-B, at this time mainly selegiline).	Selegiline	30-40	monoamine oxidase B	Homo sapiens	3-8
9274004-0	1997	Oxazolidinones, dihydrofuranones, and pyrrolidinones as inactivators and substrates of monoamine oxidase B: approaches to the design of antiparkinsonian agents.	Oxazolidinones	0-14	monoamine oxidase B	Homo sapiens	87-106
9274004-0	1997	Oxazolidinones, dihydrofuranones, and pyrrolidinones as inactivators and substrates of monoamine oxidase B: approaches to the design of antiparkinsonian agents.	dihydrofuranones	16-32	monoamine oxidase B	Homo sapiens	87-106
9274004-0	1997	Oxazolidinones, dihydrofuranones, and pyrrolidinones as inactivators and substrates of monoamine oxidase B: approaches to the design of antiparkinsonian agents.	Pyrrolidinones	38-52	monoamine oxidase B	Homo sapiens	87-106
9251066-0	1997	Simultaneous MAO-B and COMT inhibition in L-Dopa-treated patients with Parkinson"s disease.	Levodopa	42-48	monoamine oxidase B	Homo sapiens	13-18
9251066-13	1997	Entacapone decreased erythrocyte COMT activity by > 35% (p < 0.001), and platelet MAO-B activity was almost completely inhibited by selegiline (p < 0.001).	Selegiline	132-142	monoamine oxidase B	Homo sapiens	82-87
9109551-7	1997	Treatment with deprenyl, a monoamine oxidase B inhibitor, produced a complete reversal of MPTP-induced uptake inhibition, but was ineffective following exposure of cells to the MPTP metabolite, 1-methyl-4-phenylpyridinium (MPP+).	Selegiline	15-23	monoamine oxidase B	Homo sapiens	27-46
9109551-7	1997	Treatment with deprenyl, a monoamine oxidase B inhibitor, produced a complete reversal of MPTP-induced uptake inhibition, but was ineffective following exposure of cells to the MPTP metabolite, 1-methyl-4-phenylpyridinium (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	90-94	monoamine oxidase B	Homo sapiens	27-46
9125383-2	1997	This study investigates whether L-deprenyl, an irreversible and selective MAO-B inhibitor, reduces brain damage following global forebrain ischemia in adult gerbils.	Selegiline	32-42	monoamine oxidase B	Homo sapiens	74-79
9065544-1	1997	Selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase type B, is an established adjuvant to levodopa therapy in Parkinson"s disease (PD).	Selegiline	0-10	monoamine oxidase B	Homo sapiens	50-74
9089337-1	1997	Cubylcarbinylamine (1a), (4-cyclopropylcubyl)carbinylamine (1b), and (4-phenylcubyl)carbinylamine (1c) were synthesized and shown to be time-dependent, irreversible inactivators of monoamine oxidase B (MAO B).	cubylcarbinylamine	0-18	monoamine oxidase B	Homo sapiens	202-207
9089337-1	1997	Cubylcarbinylamine (1a), (4-cyclopropylcubyl)carbinylamine (1b), and (4-phenylcubyl)carbinylamine (1c) were synthesized and shown to be time-dependent, irreversible inactivators of monoamine oxidase B (MAO B).	(4-cyclopropylcubyl)carbinylamine	25-58	monoamine oxidase B	Homo sapiens	181-200
9089337-1	1997	Cubylcarbinylamine (1a), (4-cyclopropylcubyl)carbinylamine (1b), and (4-phenylcubyl)carbinylamine (1c) were synthesized and shown to be time-dependent, irreversible inactivators of monoamine oxidase B (MAO B).	(4-phenylcubyl)carbinylamine	69-97	monoamine oxidase B	Homo sapiens	181-200
9089337-1	1997	Cubylcarbinylamine (1a), (4-cyclopropylcubyl)carbinylamine (1b), and (4-phenylcubyl)carbinylamine (1c) were synthesized and shown to be time-dependent, irreversible inactivators of monoamine oxidase B (MAO B).	(4-phenylcubyl)carbinylamine	69-97	monoamine oxidase B	Homo sapiens	202-207
9129714-1	1997	Monoamine oxidase B (MAO-B) is an enzyme that has relevance for Parkinson disease (PD) because of its roles in catabolizing dopamine and potentially activating exogenous neurotoxicants.	Dopamine	124-132	monoamine oxidase B	Homo sapiens	0-19
9129714-1	1997	Monoamine oxidase B (MAO-B) is an enzyme that has relevance for Parkinson disease (PD) because of its roles in catabolizing dopamine and potentially activating exogenous neurotoxicants.	Dopamine	124-132	monoamine oxidase B	Homo sapiens	21-26
9089337-0	1997	4-substituted cubylcarbinylamines: a new class of mechanism-based monoamine oxidase B inactivators.	4-substituted cubylcarbinylamines	0-33	monoamine oxidase B	Homo sapiens	66-85
9089337-1	1997	Cubylcarbinylamine (1a), (4-cyclopropylcubyl)carbinylamine (1b), and (4-phenylcubyl)carbinylamine (1c) were synthesized and shown to be time-dependent, irreversible inactivators of monoamine oxidase B (MAO B).	cubylcarbinylamine	0-18	monoamine oxidase B	Homo sapiens	181-200
9126147-10	1997	The first agent to be tested as a candidate for neuroprotection was the MAO-B inhibitor deprenyl.	Selegiline	88-96	monoamine oxidase B	Homo sapiens	72-77
9089426-1	1997	Orally administered selegiline hydrochloride is a selective monoamine oxidase type B inhibitor at the recommended regimen of 10 mg/day, but it loses selectivity at higher doses.	Selegiline	20-44	monoamine oxidase B	Homo sapiens	60-84
9065544-1	1997	Selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase type B, is an established adjuvant to levodopa therapy in Parkinson"s disease (PD).	Selegiline	12-22	monoamine oxidase B	Homo sapiens	50-74
9076907-2	1997	We have outlined the successful management of canine PDH patients with l-deprenyl, a selective MAO-B inhibitor.	Selegiline	71-81	monoamine oxidase B	Homo sapiens	95-100
9061194-0	1997	Inactivation of monoamine oxidase B by benzyl 1-(aminomethyl) cyclopropane-1-carboxylate.	benzyl 1-(aminomethyl)cyclopropane-1-carboxylate	39-88	monoamine oxidase B	Homo sapiens	16-35
9007048-3	1997	Several reports suggest that R(-)-deprenyl (an MAO-B inhibitor and anti-Parkinsonian drug) may directly or indirectly exert antioxidant effects and thus protect neurons.	r(-)-deprenyl	29-42	monoamine oxidase B	Homo sapiens	47-52
9056051-0	1997	Pharmacokinetics and pharmacodynamics of single and multiple doses of the MAO-B inhibitor lazabemide in healthy subjects.	lazabemide	90-100	monoamine oxidase B	Homo sapiens	74-79
9056051-1	1997	AIMS: The objectives of this study were to assess the tolerability, pharmacokinetics and pharmacodynamics of the reversible monoamine oxidase B (MAO-B) inhibitor, lazabemide, in healthy subjects.	lazabemide	163-173	monoamine oxidase B	Homo sapiens	124-143
9056051-1	1997	AIMS: The objectives of this study were to assess the tolerability, pharmacokinetics and pharmacodynamics of the reversible monoamine oxidase B (MAO-B) inhibitor, lazabemide, in healthy subjects.	lazabemide	163-173	monoamine oxidase B	Homo sapiens	145-150
9056051-10	1997	Lazabemide caused a rapid and reversible inhibition of MAO-B activity in platelets.	lazabemide	0-10	monoamine oxidase B	Homo sapiens	55-60
9056051-16	1997	A dose regimen of lazebemide 100 mg twice daily is anticipated because it caused full and continuous MAO-B inhibition.	lazebemide	18-28	monoamine oxidase B	Homo sapiens	101-106
10728198-4	1997	Treatment with a combination of the AADC cofactor pyridoxine, the monoamine oxidase B inhibitor selegiline and bromocriptine was started during the fifth year of life and showed only a moderate clinical improvement in contrast to patients who have been treated since the first year of life.	Selegiline	96-106	monoamine oxidase B	Homo sapiens	66-85
8978757-1	1997	Selegiline [L-(-)-deprenyl], a monoamine oxidase B inhibitor, has been used in the treatment of Parkinson"s disease as a putative neuroprotective agent.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	31-50
8978757-1	1997	Selegiline [L-(-)-deprenyl], a monoamine oxidase B inhibitor, has been used in the treatment of Parkinson"s disease as a putative neuroprotective agent.	Selegiline	12-26	monoamine oxidase B	Homo sapiens	31-50
9013137-0	1997	Hydroxyl and peroxyl radical trapping by the monoamine oxidase-B inhibitors deprenyl and MDL 72,974A: implications for protection of biological substrates.	Hydroxyl Radical	0-8	monoamine oxidase B	Homo sapiens	45-64
9013137-0	1997	Hydroxyl and peroxyl radical trapping by the monoamine oxidase-B inhibitors deprenyl and MDL 72,974A: implications for protection of biological substrates.	perhydroxyl radical	13-28	monoamine oxidase B	Homo sapiens	45-64
9013137-1	1997	We have examined in vitro radical trapping by the monoamine oxidase-B (MAO-B) inhibitor deprenyl and compared it to the specific MAO-B inhibitor MDL 72,974A.	Selegiline	88-96	monoamine oxidase B	Homo sapiens	50-69
9013137-1	1997	We have examined in vitro radical trapping by the monoamine oxidase-B (MAO-B) inhibitor deprenyl and compared it to the specific MAO-B inhibitor MDL 72,974A.	Selegiline	88-96	monoamine oxidase B	Homo sapiens	71-76
9013137-1	1997	We have examined in vitro radical trapping by the monoamine oxidase-B (MAO-B) inhibitor deprenyl and compared it to the specific MAO-B inhibitor MDL 72,974A.	Mofegiline hydrochloride	145-156	monoamine oxidase B	Homo sapiens	129-134
9013137-7	1997	The data indicate that radical trapping by the MAO-B inhibitors provides differential protection against biological substrates and may involve trapping of secondary peroxyl radicals rather than .OH.	perhydroxyl radical	165-181	monoamine oxidase B	Homo sapiens	47-52
8978707-1	1997	L-Deprenyl is a relatively selective inhibitor of monoamine oxidase (MAO)-B that delays the emergence of disability and the progression of signs and symptoms of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	50-75
9266433-5	1997	Our research into the development of small diffusible molecules that reduce apoptosis has grown from studies of the irreversible MAO-B inhibitor (-)-deprenyl.	Selegiline	145-157	monoamine oxidase B	Homo sapiens	129-134
9116581-9	1997	The covalent labeling of human liver MAO-B was more sensitive than that of placenta MAO-A to inhibition by the imidazoline 2-(4,5-dihydroimidaz-2-yl)-quinoline (BU224).	imidazoline 2-(4,5-dihydroimidaz-2-yl)-quinoline	111-159	monoamine oxidase B	Homo sapiens	37-42
9116581-9	1997	The covalent labeling of human liver MAO-B was more sensitive than that of placenta MAO-A to inhibition by the imidazoline 2-(4,5-dihydroimidaz-2-yl)-quinoline (BU224).	BU 224	161-166	monoamine oxidase B	Homo sapiens	37-42
9116589-5	1997	The density of brain MAO-B sites labeled by [3H]Ro 19-6327 (lazabemide) in suicides was no different to that in age-matched controls.	Tritium	45-47	monoamine oxidase B	Homo sapiens	21-26
9116589-5	1997	The density of brain MAO-B sites labeled by [3H]Ro 19-6327 (lazabemide) in suicides was no different to that in age-matched controls.	lazabemide	60-70	monoamine oxidase B	Homo sapiens	21-26
8987145-1	1997	Monoamine oxidases A and B (MAOA and MAOB) are the major catabolic isoenzymes of catecholamines and serotonin in the mammalian brain.	Catecholamines	81-95	monoamine oxidase B	Homo sapiens	37-41
8987145-1	1997	Monoamine oxidases A and B (MAOA and MAOB) are the major catabolic isoenzymes of catecholamines and serotonin in the mammalian brain.	Serotonin	100-109	monoamine oxidase B	Homo sapiens	37-41
9007048-8	1997	Some different MAO-B inhibitors, namely, the aliphatic N-methylpropargylamines, e.g., (+/-)-M-2-PP [N-(2-pentyl)-N-methylpropargylamine] and N-[2-hexyl]-N-methylpropargylamine, which can also protect and rescue neurons in several in vivo and in vitro models, did not exacerbate the cytotoxicity of dopamine.	n-methylpropargylamines	55-78	monoamine oxidase B	Homo sapiens	15-20
9007048-8	1997	Some different MAO-B inhibitors, namely, the aliphatic N-methylpropargylamines, e.g., (+/-)-M-2-PP [N-(2-pentyl)-N-methylpropargylamine] and N-[2-hexyl]-N-methylpropargylamine, which can also protect and rescue neurons in several in vivo and in vitro models, did not exacerbate the cytotoxicity of dopamine.	N-methyl-N-(2-pentyl)propargylamine	86-98	monoamine oxidase B	Homo sapiens	15-20
9007048-8	1997	Some different MAO-B inhibitors, namely, the aliphatic N-methylpropargylamines, e.g., (+/-)-M-2-PP [N-(2-pentyl)-N-methylpropargylamine] and N-[2-hexyl]-N-methylpropargylamine, which can also protect and rescue neurons in several in vivo and in vitro models, did not exacerbate the cytotoxicity of dopamine.	N-Methyl-N-(2-pentyl)propargylamine	100-135	monoamine oxidase B	Homo sapiens	15-20
26964656-3	1996	In higher doses norharman binds to benzodiazepine receptors and has MAO-B inhibitory activity.	norharman	16-25	monoamine oxidase B	Homo sapiens	68-73
8978500-3	1996	Both MAO-A and MAO-B have relatively equivalent affinities for dopamine, and since PC12 primarily express the A and not the B form of the enzyme, this allowed us to distinguish the transgenic MAO activity in these cells from endogenous using the MAO-B specific substrate PEA.	Dopamine	63-71	monoamine oxidase B	Homo sapiens	15-20
9116194-2	1996	In clinical studies the monoamine oxidase-B inhibitor Selegiline appears to slow the progression of neurological deficits in PD and the cognitive decline in AD.	Selegiline	54-64	monoamine oxidase B	Homo sapiens	24-43
8959982-7	1996	Although not all features of its anti-PD action are known, studies using brain obtained at autopsy from patients who had been treated with 10 mg of selegiline showed that selective inhibition of MAO-B, with the concomitant increase of phenylethylamine and dopamine (DA) but not of serotonin or noradrenaline, in the basal ganglia may be regarded as its mode of action.	Selegiline	148-158	monoamine oxidase B	Homo sapiens	195-200
8959985-11	1996	MAO-B is essential for the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to 1-methyl-4-phenylpyridinium ion, for a component of the enzymatic conversion of dopamine to hydrogen peroxide (H2O2), and for the activation of other potential toxins such as isoquinolines and beta-carbolines.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	41-85	monoamine oxidase B	Homo sapiens	0-5
8959985-11	1996	MAO-B is essential for the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to 1-methyl-4-phenylpyridinium ion, for a component of the enzymatic conversion of dopamine to hydrogen peroxide (H2O2), and for the activation of other potential toxins such as isoquinolines and beta-carbolines.	1-Methyl-4-phenylpyridinium	89-120	monoamine oxidase B	Homo sapiens	0-5
8959985-11	1996	MAO-B is essential for the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to 1-methyl-4-phenylpyridinium ion, for a component of the enzymatic conversion of dopamine to hydrogen peroxide (H2O2), and for the activation of other potential toxins such as isoquinolines and beta-carbolines.	Dopamine	169-177	monoamine oxidase B	Homo sapiens	0-5
8959985-11	1996	MAO-B is essential for the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to 1-methyl-4-phenylpyridinium ion, for a component of the enzymatic conversion of dopamine to hydrogen peroxide (H2O2), and for the activation of other potential toxins such as isoquinolines and beta-carbolines.	Hydrogen Peroxide	181-198	monoamine oxidase B	Homo sapiens	0-5
8959985-11	1996	MAO-B is essential for the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to 1-methyl-4-phenylpyridinium ion, for a component of the enzymatic conversion of dopamine to hydrogen peroxide (H2O2), and for the activation of other potential toxins such as isoquinolines and beta-carbolines.	Hydrogen Peroxide	200-204	monoamine oxidase B	Homo sapiens	0-5
8959985-11	1996	MAO-B is essential for the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to 1-methyl-4-phenylpyridinium ion, for a component of the enzymatic conversion of dopamine to hydrogen peroxide (H2O2), and for the activation of other potential toxins such as isoquinolines and beta-carbolines.	Isoquinolines	264-277	monoamine oxidase B	Homo sapiens	0-5
8959985-11	1996	MAO-B is essential for the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to 1-methyl-4-phenylpyridinium ion, for a component of the enzymatic conversion of dopamine to hydrogen peroxide (H2O2), and for the activation of other potential toxins such as isoquinolines and beta-carbolines.	Carbolines	282-297	monoamine oxidase B	Homo sapiens	0-5
8959985-12	1996	Thus, the inhibition of MAO-B by drugs such as selegiline may protect against activation of some toxins and free radicals formed from the MAO-B oxidation of dopamine.	Selegiline	47-57	monoamine oxidase B	Homo sapiens	24-29
8959985-12	1996	Thus, the inhibition of MAO-B by drugs such as selegiline may protect against activation of some toxins and free radicals formed from the MAO-B oxidation of dopamine.	Selegiline	47-57	monoamine oxidase B	Homo sapiens	138-143
8959985-12	1996	Thus, the inhibition of MAO-B by drugs such as selegiline may protect against activation of some toxins and free radicals formed from the MAO-B oxidation of dopamine.	Dopamine	157-165	monoamine oxidase B	Homo sapiens	24-29
8959985-12	1996	Thus, the inhibition of MAO-B by drugs such as selegiline may protect against activation of some toxins and free radicals formed from the MAO-B oxidation of dopamine.	Dopamine	157-165	monoamine oxidase B	Homo sapiens	138-143
8941389-0	1996	Synthesis and selective monoamine oxidase B-inhibiting properties of 1-methyl-1,2,3,6-tetrahydropyrid-4-yl carbamate derivatives: potential prodrugs of (R)- and (S)-nordeprenyl.	1-methyl-1,2,3,6-tetrahydropyrid-4-yl carbamate	69-116	monoamine oxidase B	Homo sapiens	24-43
8959986-1	1996	(-)-Deprenyl has been used to irreversibly inhibit monoamine oxidase B (MAO-B) in Parkinson"s disease (PD) and Alzheimer"s disease (AD) as a possible means of improving dopaminergic neurotransmission or of reducing neuronal necrosis caused by oxidative radical damage.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	51-70
8959986-1	1996	(-)-Deprenyl has been used to irreversibly inhibit monoamine oxidase B (MAO-B) in Parkinson"s disease (PD) and Alzheimer"s disease (AD) as a possible means of improving dopaminergic neurotransmission or of reducing neuronal necrosis caused by oxidative radical damage.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	72-77
8870990-0	1996	Synthesis and monoamine oxidase B catalyzed oxidation of C-4 heteroaromatic substituted 1,2,3,6-tetrahydropyridine derivatives.	1,2,3,6-Tetrahydropyridine	88-114	monoamine oxidase B	Homo sapiens	14-33
8998375-8	1996	DATA SYNTHESIS: Selegiline is a selective, irreversible inhibitor of monoamine oxidase type B.	Selegiline	16-26	monoamine oxidase B	Homo sapiens	69-93
9086498-13	1996	Platelet MAO-B activity seems to be less sensitive to styrene exposure.	Styrene	54-61	monoamine oxidase B	Homo sapiens	9-14
8809158-0	1996	Assessment of structural requirements for the monoamine oxidase-B-catalyzed oxidation of 1,4-disubstituted-1,2,3,6-tetrahydropyridine derivatives related to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	1,4-disubstituted-1,2,3,6-tetrahydropyridine	89-133	monoamine oxidase B	Homo sapiens	46-65
8809158-0	1996	Assessment of structural requirements for the monoamine oxidase-B-catalyzed oxidation of 1,4-disubstituted-1,2,3,6-tetrahydropyridine derivatives related to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	172-216	monoamine oxidase B	Homo sapiens	46-65
8889283-11	1996	Moclobemide alone exerted a slight inhibition of platelet MAO-B activity.	Moclobemide	0-11	monoamine oxidase B	Homo sapiens	58-63
8994331-1	1996	BACKGROUND: To improve dose-related fluctuations in patients with Parkinson"s disease, the efficacy of selegiline, a selective inhibitor of monoamine oxidase B, was determined.	Selegiline	103-113	monoamine oxidase B	Homo sapiens	140-159
8870990-1	1996	The monoamine oxidase B (MAO-B) catalyzed oxidation of amines has been proposed to proceed via a polar pathway, an initial single-electron transfer pathway and an initial hydrogen atom transfer pathway.	Amines	55-61	monoamine oxidase B	Homo sapiens	4-23
8870990-1	1996	The monoamine oxidase B (MAO-B) catalyzed oxidation of amines has been proposed to proceed via a polar pathway, an initial single-electron transfer pathway and an initial hydrogen atom transfer pathway.	Amines	55-61	monoamine oxidase B	Homo sapiens	25-30
8870990-1	1996	The monoamine oxidase B (MAO-B) catalyzed oxidation of amines has been proposed to proceed via a polar pathway, an initial single-electron transfer pathway and an initial hydrogen atom transfer pathway.	Hydrogen	171-179	monoamine oxidase B	Homo sapiens	4-23
8870990-1	1996	The monoamine oxidase B (MAO-B) catalyzed oxidation of amines has been proposed to proceed via a polar pathway, an initial single-electron transfer pathway and an initial hydrogen atom transfer pathway.	Hydrogen	171-179	monoamine oxidase B	Homo sapiens	25-30
8870990-3	1996	The studies summarized in this paper were undertaken to explore further the structural features that determine the MAO-B substrate and/or inactivator properties of various 1,4-disubstituted tetrahydropyridine derivatives.	1,4-disubstituted tetrahydropyridine	172-208	monoamine oxidase B	Homo sapiens	115-120
8870990-4	1996	We report here the results of our studies on the synthesis and MAO-B catalyzed oxidation of 1-methyl- and 1-cyclopropyl-1,2,3,6-tetrahydropyridine derivatives bearing a variety of heteroaromatic groups at C-4.	1-methyl- and 1-cyclopropyl-1,2,3,6-tetrahydropyridine	92-146	monoamine oxidase B	Homo sapiens	63-68
8870990-5	1996	All of the N-cyclopropyltetrahydropyridine analogs were time and concentration dependent inhibitors of MAO-B while all of the N-methyltetrahydropyridine analogs and the N-cyclopropyl-4-(1-methyl-2-pyrryl)tetrahydropyridine analog were substrates.	1-cyclopropylpiperidine	11-42	monoamine oxidase B	Homo sapiens	103-108
8695909-1	1996	Bacterial cells respond to monoamine compounds, such as tyramine, dopamine, octopamine, or norepinephrine, and induce the syntheses of tyramine oxidase encoded by tynA and monoamine oxidase encoded by maoA.	monoamine	27-36	monoamine oxidase B	Homo sapiens	135-151
8780511-0	1996	Observation of a flavin semiquinone in the resting state of monoamine oxidase B by electron paramagnetic resonance and electron nuclear double resonance spectroscopy.	flavin semiquinone	17-35	monoamine oxidase B	Homo sapiens	60-79
8780511-3	1996	X-Band and Q-band electron paramagnetic resonance (EPR) and electron nuclear double resonance (ENDOR) spectroscopic techniques are employed to characterize a signal assigned as a stable red anionic semiquinone radical in the resting state of MAO B.	semiquinone radicals	198-217	monoamine oxidase B	Homo sapiens	242-247
8780511-7	1996	These results suggest that the two flavin prosthetic groups that exist in catalytically active monoamine oxidase B are physically distinct.	4,6-dinitro-o-cresol	35-41	monoamine oxidase B	Homo sapiens	95-114
8695909-1	1996	Bacterial cells respond to monoamine compounds, such as tyramine, dopamine, octopamine, or norepinephrine, and induce the syntheses of tyramine oxidase encoded by tynA and monoamine oxidase encoded by maoA.	Octopamine	76-86	monoamine oxidase B	Homo sapiens	135-151
8695909-1	1996	Bacterial cells respond to monoamine compounds, such as tyramine, dopamine, octopamine, or norepinephrine, and induce the syntheses of tyramine oxidase encoded by tynA and monoamine oxidase encoded by maoA.	Tyramine	56-64	monoamine oxidase B	Homo sapiens	135-151
8695909-1	1996	Bacterial cells respond to monoamine compounds, such as tyramine, dopamine, octopamine, or norepinephrine, and induce the syntheses of tyramine oxidase encoded by tynA and monoamine oxidase encoded by maoA.	Dopamine	66-74	monoamine oxidase B	Homo sapiens	135-151
8800629-10	1996	As a selective monoamine oxidase type B (MAO-B) inhibitor, selegiline (deprenyl) is free of the "cheese-effect" when employed in recommended dosages.	Selegiline	59-69	monoamine oxidase B	Homo sapiens	15-39
8798928-6	1996	The method was successfully applied to the determination of PEA urinary excretion in Parkinsonian patients after oral administration of the monoamine oxidase B (MAO-B) inhibitor, selegiline.	Selegiline	179-189	monoamine oxidase B	Homo sapiens	140-159
8798928-6	1996	The method was successfully applied to the determination of PEA urinary excretion in Parkinsonian patients after oral administration of the monoamine oxidase B (MAO-B) inhibitor, selegiline.	Selegiline	179-189	monoamine oxidase B	Homo sapiens	161-166
8800629-10	1996	As a selective monoamine oxidase type B (MAO-B) inhibitor, selegiline (deprenyl) is free of the "cheese-effect" when employed in recommended dosages.	Selegiline	59-69	monoamine oxidase B	Homo sapiens	41-46
8800629-10	1996	As a selective monoamine oxidase type B (MAO-B) inhibitor, selegiline (deprenyl) is free of the "cheese-effect" when employed in recommended dosages.	Selegiline	71-79	monoamine oxidase B	Homo sapiens	41-46
8860658-1	1996	Monoamine oxidases (MAO-A and MAO-B) are enzymes that play a key role in the degradation of endogenous and dietary monoamines.	monoamines	115-125	monoamine oxidase B	Homo sapiens	30-35
8628464-2	1996	The oxidative degradation of dopamine, catalyzed by monoamine oxidase type B (MAO-B), produces free radicals and thus could be implicated in the degenerative process.	Dopamine	29-37	monoamine oxidase B	Homo sapiens	52-76
8628464-2	1996	The oxidative degradation of dopamine, catalyzed by monoamine oxidase type B (MAO-B), produces free radicals and thus could be implicated in the degenerative process.	Dopamine	29-37	monoamine oxidase B	Homo sapiens	78-83
8628464-12	1996	We conclude that the presence of MAO-B in dopamine-containing neurons does not contribute to vulnerability in PD.	Dopamine	42-50	monoamine oxidase B	Homo sapiens	33-38
8627546-1	1996	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces a Parkinson-like syndrome through biotransformation by monoamine oxidase B to the neurotoxic metabolite 1-methyl-4-phenylpyridine.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-44	monoamine oxidase B	Homo sapiens	115-134
8627546-1	1996	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces a Parkinson-like syndrome through biotransformation by monoamine oxidase B to the neurotoxic metabolite 1-methyl-4-phenylpyridine.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	46-50	monoamine oxidase B	Homo sapiens	115-134
8627546-1	1996	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces a Parkinson-like syndrome through biotransformation by monoamine oxidase B to the neurotoxic metabolite 1-methyl-4-phenylpyridine.	1-Methyl-4-phenylpyridinium	164-189	monoamine oxidase B	Homo sapiens	115-134
9148606-4	1996	Isatin is a selective inhibitor of monoamine oxidase B.	Isatin	0-6	monoamine oxidase B	Homo sapiens	35-54
11862265-17	1996	The prolonged half-lives of selegiline and N-desmethylselegiline with multiple dosing may be the result of binding to the mitochondrial monoamine oxidase type B pool.	Selegiline	28-38	monoamine oxidase B	Homo sapiens	136-160
11862265-17	1996	The prolonged half-lives of selegiline and N-desmethylselegiline with multiple dosing may be the result of binding to the mitochondrial monoamine oxidase type B pool.	desmethylselegiline	43-64	monoamine oxidase B	Homo sapiens	136-160
8661341-4	1996	As expected, the development of the fluorescence was inhibited by both clorgyline (an MAO-A inhibitor) and deprenyl (an MAO-B inhibitor).	Selegiline	107-115	monoamine oxidase B	Homo sapiens	120-125
8713690-5	1996	Consequently, selegiline (deprenyl), a selective MAO-B inhibitor, was developed for the treatment of idiopathic Parkinson"s disease.	Selegiline	14-24	monoamine oxidase B	Homo sapiens	49-54
8713690-5	1996	Consequently, selegiline (deprenyl), a selective MAO-B inhibitor, was developed for the treatment of idiopathic Parkinson"s disease.	Selegiline	26-34	monoamine oxidase B	Homo sapiens	49-54
8665924-2	1996	The pseudosubstrate inhibitor N-[2-aminoethyl]-5-chloro-2-pyridine carboxamide HCl (lazabemide) can be irreversibly linked to MAO-B by reduction of the enzyme-inhibitor complex with NaBH(3)CN.	n-[2-aminoethyl]-5-chloro-2-pyridine carboxamide hcl	30-82	monoamine oxidase B	Homo sapiens	126-131
8665924-0	1996	Investigation on the structure of the active site of monoamine oxidase-B by affinity labeling with the selective inhibitor lazabemide and by site-directed mutagenesis.	lazabemide	123-133	monoamine oxidase B	Homo sapiens	53-72
8665924-2	1996	The pseudosubstrate inhibitor N-[2-aminoethyl]-5-chloro-2-pyridine carboxamide HCl (lazabemide) can be irreversibly linked to MAO-B by reduction of the enzyme-inhibitor complex with NaBH(3)CN.	lazabemide	84-94	monoamine oxidase B	Homo sapiens	126-131
8665924-2	1996	The pseudosubstrate inhibitor N-[2-aminoethyl]-5-chloro-2-pyridine carboxamide HCl (lazabemide) can be irreversibly linked to MAO-B by reduction of the enzyme-inhibitor complex with NaBH(3)CN.	sodium cyanoborohydride	182-191	monoamine oxidase B	Homo sapiens	126-131
8665924-3	1996	Analysis of the flavin spectrum of [(3)H]lazabemide-labeled human MAO-B indicated that insertion of the inhibitor did not occur into the isoalloxazine ring of FAD.	4,6-dinitro-o-cresol	16-22	monoamine oxidase B	Homo sapiens	66-71
8665924-3	1996	Analysis of the flavin spectrum of [(3)H]lazabemide-labeled human MAO-B indicated that insertion of the inhibitor did not occur into the isoalloxazine ring of FAD.	[(3)h]lazabemide	35-51	monoamine oxidase B	Homo sapiens	66-71
8665924-6	1996	These results indicate that [(3)H]lazabemide is incorporated into the MAO-B peptide stretch containing the FAD-modified Cys397.	[(3)h]lazabemide	28-44	monoamine oxidase B	Homo sapiens	70-75
8665924-6	1996	These results indicate that [(3)H]lazabemide is incorporated into the MAO-B peptide stretch containing the FAD-modified Cys397.	Flavin-Adenine Dinucleotide	107-110	monoamine oxidase B	Homo sapiens	70-75
8665924-8	1996	Substitution of His382 of MAO-B with an Arg greatly reduced the enzymic activity, suggesting that this residue may represent a nucleophile relevant for the MAO-B catalytic mechanism.	Arginine	40-43	monoamine oxidase B	Homo sapiens	26-31
8665924-8	1996	Substitution of His382 of MAO-B with an Arg greatly reduced the enzymic activity, suggesting that this residue may represent a nucleophile relevant for the MAO-B catalytic mechanism.	Arginine	40-43	monoamine oxidase B	Homo sapiens	156-161
8665924-13	1996	We also report that mutation of MAO-B Thr158 (to Ala) resulted in a dramatic loss of enzymic activity.	Alanine	49-52	monoamine oxidase B	Homo sapiens	32-37
8965658-0	1996	Detection of MAO-A and MAO-B mRNAs in monkey brainstem by cross-hybridization with human oligonucleotide probes.	Oligonucleotides	89-104	monoamine oxidase B	Homo sapiens	23-28
8605171-0	1996	Deuterium isotope effect studies on the MAO-B catalyzed oxidation of 4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine.	Deuterium	0-9	monoamine oxidase B	Homo sapiens	40-45
8605171-0	1996	Deuterium isotope effect studies on the MAO-B catalyzed oxidation of 4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine.	4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine	69-118	monoamine oxidase B	Homo sapiens	40-45
8605171-1	1996	Previous studies have established that 1-cyclopropyl-4-phenyl-1,2,3,6-tetrahydropyridine is an efficient time- and concentration-dependent inhibitor of the flavin-containing enzyme monoamine oxidase B (MAO-B).	1-cyclopropyl-4-phenyl-1,2,3,6-tetrahydropyridine	39-88	monoamine oxidase B	Homo sapiens	181-200
8605171-1	1996	Previous studies have established that 1-cyclopropyl-4-phenyl-1,2,3,6-tetrahydropyridine is an efficient time- and concentration-dependent inhibitor of the flavin-containing enzyme monoamine oxidase B (MAO-B).	1-cyclopropyl-4-phenyl-1,2,3,6-tetrahydropyridine	39-88	monoamine oxidase B	Homo sapiens	202-207
8605171-1	1996	Previous studies have established that 1-cyclopropyl-4-phenyl-1,2,3,6-tetrahydropyridine is an efficient time- and concentration-dependent inhibitor of the flavin-containing enzyme monoamine oxidase B (MAO-B).	4,6-dinitro-o-cresol	156-162	monoamine oxidase B	Homo sapiens	181-200
8605171-1	1996	Previous studies have established that 1-cyclopropyl-4-phenyl-1,2,3,6-tetrahydropyridine is an efficient time- and concentration-dependent inhibitor of the flavin-containing enzyme monoamine oxidase B (MAO-B).	4,6-dinitro-o-cresol	156-162	monoamine oxidase B	Homo sapiens	202-207
8605171-3	1996	More recently we have found that, in addition to being an inhibitor, the corresponding 1-cyclopropyl-4-benzyl-1,2,3,6-tetrahydropyridine species is an excellent MAO-B substrate, behavior which may not be consistent with the obligatory formation of a cyclopropylaminyl radical cation intermediate.	4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine	87-136	monoamine oxidase B	Homo sapiens	161-166
8605171-3	1996	More recently we have found that, in addition to being an inhibitor, the corresponding 1-cyclopropyl-4-benzyl-1,2,3,6-tetrahydropyridine species is an excellent MAO-B substrate, behavior which may not be consistent with the obligatory formation of a cyclopropylaminyl radical cation intermediate.	cyclopropylaminyl radical	250-275	monoamine oxidase B	Homo sapiens	161-166
8605171-7	1996	The results are discussed in terms of possible mechanisms for the MAO-B catalyzed oxidation of 1,4-disubstituted 1,2,3,6-tetrahydropyridines.	1,4-disubstituted 1,2,3,6-tetrahydropyridines	95-140	monoamine oxidase B	Homo sapiens	66-71
8613523-8	1996	In contrast, the only biochemical abnormalities detected in subjects with the MAO-B gene deletion are a complete absence of platelet MAO-B activity and an increased urinary excretion of phenylethylamine.	Phenethylamines	186-202	monoamine oxidase B	Homo sapiens	78-83
8618686-6	1996	Chronic treatment with the MAO-B inhibitor, deprenyl (N=16), was not associated with any differences in serum malondialdehyde or plasma 5-S-cysteinyl-dopa concentrations compared with those not treated with deprenyl (N=11).	Selegiline	44-52	monoamine oxidase B	Homo sapiens	27-32
8678123-1	1996	The monoamine oxidases (MAO-A and MAO-B) are the enzymes primarily responsible for the degradation of amine neurotransmitters, such as dopamine, norepinephrine, and serotonin.	Amines	8-13	monoamine oxidase B	Homo sapiens	34-39
8678123-1	1996	The monoamine oxidases (MAO-A and MAO-B) are the enzymes primarily responsible for the degradation of amine neurotransmitters, such as dopamine, norepinephrine, and serotonin.	Dopamine	135-143	monoamine oxidase B	Homo sapiens	34-39
8678123-1	1996	The monoamine oxidases (MAO-A and MAO-B) are the enzymes primarily responsible for the degradation of amine neurotransmitters, such as dopamine, norepinephrine, and serotonin.	Norepinephrine	145-159	monoamine oxidase B	Homo sapiens	34-39
8678123-1	1996	The monoamine oxidases (MAO-A and MAO-B) are the enzymes primarily responsible for the degradation of amine neurotransmitters, such as dopamine, norepinephrine, and serotonin.	Serotonin	165-174	monoamine oxidase B	Homo sapiens	34-39
8613523-9	1996	The differences in neurochemical profiles indicate that, under normal conditions, MAO-A is considerably more important than MAO-B in the metabolism of biogenic amines, a factor likely to contribute to the different clinical phenotypes.	Amines	160-166	monoamine oxidase B	Homo sapiens	124-129
8742074-2	1996	E-2,5-Dimethoxycinnamylamine hydrochloride was designed and synthesized and was found to be an excellent substrate for MAO B (Km = 218 microM, Kcat = 435 min-1).	e-2,5-dimethoxycinnamylamine hydrochloride	0-42	monoamine oxidase B	Homo sapiens	119-124
8929994-3	1996	We have carried out allelic association studies of PD with monoamine oxidase type A (MAOA) and monoamine oxidase type B (MAOB) gene loci using dinucleotide repeat polymorphisms.	Dinucleoside Phosphates	143-155	monoamine oxidase B	Homo sapiens	95-119
8929994-3	1996	We have carried out allelic association studies of PD with monoamine oxidase type A (MAOA) and monoamine oxidase type B (MAOB) gene loci using dinucleotide repeat polymorphisms.	Dinucleoside Phosphates	143-155	monoamine oxidase B	Homo sapiens	121-125
8988458-1	1996	There have been many claims that the selective monoamine oxidase type B (MAO-B) inhibitor selegiline may have distinct properties in slowing the progression of Parkinson"s disease (PD).	Selegiline	90-100	monoamine oxidase B	Homo sapiens	47-71
8791022-5	1996	The addition of direct-acting dopamine agonists or the MAO-B inhibitor selegiline is helpful for short-term improvement.	Selegiline	71-81	monoamine oxidase B	Homo sapiens	55-60
8573115-0	1996	Human anti-mitochondria autoantibodies appearing in iproniazid-induced immunoallergic hepatitis recognize human liver monoamine oxidase B.	Iproniazid	52-62	monoamine oxidase B	Homo sapiens	118-137
8573115-3	1996	Moreover the enzymatic activity of MAO-B towards phenylethylamine and tyramine is also suppressed after this immunoprecipitation, contrary to the MAO-A activity towards 5-hydroxy-tryptamine.	Phenethylamines	49-65	monoamine oxidase B	Homo sapiens	35-40
8573115-3	1996	Moreover the enzymatic activity of MAO-B towards phenylethylamine and tyramine is also suppressed after this immunoprecipitation, contrary to the MAO-A activity towards 5-hydroxy-tryptamine.	Tyramine	70-78	monoamine oxidase B	Homo sapiens	35-40
8573115-3	1996	Moreover the enzymatic activity of MAO-B towards phenylethylamine and tyramine is also suppressed after this immunoprecipitation, contrary to the MAO-A activity towards 5-hydroxy-tryptamine.	Serotonin	169-189	monoamine oxidase B	Homo sapiens	35-40
8836930-5	1996	In contrast, increases (2-3-fold) in both reporter gene expression and enzyme activity were observed after ethanol treatment of cells transfected with MAO-B fragments.	Ethanol	107-114	monoamine oxidase B	Homo sapiens	151-156
8836930-6	1996	Gel retardation analysis showed that ethanol caused changes in transcription factor binding to the MAO-B core promoter in both the SH-SY5Y and 1242 MG cell lines in a cell-type specific fashion.	Ethanol	37-44	monoamine oxidase B	Homo sapiens	99-104
8988458-1	1996	There have been many claims that the selective monoamine oxidase type B (MAO-B) inhibitor selegiline may have distinct properties in slowing the progression of Parkinson"s disease (PD).	Selegiline	90-100	monoamine oxidase B	Homo sapiens	73-78
8988458-12	1996	Under treatment with the MAO-B inhibitor selegiline, the degradation of putrescine via MAO, a key factor in regulating the polyamine metabolism, might be diminished in the Parkinsonian brain, which in turn would suppress the polyamine synthesis.	Selegiline	41-51	monoamine oxidase B	Homo sapiens	25-30
8988458-12	1996	Under treatment with the MAO-B inhibitor selegiline, the degradation of putrescine via MAO, a key factor in regulating the polyamine metabolism, might be diminished in the Parkinsonian brain, which in turn would suppress the polyamine synthesis.	Putrescine	72-82	monoamine oxidase B	Homo sapiens	25-30
8988458-12	1996	Under treatment with the MAO-B inhibitor selegiline, the degradation of putrescine via MAO, a key factor in regulating the polyamine metabolism, might be diminished in the Parkinsonian brain, which in turn would suppress the polyamine synthesis.	Polyamines	123-132	monoamine oxidase B	Homo sapiens	25-30
8988458-12	1996	Under treatment with the MAO-B inhibitor selegiline, the degradation of putrescine via MAO, a key factor in regulating the polyamine metabolism, might be diminished in the Parkinsonian brain, which in turn would suppress the polyamine synthesis.	Polyamines	225-234	monoamine oxidase B	Homo sapiens	25-30
8988458-14	1996	On the other hand, since N1-acetylated spermine and spermidine are also good substrates of MAO-B, it is likely that these compounds will be present in the brain in increased concentrations.	n1-acetylated spermine	25-47	monoamine oxidase B	Homo sapiens	91-96
8988458-14	1996	On the other hand, since N1-acetylated spermine and spermidine are also good substrates of MAO-B, it is likely that these compounds will be present in the brain in increased concentrations.	Spermidine	52-62	monoamine oxidase B	Homo sapiens	91-96
8988460-1	1996	(-)-deprenyl cannot be considered as a simple, selective inhibitor of MAO-B.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	70-75
8988460-3	1996	The MAO-B inhibition could result in a potentiation of the effect and the reduction of the dose of L-dopa, including the restoration of the sensitivity to L-dopa treatment, when the response to the drug has already been diminished or lost.	Levodopa	99-105	monoamine oxidase B	Homo sapiens	4-9
8988460-3	1996	The MAO-B inhibition could result in a potentiation of the effect and the reduction of the dose of L-dopa, including the restoration of the sensitivity to L-dopa treatment, when the response to the drug has already been diminished or lost.	Levodopa	155-161	monoamine oxidase B	Homo sapiens	4-9
8988460-9	1996	The most widely used MAO-B inhibitor in the therapy is (-)-deprenyl and it lacks the "cheese reaction".	Selegiline	55-67	monoamine oxidase B	Homo sapiens	21-26
8988461-1	1996	(-)-Deprenyl stereospecifically reduces neuronal death even after neurons have sustained seemingly lethal damage at concentrations too small to cause monoamine oxidase-B (MAO-B) inhibition.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	150-169
8988461-1	1996	(-)-Deprenyl stereospecifically reduces neuronal death even after neurons have sustained seemingly lethal damage at concentrations too small to cause monoamine oxidase-B (MAO-B) inhibition.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	171-176
8988463-1	1996	Selegiline is a relatively selective inhibitor of monoamine oxidase type B that has been used in Parkinson"s disease as an adjunct to levodopa and as putative neuroprotective therapy.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	50-74
8988463-1	1996	Selegiline is a relatively selective inhibitor of monoamine oxidase type B that has been used in Parkinson"s disease as an adjunct to levodopa and as putative neuroprotective therapy.	Levodopa	134-142	monoamine oxidase B	Homo sapiens	50-74
8614567-2	1995	Further, selegiline, a monoamine oxidase B (MAO) inhibitor (0.125-0.250 microM) enhanced the number of tyrosine hydroxylase (TH)-positive neurons, augmented the high affinity uptake of dopamine (DA), and averted the neurotoxic effects of CSF of PD patients on rat mesencephalic neurons in culture.	Selegiline	9-19	monoamine oxidase B	Homo sapiens	23-42
8632725-7	1996	Furthermore, (AB161-375)A was more sensitive to the MAO-B specific inhibitor deprenyl (IC50 2.7 +/- 0.4 x 10(-8) M) than to the MAO-A specific inhibitor clorgyline (IC50 5.4 +/- 0.8 x 10(-7) M).	Selegiline	77-85	monoamine oxidase B	Homo sapiens	52-57
8876663-3	1996	[3H]Ro41-1049 and [3H]lazabemide, two recently characterized selective radioligands were used to map MAO-A and MAO-B respectively.	[3h]lazabemide	18-32	monoamine oxidase B	Homo sapiens	111-116
8614567-2	1995	Further, selegiline, a monoamine oxidase B (MAO) inhibitor (0.125-0.250 microM) enhanced the number of tyrosine hydroxylase (TH)-positive neurons, augmented the high affinity uptake of dopamine (DA), and averted the neurotoxic effects of CSF of PD patients on rat mesencephalic neurons in culture.	Selegiline	9-19	monoamine oxidase B	Homo sapiens	44-47
7499273-1	1995	Relationship to subtypes of imidazoline-binding proteins and tissue-specific interaction of imidazoline ligands with monoamine oxidase B.	Imidazolines	28-39	monoamine oxidase B	Homo sapiens	117-136
8614567-2	1995	Further, selegiline, a monoamine oxidase B (MAO) inhibitor (0.125-0.250 microM) enhanced the number of tyrosine hydroxylase (TH)-positive neurons, augmented the high affinity uptake of dopamine (DA), and averted the neurotoxic effects of CSF of PD patients on rat mesencephalic neurons in culture.	Dopamine	185-193	monoamine oxidase B	Homo sapiens	23-42
7499273-1	1995	Relationship to subtypes of imidazoline-binding proteins and tissue-specific interaction of imidazoline ligands with monoamine oxidase B.	Imidazolines	92-103	monoamine oxidase B	Homo sapiens	117-136
7499273-9	1995	Restricted access to the imidazoline binding domain on platelet MAO-B was not altered by membrane washing with 500 mM KCl or by solubilization and partial purification of the enzyme suggesting that there are distinct subpopulations of MAO.	Imidazolines	25-36	monoamine oxidase B	Homo sapiens	64-69
8614567-2	1995	Further, selegiline, a monoamine oxidase B (MAO) inhibitor (0.125-0.250 microM) enhanced the number of tyrosine hydroxylase (TH)-positive neurons, augmented the high affinity uptake of dopamine (DA), and averted the neurotoxic effects of CSF of PD patients on rat mesencephalic neurons in culture.	Dopamine	185-193	monoamine oxidase B	Homo sapiens	44-47
8614567-2	1995	Further, selegiline, a monoamine oxidase B (MAO) inhibitor (0.125-0.250 microM) enhanced the number of tyrosine hydroxylase (TH)-positive neurons, augmented the high affinity uptake of dopamine (DA), and averted the neurotoxic effects of CSF of PD patients on rat mesencephalic neurons in culture.	Dopamine	195-197	monoamine oxidase B	Homo sapiens	44-47
8614567-3	1995	The neuroprotective effects of selegiline may be related either to its ability to inhibit MAO B, preventing the generation of free radicals, or to neuronal rescue property due to unknown mechanisms.	Selegiline	31-41	monoamine oxidase B	Homo sapiens	90-95
7559533-0	1995	Flavinylation of monoamine oxidase B. Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of biogenic and xenobiotic amines.	xenobiotic amines	118-135	monoamine oxidase B	Homo sapiens	59-64
8998478-0	1995	[123I/18F] N-(2-aminoethyl)-5-halogeno-2-pyridinecarbox-amides, site specific tracers for MAO-B mapping with SPECT and PET.	[123i/18f] n-(2-aminoethyl)-5-halogeno-2-pyridinecarbox-amides	0-62	monoamine oxidase B	Homo sapiens	90-95
7559533-2	1995	In this study, we developed a novel riboflavin-depleted (Rib-) COS-7 cell line to study the flavinylation of MAO B.	Riboflavin	36-46	monoamine oxidase B	Homo sapiens	109-114
7559533-4	1995	We found that MAO B is expressed equally in the presence or absence of FAD and that apoMAO B can be inserted into the outer mitochondrial membrane.	Flavin-Adenine Dinucleotide	71-74	monoamine oxidase B	Homo sapiens	14-19
7559533-5	1995	Flavinylation of MAO B was achieved by introducing MAO B cDNA and different flavin derivatives simultaneously into Rib- COS-7 cells via electroporation.	4,6-dinitro-o-cresol	76-82	monoamine oxidase B	Homo sapiens	17-22
7559533-6	1995	Since the addition of riboflavin, FMN, or FAD resulted in equal levels of MAO B activity, we conclude that the flavin which initially binds to apoMAO B is FAD.	Riboflavin	22-32	monoamine oxidase B	Homo sapiens	74-79
7559533-6	1995	Since the addition of riboflavin, FMN, or FAD resulted in equal levels of MAO B activity, we conclude that the flavin which initially binds to apoMAO B is FAD.	Flavin Mononucleotide	34-37	monoamine oxidase B	Homo sapiens	74-79
7559533-6	1995	Since the addition of riboflavin, FMN, or FAD resulted in equal levels of MAO B activity, we conclude that the flavin which initially binds to apoMAO B is FAD.	Flavin-Adenine Dinucleotide	42-45	monoamine oxidase B	Homo sapiens	74-79
7559533-6	1995	Since the addition of riboflavin, FMN, or FAD resulted in equal levels of MAO B activity, we conclude that the flavin which initially binds to apoMAO B is FAD.	4,6-dinitro-o-cresol	26-32	monoamine oxidase B	Homo sapiens	74-79
7559533-6	1995	Since the addition of riboflavin, FMN, or FAD resulted in equal levels of MAO B activity, we conclude that the flavin which initially binds to apoMAO B is FAD.	apomao b	143-151	monoamine oxidase B	Homo sapiens	74-79
7559533-6	1995	Since the addition of riboflavin, FMN, or FAD resulted in equal levels of MAO B activity, we conclude that the flavin which initially binds to apoMAO B is FAD.	Flavin-Adenine Dinucleotide	155-158	monoamine oxidase B	Homo sapiens	74-79
7559533-7	1995	In our previous work, we used site-directed mutagenesis to show that Glu34 in the dinucleotide-binding motif of MAO B is essential for MAO B activity, and we postulated that this residue is involved in FAD binding.	Dinucleoside Phosphates	82-94	monoamine oxidase B	Homo sapiens	112-117
7559533-7	1995	In our previous work, we used site-directed mutagenesis to show that Glu34 in the dinucleotide-binding motif of MAO B is essential for MAO B activity, and we postulated that this residue is involved in FAD binding.	Dinucleoside Phosphates	82-94	monoamine oxidase B	Homo sapiens	135-140
7559533-10	1995	Thus, FAD binds to MAO B in a dual manner at Glu34 noncovalently and Cys397 covalently.	Flavin-Adenine Dinucleotide	6-9	monoamine oxidase B	Homo sapiens	19-24
7562919-0	1995	Inhibition of monoamine oxidase-B by 5H-indeno[1,2-c]pyridazines: biological activities, quantitative structure-activity relationships (QSARs) and 3D-QSARs.	5h-indeno[1,2-c]pyridazines	37-64	monoamine oxidase B	Homo sapiens	14-33
7487655-3	1995	The optimal independent roles of the ergot derivatives bromocriptine and pergolide, and the MAOb inhibitor selegiline, are not yet generally agreed although they are accepted as useful in supplementing the effects of levodopa.	Selegiline	107-117	monoamine oxidase B	Homo sapiens	92-96
8535333-15	1995	This new ligand labeled with 123I should therefore be a suitable tool for SPECT exploration of MAO B in the human brain.	Iodine-123	29-33	monoamine oxidase B	Homo sapiens	95-100
7554709-0	1995	Pharmacokinetics and pharmacodynamics of the monoamine oxidase B inhibitor mofegiline assessed during a phase I dose tolerance trial.	mofegiline	75-85	monoamine oxidase B	Homo sapiens	45-64
7554709-4	1995	Mofegiline rapidly and markedly inhibited platelet monoamine oxidase B (MAOB) activity, which returned to baseline within 14 days.	mofegiline	0-10	monoamine oxidase B	Homo sapiens	51-70
7554709-4	1995	Mofegiline rapidly and markedly inhibited platelet monoamine oxidase B (MAOB) activity, which returned to baseline within 14 days.	mofegiline	0-10	monoamine oxidase B	Homo sapiens	72-76
7593732-2	1995	Selegiline (L-deprenyl), a selective inhibitor of MAO-B, ameliorates the "wearing off" akinesia and delays the need for levodopa in mild, previously untreated Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	50-55
7593732-2	1995	Selegiline (L-deprenyl), a selective inhibitor of MAO-B, ameliorates the "wearing off" akinesia and delays the need for levodopa in mild, previously untreated Parkinson"s disease.	Selegiline	12-22	monoamine oxidase B	Homo sapiens	50-55
7626622-8	1995	Variant MAO B enzymes were then characterized with respect to enzymatic activity and [14C]FAD incorporation.	Carbon-14	86-89	monoamine oxidase B	Homo sapiens	8-13
7626622-0	1995	Mutagenesis at a highly conserved tyrosine in monoamine oxidase B affects FAD incorporation and catalytic activity.	Tyrosine	34-42	monoamine oxidase B	Homo sapiens	46-65
7626622-1	1995	Monoamine oxidase B (MAO B), an integral protein of the outer mitochondrial membrane, catalyzes the oxidative deamination of various neuroactive and vasoactive amines.	Amines	160-166	monoamine oxidase B	Homo sapiens	0-19
7555990-3	1995	Deprenyl is an irreversible inhibitor of monoamine oxidase type B (MAO-B) with a very high affinity for the enzyme.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	41-65
7626622-1	1995	Monoamine oxidase B (MAO B), an integral protein of the outer mitochondrial membrane, catalyzes the oxidative deamination of various neuroactive and vasoactive amines.	Amines	160-166	monoamine oxidase B	Homo sapiens	21-26
7626622-2	1995	A covalently bound FAD cofactor at Cys-397 of human MAO B is required for the oxidation of the amine substrates.	Cysteine	35-38	monoamine oxidase B	Homo sapiens	52-57
7626622-2	1995	A covalently bound FAD cofactor at Cys-397 of human MAO B is required for the oxidation of the amine substrates.	Amines	95-100	monoamine oxidase B	Homo sapiens	52-57
7626622-3	1995	In addition to the covalent binding site, MAO B also contains a noncovalent FAD binding region (residues 6-34) known as the dinucleotide binding motif.	Dinucleoside Phosphates	124-136	monoamine oxidase B	Homo sapiens	42-47
7548753-0	1995	Probing the mechanism of bioactivation of MPTP type analogs by monoamine oxidase B: structure-activity studies on substituted 4-phenoxy-, 4-phenyl-, and 4-thiophenoxy-1-cyclopropyl-1,2,3,6-tetrahydropyridines.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	42-46	monoamine oxidase B	Homo sapiens	63-82
7548753-0	1995	Probing the mechanism of bioactivation of MPTP type analogs by monoamine oxidase B: structure-activity studies on substituted 4-phenoxy-, 4-phenyl-, and 4-thiophenoxy-1-cyclopropyl-1,2,3,6-tetrahydropyridines.	4-phenoxy-, 4-phenyl-, and 4-thiophenoxy-1-cyclopropyl-1,2,3,6-tetrahydropyridines	126-208	monoamine oxidase B	Homo sapiens	63-82
7548753-1	1995	Previous studies have shown that 4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine is an excellent monoamine oxidase B (MAO-B) substrate (kappa cat/KM = 1538 min-1 mM-1) although the corresponding 4-phenyl analog displays MAO-B inactivating properties only.	4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine	33-82	monoamine oxidase B	Homo sapiens	99-118
7548753-1	1995	Previous studies have shown that 4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine is an excellent monoamine oxidase B (MAO-B) substrate (kappa cat/KM = 1538 min-1 mM-1) although the corresponding 4-phenyl analog displays MAO-B inactivating properties only.	4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine	33-82	monoamine oxidase B	Homo sapiens	120-125
7548753-1	1995	Previous studies have shown that 4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine is an excellent monoamine oxidase B (MAO-B) substrate (kappa cat/KM = 1538 min-1 mM-1) although the corresponding 4-phenyl analog displays MAO-B inactivating properties only.	4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine	33-82	monoamine oxidase B	Homo sapiens	222-227
7548753-2	1995	This behavior led us to speculate that the pathway for the MAO-B catalyzed oxidation of these tetrahydropyridines may not necessarily proceed via an initial single electron transfer step as proposed by others but rather through an initial alpha-carbon hydrogen atom abstraction step.	Pyrrolidines	94-113	monoamine oxidase B	Homo sapiens	59-64
7548753-2	1995	This behavior led us to speculate that the pathway for the MAO-B catalyzed oxidation of these tetrahydropyridines may not necessarily proceed via an initial single electron transfer step as proposed by others but rather through an initial alpha-carbon hydrogen atom abstraction step.	Carbon	245-251	monoamine oxidase B	Homo sapiens	59-64
7548753-2	1995	This behavior led us to speculate that the pathway for the MAO-B catalyzed oxidation of these tetrahydropyridines may not necessarily proceed via an initial single electron transfer step as proposed by others but rather through an initial alpha-carbon hydrogen atom abstraction step.	Hydrogen	252-260	monoamine oxidase B	Homo sapiens	59-64
7587975-1	1995	Selegiline, an irreversible monoamine oxidase-B (MAO-B) inhibitor, is under investigation as a treatment for cocaine relapse prevention.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	28-47
7587975-1	1995	Selegiline, an irreversible monoamine oxidase-B (MAO-B) inhibitor, is under investigation as a treatment for cocaine relapse prevention.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	49-54
7587975-1	1995	Selegiline, an irreversible monoamine oxidase-B (MAO-B) inhibitor, is under investigation as a treatment for cocaine relapse prevention.	Cocaine	109-116	monoamine oxidase B	Homo sapiens	49-54
7555990-3	1995	Deprenyl is an irreversible inhibitor of monoamine oxidase type B (MAO-B) with a very high affinity for the enzyme.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	67-72
7581172-0	1995	Synthesis and characterization of [125I]N-(2-aminoethyl)-4-iodobenzamide as a selective monoamine oxidase B inhibitor.	[125i]n-(2-aminoethyl)-4-iodobenzamide	34-72	monoamine oxidase B	Homo sapiens	88-107
7790952-1	1995	UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration.	Carbon-11	82-85	monoamine oxidase B	Homo sapiens	46-65
7790952-1	1995	UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration.	Carbon-11	82-85	monoamine oxidase B	Homo sapiens	67-72
7790952-1	1995	UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration.	Carbon-11	82-85	monoamine oxidase B	Homo sapiens	225-230
7790952-1	1995	UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration.	Selegiline	86-96	monoamine oxidase B	Homo sapiens	46-65
7790952-1	1995	UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration.	Selegiline	86-96	monoamine oxidase B	Homo sapiens	67-72
7790952-1	1995	UNLABELLED: Recent human PET studies with the monoamine oxidase B (MAO B) tracer [11C]L-deprenyl show that the rapid rate of radiotracer trapping relative to transport reduces the sensitivity of the tracer in regions of high MAO B concentration.	Selegiline	86-96	monoamine oxidase B	Homo sapiens	225-230
7790952-11	1995	CONCLUSION: This study demonstrates that deuterium substitution causes a significant reduction in the rate of trapping of labeled deprenyl, providing a direct link between radiotracer uptake and MAO B in the human brain and enhancing tracer sensitivity to changes in MAO B concentration.	Deuterium	41-50	monoamine oxidase B	Homo sapiens	195-200
7790952-11	1995	CONCLUSION: This study demonstrates that deuterium substitution causes a significant reduction in the rate of trapping of labeled deprenyl, providing a direct link between radiotracer uptake and MAO B in the human brain and enhancing tracer sensitivity to changes in MAO B concentration.	Deuterium	41-50	monoamine oxidase B	Homo sapiens	267-272
7790952-11	1995	CONCLUSION: This study demonstrates that deuterium substitution causes a significant reduction in the rate of trapping of labeled deprenyl, providing a direct link between radiotracer uptake and MAO B in the human brain and enhancing tracer sensitivity to changes in MAO B concentration.	Selegiline	130-138	monoamine oxidase B	Homo sapiens	195-200
7790952-11	1995	CONCLUSION: This study demonstrates that deuterium substitution causes a significant reduction in the rate of trapping of labeled deprenyl, providing a direct link between radiotracer uptake and MAO B in the human brain and enhancing tracer sensitivity to changes in MAO B concentration.	Selegiline	130-138	monoamine oxidase B	Homo sapiens	267-272
7581172-1	1995	We described the radiosynthesis of an analog of Ro 16-6491, [125I]N-(2-aminoethyl)-4-iodobenzamide, for SPECT exploration of the monoamine oxidase B (MAO-B) in human brain.	ro 16	48-53	monoamine oxidase B	Homo sapiens	129-148
7581172-1	1995	We described the radiosynthesis of an analog of Ro 16-6491, [125I]N-(2-aminoethyl)-4-iodobenzamide, for SPECT exploration of the monoamine oxidase B (MAO-B) in human brain.	ro 16	48-53	monoamine oxidase B	Homo sapiens	150-155
7616414-1	1995	L-Deprenyl (selegiline) is an irreversible inhibitor of monoamine oxidase type B, but also exerts several effects on dopamine and noradrenaline systems independent of monoamine oxidase type B inhibition.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	56-80
7616414-1	1995	L-Deprenyl (selegiline) is an irreversible inhibitor of monoamine oxidase type B, but also exerts several effects on dopamine and noradrenaline systems independent of monoamine oxidase type B inhibition.	Selegiline	12-22	monoamine oxidase B	Homo sapiens	56-80
8544935-1	1995	In the metabolism of one of the main CNS neurotransmitters dopamine very important roles are played by four enzymes: two synthetizing dopamine: TH and DDC, and two enzymes breaking down dopamine: MAO-B and COMT.	Dopamine	59-67	monoamine oxidase B	Homo sapiens	196-201
7581172-1	1995	We described the radiosynthesis of an analog of Ro 16-6491, [125I]N-(2-aminoethyl)-4-iodobenzamide, for SPECT exploration of the monoamine oxidase B (MAO-B) in human brain.	N-(2-Aminoethyl)-4-iodobenzamide	66-98	monoamine oxidase B	Homo sapiens	129-148
7581172-1	1995	We described the radiosynthesis of an analog of Ro 16-6491, [125I]N-(2-aminoethyl)-4-iodobenzamide, for SPECT exploration of the monoamine oxidase B (MAO-B) in human brain.	N-(2-Aminoethyl)-4-iodobenzamide	66-98	monoamine oxidase B	Homo sapiens	150-155
7581172-4	1995	In comparison with Ro 16-6491, the in vitro studies showed a good selectivity of stable N-(2-aminoethyl)-4-iodobenzamide for MAO-B but a slightly lower affinity.	ro 16	19-24	monoamine oxidase B	Homo sapiens	125-130
7581172-4	1995	In comparison with Ro 16-6491, the in vitro studies showed a good selectivity of stable N-(2-aminoethyl)-4-iodobenzamide for MAO-B but a slightly lower affinity.	N-(2-Aminoethyl)-4-iodobenzamide	88-120	monoamine oxidase B	Homo sapiens	125-130
7601156-5	1995	Whereas exchange of the ADP-binding sequence did not modify the catalytic properties of either MAO isoforms, chimeras with increasing length of the NH2-terminus of MAO-A (up to residue 256) showed a marked decrease in affinity towards the MAO-B substrate phenylethylamine and the inhibitor N-(2-aminoethyl)-5-chloro-2-pyridine carboxamide .	Phenethylamines	255-271	monoamine oxidase B	Homo sapiens	239-244
7601156-5	1995	Whereas exchange of the ADP-binding sequence did not modify the catalytic properties of either MAO isoforms, chimeras with increasing length of the NH2-terminus of MAO-A (up to residue 256) showed a marked decrease in affinity towards the MAO-B substrate phenylethylamine and the inhibitor N-(2-aminoethyl)-5-chloro-2-pyridine carboxamide .	lazabemide	290-338	monoamine oxidase B	Homo sapiens	239-244
7727530-8	1995	From substrate specificity and inhibitor susceptibility, it is suggested that the monoamine oxidase from A. niger (MAO-N) is a prototype of the two mammalian enzymes, MAO-A and MAO-B.	mao-n	115-120	monoamine oxidase B	Homo sapiens	177-182
7770050-6	1995	Analysis of the deduced amino acid sequence indicates that MAO-N is structurally related to the human monoamine oxidases MAO-A and MAO-B.	spizofurone	59-64	monoamine oxidase B	Homo sapiens	131-136
7618127-5	1995	Activity of monoamine oxidase B (MAO-B) in platelets was found to be inversely correlated with the levels of exposure to styrene, suggesting that this biochemical measurement may be a useful effect-related biomarker, though additional studies are needed to understand the mechanistic implications of these findings.	Styrene	121-128	monoamine oxidase B	Homo sapiens	12-31
7618127-5	1995	Activity of monoamine oxidase B (MAO-B) in platelets was found to be inversely correlated with the levels of exposure to styrene, suggesting that this biochemical measurement may be a useful effect-related biomarker, though additional studies are needed to understand the mechanistic implications of these findings.	Styrene	121-128	monoamine oxidase B	Homo sapiens	33-38
7618158-4	1995	Since DBH is an expression of catecholamine release, the relative increase in such activity could be envisaged as a compensatory mechanism to a reduced turnover rate as reflected by MAO-B activity.	Catecholamines	30-43	monoamine oxidase B	Homo sapiens	182-187
7783122-0	1995	Studies on the monoamine oxidase (MAO)-catalyzed oxidation of phenyl-substituted 1-methyl-4-phenoxy-1,2,3,6-tetrahydropyridine derivatives: factors contributing to MAO-A and MAO-B selectivity.	phenyl-substituted 1-methyl-4-phenoxy-1,2,3,6-tetrahydropyridine	62-126	monoamine oxidase B	Homo sapiens	174-179
7651456-7	1995	The acute inhibition of amino acid decarboxylase, monoamine oxidase-B, and COMT is well tolerated and prolongs the L-DOPA response in PD patients.	Levodopa	115-121	monoamine oxidase B	Homo sapiens	50-69
7840641-0	1995	Characterization of a dinucleotide-binding site in monoamine oxidase B by site-directed mutagenesis.	Dinucleoside Phosphates	22-34	monoamine oxidase B	Homo sapiens	51-70
7830050-1	1995	L-3,4-Dihydroxyphenylalanine (L-dopa) is toxic for human neuroblastoma cells NB69 and its toxicity is related to several mechanisms including quinone formation and enhanced production of free radicals related to the metabolism of dopamine via monoamine oxidase type B.	Levodopa	0-28	monoamine oxidase B	Homo sapiens	243-267
7830050-1	1995	L-3,4-Dihydroxyphenylalanine (L-dopa) is toxic for human neuroblastoma cells NB69 and its toxicity is related to several mechanisms including quinone formation and enhanced production of free radicals related to the metabolism of dopamine via monoamine oxidase type B.	Levodopa	30-36	monoamine oxidase B	Homo sapiens	243-267
7830050-1	1995	L-3,4-Dihydroxyphenylalanine (L-dopa) is toxic for human neuroblastoma cells NB69 and its toxicity is related to several mechanisms including quinone formation and enhanced production of free radicals related to the metabolism of dopamine via monoamine oxidase type B.	Free Radicals	187-200	monoamine oxidase B	Homo sapiens	243-267
7830050-1	1995	L-3,4-Dihydroxyphenylalanine (L-dopa) is toxic for human neuroblastoma cells NB69 and its toxicity is related to several mechanisms including quinone formation and enhanced production of free radicals related to the metabolism of dopamine via monoamine oxidase type B.	Dopamine	230-238	monoamine oxidase B	Homo sapiens	243-267
7756620-1	1995	Using immunohistochemistry, we investigated in the cat the effects of MPTP, a Parkinsonian syndrome-inducing substance, on brain type B monoamine oxidase (MAO-B) which is responsible for the conversion of MPTP to its neurotoxic product (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	70-74	monoamine oxidase B	Homo sapiens	155-160
7756620-1	1995	Using immunohistochemistry, we investigated in the cat the effects of MPTP, a Parkinsonian syndrome-inducing substance, on brain type B monoamine oxidase (MAO-B) which is responsible for the conversion of MPTP to its neurotoxic product (MPP+).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	205-209	monoamine oxidase B	Homo sapiens	155-160
7756620-4	1995	In addition, the MPTP-induced paradoxical sleep suppression might be related to this raphe MAO-B loss.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	17-21	monoamine oxidase B	Homo sapiens	91-96
7872875-2	1995	OBJECTIVES: To determine whether cerebrospinal fluid (CSF) homovanillic acid (HVA) concentration in subjects with early, mild Parkinson"s disease (PD) treated with the monoamine oxidase type B inhibitor selegiline hydrochloride differs from that of control subjects receiving placebo.	Selegiline	203-227	monoamine oxidase B	Homo sapiens	168-192
7617809-1	1995	The effect of haloperidol and its metabolites on human platelet monoamine oxidase B (MAO-B) and human placenta monoamine oxidase A (MAO-A) in vitro has been investigated.	Haloperidol	14-25	monoamine oxidase B	Homo sapiens	85-90
7617809-3	1995	HP+ appeared to be a reversible, uncompetitive and selective MAO-B inhibitor with a Ki of 0.83 microM.	histidylproline	0-3	monoamine oxidase B	Homo sapiens	61-66
7617809-4	1995	HTP was found to be an irreversible, uncompetitive and selective MAO-B inhibitor (Ki of 1.84 microM).	htp	0-3	monoamine oxidase B	Homo sapiens	65-70
7828725-0	1995	Inhibition of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine metabolic activity of porcine FAD-containing monooxygenase by selective monoamine oxidase-B inhibitors.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	14-58	monoamine oxidase B	Homo sapiens	131-150
7828725-1	1995	The MPTP metabolic activity of porcine FAD-containing monooxygenase (FMO) (EC 1.14.13.8) was inhibited considerably by deprenyl and pargyline, selective MAO-B inhibitors, and they showed typical competitive inhibition.	Selegiline	119-127	monoamine oxidase B	Homo sapiens	153-158
7840641-1	1995	Monoamine oxidase B (MAO B), an integral protein of the outer mitochondrial membrane, catalyzes the oxidative deamination of neuroactive and vasoactive amines.	Amines	152-158	monoamine oxidase B	Homo sapiens	0-19
7840641-1	1995	Monoamine oxidase B (MAO B), an integral protein of the outer mitochondrial membrane, catalyzes the oxidative deamination of neuroactive and vasoactive amines.	Amines	152-158	monoamine oxidase B	Homo sapiens	21-26
7840641-3	1995	In this study, we have examined the role of one amino acid (Glu34) in human MAO B that is thought to play a crucial role in binding to the 2"-hydroxy group of ribose in the AMP moiety of FAD.	Ribose	159-165	monoamine oxidase B	Homo sapiens	76-81
7840641-3	1995	In this study, we have examined the role of one amino acid (Glu34) in human MAO B that is thought to play a crucial role in binding to the 2"-hydroxy group of ribose in the AMP moiety of FAD.	Adenosine Monophosphate	173-176	monoamine oxidase B	Homo sapiens	76-81
7840641-3	1995	In this study, we have examined the role of one amino acid (Glu34) in human MAO B that is thought to play a crucial role in binding to the 2"-hydroxy group of ribose in the AMP moiety of FAD.	Flavin-Adenine Dinucleotide	187-190	monoamine oxidase B	Homo sapiens	76-81
7840641-4	1995	Glu34 is located within a region of the MAO B molecule of high sequence identity to the dinucleotide-binding site in other flavoproteins.	Dinucleoside Phosphates	88-100	monoamine oxidase B	Homo sapiens	40-45
7840641-5	1995	In MAO B, this region is postulated to consist of a beta 1-sheet-alpha-helix-beta 2-sheet motif which culminates with a Glu at the C-terminal end of the second beta-sheet.	Glutamic Acid	120-123	monoamine oxidase B	Homo sapiens	3-8
8695059-2	1995	Qualitative and quantitative analysis for MAO-B was provided by kinetic studies with a specific radioligand, [3H]lazabemide.	[3h]lazabemide	109-123	monoamine oxidase B	Homo sapiens	42-47
7697377-0	1995	Responses of forebrain neurons to the MAO-B blocker L-deprenyl.	Selegiline	52-62	monoamine oxidase B	Homo sapiens	38-43
8847600-0	1995	SAR studies of fluorine-substituted benzylamines and substituted 2-phenylethylamines as substrates and inactivators of monoamine oxidase B.	Fluorine	15-23	monoamine oxidase B	Homo sapiens	119-138
8847600-0	1995	SAR studies of fluorine-substituted benzylamines and substituted 2-phenylethylamines as substrates and inactivators of monoamine oxidase B.	Benzylamines	36-48	monoamine oxidase B	Homo sapiens	119-138
8847600-0	1995	SAR studies of fluorine-substituted benzylamines and substituted 2-phenylethylamines as substrates and inactivators of monoamine oxidase B.	phenethylamine	65-84	monoamine oxidase B	Homo sapiens	119-138
8527006-2	1995	We have previously identified one of them, isatin, which is a selective inhibitor of MAO B.	Isatin	43-49	monoamine oxidase B	Homo sapiens	85-90
7618520-0	1995	Aliphatic propargylamines, a new series of potent selective, irreversible non-amphetamine-like MAO-B inhibitors.	aliphatic propargylamines	0-25	monoamine oxidase B	Homo sapiens	95-100
7618520-0	1995	Aliphatic propargylamines, a new series of potent selective, irreversible non-amphetamine-like MAO-B inhibitors.	Amphetamine	78-89	monoamine oxidase B	Homo sapiens	95-100
7618520-2	1995	1-Deprenyl, a selective irreversible MAO-B inhibitor, has been shown to prolong the onset of disability in Parkinson"s patients and to improve cognitive behavior in Alzheimer"s disease.	1-deprenyl	0-10	monoamine oxidase B	Homo sapiens	37-42
7618520-5	1995	It is yet to be established whether or not the effects are unique to 1-deprenyl; a drug which possesses, in addition to inhibition of MAO-B activity, an amphetamine moiety.	1-deprenyl	69-79	monoamine oxidase B	Homo sapiens	134-139
7618520-6	1995	Based on the fact that several N-methylpropargylamine derivatives have been shown to be MAO inhibitors and that aliphatic amines are typical MAO-B substrates with a high affinity for the enzyme, we have synthesized a series of aliphatic propargylamines which have turned out to be highly potent, selective and irreversible MAO-B inhibitors, structurally unrelated to amphetamine.	diethanolamine	112-128	monoamine oxidase B	Homo sapiens	141-146
7618520-6	1995	Based on the fact that several N-methylpropargylamine derivatives have been shown to be MAO inhibitors and that aliphatic amines are typical MAO-B substrates with a high affinity for the enzyme, we have synthesized a series of aliphatic propargylamines which have turned out to be highly potent, selective and irreversible MAO-B inhibitors, structurally unrelated to amphetamine.	diethanolamine	112-128	monoamine oxidase B	Homo sapiens	323-328
7618520-6	1995	Based on the fact that several N-methylpropargylamine derivatives have been shown to be MAO inhibitors and that aliphatic amines are typical MAO-B substrates with a high affinity for the enzyme, we have synthesized a series of aliphatic propargylamines which have turned out to be highly potent, selective and irreversible MAO-B inhibitors, structurally unrelated to amphetamine.	aliphatic propargylamines	227-252	monoamine oxidase B	Homo sapiens	141-146
7618520-6	1995	Based on the fact that several N-methylpropargylamine derivatives have been shown to be MAO inhibitors and that aliphatic amines are typical MAO-B substrates with a high affinity for the enzyme, we have synthesized a series of aliphatic propargylamines which have turned out to be highly potent, selective and irreversible MAO-B inhibitors, structurally unrelated to amphetamine.	aliphatic propargylamines	227-252	monoamine oxidase B	Homo sapiens	323-328
7618520-10	1995	Inhibitors with relatively short carbon chain lengths (i.e. four to six carbons) were found to be more potent at inhibiting brain MAO-B activity in vivo especially after oral administration.	Carbon	33-39	monoamine oxidase B	Homo sapiens	130-135
7618520-10	1995	Inhibitors with relatively short carbon chain lengths (i.e. four to six carbons) were found to be more potent at inhibiting brain MAO-B activity in vivo especially after oral administration.	Carbon	72-79	monoamine oxidase B	Homo sapiens	130-135
7669938-4	1995	(-)deprenyl, the first selective inhibitor of MAO-B described in literature, has become the universally used research tool for selectively blocking B-type MAO.	Selegiline	3-11	monoamine oxidase B	Homo sapiens	46-51
8748632-1	1995	The addition of a dopamine agonist and of a monoamine oxidase type B inhibitor to I-dopa has been suggested in the therapy of Parkinson"s disease.	i-dopa	82-88	monoamine oxidase B	Homo sapiens	44-68
8748635-4	1995	High concentrations of the dopamimetic substances L-DOPA slightly and the monoamine oxidase B inhibitor selegiline more effectively inhibit SOD activity.	Selegiline	104-114	monoamine oxidase B	Homo sapiens	74-93
8748635-5	1995	The MAO-B inhibitor RO 16-6491 (N-(2-aminoethyl)-4-chlorobenzamide hydrochloride) has no effect on SOD enzyme activity.	Ro 16-6491	20-30	monoamine oxidase B	Homo sapiens	4-9
8748607-3	1995	Moreover, there is evidence suggesting that MAO-B inhibition might protect DA neurons from oxidative stress.	Dopamine	75-77	monoamine oxidase B	Homo sapiens	44-49
7695025-8	1994	However, MAO B activity obtained during medium- and long-term abstinence was significantly lowered in patients with high novelty-seeking and impulsiveness scores in the TPQ, a history of suicide attempts, or an alcoholic mother.	6-hydroxydopa quinone	169-172	monoamine oxidase B	Homo sapiens	9-14
7711493-3	1995	The administration of PEA or of its precursor L-phenylalanine improves mood in depressed patients treated with a selective monoamine oxidase B inhibitor.	Phenethylamines	22-25	monoamine oxidase B	Homo sapiens	123-142
7711493-3	1995	The administration of PEA or of its precursor L-phenylalanine improves mood in depressed patients treated with a selective monoamine oxidase B inhibitor.	Phenylalanine	46-61	monoamine oxidase B	Homo sapiens	123-142
8584655-1	1995	We have observed that the survival of dopamine neuroblastoma (SH-SY5Y) cells in co-cultures with C-6 glioma in serum-deprived media is slightly but significantly enhanced by R-(-)-deprenyl, a selective monoamine oxidase B inhibitor.	Dopamine	38-46	monoamine oxidase B	Homo sapiens	202-221
8584655-1	1995	We have observed that the survival of dopamine neuroblastoma (SH-SY5Y) cells in co-cultures with C-6 glioma in serum-deprived media is slightly but significantly enhanced by R-(-)-deprenyl, a selective monoamine oxidase B inhibitor.	r-(-)-deprenyl	174-188	monoamine oxidase B	Homo sapiens	202-221
7993913-0	1994	Hydrogen tunneling in the flavoenzyme monoamine oxidase B.	Hydrogen	0-8	monoamine oxidase B	Homo sapiens	38-57
7993913-1	1994	Competitive kH/kT and kD/kT kinetic isotope effects on p-methoxybenzylamine oxidation by the 8 alpha-S-cysteinyl flavin adenine dinucleotide (FAD)-dependent enzyme monoamine oxidase B (MAO-B) have been measured as a function of temperature.	4-methoxybenzylamine	55-75	monoamine oxidase B	Homo sapiens	164-183
7993913-1	1994	Competitive kH/kT and kD/kT kinetic isotope effects on p-methoxybenzylamine oxidation by the 8 alpha-S-cysteinyl flavin adenine dinucleotide (FAD)-dependent enzyme monoamine oxidase B (MAO-B) have been measured as a function of temperature.	4-methoxybenzylamine	55-75	monoamine oxidase B	Homo sapiens	185-190
7993913-1	1994	Competitive kH/kT and kD/kT kinetic isotope effects on p-methoxybenzylamine oxidation by the 8 alpha-S-cysteinyl flavin adenine dinucleotide (FAD)-dependent enzyme monoamine oxidase B (MAO-B) have been measured as a function of temperature.	8 alpha-s-cysteinyl flavin adenine dinucleotide	93-140	monoamine oxidase B	Homo sapiens	164-183
7993913-1	1994	Competitive kH/kT and kD/kT kinetic isotope effects on p-methoxybenzylamine oxidation by the 8 alpha-S-cysteinyl flavin adenine dinucleotide (FAD)-dependent enzyme monoamine oxidase B (MAO-B) have been measured as a function of temperature.	8 alpha-s-cysteinyl flavin adenine dinucleotide	93-140	monoamine oxidase B	Homo sapiens	185-190
7993913-1	1994	Competitive kH/kT and kD/kT kinetic isotope effects on p-methoxybenzylamine oxidation by the 8 alpha-S-cysteinyl flavin adenine dinucleotide (FAD)-dependent enzyme monoamine oxidase B (MAO-B) have been measured as a function of temperature.	Flavin-Adenine Dinucleotide	142-145	monoamine oxidase B	Homo sapiens	164-183
7993913-1	1994	Competitive kH/kT and kD/kT kinetic isotope effects on p-methoxybenzylamine oxidation by the 8 alpha-S-cysteinyl flavin adenine dinucleotide (FAD)-dependent enzyme monoamine oxidase B (MAO-B) have been measured as a function of temperature.	Flavin-Adenine Dinucleotide	142-145	monoamine oxidase B	Homo sapiens	185-190
7995014-2	1994	Although not all features of its antiParkinson action are known, studies that used brains obtained at autopsy from patients who took l-deprenyl show that the selective inhibition of MAO-B with a concomitant increase of phenylethylamine and dopamine, but not of serotonin or noradrenaline, in the basal ganglia may be responsible for its mode of action.	Selegiline	133-143	monoamine oxidase B	Homo sapiens	182-187
7995014-2	1994	Although not all features of its antiParkinson action are known, studies that used brains obtained at autopsy from patients who took l-deprenyl show that the selective inhibition of MAO-B with a concomitant increase of phenylethylamine and dopamine, but not of serotonin or noradrenaline, in the basal ganglia may be responsible for its mode of action.	Dopamine	240-248	monoamine oxidase B	Homo sapiens	182-187
7995014-2	1994	Although not all features of its antiParkinson action are known, studies that used brains obtained at autopsy from patients who took l-deprenyl show that the selective inhibition of MAO-B with a concomitant increase of phenylethylamine and dopamine, but not of serotonin or noradrenaline, in the basal ganglia may be responsible for its mode of action.	Serotonin	261-270	monoamine oxidase B	Homo sapiens	182-187
7995014-2	1994	Although not all features of its antiParkinson action are known, studies that used brains obtained at autopsy from patients who took l-deprenyl show that the selective inhibition of MAO-B with a concomitant increase of phenylethylamine and dopamine, but not of serotonin or noradrenaline, in the basal ganglia may be responsible for its mode of action.	Norepinephrine	274-287	monoamine oxidase B	Homo sapiens	182-187
7995015-1	1994	l-Deprenyl is a selective, irreversible monoamine oxidase (MAO) type B inhibitor.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	40-70
7995015-2	1994	Dopamine is a relatively good MAO-B substrate in the human brain.	Dopamine	0-8	monoamine oxidase B	Homo sapiens	30-35
7995015-3	1994	Because Parkinson"s disease is characterized by a decrease in dopaminergic neurotransmission in the basal ganglia, the selective inhibition of MAO-B should lead to diminished metabolism of dopamine in the nigrostriatal system and a significant increase in the concentration of the neurotransmitter.	Dopamine	62-70	monoamine oxidase B	Homo sapiens	143-148
7995015-4	1994	MAO-B inhibition explains the clinical efficacy of l-deprenyl in the treatment of Parkinson"s disease and the prevention of the conversion of protoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is oxidized by MAO-B and can cause a parkinsonian syndrome, to their active neurotoxin.	Selegiline	51-61	monoamine oxidase B	Homo sapiens	0-5
7995015-4	1994	MAO-B inhibition explains the clinical efficacy of l-deprenyl in the treatment of Parkinson"s disease and the prevention of the conversion of protoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is oxidized by MAO-B and can cause a parkinsonian syndrome, to their active neurotoxin.	Selegiline	51-61	monoamine oxidase B	Homo sapiens	227-232
7995015-4	1994	MAO-B inhibition explains the clinical efficacy of l-deprenyl in the treatment of Parkinson"s disease and the prevention of the conversion of protoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is oxidized by MAO-B and can cause a parkinsonian syndrome, to their active neurotoxin.	protoxins	142-151	monoamine oxidase B	Homo sapiens	0-5
7995015-4	1994	MAO-B inhibition explains the clinical efficacy of l-deprenyl in the treatment of Parkinson"s disease and the prevention of the conversion of protoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is oxidized by MAO-B and can cause a parkinsonian syndrome, to their active neurotoxin.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	160-204	monoamine oxidase B	Homo sapiens	0-5
7995015-4	1994	MAO-B inhibition explains the clinical efficacy of l-deprenyl in the treatment of Parkinson"s disease and the prevention of the conversion of protoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is oxidized by MAO-B and can cause a parkinsonian syndrome, to their active neurotoxin.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	160-204	monoamine oxidase B	Homo sapiens	227-232
7995015-5	1994	In addition, l-deprenyl appears to exhibit other biochemical actions that are independent of its MAO-B activity.	Selegiline	13-23	monoamine oxidase B	Homo sapiens	97-102
7696527-0	1994	Mechanistic studies on the monoamine oxidase B catalyzed oxidation of 1,4-disubstituted tetrahydropyridines.	1,4-disubstituted tetrahydropyridines	70-107	monoamine oxidase B	Homo sapiens	27-46
7721026-3	1994	1-Deprenyl (selegiline), an archetypical MAO-B inhibitor, alone does not seem to exert an antidepressive effect, however, it may become useful when administered in combination with amine neurotransmitter precursors.	1-deprenyl	0-10	monoamine oxidase B	Homo sapiens	41-46
7721026-3	1994	1-Deprenyl (selegiline), an archetypical MAO-B inhibitor, alone does not seem to exert an antidepressive effect, however, it may become useful when administered in combination with amine neurotransmitter precursors.	Selegiline	12-22	monoamine oxidase B	Homo sapiens	41-46
7721026-4	1994	MAO-B inhibitors are useful adjunct drugs to 1-DOPA in the symptomatic treatment of Parkinson"s disease.	1-dopa	45-51	monoamine oxidase B	Homo sapiens	0-5
7721026-7	1994	MAO-B inhibitors can selectively and dramatically increase the level of beta-phenylethylamine, which has been shown to potentiate dopamine and noradrenaline function in the central nervous system.	phenethylamine	72-93	monoamine oxidase B	Homo sapiens	0-5
7721026-7	1994	MAO-B inhibitors can selectively and dramatically increase the level of beta-phenylethylamine, which has been shown to potentiate dopamine and noradrenaline function in the central nervous system.	Dopamine	130-138	monoamine oxidase B	Homo sapiens	0-5
7721026-7	1994	MAO-B inhibitors can selectively and dramatically increase the level of beta-phenylethylamine, which has been shown to potentiate dopamine and noradrenaline function in the central nervous system.	Norepinephrine	143-156	monoamine oxidase B	Homo sapiens	0-5
7696527-1	1994	Previous studies have established that 1-cyclopropyl-4-phenyl-1,2,3,6- tetrahydropyridine (6) is an efficient time and concentration dependent inhibitor of the flavin containing enzyme monoamine oxidase B (MAO-B).	1-cyclopropyl-4-phenyl-1,2,3,6-tetrahydropyridine	39-89	monoamine oxidase B	Homo sapiens	185-204
7696527-1	1994	Previous studies have established that 1-cyclopropyl-4-phenyl-1,2,3,6- tetrahydropyridine (6) is an efficient time and concentration dependent inhibitor of the flavin containing enzyme monoamine oxidase B (MAO-B).	1-cyclopropyl-4-phenyl-1,2,3,6-tetrahydropyridine	39-89	monoamine oxidase B	Homo sapiens	206-211
7696527-1	1994	Previous studies have established that 1-cyclopropyl-4-phenyl-1,2,3,6- tetrahydropyridine (6) is an efficient time and concentration dependent inhibitor of the flavin containing enzyme monoamine oxidase B (MAO-B).	4,6-dinitro-o-cresol	160-166	monoamine oxidase B	Homo sapiens	185-204
7696527-1	1994	Previous studies have established that 1-cyclopropyl-4-phenyl-1,2,3,6- tetrahydropyridine (6) is an efficient time and concentration dependent inhibitor of the flavin containing enzyme monoamine oxidase B (MAO-B).	4,6-dinitro-o-cresol	160-166	monoamine oxidase B	Homo sapiens	206-211
7696527-4	1994	We now have examined the MAO-B inactivator and substrate properties of 4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine (11).	4-benzyl-1-cyclopropyl-1,2,3,6-tetrahydropyridine	71-120	monoamine oxidase B	Homo sapiens	25-30
7696527-7	1994	These results are discussed in terms of possible catalytic pathways for the MAO-B catalyzed oxidation of 1,4-disubstituted-1,2,3,6- tetrahydropyridines.	1,4-disubstituted-1,2,3,6- tetrahydropyridines	105-151	monoamine oxidase B	Homo sapiens	76-81
7953696-0	1994	The MAO-B inhibitor deprenyl, but not the MAO-A inhibitor clorgyline, potentiates the neurotoxicity of p-chloroamphetamine.	Selegiline	20-28	monoamine oxidase B	Homo sapiens	4-9
7839316-0	1994	Slow recovery of human brain MAO B after L-deprenyl (Selegeline) withdrawal.	Selegiline	41-51	monoamine oxidase B	Homo sapiens	29-34
7839316-0	1994	Slow recovery of human brain MAO B after L-deprenyl (Selegeline) withdrawal.	selegeline	53-63	monoamine oxidase B	Homo sapiens	29-34
7839316-1	1994	L-Deprenyl (Selegeline) is an enzyme-activated irreversible inhibitor of monoamine oxidase B (MAO B; EC 1.4.3.4).	Selegiline	0-10	monoamine oxidase B	Homo sapiens	73-92
7839316-1	1994	L-Deprenyl (Selegeline) is an enzyme-activated irreversible inhibitor of monoamine oxidase B (MAO B; EC 1.4.3.4).	Selegiline	0-10	monoamine oxidase B	Homo sapiens	94-99
7839316-1	1994	L-Deprenyl (Selegeline) is an enzyme-activated irreversible inhibitor of monoamine oxidase B (MAO B; EC 1.4.3.4).	selegeline	12-22	monoamine oxidase B	Homo sapiens	73-92
7839316-1	1994	L-Deprenyl (Selegeline) is an enzyme-activated irreversible inhibitor of monoamine oxidase B (MAO B; EC 1.4.3.4).	selegeline	12-22	monoamine oxidase B	Homo sapiens	94-99
7839316-4	1994	We have measured a 40 day half-time for brain MAO B synthesis in Parkinson"s disease and in normal subjects after withdrawal from L-deprenyl.	Selegiline	130-140	monoamine oxidase B	Homo sapiens	46-51
7839316-7	1994	The slow turnover of brain MAO B suggests that the current clinical dose of L-deprenyl may be excessive and that the clinical efficacy of reduced dosing should be evaluated.	Selegiline	76-86	monoamine oxidase B	Homo sapiens	27-32
7821682-0	1994	Biochemical and pharmacological evaluation of 2,4-difluorobenzyldimethylsilylmethanamine, a new highly selective inhibitor of monoamine oxidase-B.	2,4-difluorobenzyldimethylsilylmethanamine	46-88	monoamine oxidase B	Homo sapiens	126-145
8000982-1	1994	The use of the combination of fluoxetine, an anti-depressant serotonin uptake inhibitor, and selegiline, a monoamine oxidase -B inhibitor, was reviewed in a large population of patients with Parkinson"s disease.	Selegiline	93-103	monoamine oxidase B	Homo sapiens	107-127
7955818-1	1994	The effects of monoamine oxidase B (MAO-B) inhibition by mofegiline on the pharmacokinetics of p-tyramine and its major metabolite, p-hydroxyphenylacetic acid, were investigated in 24 healthy male volunteers.	mofegiline	57-67	monoamine oxidase B	Homo sapiens	36-41
7955818-1	1994	The effects of monoamine oxidase B (MAO-B) inhibition by mofegiline on the pharmacokinetics of p-tyramine and its major metabolite, p-hydroxyphenylacetic acid, were investigated in 24 healthy male volunteers.	Tyramine	95-105	monoamine oxidase B	Homo sapiens	36-41
7955818-6	1994	The data suggest that mofegiline maintains its selectivity for MAO-B in the intestine and liver at doses up to and including 24 mg.	mofegiline	22-32	monoamine oxidase B	Homo sapiens	63-68
8000101-1	1994	To confirm the clinical utility of selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase B, as an anti-Parkinson"s disease (PD) agent, the first Japanese multi-center, double-blind comparative study of this drug was conducted.	Selegiline	35-45	monoamine oxidase B	Homo sapiens	85-104
8000101-1	1994	To confirm the clinical utility of selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase B, as an anti-Parkinson"s disease (PD) agent, the first Japanese multi-center, double-blind comparative study of this drug was conducted.	Selegiline	47-57	monoamine oxidase B	Homo sapiens	85-104
7816197-4	1994	Using tritiated monoamine oxidase inhibitors (Ro41-1049 and lazabemide)--as high affinity substrates selective for monoamine oxidases A and B, respectively--it was found that monoamine oxidase B activity increased up to three-fold exclusively in temporal, parietal and frontal cortices of Alzheimer disease cases compared with controls.	Ro 41-1049	46-55	monoamine oxidase B	Homo sapiens	175-194
7816197-4	1994	Using tritiated monoamine oxidase inhibitors (Ro41-1049 and lazabemide)--as high affinity substrates selective for monoamine oxidases A and B, respectively--it was found that monoamine oxidase B activity increased up to three-fold exclusively in temporal, parietal and frontal cortices of Alzheimer disease cases compared with controls.	lazabemide	60-70	monoamine oxidase B	Homo sapiens	175-194
7816197-10	1994	The up-regulation of monoamine oxidase B in plaque-associated astrocytes in Alzheimer"s disease--in analogy to its proposed role in neurodegenerative disorders such as Parkinson"s disease--might, indirectly, be a potential source of cytotoxic free radicals.	Free Radicals	243-256	monoamine oxidase B	Homo sapiens	21-40
7816197-11	1994	Lazabemide, a selective reversible monoamine oxidase B inhibitor, is currently under clinical evaluation for the treatment of Parkinson"s and Alzheimer"s diseases.	lazabemide	0-10	monoamine oxidase B	Homo sapiens	35-54
8071874-1	1994	It is now generally accepted that the nigrostriatal degenerative properties of the parkinsonian-inducing agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine are mediated by the brain monoamine oxidase B generated 1-methyl-4-phenylpyridinium metabolite (MPP+).	methyl-4-phenyl-1,2,3,6-tetrahydropyridine	113-155	monoamine oxidase B	Homo sapiens	182-201
8071874-1	1994	It is now generally accepted that the nigrostriatal degenerative properties of the parkinsonian-inducing agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine are mediated by the brain monoamine oxidase B generated 1-methyl-4-phenylpyridinium metabolite (MPP+).	1-Methyl-4-phenylpyridinium	212-239	monoamine oxidase B	Homo sapiens	182-201
8071874-1	1994	It is now generally accepted that the nigrostriatal degenerative properties of the parkinsonian-inducing agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine are mediated by the brain monoamine oxidase B generated 1-methyl-4-phenylpyridinium metabolite (MPP+).	mangion-purified polysaccharide (Candida albicans)	252-255	monoamine oxidase B	Homo sapiens	182-201
7981318-0	1994	An enzymatic assay for the MAO-B inhibitor selegiline in plasma.	Selegiline	43-53	monoamine oxidase B	Homo sapiens	27-32
7953696-0	1994	The MAO-B inhibitor deprenyl, but not the MAO-A inhibitor clorgyline, potentiates the neurotoxicity of p-chloroamphetamine.	p-Chloroamphetamine	103-122	monoamine oxidase B	Homo sapiens	4-9
7953696-4	1994	However, co-administration of the MAO-B selective inhibitor deprenyl (1 mg/kg) or the non-selective inhibitor pargyline (50 mg/kg) produced significant decreases in radioligand binding.	Selegiline	60-68	monoamine oxidase B	Homo sapiens	34-39
7953696-9	1994	Administration of deprenyl or pargyline, together with pCA, itself a MAO-A inhibitor, will lead to inhibition of both MAO-A and MAO-B activities.	Selegiline	18-26	monoamine oxidase B	Homo sapiens	128-133
7953696-9	1994	Administration of deprenyl or pargyline, together with pCA, itself a MAO-A inhibitor, will lead to inhibition of both MAO-A and MAO-B activities.	Pargyline	30-39	monoamine oxidase B	Homo sapiens	128-133
7993928-1	1994	Both low and high platelet MAO-B (pMAO-B) activity is considered an indicator of increased vulnerability in psychopathology.	pmao-b	34-40	monoamine oxidase B	Homo sapiens	27-32
7917773-0	1994	Pharmacodynamics of lazabemide, a reversible and selective inhibitor of monoamine oxidase B.	lazabemide	20-30	monoamine oxidase B	Homo sapiens	72-91
7917773-2	1994	The inhibition of monoamine oxidase B (MAO-B) by lazabemide was measured in platelets collected from 35 young (19-36 years) and 40 older (60-78 years) healthy volunteers after single (100-300 mg) and multiple (100-350 mg twice daily) oral doses respectively.	lazabemide	49-59	monoamine oxidase B	Homo sapiens	18-37
7917773-2	1994	The inhibition of monoamine oxidase B (MAO-B) by lazabemide was measured in platelets collected from 35 young (19-36 years) and 40 older (60-78 years) healthy volunteers after single (100-300 mg) and multiple (100-350 mg twice daily) oral doses respectively.	lazabemide	49-59	monoamine oxidase B	Homo sapiens	39-44
8044048-0	1994	Phenylethylamine relieves depression after selective MAO-B inhibition.	Phenethylamines	0-16	monoamine oxidase B	Homo sapiens	53-58
8158148-0	1994	Oxidation products arising from the action of monoamine oxidase B on 1-methyl-4-benzyl-1,2,3,6-tetrahydropyridine, a nonneurotoxic analogue of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	4-benzyl-1-methyl-1,2,3,6-tetrahydropyridine	69-113	monoamine oxidase B	Homo sapiens	46-65
8158148-0	1994	Oxidation products arising from the action of monoamine oxidase B on 1-methyl-4-benzyl-1,2,3,6-tetrahydropyridine, a nonneurotoxic analogue of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	143-187	monoamine oxidase B	Homo sapiens	46-65
8158148-1	1994	1-Methyl-4-benzyl-1,2,3,6-tetrahydropyridine (MBzTP), an analogue of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, despite its rapid oxidation by monoamine oxidase B (MAO B), is not neurotoxic.	4-benzyl-1-methyl-1,2,3,6-tetrahydropyridine	0-44	monoamine oxidase B	Homo sapiens	161-180
8158148-1	1994	1-Methyl-4-benzyl-1,2,3,6-tetrahydropyridine (MBzTP), an analogue of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, despite its rapid oxidation by monoamine oxidase B (MAO B), is not neurotoxic.	4-benzyl-1-methyl-1,2,3,6-tetrahydropyridine	0-44	monoamine oxidase B	Homo sapiens	182-187
8158148-1	1994	1-Methyl-4-benzyl-1,2,3,6-tetrahydropyridine (MBzTP), an analogue of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, despite its rapid oxidation by monoamine oxidase B (MAO B), is not neurotoxic.	4-benzyl-1-methyl-1,2,3,6-tetrahydropyridine	46-51	monoamine oxidase B	Homo sapiens	161-180
8158148-1	1994	1-Methyl-4-benzyl-1,2,3,6-tetrahydropyridine (MBzTP), an analogue of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, despite its rapid oxidation by monoamine oxidase B (MAO B), is not neurotoxic.	4-benzyl-1-methyl-1,2,3,6-tetrahydropyridine	46-51	monoamine oxidase B	Homo sapiens	182-187
8158148-1	1994	1-Methyl-4-benzyl-1,2,3,6-tetrahydropyridine (MBzTP), an analogue of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, despite its rapid oxidation by monoamine oxidase B (MAO B), is not neurotoxic.	neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine	73-128	monoamine oxidase B	Homo sapiens	161-180
8158148-1	1994	1-Methyl-4-benzyl-1,2,3,6-tetrahydropyridine (MBzTP), an analogue of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, despite its rapid oxidation by monoamine oxidase B (MAO B), is not neurotoxic.	neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine	73-128	monoamine oxidase B	Homo sapiens	182-187
8158148-4	1994	Incubation of MBzTP with purified MAO B yields first the dihydropyridinium form, then a mixture of the pyridinium form and another unidentified product, in proportions that depend on the concentrations of MAO B and oxygen.	4-benzyl-1-methyl-1,2,3,6-tetrahydropyridine	14-19	monoamine oxidase B	Homo sapiens	34-39
8158148-4	1994	Incubation of MBzTP with purified MAO B yields first the dihydropyridinium form, then a mixture of the pyridinium form and another unidentified product, in proportions that depend on the concentrations of MAO B and oxygen.	4-benzyl-1-methyl-1,2,3,6-tetrahydropyridine	14-19	monoamine oxidase B	Homo sapiens	205-210
8158148-4	1994	Incubation of MBzTP with purified MAO B yields first the dihydropyridinium form, then a mixture of the pyridinium form and another unidentified product, in proportions that depend on the concentrations of MAO B and oxygen.	dihydropyridinium	57-74	monoamine oxidase B	Homo sapiens	34-39
8158148-4	1994	Incubation of MBzTP with purified MAO B yields first the dihydropyridinium form, then a mixture of the pyridinium form and another unidentified product, in proportions that depend on the concentrations of MAO B and oxygen.	pyridine	64-74	monoamine oxidase B	Homo sapiens	34-39
8158148-4	1994	Incubation of MBzTP with purified MAO B yields first the dihydropyridinium form, then a mixture of the pyridinium form and another unidentified product, in proportions that depend on the concentrations of MAO B and oxygen.	Oxygen	215-221	monoamine oxidase B	Homo sapiens	34-39
8155011-2	1994	BACKGROUND: Lazabemide (Ro 19-6327) is a short-acting, reversible, highly selective inhibitor of monoamine oxidase type B, that, unlike selegiline (deprenyl), is not metabolized to active compounds.	lazabemide	12-22	monoamine oxidase B	Homo sapiens	97-121
8155011-2	1994	BACKGROUND: Lazabemide (Ro 19-6327) is a short-acting, reversible, highly selective inhibitor of monoamine oxidase type B, that, unlike selegiline (deprenyl), is not metabolized to active compounds.	lazabemide	24-34	monoamine oxidase B	Homo sapiens	97-121
8155011-11	1994	CONCLUSIONS: The overall safety of lazabemide observed in this short-term study justifies further long-term investigations to determine if this monoamine oxidase type B inhibitor is a useful adjuvant to levodopa therapy in Parkinson"s disease.	lazabemide	35-45	monoamine oxidase B	Homo sapiens	144-168
8151621-2	1994	The expected dihydropyridinium metabolites generated from these MAO-A- and MAO-B-catalyzed oxidations of the 4-(aryloxy)tetrahydropyridine analogs were found to undergo rapid hydrolytic cleavage to yield the corresponding arenol and 1-methyl-2,3-dihydro-4-pyridone, a species that could be monitored spectrophotometrically.	dihydropyridinium	13-30	monoamine oxidase B	Homo sapiens	75-80
8151621-2	1994	The expected dihydropyridinium metabolites generated from these MAO-A- and MAO-B-catalyzed oxidations of the 4-(aryloxy)tetrahydropyridine analogs were found to undergo rapid hydrolytic cleavage to yield the corresponding arenol and 1-methyl-2,3-dihydro-4-pyridone, a species that could be monitored spectrophotometrically.	4-(aryloxy)tetrahydropyridine	109-138	monoamine oxidase B	Homo sapiens	75-80
8161354-4	1994	Incubation with clorgyline and deprenyl, probe inhibitors of MAO-A and MAO-B, respectively, showed that [14C]sumatriptan was metabolized by MAO-A; there was no evidence of P450 involvement in its metabolism.	Carbon-14	105-108	monoamine oxidase B	Homo sapiens	71-76
8151621-2	1994	The expected dihydropyridinium metabolites generated from these MAO-A- and MAO-B-catalyzed oxidations of the 4-(aryloxy)tetrahydropyridine analogs were found to undergo rapid hydrolytic cleavage to yield the corresponding arenol and 1-methyl-2,3-dihydro-4-pyridone, a species that could be monitored spectrophotometrically.	Arenol	222-228	monoamine oxidase B	Homo sapiens	75-80
8151621-2	1994	The expected dihydropyridinium metabolites generated from these MAO-A- and MAO-B-catalyzed oxidations of the 4-(aryloxy)tetrahydropyridine analogs were found to undergo rapid hydrolytic cleavage to yield the corresponding arenol and 1-methyl-2,3-dihydro-4-pyridone, a species that could be monitored spectrophotometrically.	1-methyl-2,3-dihydro-4-pyridone	233-264	monoamine oxidase B	Homo sapiens	75-80
8151621-3	1994	We have exploited this reaction sequence to probe the active sites of beef liver MAO-B and human placental MAO-A with a variety of 4-(aryloxy)-1-methyl-1,2,3,6-tetrahydropyridine derivatives.	4-(aryloxy)-1-methyl-1,2,3,6-tetrahydropyridine	131-178	monoamine oxidase B	Homo sapiens	81-86
8151621-4	1994	The results are discussed in relationship to recently published reports describing the MAO-A vs MAO-B selectivity of various 4-(arylmethyl)tetrahydropyridine derivatives.	4-(arylmethyl)tetrahydropyridine	125-157	monoamine oxidase B	Homo sapiens	96-101
8161354-4	1994	Incubation with clorgyline and deprenyl, probe inhibitors of MAO-A and MAO-B, respectively, showed that [14C]sumatriptan was metabolized by MAO-A; there was no evidence of P450 involvement in its metabolism.	Clorgyline	16-26	monoamine oxidase B	Homo sapiens	71-76
8161354-4	1994	Incubation with clorgyline and deprenyl, probe inhibitors of MAO-A and MAO-B, respectively, showed that [14C]sumatriptan was metabolized by MAO-A; there was no evidence of P450 involvement in its metabolism.	Selegiline	31-39	monoamine oxidase B	Homo sapiens	71-76
8161354-4	1994	Incubation with clorgyline and deprenyl, probe inhibitors of MAO-A and MAO-B, respectively, showed that [14C]sumatriptan was metabolized by MAO-A; there was no evidence of P450 involvement in its metabolism.	Sumatriptan	109-120	monoamine oxidase B	Homo sapiens	71-76
8289189-1	1994	1-Methyl-1,2,3,6-tetrahydrostilbazole (MTHS) and its analogs are oxidized by monoamine oxidase (MAO) A at slow rates comparable to that for the structurally similar neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, but the rates of oxidation by MAO B vary over a wide range depending on the structure of the analog.	1-methyl-1,2,3,6-tetrahydrostilbazole	0-37	monoamine oxidase B	Homo sapiens	253-258
8289189-1	1994	1-Methyl-1,2,3,6-tetrahydrostilbazole (MTHS) and its analogs are oxidized by monoamine oxidase (MAO) A at slow rates comparable to that for the structurally similar neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, but the rates of oxidation by MAO B vary over a wide range depending on the structure of the analog.	1-methyl-1,2,3,6-tetrahydrostilbazole	39-43	monoamine oxidase B	Homo sapiens	253-258
8289189-4	1994	The corresponding pyridinium forms of trans-MTHS and its analogs were more potent inhibitors of MAO A (Ki values between 0.3 and 5 microM) than of MAO B, for which the Ki values varied greatly.	pyridine	18-28	monoamine oxidase B	Homo sapiens	147-152
9358191-5	1994	Selegiline is a monoamine oxidase-B inhibitor; once thought to affect the pathogenesis of idiopathic parkinsonism, it is now known to offer only symptomatic relief.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	16-35
7896422-0	1994	Platelet monoamine oxidase B activity in workers exposed to styrene.	Styrene	60-67	monoamine oxidase B	Homo sapiens	9-28
8828003-4	1994	Although the molecular identity of the I1 binding site remains unknown, an I2 receptive site has been reported to be encoded by monoamine oxidase genes (both MAO-A and MAO-B), suggesting a novel explanation for the antidepressant efficacy of idazoxan, a prototypic I2 ligand.	Idazoxan	242-250	monoamine oxidase B	Homo sapiens	168-173
7896422-1	1994	A cross-sectional study was conducted to evaluate monoamine oxidase type B (MAO-B) activity in platelets as a biomarker of effect of styrene and perchloroethylene exposures.	Styrene	133-140	monoamine oxidase B	Homo sapiens	50-74
7896422-1	1994	A cross-sectional study was conducted to evaluate monoamine oxidase type B (MAO-B) activity in platelets as a biomarker of effect of styrene and perchloroethylene exposures.	Styrene	133-140	monoamine oxidase B	Homo sapiens	76-81
7896422-1	1994	A cross-sectional study was conducted to evaluate monoamine oxidase type B (MAO-B) activity in platelets as a biomarker of effect of styrene and perchloroethylene exposures.	Tetrachloroethylene	145-162	monoamine oxidase B	Homo sapiens	50-74
7896422-1	1994	A cross-sectional study was conducted to evaluate monoamine oxidase type B (MAO-B) activity in platelets as a biomarker of effect of styrene and perchloroethylene exposures.	Tetrachloroethylene	145-162	monoamine oxidase B	Homo sapiens	76-81
7896422-2	1994	MAO-B is an enzyme system involved in dopamine catabolism, the impairment of which has been postulated as a mechanism of styrene-induced neurotoxicity.	Dopamine	38-46	monoamine oxidase B	Homo sapiens	0-5
7896422-2	1994	MAO-B is an enzyme system involved in dopamine catabolism, the impairment of which has been postulated as a mechanism of styrene-induced neurotoxicity.	Styrene	121-128	monoamine oxidase B	Homo sapiens	0-5
7896422-3	1994	We previously observed an inverse association between blood styrene and MAO-B among reinforced plastics manufacturing workers.	Styrene	60-67	monoamine oxidase B	Homo sapiens	72-77
7896422-7	1994	MAO-B activity (pmol/10(8) cells/h) was measured in peripheral blood platelets, using phenylethylamine as substrate.	Phenethylamines	86-102	monoamine oxidase B	Homo sapiens	0-5
7896422-9	1994	Despite the absence of gross differences among the groups, styrene exposure was inversely related to MAO-B.	Styrene	59-66	monoamine oxidase B	Homo sapiens	101-106
7896422-11	1994	The Spearman rank correlation coefficient for styrene with MAO-B was -0.41.	Styrene	46-53	monoamine oxidase B	Homo sapiens	59-64
7931223-2	1994	Among these derivatives U-1424 [N-methyl-N-propargyl-(2-furyl-1-methyl)-ethyl ammonium] and J-508 [N-methyl-N-propargyl-(1-indanyl) ammonium] preserved the selectivity to MAO-B, but the former is slightly less potent inhibitor of the enzyme, while J-508 is more effective than the parent compound.	n-methyl-n-propargyl-(2-furyl-1-methyl)-ethyl ammonium	32-86	monoamine oxidase B	Homo sapiens	171-176
7884399-1	1994	Attempts to lessen the progression of Parkinson"s Disease (PD) have made use of 2 strategies: inhibition of monoamine oxidase type B with deprenyl (selegiline) and the free radical trapping agent alpha-tocopherol (vitamin E).	Selegiline	138-146	monoamine oxidase B	Homo sapiens	108-132
7884399-1	1994	Attempts to lessen the progression of Parkinson"s Disease (PD) have made use of 2 strategies: inhibition of monoamine oxidase type B with deprenyl (selegiline) and the free radical trapping agent alpha-tocopherol (vitamin E).	Selegiline	148-158	monoamine oxidase B	Homo sapiens	108-132
7931223-2	1994	Among these derivatives U-1424 [N-methyl-N-propargyl-(2-furyl-1-methyl)-ethyl ammonium] and J-508 [N-methyl-N-propargyl-(1-indanyl) ammonium] preserved the selectivity to MAO-B, but the former is slightly less potent inhibitor of the enzyme, while J-508 is more effective than the parent compound.	n-methyl-n-propargyl-(1-indanyl) ammonium	99-140	monoamine oxidase B	Homo sapiens	171-176
7931223-8	1994	PFD is slightly less potent inhibitor of MAO-B in vitro than deprenyl but it maintains a more prolonged concentration in tissues.	pfd	0-3	monoamine oxidase B	Homo sapiens	41-46
7931231-1	1994	In this paper we present results from a double blind cross over trial with deprenyl, a selective and irreversible monoamine oxidase-B (MAO-B) inhibitor, in 10 patients suffering from amyotrophic lateral sclerosis.	Selegiline	75-83	monoamine oxidase B	Homo sapiens	114-133
7931231-1	1994	In this paper we present results from a double blind cross over trial with deprenyl, a selective and irreversible monoamine oxidase-B (MAO-B) inhibitor, in 10 patients suffering from amyotrophic lateral sclerosis.	Selegiline	75-83	monoamine oxidase B	Homo sapiens	135-140
7931231-6	1994	MAO-B activity in blood platelets was completely inhibited during treatment with deprenyl.	Selegiline	81-89	monoamine oxidase B	Homo sapiens	0-5
7931241-3	1994	However, unlike clorgyline, it was selective towards MAO-B, both in its initial, non-covalent, binding to the enzyme and as an irreversible inhibitor.	Clorgyline	16-26	monoamine oxidase B	Homo sapiens	53-58
7931232-7	1994	Moreover, the concentration of MAO-B was highly correlated with glial cell counts in thionine stained sections in various regions of the spinal cord, both in controls and ALS cases.	thionine	85-93	monoamine oxidase B	Homo sapiens	31-36
7931233-1	1994	Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night.	Selegiline	63-73	monoamine oxidase B	Homo sapiens	46-51
7931233-1	1994	Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night.	Selegiline	63-73	monoamine oxidase B	Homo sapiens	164-169
7931233-1	1994	Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night.	Selegiline	75-85	monoamine oxidase B	Homo sapiens	46-51
7931233-1	1994	Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night.	Selegiline	75-85	monoamine oxidase B	Homo sapiens	164-169
7931235-2	1994	In addition, the rational for using selegiline as a neuroprotector in Parkinson"s disease may also be applicable in Alzheimer"s disease in which a dramatic increase in the MAO-B activity has been reported.	Selegiline	36-46	monoamine oxidase B	Homo sapiens	172-177
7931238-4	1994	The kinetic behaviour of the parent amines as MAO A and MAO B inhibitors and substrates was determined.	Amines	36-42	monoamine oxidase B	Homo sapiens	56-61
7931241-11	1994	In the case of MAO-B inhibition, the 2 and 3 carbon-chain compounds had similar inhibitory potencies but this increased substantially when the chain length was increased to 4 carbons.	Carbon	45-51	monoamine oxidase B	Homo sapiens	15-20
7931238-6	1994	These parameters will allow us to establish the correlation with structural features that predetermine one compound to be a good MAO substrate or a good MAO A and MAO B inhibitor.	predetermine	90-102	monoamine oxidase B	Homo sapiens	163-168
7931241-11	1994	In the case of MAO-B inhibition, the 2 and 3 carbon-chain compounds had similar inhibitory potencies but this increased substantially when the chain length was increased to 4 carbons.	Carbon	175-182	monoamine oxidase B	Homo sapiens	15-20
7931243-0	1994	Kinetics of inhibition of MAO-B by N-(2-aminoethyl)-p-chlorobenzamide (Ro 16-6491) and analogues.	4-CHLORO-N-(2-HYDROXYETHYL)BENZAMIDE	35-69	monoamine oxidase B	Homo sapiens	26-31
7931256-1	1994	Straight and branched chain aliphatic monoamines, which are not normal tissue constituents, are deaminated selectively by type B monoamine oxidase (MAO-B).	aliphatic monoamines	28-48	monoamine oxidase B	Homo sapiens	148-153
7931256-3	1994	An anticonvulsant prodrug, Milacemide [2-(N-pentyl)glycinamide] is deaminated by MAO-B and this facilitates a mechanism of delivering glycine into the CNS.	milacemide	27-37	monoamine oxidase B	Homo sapiens	81-86
7931243-1	1994	Ro 16-6491 is known to be a potent reversible inhibitor of human brain MAO-B.	Ro 16-6491	0-10	monoamine oxidase B	Homo sapiens	71-76
7931256-3	1994	An anticonvulsant prodrug, Milacemide [2-(N-pentyl)glycinamide] is deaminated by MAO-B and this facilitates a mechanism of delivering glycine into the CNS.	2-(n-pentyl)glycinamide	39-62	monoamine oxidase B	Homo sapiens	81-86
7931245-2	1994	The selectivity of MAO-B inhibition of L, selegiline and MDL 72974 was also measured in vitro in human brain tissue as well as ex vivo in rat brain and liver after acute and subchronic administration.	Selegiline	42-52	monoamine oxidase B	Homo sapiens	19-24
7931256-3	1994	An anticonvulsant prodrug, Milacemide [2-(N-pentyl)glycinamide] is deaminated by MAO-B and this facilitates a mechanism of delivering glycine into the CNS.	Glycine	134-141	monoamine oxidase B	Homo sapiens	81-86
7931256-4	1994	We have found that 2-propyl-pentylamine (2-propyl-1-aminopentane) and N-(2-propylpentyl)glycinamide are also converted by MAO-B to valproic acid and glycine both in vitro and in vivo; these compounds, however, cause severe tremor.	2-Propyl-1-aminopentane	19-39	monoamine oxidase B	Homo sapiens	122-127
7931257-2	1994	Potent inhibition of MAO-B and SSAO occurred with fluoroallylamines whereas chloroallylamines, such as MDL 72274A ((E)-2-phenyl-3-chloroallylamine hydrochloride), were selective and potent inhibitors of SSAO.	fluoroallylamines	50-67	monoamine oxidase B	Homo sapiens	21-26
7931256-4	1994	We have found that 2-propyl-pentylamine (2-propyl-1-aminopentane) and N-(2-propylpentyl)glycinamide are also converted by MAO-B to valproic acid and glycine both in vitro and in vivo; these compounds, however, cause severe tremor.	2-propyl-1-aminopentane	41-64	monoamine oxidase B	Homo sapiens	122-127
7931256-4	1994	We have found that 2-propyl-pentylamine (2-propyl-1-aminopentane) and N-(2-propylpentyl)glycinamide are also converted by MAO-B to valproic acid and glycine both in vitro and in vivo; these compounds, however, cause severe tremor.	N-(2-propylpentyl)glycinamide	70-99	monoamine oxidase B	Homo sapiens	122-127
7931257-3	1994	MDL 72974A (E)-2-(4-fluorophenethyl)-3-fluoroallylamine hydrochloride is a potent (IC50 = 10(-9) M) inhibitor of both MAO-B and SSAO, with 190-fold lower affinity for MAO-A.	mofegiline	0-10	monoamine oxidase B	Homo sapiens	118-123
7931256-4	1994	We have found that 2-propyl-pentylamine (2-propyl-1-aminopentane) and N-(2-propylpentyl)glycinamide are also converted by MAO-B to valproic acid and glycine both in vitro and in vivo; these compounds, however, cause severe tremor.	Valproic Acid	131-144	monoamine oxidase B	Homo sapiens	122-127
7931257-3	1994	MDL 72974A (E)-2-(4-fluorophenethyl)-3-fluoroallylamine hydrochloride is a potent (IC50 = 10(-9) M) inhibitor of both MAO-B and SSAO, with 190-fold lower affinity for MAO-A.	e)-2-(4-fluorophenethyl)-3-fluoroallylamine hydrochloride	12-69	monoamine oxidase B	Homo sapiens	118-123
7931257-7	1994	MAO-B inhibitors, such as MDL 72974A and L-deprenyl, offer the potential of being neuroprotective in Parkinson"s Disease and other neurogenerative disorders.	mofegiline	26-36	monoamine oxidase B	Homo sapiens	0-5
7931256-4	1994	We have found that 2-propyl-pentylamine (2-propyl-1-aminopentane) and N-(2-propylpentyl)glycinamide are also converted by MAO-B to valproic acid and glycine both in vitro and in vivo; these compounds, however, cause severe tremor.	Glycine	149-156	monoamine oxidase B	Homo sapiens	122-127
7931257-7	1994	MAO-B inhibitors, such as MDL 72974A and L-deprenyl, offer the potential of being neuroprotective in Parkinson"s Disease and other neurogenerative disorders.	Selegiline	41-51	monoamine oxidase B	Homo sapiens	0-5
7931256-5	1994	By attaching a propargylamine group the resultant series of aliphatic propargylamine derivatives have been shown to be very potent selective MAO-B inhibitors.	propargylamine	15-29	monoamine oxidase B	Homo sapiens	141-146
7931256-5	1994	By attaching a propargylamine group the resultant series of aliphatic propargylamine derivatives have been shown to be very potent selective MAO-B inhibitors.	aliphatic propargylamine	60-84	monoamine oxidase B	Homo sapiens	141-146
7931267-2	1994	Ethanol (ETOH) in vitro displays a competitive inhibition of human platelet MAO-B with a Ki of 270 +/- 30 mM.	Ethanol	0-7	monoamine oxidase B	Homo sapiens	76-81
7931256-7	1994	The relatively short chain aliphatic propargylamines, i.e. N-2-pentyl-N-methylpropargylamine and N-2-hexyl-N-methylpropargylamine, are 4 to 5 times more potent and more selective than selegiline (1-deprenyl) with respect to the inhibition of MAO-B in brain following oral administration.	aliphatic propargylamines	27-52	monoamine oxidase B	Homo sapiens	242-247
7931256-7	1994	The relatively short chain aliphatic propargylamines, i.e. N-2-pentyl-N-methylpropargylamine and N-2-hexyl-N-methylpropargylamine, are 4 to 5 times more potent and more selective than selegiline (1-deprenyl) with respect to the inhibition of MAO-B in brain following oral administration.	n-2-pentyl-n-methylpropargylamine	59-92	monoamine oxidase B	Homo sapiens	242-247
7821334-2	1994	Monoamine oxidase type B is an active form in brain, and its preferential substrate is dopamine that is the most constantly reduced monoamine in Parkinson"s disease brain.	Dopamine	87-95	monoamine oxidase B	Homo sapiens	0-24
7931267-2	1994	Ethanol (ETOH) in vitro displays a competitive inhibition of human platelet MAO-B with a Ki of 270 +/- 30 mM.	Ethanol	9-13	monoamine oxidase B	Homo sapiens	76-81
8293522-4	1993	A selective interaction with MAO-A in the accumulation of [11C]fluorclorgyline was confirmed by a competition experiment performed with the MAO-A specific inhibitor,clorgyline, and MAO-B specific inhibitor, l-deprenyl.	[11c]fluorclorgyline	58-78	monoamine oxidase B	Homo sapiens	181-186
7980742-10	1993	Recently decreased monoamine oxidase type B activity in peripheral blood cells has been investigated as biochemical indicator of neurotoxicity of styrene in workers.	Styrene	146-153	monoamine oxidase B	Homo sapiens	19-43
7931256-7	1994	The relatively short chain aliphatic propargylamines, i.e. N-2-pentyl-N-methylpropargylamine and N-2-hexyl-N-methylpropargylamine, are 4 to 5 times more potent and more selective than selegiline (1-deprenyl) with respect to the inhibition of MAO-B in brain following oral administration.	N-2-hexyl-N-methylpropargylamine	97-129	monoamine oxidase B	Homo sapiens	242-247
8246228-0	1993	Transformation of heterocyclic reversible monoamine oxidase-B inactivators into irreversible inactivators by N-methylation.	Nitrogen	109-110	monoamine oxidase B	Homo sapiens	42-61
8246228-1	1993	3-[4-[(3-Chlorophenyl)methoxy]phenyl]-5-[(methylamino)methyl]- 2-oxazolidinone (1) is a secondary amine known to be a potent time-dependent irreversible inactivator of monoamine oxidase B (MAO-B).	MD 780236	0-78	monoamine oxidase B	Homo sapiens	168-187
8246228-1	1993	3-[4-[(3-Chlorophenyl)methoxy]phenyl]-5-[(methylamino)methyl]- 2-oxazolidinone (1) is a secondary amine known to be a potent time-dependent irreversible inactivator of monoamine oxidase B (MAO-B).	MD 780236	0-78	monoamine oxidase B	Homo sapiens	189-194
8246228-1	1993	3-[4-[(3-Chlorophenyl)methoxy]phenyl]-5-[(methylamino)methyl]- 2-oxazolidinone (1) is a secondary amine known to be a potent time-dependent irreversible inactivator of monoamine oxidase B (MAO-B).	Amines	98-103	monoamine oxidase B	Homo sapiens	168-187
8246228-1	1993	3-[4-[(3-Chlorophenyl)methoxy]phenyl]-5-[(methylamino)methyl]- 2-oxazolidinone (1) is a secondary amine known to be a potent time-dependent irreversible inactivator of monoamine oxidase B (MAO-B).	Amines	98-103	monoamine oxidase B	Homo sapiens	189-194
8293522-4	1993	A selective interaction with MAO-A in the accumulation of [11C]fluorclorgyline was confirmed by a competition experiment performed with the MAO-A specific inhibitor,clorgyline, and MAO-B specific inhibitor, l-deprenyl.	Clorgyline	68-78	monoamine oxidase B	Homo sapiens	181-186
8293522-4	1993	A selective interaction with MAO-A in the accumulation of [11C]fluorclorgyline was confirmed by a competition experiment performed with the MAO-A specific inhibitor,clorgyline, and MAO-B specific inhibitor, l-deprenyl.	Selegiline	207-217	monoamine oxidase B	Homo sapiens	181-186
8363632-3	1993	A new parameter, the specificity index is defined and used in a model which describes the specific and non-specific binding of (-)-deprenyl to MAO B and MAO A, respectively.	Selegiline	127-139	monoamine oxidase B	Homo sapiens	143-148
8242348-2	1993	Activities of both MAOA and MAOB were significantly increased in frontal cortex and caudate nucleus, two brain regions shown previously to be the site of functional and morphological alterations of astrocytes and increased concentrations of the acid metabolites of dopamine and serotonin.	Dopamine	265-273	monoamine oxidase B	Homo sapiens	28-32
8242348-2	1993	Activities of both MAOA and MAOB were significantly increased in frontal cortex and caudate nucleus, two brain regions shown previously to be the site of functional and morphological alterations of astrocytes and increased concentrations of the acid metabolites of dopamine and serotonin.	Serotonin	278-287	monoamine oxidase B	Homo sapiens	28-32
8395564-5	1993	In an age-selected group (range, 10-89 years), the density of monoamine oxidase (MAO)-B sites labeled by [3H]Ro 19-6327 (lazabemide) also showed a positive correlation with age (r = 0.80; p &lt; 0.005).	Tritium	106-108	monoamine oxidase B	Homo sapiens	62-87
8395564-5	1993	In an age-selected group (range, 10-89 years), the density of monoamine oxidase (MAO)-B sites labeled by [3H]Ro 19-6327 (lazabemide) also showed a positive correlation with age (r = 0.80; p &lt; 0.005).	lazabemide	121-131	monoamine oxidase B	Homo sapiens	62-87
8395564-6	1993	In these subjects, the density of I2-imidazoline sites correlated well with the density of MAO-B sites (r = 0.70; p &lt; 0.005).	i2-imidazoline	34-48	monoamine oxidase B	Homo sapiens	91-96
8395564-8	1993	In the human frontal cortex, idazoxan displayed very low affinity (Ki = 89 microM) against the binding of [3H]Ro 19-6327 to MAO-B, which discounted a direct interaction of [3H]idazoxan with the active center of the enzyme and indicated that the I2-imidazoline site cannot be identified with MAO-B.	Idazoxan	29-37	monoamine oxidase B	Homo sapiens	124-129
8395564-8	1993	In the human frontal cortex, idazoxan displayed very low affinity (Ki = 89 microM) against the binding of [3H]Ro 19-6327 to MAO-B, which discounted a direct interaction of [3H]idazoxan with the active center of the enzyme and indicated that the I2-imidazoline site cannot be identified with MAO-B.	Idazoxan	29-37	monoamine oxidase B	Homo sapiens	291-296
8395564-8	1993	In the human frontal cortex, idazoxan displayed very low affinity (Ki = 89 microM) against the binding of [3H]Ro 19-6327 to MAO-B, which discounted a direct interaction of [3H]idazoxan with the active center of the enzyme and indicated that the I2-imidazoline site cannot be identified with MAO-B.	Tritium	107-109	monoamine oxidase B	Homo sapiens	124-129
8377010-5	1993	(-)-Deprenyl, a specific monoamine oxidase (MAO) B inhibitor, has been used as an effective antiparkinsonian drug, and it has been reported to possess neuroprotective and neurorescue properties.	Selegiline	0-12	monoamine oxidase B	Homo sapiens	25-50
8377010-7	1993	The effect seems to be specific to MAO B inhibitors because (+)-deprenyl and clorgyline exhibit no effect.	Selegiline	60-72	monoamine oxidase B	Homo sapiens	35-40
8377010-7	1993	The effect seems to be specific to MAO B inhibitors because (+)-deprenyl and clorgyline exhibit no effect.	Clorgyline	77-87	monoamine oxidase B	Homo sapiens	35-40
8413955-0	1993	Monoamine oxidase B (MAO B) inhibitor therapy in Parkinson"s disease: the degree and reversibility of human brain MAO B inhibition by Ro 19 6327.	lazabemide	134-144	monoamine oxidase B	Homo sapiens	0-19
8413955-0	1993	Monoamine oxidase B (MAO B) inhibitor therapy in Parkinson"s disease: the degree and reversibility of human brain MAO B inhibition by Ro 19 6327.	lazabemide	134-144	monoamine oxidase B	Homo sapiens	114-119
8413955-2	1993	Ro 19 6327 is a highly selective inhibitor of MAO B currently under clinical investigation.	lazabemide	0-10	monoamine oxidase B	Homo sapiens	46-51
8413955-3	1993	We used positron emission tomography (PET) and the MAO B tracer [11C]L-deprenyl to determine the degree and reversibility of human brain MAO B inhibition by Ro 19 6327 in six early Parkinson"s disease patients who were treated with different doses of Ro 19 6327 (25 mg [n = 3], 50 mg [n = 2], and 100 mg [n = 1]; 0.34 to 1.4 mg/kg) every 12 hours for 1 week.	lazabemide	157-167	monoamine oxidase B	Homo sapiens	137-142
8413955-7	1993	Thus, 0.4 mg/kg or greater of Ro 19 6327 given every 12 hours is the minimum dose necessary to provide > 90% inhibition of brain MAO B in patients with early PD.	lazabemide	30-40	monoamine oxidase B	Homo sapiens	129-134
8259692-3	1993	This is attributed to a primary amine metabolite which inhibits MAO B in vitro, but which is not detected in human plasma in vivo.	Amines	32-37	monoamine oxidase B	Homo sapiens	64-69
8259692-4	1993	A secondary amine metabolite, also present in rat but not human plasma, inhibitors MAO B in vivo but not in vitro.	Amines	12-17	monoamine oxidase B	Homo sapiens	83-88
8363648-0	1993	Effect of structural modification of alkyl N-propargylamines on the selective inhibition of monoamine oxidase B activity.	alkyl n-propargylamines	37-60	monoamine oxidase B	Homo sapiens	92-111
8363648-1	1993	A series of alkyl N-methyl-propargylamine derivatives has been discovered recently to be very potent selective irreversible monoamine oxidase B inhibitors (MAO-B).	alkyl n-methyl-propargylamine	12-41	monoamine oxidase B	Homo sapiens	124-143
8363648-1	1993	A series of alkyl N-methyl-propargylamine derivatives has been discovered recently to be very potent selective irreversible monoamine oxidase B inhibitors (MAO-B).	alkyl n-methyl-propargylamine	12-41	monoamine oxidase B	Homo sapiens	156-161
8363648-8	1993	Other branched alkyl N-methylpropargylamines, e.g. N-methyl-N-(3-pentyl)propargylamine, appeared to be slightly less selective in the inhibition of MAO-B activity.	alkyl n-methylpropargylamines	15-44	monoamine oxidase B	Homo sapiens	148-153
8363648-8	1993	Other branched alkyl N-methylpropargylamines, e.g. N-methyl-N-(3-pentyl)propargylamine, appeared to be slightly less selective in the inhibition of MAO-B activity.	N-methyl-N-(3-pentyl)propargylamine	51-86	monoamine oxidase B	Homo sapiens	148-153
8363648-9	1993	Some of these alkyl propargylamine MAO-B inhibitors, which do not possess the amphetamine-like moiety of L-deprenyl, may have significant neuropsychopharmacological implications.	Amphetamine	78-89	monoamine oxidase B	Homo sapiens	35-40
8102552-1	1993	The goal of this study was to determine whether selegiline (L-deprenyl), a selective monoamine oxidase B inhibitor and antioxidant, would improve neuroleptic-induced tardive dyskinesia (TD).	Selegiline	48-58	monoamine oxidase B	Homo sapiens	85-104
8510099-2	1993	A family of N-methylated and N,N-dimethylated alkyl and arylalkylamines was prepared and more than half of the analogues were shown to be time-dependent pseudo-first-order inhibitors of monoamine oxidase-B.	Nitrogen	12-13	monoamine oxidase B	Homo sapiens	186-205
8510099-2	1993	A family of N-methylated and N,N-dimethylated alkyl and arylalkylamines was prepared and more than half of the analogues were shown to be time-dependent pseudo-first-order inhibitors of monoamine oxidase-B.	n,n-dimethylated alkyl and arylalkylamines	29-71	monoamine oxidase B	Homo sapiens	186-205
8316221-1	1993	Nine cysteines are found in the deduced amino acid sequences of both human liver monoamine oxidase (MAO)-A and MAO-B.	Cysteine	5-14	monoamine oxidase B	Homo sapiens	111-116
8316221-4	1993	Catalytic activities were retained in seven MAO-A cysteine to serine mutants (mutations at residues 165, 210, 266, 306, 321, 323, and 398) and in six MAO-B cysteine to serine mutants (mutations at residues 5, 172, 192, 297, 312, and 389).	Cysteine	156-164	monoamine oxidase B	Homo sapiens	150-155
8316221-4	1993	Catalytic activities were retained in seven MAO-A cysteine to serine mutants (mutations at residues 165, 210, 266, 306, 321, 323, and 398) and in six MAO-B cysteine to serine mutants (mutations at residues 5, 172, 192, 297, 312, and 389).	Serine	168-174	monoamine oxidase B	Homo sapiens	150-155
8316221-6	1993	Substitution of MAO-A Cys-374 and -406 and MAO-B Cys-156, -365, and -397 with serine resulted in complete loss of MAO-A and -B catalytic activity.	Cysteine	49-52	monoamine oxidase B	Homo sapiens	43-48
8316221-6	1993	Substitution of MAO-A Cys-374 and -406 and MAO-B Cys-156, -365, and -397 with serine resulted in complete loss of MAO-A and -B catalytic activity.	Serine	78-84	monoamine oxidase B	Homo sapiens	43-48
8316221-8	1993	The loss of catalytic activity in the MAO-A Ser-406 and MAO-B Ser-397 mutants may be due to the prevention of covalent binding of the enzyme to the cofactor FAD, which is necessary for catalytic activity.	Serine	62-65	monoamine oxidase B	Homo sapiens	56-61
8316221-9	1993	The loss of catalytic activity of MAO-A Ser-374 and MAO-B Ser-156 and -365 suggests that these cysteines are important for catalytic activity, but whether they are involved in forming the active site or are important for the appropriate conformation of MAO-A and -B remains to be studied.	Serine	58-61	monoamine oxidase B	Homo sapiens	52-57
8316221-9	1993	The loss of catalytic activity of MAO-A Ser-374 and MAO-B Ser-156 and -365 suggests that these cysteines are important for catalytic activity, but whether they are involved in forming the active site or are important for the appropriate conformation of MAO-A and -B remains to be studied.	Cysteine	95-104	monoamine oxidase B	Homo sapiens	52-57
8393868-1	1993	The neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to generate reactive oxygen species during its interaction with monoamine oxidase type B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	18-62	monoamine oxidase B	Homo sapiens	149-173
8393868-1	1993	The neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to generate reactive oxygen species during its interaction with monoamine oxidase type B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	18-62	monoamine oxidase B	Homo sapiens	175-180
8393868-1	1993	The neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to generate reactive oxygen species during its interaction with monoamine oxidase type B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	64-68	monoamine oxidase B	Homo sapiens	149-173
8393868-1	1993	The neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to generate reactive oxygen species during its interaction with monoamine oxidase type B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	64-68	monoamine oxidase B	Homo sapiens	175-180
8393868-1	1993	The neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to generate reactive oxygen species during its interaction with monoamine oxidase type B (MAO-B).	Reactive Oxygen Species	97-120	monoamine oxidase B	Homo sapiens	149-173
8393868-1	1993	The neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to generate reactive oxygen species during its interaction with monoamine oxidase type B (MAO-B).	Reactive Oxygen Species	97-120	monoamine oxidase B	Homo sapiens	175-180
8393868-2	1993	The kinetic parameters, Km and Vmax, for MAO-B-catalyzed oxidation of MPTP to the corresponding species MPDP+ were found to be 0.194 mM and 0.335 microM/min, respectively.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	70-74	monoamine oxidase B	Homo sapiens	41-46
8393868-2	1993	The kinetic parameters, Km and Vmax, for MAO-B-catalyzed oxidation of MPTP to the corresponding species MPDP+ were found to be 0.194 mM and 0.335 microM/min, respectively.	1-methyl-4-phenyl-2,3-dihydropyridinium	104-109	monoamine oxidase B	Homo sapiens	41-46
8393868-5	1993	Catalase, a scavenger of hydrogen peroxide (H2O2), inhibited the DMPO-OH spin adduct formation in a dose-dependent manner, indicating that H2O2 is produced in the MAO-B catalyzed oxidation of MPTP.	Hydrogen Peroxide	25-42	monoamine oxidase B	Homo sapiens	163-168
8393868-5	1993	Catalase, a scavenger of hydrogen peroxide (H2O2), inhibited the DMPO-OH spin adduct formation in a dose-dependent manner, indicating that H2O2 is produced in the MAO-B catalyzed oxidation of MPTP.	Hydrogen Peroxide	44-48	monoamine oxidase B	Homo sapiens	163-168
8393868-5	1993	Catalase, a scavenger of hydrogen peroxide (H2O2), inhibited the DMPO-OH spin adduct formation in a dose-dependent manner, indicating that H2O2 is produced in the MAO-B catalyzed oxidation of MPTP.	Hydrogen Peroxide	139-143	monoamine oxidase B	Homo sapiens	163-168
8393868-5	1993	Catalase, a scavenger of hydrogen peroxide (H2O2), inhibited the DMPO-OH spin adduct formation in a dose-dependent manner, indicating that H2O2 is produced in the MAO-B catalyzed oxidation of MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	192-196	monoamine oxidase B	Homo sapiens	163-168
8393868-8	1993	These data suggest that superoxide radicals are produced during the oxidation of MPTP by MAO-B and that the generation of H2O2 and .OH was secondary to the production of .O2-.	Superoxides	24-34	monoamine oxidase B	Homo sapiens	89-94
8393868-8	1993	These data suggest that superoxide radicals are produced during the oxidation of MPTP by MAO-B and that the generation of H2O2 and .OH was secondary to the production of .O2-.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	81-85	monoamine oxidase B	Homo sapiens	89-94
8374913-1	1993	Selegiline (deprenyl) and lazabemide (Ro 19-6327) are inhibitors of monoamine oxidase-B but differ in several other pharmacological properties.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	68-87
8374913-1	1993	Selegiline (deprenyl) and lazabemide (Ro 19-6327) are inhibitors of monoamine oxidase-B but differ in several other pharmacological properties.	Selegiline	12-20	monoamine oxidase B	Homo sapiens	68-87
8374913-1	1993	Selegiline (deprenyl) and lazabemide (Ro 19-6327) are inhibitors of monoamine oxidase-B but differ in several other pharmacological properties.	lazabemide	26-36	monoamine oxidase B	Homo sapiens	68-87
8374913-1	1993	Selegiline (deprenyl) and lazabemide (Ro 19-6327) are inhibitors of monoamine oxidase-B but differ in several other pharmacological properties.	lazabemide	38-48	monoamine oxidase B	Homo sapiens	68-87
8374913-5	1993	This work confirms that the symptomatic effects of selegiline against Parkinsonism are small and are likely due to its inhibition of monoamine oxidase-B.	Selegiline	51-61	monoamine oxidase B	Homo sapiens	133-152
8410065-1	1993	Monoamine oxidase type B (MAO-B), which catalyses the breakdown of dopamine (DA) in human brain, is said to be involved in the pathophysiology of Parkinson"s disease (PD).	Dopamine	67-75	monoamine oxidase B	Homo sapiens	0-24
8410065-1	1993	Monoamine oxidase type B (MAO-B), which catalyses the breakdown of dopamine (DA) in human brain, is said to be involved in the pathophysiology of Parkinson"s disease (PD).	Dopamine	67-75	monoamine oxidase B	Homo sapiens	26-31
8410065-1	1993	Monoamine oxidase type B (MAO-B), which catalyses the breakdown of dopamine (DA) in human brain, is said to be involved in the pathophysiology of Parkinson"s disease (PD).	Dopamine	77-79	monoamine oxidase B	Homo sapiens	0-24
8410065-1	1993	Monoamine oxidase type B (MAO-B), which catalyses the breakdown of dopamine (DA) in human brain, is said to be involved in the pathophysiology of Parkinson"s disease (PD).	Dopamine	77-79	monoamine oxidase B	Homo sapiens	26-31
8406673-5	1993	Regional increases of MAO-B concentration were found in ALS lumbar sections with quantitative 3H-L-deprenyl autoradiography.	3h-l-deprenyl	94-107	monoamine oxidase B	Homo sapiens	22-27
8102552-1	1993	The goal of this study was to determine whether selegiline (L-deprenyl), a selective monoamine oxidase B inhibitor and antioxidant, would improve neuroleptic-induced tardive dyskinesia (TD).	Selegiline	60-70	monoamine oxidase B	Homo sapiens	85-104
8487265-1	1993	The introduction of a methylene bridge between the phenyl and tetrahydropyridyl moieties of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) results in increased selectivity for monoamine oxidase B (MAO B) over monoamine oxidase A (MAO A).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	92-136	monoamine oxidase B	Homo sapiens	181-200
8314932-2	1993	Incubation of dopamine with monoamine oxidase B gave the same product which was identified as 3,4-dihydroxyphenylacetaldehyde.	Dopamine	14-22	monoamine oxidase B	Homo sapiens	28-47
8314932-2	1993	Incubation of dopamine with monoamine oxidase B gave the same product which was identified as 3,4-dihydroxyphenylacetaldehyde.	3,4-dihydroxyphenylacetaldehyde	94-125	monoamine oxidase B	Homo sapiens	28-47
8487265-1	1993	The introduction of a methylene bridge between the phenyl and tetrahydropyridyl moieties of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) results in increased selectivity for monoamine oxidase B (MAO B) over monoamine oxidase A (MAO A).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	92-136	monoamine oxidase B	Homo sapiens	202-207
8487265-1	1993	The introduction of a methylene bridge between the phenyl and tetrahydropyridyl moieties of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) results in increased selectivity for monoamine oxidase B (MAO B) over monoamine oxidase A (MAO A).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	138-142	monoamine oxidase B	Homo sapiens	181-200
8487265-1	1993	The introduction of a methylene bridge between the phenyl and tetrahydropyridyl moieties of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) results in increased selectivity for monoamine oxidase B (MAO B) over monoamine oxidase A (MAO A).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	138-142	monoamine oxidase B	Homo sapiens	202-207
8487265-6	1993	Similarly, all thienyl analogs were found to be more effective substrates of MAO B.	thienyl	15-22	monoamine oxidase B	Homo sapiens	77-82
8487265-7	1993	In contrast to the naphthalenes, the conformationally restrained thiophenes 9a and 10a were found to be poor substrates of MAO B, relative to benzylamine, the reference substrate.	Naphthalenes	19-31	monoamine oxidase B	Homo sapiens	123-128
8487265-7	1993	In contrast to the naphthalenes, the conformationally restrained thiophenes 9a and 10a were found to be poor substrates of MAO B, relative to benzylamine, the reference substrate.	Thiophenes	65-75	monoamine oxidase B	Homo sapiens	123-128
8487265-7	1993	In contrast to the naphthalenes, the conformationally restrained thiophenes 9a and 10a were found to be poor substrates of MAO B, relative to benzylamine, the reference substrate.	benzylamine	142-153	monoamine oxidase B	Homo sapiens	123-128
8489556-0	1993	Pharmacokinetics of and monoamine oxidase B inhibition by (E)-4-fluoro-beta-fluoromethylene benzene butanamine in man.	(e)-4-fluoro-beta-fluoromethylene benzene butanamine	58-110	monoamine oxidase B	Homo sapiens	24-43
8489205-2	1993	The monoamine oxidase type B inhibitor deprenyl (selegiline) has been demonstrated to delay the emergence of disability in early untreated Parkinson"s disease.	Selegiline	39-47	monoamine oxidase B	Homo sapiens	4-28
8489205-2	1993	The monoamine oxidase type B inhibitor deprenyl (selegiline) has been demonstrated to delay the emergence of disability in early untreated Parkinson"s disease.	Selegiline	49-59	monoamine oxidase B	Homo sapiens	4-28
8489205-3	1993	Lazabemide (RO19-6327) is a short-acting, reversible, highly selective inhibitor of monoamine oxidase type B which, unlike deprenyl, is not metabolized to active compounds.	lazabemide	0-10	monoamine oxidase B	Homo sapiens	84-108
8489205-3	1993	Lazabemide (RO19-6327) is a short-acting, reversible, highly selective inhibitor of monoamine oxidase type B which, unlike deprenyl, is not metabolized to active compounds.	lazabemide	12-21	monoamine oxidase B	Homo sapiens	84-108
8489205-11	1993	The overall safety and benefits of lazabemide observed in this short-term study justify further long-term investigations to determine if this monoamine oxidase type B inhibitor can slow the clinical progression of Parkinson"s disease.	lazabemide	35-45	monoamine oxidase B	Homo sapiens	142-166
8489207-1	1993	Monoamine oxidase B (MAO-B) is implicated in the cause of Parkinson"s disease (PD) because of its role in metabolizing the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and forming H2O2 during dopamine metabolism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	134-178	monoamine oxidase B	Homo sapiens	0-19
8489207-1	1993	Monoamine oxidase B (MAO-B) is implicated in the cause of Parkinson"s disease (PD) because of its role in metabolizing the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and forming H2O2 during dopamine metabolism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	134-178	monoamine oxidase B	Homo sapiens	21-26
8489207-1	1993	Monoamine oxidase B (MAO-B) is implicated in the cause of Parkinson"s disease (PD) because of its role in metabolizing the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and forming H2O2 during dopamine metabolism.	Hydrogen Peroxide	192-196	monoamine oxidase B	Homo sapiens	0-19
8489207-1	1993	Monoamine oxidase B (MAO-B) is implicated in the cause of Parkinson"s disease (PD) because of its role in metabolizing the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and forming H2O2 during dopamine metabolism.	Hydrogen Peroxide	192-196	monoamine oxidase B	Homo sapiens	21-26
8489207-1	1993	Monoamine oxidase B (MAO-B) is implicated in the cause of Parkinson"s disease (PD) because of its role in metabolizing the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and forming H2O2 during dopamine metabolism.	Dopamine	204-212	monoamine oxidase B	Homo sapiens	0-19
8489207-1	1993	Monoamine oxidase B (MAO-B) is implicated in the cause of Parkinson"s disease (PD) because of its role in metabolizing the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and forming H2O2 during dopamine metabolism.	Dopamine	204-212	monoamine oxidase B	Homo sapiens	21-26
7682224-1	1993	It is known that histamine (HA) and type B monoamine oxidase (MAO-B), an enzyme involved in its metabolism, are present in the posterior hypothalamus, but the sites where MAO-B intervenes in HA metabolism remain uncertain.	Histamine	17-26	monoamine oxidase B	Homo sapiens	171-176
7682224-4	1993	MAO-B-ir staining was detected in the vast majority of HA-ir neurons, suggesting that the degradation of tele-methylhistamine (t-MHA), the direct metabolite of HA, may occur within these cells.	tele-methylhistamine	105-125	monoamine oxidase B	Homo sapiens	0-8
7682224-4	1993	MAO-B-ir staining was detected in the vast majority of HA-ir neurons, suggesting that the degradation of tele-methylhistamine (t-MHA), the direct metabolite of HA, may occur within these cells.	tele-methylhistamine	127-132	monoamine oxidase B	Homo sapiens	0-8
8489556-1	1993	MDL 72974A ((E)-4-fluoro-beta-fluoromethylene benzene butanamine HCl salt, CAS 120635-25-8) is a new irreversible inhibitor of the B form of monoamine oxidase (MAO-B).	(e)-4-fluoro-beta-fluoromethylene benzene butanamine hcl salt	12-73	monoamine oxidase B	Homo sapiens	160-165
8474100-0	1993	Inactivation of monoamine oxidase B by analogues of the anticonvulsant agent milacemide (2-(n-pentylamino)acetamide).	milacemide	77-87	monoamine oxidase B	Homo sapiens	16-35
8452568-4	1993	MPTP toxicity was shown to be reduced by monoamine oxidase B inhibitors, pargyline (P &lt; 0.01) and selegiline (P &lt; 0.05), indicating that toxicity was due to metabolism of MPTP rather than the parent compound.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	41-60
8452568-4	1993	MPTP toxicity was shown to be reduced by monoamine oxidase B inhibitors, pargyline (P &lt; 0.01) and selegiline (P &lt; 0.05), indicating that toxicity was due to metabolism of MPTP rather than the parent compound.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	177-181	monoamine oxidase B	Homo sapiens	41-60
8474100-0	1993	Inactivation of monoamine oxidase B by analogues of the anticonvulsant agent milacemide (2-(n-pentylamino)acetamide).	milacemide	89-115	monoamine oxidase B	Homo sapiens	16-35
8474100-1	1993	Analogues of the anticonvulsant agent milacemide (1,2-(n-pentylamino)acetamide), in which the carboxamide group is changed to a nitrile (2), a carbethoxy group (3), a carboxylic acid (4), a cyanomethyl group (5), and a trifluoromethyl group (6), were synthesized and tested as substrates and inactivators of monoamine oxidase B (MAO B).	milacemide	38-48	monoamine oxidase B	Homo sapiens	308-327
8474100-1	1993	Analogues of the anticonvulsant agent milacemide (1,2-(n-pentylamino)acetamide), in which the carboxamide group is changed to a nitrile (2), a carbethoxy group (3), a carboxylic acid (4), a cyanomethyl group (5), and a trifluoromethyl group (6), were synthesized and tested as substrates and inactivators of monoamine oxidase B (MAO B).	milacemide	38-48	monoamine oxidase B	Homo sapiens	329-334
8428624-1	1993	Monoamine oxidase (MAO)-A and MAO-B are FAD-containing mitochondrial enzymes which catabolize biogenic and xenobiotic amines.	Flavin-Adenine Dinucleotide	40-43	monoamine oxidase B	Homo sapiens	30-35
8428624-1	1993	Monoamine oxidase (MAO)-A and MAO-B are FAD-containing mitochondrial enzymes which catabolize biogenic and xenobiotic amines.	xenobiotic amines	107-124	monoamine oxidase B	Homo sapiens	30-35
8428624-7	1993	Substitution of Cys-397 of MAO-B, i.e. the residue covalently anchoring FAD, with an Ala or a His residue resulted in the total loss of enzymatic activity, suggesting that the covalent coupling of FAD to MAO occurs specifically at the-SH group of cysteine.	Cysteine	16-19	monoamine oxidase B	Homo sapiens	27-32
8428624-7	1993	Substitution of Cys-397 of MAO-B, i.e. the residue covalently anchoring FAD, with an Ala or a His residue resulted in the total loss of enzymatic activity, suggesting that the covalent coupling of FAD to MAO occurs specifically at the-SH group of cysteine.	Flavin-Adenine Dinucleotide	72-75	monoamine oxidase B	Homo sapiens	27-32
8428624-7	1993	Substitution of Cys-397 of MAO-B, i.e. the residue covalently anchoring FAD, with an Ala or a His residue resulted in the total loss of enzymatic activity, suggesting that the covalent coupling of FAD to MAO occurs specifically at the-SH group of cysteine.	Alanine	85-88	monoamine oxidase B	Homo sapiens	27-32
8428624-7	1993	Substitution of Cys-397 of MAO-B, i.e. the residue covalently anchoring FAD, with an Ala or a His residue resulted in the total loss of enzymatic activity, suggesting that the covalent coupling of FAD to MAO occurs specifically at the-SH group of cysteine.	Histidine	94-97	monoamine oxidase B	Homo sapiens	27-32
8428624-7	1993	Substitution of Cys-397 of MAO-B, i.e. the residue covalently anchoring FAD, with an Ala or a His residue resulted in the total loss of enzymatic activity, suggesting that the covalent coupling of FAD to MAO occurs specifically at the-SH group of cysteine.	Flavin-Adenine Dinucleotide	197-200	monoamine oxidase B	Homo sapiens	27-32
8428624-7	1993	Substitution of Cys-397 of MAO-B, i.e. the residue covalently anchoring FAD, with an Ala or a His residue resulted in the total loss of enzymatic activity, suggesting that the covalent coupling of FAD to MAO occurs specifically at the-SH group of cysteine.	Cysteine	247-255	monoamine oxidase B	Homo sapiens	27-32
8294896-1	1993	MDL 72,974A [(E)-2-(4-fluorophenethyl)-3-fluoroallylamine, hydrochloride] was designed to be a selective, mechanism-based irreversible inhibitor of monoamine oxidase type B (MAO-B).	mofegiline	13-57	monoamine oxidase B	Homo sapiens	148-172
8093582-1	1993	The discovery of a selective striatal dopamine deficiency in Parkinson"s disease has led to dopamine replacement therapies including L-DOPA, dopamine full and partial agonists, and MAO-B inhibitors.	Dopamine	38-46	monoamine oxidase B	Homo sapiens	181-186
7805584-11	1993	Astrocytic metabolism of monoamine neurotransmitters may also be increased as a result of increased activities of monoamine oxidase MAOB.	monoamine	25-34	monoamine oxidase B	Homo sapiens	132-136
7510793-0	1993	The anti-ulcer drug ranitidine hydrochloride and its synthetic intermediates are inactivators of monoamine oxidase-B.	Ranitidine	20-44	monoamine oxidase B	Homo sapiens	97-116
8390270-1	1993	The "cheese effect", potentiation of sympathomimetic action of indirectly acting amines such as tyramine, the main side effect of irreversible non-selective and selective monoamine oxidase (MAO) A inhibitors, has largely been eliminated in the new generation of reversible selective MAO-A and B and irreversible MAO-B inhibitors.	Amines	81-87	monoamine oxidase B	Homo sapiens	312-317
8390270-1	1993	The "cheese effect", potentiation of sympathomimetic action of indirectly acting amines such as tyramine, the main side effect of irreversible non-selective and selective monoamine oxidase (MAO) A inhibitors, has largely been eliminated in the new generation of reversible selective MAO-A and B and irreversible MAO-B inhibitors.	Tyramine	96-104	monoamine oxidase B	Homo sapiens	312-317
8439389-1	1993	An increase in platelet monoamine oxidase (MAO) B activity in drug-free parkinsonians (n = 6) compared with healthy controls (n = 10) has been confirmed using both phenylethylamine (PEA) and dopamine as substrates, reaching statistical significance in the case of PEA oxidising activity (p < 0.05).	Phenethylamines	164-180	monoamine oxidase B	Homo sapiens	24-49
8294896-1	1993	MDL 72,974A [(E)-2-(4-fluorophenethyl)-3-fluoroallylamine, hydrochloride] was designed to be a selective, mechanism-based irreversible inhibitor of monoamine oxidase type B (MAO-B).	mofegiline	13-57	monoamine oxidase B	Homo sapiens	174-179
8439389-1	1993	An increase in platelet monoamine oxidase (MAO) B activity in drug-free parkinsonians (n = 6) compared with healthy controls (n = 10) has been confirmed using both phenylethylamine (PEA) and dopamine as substrates, reaching statistical significance in the case of PEA oxidising activity (p < 0.05).	Phenethylamines	182-185	monoamine oxidase B	Homo sapiens	24-49
8439389-1	1993	An increase in platelet monoamine oxidase (MAO) B activity in drug-free parkinsonians (n = 6) compared with healthy controls (n = 10) has been confirmed using both phenylethylamine (PEA) and dopamine as substrates, reaching statistical significance in the case of PEA oxidising activity (p < 0.05).	Dopamine	191-199	monoamine oxidase B	Homo sapiens	24-49
8294896-1	1993	MDL 72,974A [(E)-2-(4-fluorophenethyl)-3-fluoroallylamine, hydrochloride] was designed to be a selective, mechanism-based irreversible inhibitor of monoamine oxidase type B (MAO-B).	hydrochloride	59-72	monoamine oxidase B	Homo sapiens	148-172
8294896-1	1993	MDL 72,974A [(E)-2-(4-fluorophenethyl)-3-fluoroallylamine, hydrochloride] was designed to be a selective, mechanism-based irreversible inhibitor of monoamine oxidase type B (MAO-B).	hydrochloride	59-72	monoamine oxidase B	Homo sapiens	174-179
8469735-1	1993	Specific 2-propynylamine inhibitors of monoamine oxidase (MAO) pargyline and especially chlorgyline, a selective inhibitor of MAO A (but not deprenyl, a selective inhibitor of MAO B) increase the radioprotective effect of small doses of O-methyltyramine and phenylephrine and do not change the efficacy of large doses.	propargylamine	9-24	monoamine oxidase B	Homo sapiens	176-181
8469735-1	1993	Specific 2-propynylamine inhibitors of monoamine oxidase (MAO) pargyline and especially chlorgyline, a selective inhibitor of MAO A (but not deprenyl, a selective inhibitor of MAO B) increase the radioprotective effect of small doses of O-methyltyramine and phenylephrine and do not change the efficacy of large doses.	Clorgyline	88-99	monoamine oxidase B	Homo sapiens	176-181
1433219-0	1992	Synthesis of novel MPTP analogs as potential monoamine oxidase B (MAO-B) inhibitors.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	19-23	monoamine oxidase B	Homo sapiens	45-64
8302308-0	1993	The relevance of glial monoamine oxidase-B and polyamines to the action of selegiline in Parkinson"s disease.	Selegiline	75-85	monoamine oxidase B	Homo sapiens	23-42
8302308-3	1993	Methylhistamine as well as N-acetylated polyamine derivatives are selective substrates for monoamine oxidase type B (MAO-B).	Methylhistamines	0-15	monoamine oxidase B	Homo sapiens	91-115
8302308-3	1993	Methylhistamine as well as N-acetylated polyamine derivatives are selective substrates for monoamine oxidase type B (MAO-B).	Methylhistamines	0-15	monoamine oxidase B	Homo sapiens	117-122
8302308-3	1993	Methylhistamine as well as N-acetylated polyamine derivatives are selective substrates for monoamine oxidase type B (MAO-B).	n-acetylated polyamine	27-49	monoamine oxidase B	Homo sapiens	91-115
8302308-3	1993	Methylhistamine as well as N-acetylated polyamine derivatives are selective substrates for monoamine oxidase type B (MAO-B).	n-acetylated polyamine	27-49	monoamine oxidase B	Homo sapiens	117-122
8302308-4	1993	Theoretically at least, MAO-B inhibition by selegiline could result in the increase in the levels of polyamines and their N-acetyl derivatives.	Selegiline	44-54	monoamine oxidase B	Homo sapiens	24-29
8302308-4	1993	Theoretically at least, MAO-B inhibition by selegiline could result in the increase in the levels of polyamines and their N-acetyl derivatives.	Polyamines	101-111	monoamine oxidase B	Homo sapiens	24-29
8302308-4	1993	Theoretically at least, MAO-B inhibition by selegiline could result in the increase in the levels of polyamines and their N-acetyl derivatives.	n-acetyl	122-130	monoamine oxidase B	Homo sapiens	24-29
8302302-5	1993	Selective inhibitors of monoamine oxidase type B (MAO-B) have been chosen for study because of their capacity to interfere with the oxidative metabolism of dopamine and so diminish the likelihood that free radicals will be formed.	Dopamine	156-164	monoamine oxidase B	Homo sapiens	24-48
8302302-5	1993	Selective inhibitors of monoamine oxidase type B (MAO-B) have been chosen for study because of their capacity to interfere with the oxidative metabolism of dopamine and so diminish the likelihood that free radicals will be formed.	Dopamine	156-164	monoamine oxidase B	Homo sapiens	50-55
8302302-6	1993	Initial studies demonstrate that the MAO-B inhibitor L-deprenyl (selegiline) delays the development of disability in otherwise untreated patients with early Parkinson"s disease.	Selegiline	53-63	monoamine oxidase B	Homo sapiens	37-42
8302302-6	1993	Initial studies demonstrate that the MAO-B inhibitor L-deprenyl (selegiline) delays the development of disability in otherwise untreated patients with early Parkinson"s disease.	Selegiline	65-75	monoamine oxidase B	Homo sapiens	37-42
1433219-0	1992	Synthesis of novel MPTP analogs as potential monoamine oxidase B (MAO-B) inhibitors.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	19-23	monoamine oxidase B	Homo sapiens	66-71
1433219-1	1992	The nigrostriatal toxin 1-methyl-4-phenyl-1,2,3,6-tetahydropyridine (MPTP) is an excellent substrate and a weak inactivator of the flavoenzyme monoamine oxidase B (MAO-B).	1-methyl-4-phenyl-1,2,3,6-tetahydropyridine	24-67	monoamine oxidase B	Homo sapiens	143-162
1433219-1	1992	The nigrostriatal toxin 1-methyl-4-phenyl-1,2,3,6-tetahydropyridine (MPTP) is an excellent substrate and a weak inactivator of the flavoenzyme monoamine oxidase B (MAO-B).	1-methyl-4-phenyl-1,2,3,6-tetahydropyridine	24-67	monoamine oxidase B	Homo sapiens	164-169
1433219-1	1992	The nigrostriatal toxin 1-methyl-4-phenyl-1,2,3,6-tetahydropyridine (MPTP) is an excellent substrate and a weak inactivator of the flavoenzyme monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	69-73	monoamine oxidase B	Homo sapiens	143-162
1433219-1	1992	The nigrostriatal toxin 1-methyl-4-phenyl-1,2,3,6-tetahydropyridine (MPTP) is an excellent substrate and a weak inactivator of the flavoenzyme monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	69-73	monoamine oxidase B	Homo sapiens	164-169
1433219-2	1992	In an attempt to develop novel mechanism-based inactivators of MAO-B, we have synthesized analogs of MPTP bearing a variety of functional groups at either the N or the C(4) position and have examined their interactions with a purified MAO-B preparation isolated from beef liver.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	101-105	monoamine oxidase B	Homo sapiens	63-68
1433219-7	1992	The results of these studies provide additional insights into the steric features of the active site of MAO-B and predict that the area in which the C(4) substituent of the tetrahydropyridine ring resides lacks a reactive nucleophilic group.	Pyrrolidines	173-191	monoamine oxidase B	Homo sapiens	104-109
1515348-9	1992	The MAO-B activity decreased with increasing blood styrene concentration; the mean (SE) MAO-B values for the four groups were 34.2 (3.0), 28.1 (5.3), 20.1 (4.8), and 16.9 (7.7) pmol/10(7) cells/min.	Styrene	51-58	monoamine oxidase B	Homo sapiens	4-9
1488910-1	1992	The combination of C-11-labelled Selegiline with PET gives the possibility of a non-invasive method for the determination of the distribution, activity and turnover of MAO-B enzyme and all the enzyme-related changes in the brain as well as for the early detection of Parkinson"s disease.	Selegiline	33-43	monoamine oxidase B	Homo sapiens	168-173
1513186-3	1992	(-)Deprenyl was the first selective inhibitor of MAO-B described in literature, became the worldwide research tool used for blocking selectively B-type MAO, and is still the only MAO-B inhibitor in clinical use.	Selegiline	3-11	monoamine oxidase B	Homo sapiens	49-54
1513186-3	1992	(-)Deprenyl was the first selective inhibitor of MAO-B described in literature, became the worldwide research tool used for blocking selectively B-type MAO, and is still the only MAO-B inhibitor in clinical use.	Selegiline	3-11	monoamine oxidase B	Homo sapiens	179-184
1510706-1	1992	Isatin is an endogenous compound which acts as a selective inhibitor of monoamine oxidase (MAO) B.	Isatin	0-6	monoamine oxidase B	Homo sapiens	72-97
1446001-2	1992	In addition to its excellent substrate properties, MPTP is a mechanism-based inactivator of monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	51-55	monoamine oxidase B	Homo sapiens	92-111
1446001-2	1992	In addition to its excellent substrate properties, MPTP is a mechanism-based inactivator of monoamine oxidase B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	51-55	monoamine oxidase B	Homo sapiens	113-118
1446001-3	1992	In an attempt to exploit the special interactions between this cyclic tertiary allylamine and MAO-B, we have initiated studies to evaluate the enzymatic and biological properties of MPTP analogs bearing functional groups which are known to mediate the metabolism-dependent inactivation of this enzyme.	Allylamine	79-89	monoamine oxidase B	Homo sapiens	94-99
1446001-3	1992	In an attempt to exploit the special interactions between this cyclic tertiary allylamine and MAO-B, we have initiated studies to evaluate the enzymatic and biological properties of MPTP analogs bearing functional groups which are known to mediate the metabolism-dependent inactivation of this enzyme.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	182-186	monoamine oxidase B	Homo sapiens	94-99
1515348-11	1992	The findings for MAO-B activity are consistent with previously reported experimental data, and suggest that MAO-B may be a useful marker of styrene neurotoxicity.	Styrene	140-147	monoamine oxidase B	Homo sapiens	108-113
1436479-2	1992	[3H]L-Deprenyl, an irreversible and selective monoamine oxidase-B inhibitor, was used as ligand and the autoradiographs were analysed by computer-assisted densitometry.	[3h]l-deprenyl	0-14	monoamine oxidase B	Homo sapiens	46-65
1641061-0	1992	Interactions of the neurotoxin MPTP and its demethylated derivative (PTP) with monoamine oxidase-B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	31-35	monoamine oxidase B	Homo sapiens	79-98
1641061-6	1992	The conversion of MPTP to its corresponding pyridinium-ion derivative through the action of MAO-B is known to be essential for its neurotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	18-22	monoamine oxidase B	Homo sapiens	92-97
1634730-4	1992	(-)Deprenyl, the first selective inhibitor of MAO-B described in literature, has become the universally used research tool for selectively blocking B-type MAO.	Selegiline	3-11	monoamine oxidase B	Homo sapiens	46-51
1641061-6	1992	The conversion of MPTP to its corresponding pyridinium-ion derivative through the action of MAO-B is known to be essential for its neurotoxicity.	pyridine	44-54	monoamine oxidase B	Homo sapiens	92-97
1417423-3	1992	MPTP toxicity is actually provoked by MPP+ which results after oxidation by MAO-B.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	0-4	monoamine oxidase B	Homo sapiens	76-81
1641061-8	1992	Studies of the changes in absorbance spectra during the MAO-B catalysed oxidation were consistent with the formation of the corresponding pyridinium-ion derivative (MPP+), which is known to be the effective neurotoxin, as the end-product when MPTP was oxidized.	pyridine	138-148	monoamine oxidase B	Homo sapiens	56-61
1641061-8	1992	Studies of the changes in absorbance spectra during the MAO-B catalysed oxidation were consistent with the formation of the corresponding pyridinium-ion derivative (MPP+), which is known to be the effective neurotoxin, as the end-product when MPTP was oxidized.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	243-247	monoamine oxidase B	Homo sapiens	56-61
10146952-1	1992	Selegiline (deprenyl) is a selective, irreversible cerebral monoamine oxidase type B inhibitor (MAO-B) that is used in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	60-84
10146952-1	1992	Selegiline (deprenyl) is a selective, irreversible cerebral monoamine oxidase type B inhibitor (MAO-B) that is used in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	96-101
10146952-1	1992	Selegiline (deprenyl) is a selective, irreversible cerebral monoamine oxidase type B inhibitor (MAO-B) that is used in the treatment of Parkinson"s disease.	Selegiline	12-20	monoamine oxidase B	Homo sapiens	60-84
10146952-1	1992	Selegiline (deprenyl) is a selective, irreversible cerebral monoamine oxidase type B inhibitor (MAO-B) that is used in the treatment of Parkinson"s disease.	Selegiline	12-20	monoamine oxidase B	Homo sapiens	96-101
1321029-1	1992	Distribution of the enzyme monoamine oxidase B (MAO-B) and the peripheral benzodiazepine binding site (omega 3 site) was studied by quantitative autoradiography using [3H]L-deprenyl and [3H]PK 11195, two tentative glial markers, as ligands.	Tritium	168-170	monoamine oxidase B	Homo sapiens	27-46
1394694-1	1992	A new series of iodinated analogues of N-(2-aminoethyl)benzamide was synthesized and evaluated for inhibitory potency and specificity toward monoamine oxidase type-B (MAO-B).	N-(2-aminoethyl)benzamide	39-64	monoamine oxidase B	Homo sapiens	167-172
1394694-2	1992	Among them, N-(2-aminoethyl)-2-chloro-4-iodobenzamide hydrochloride (2d) showed high inhibitory potency and selectivity against MAO-B.	n-(2-aminoethyl)-2-chloro-4-iodobenzamide hydrochloride	12-67	monoamine oxidase B	Homo sapiens	128-133
1394694-0	1992	Synthesis and evaluation of iodinated benzamide derivatives as selective and reversible monoamine oxidase B inhibitors.	benzamide	38-47	monoamine oxidase B	Homo sapiens	88-107
1394694-1	1992	A new series of iodinated analogues of N-(2-aminoethyl)benzamide was synthesized and evaluated for inhibitory potency and specificity toward monoamine oxidase type-B (MAO-B).	N-(2-aminoethyl)benzamide	39-64	monoamine oxidase B	Homo sapiens	141-165
1321029-1	1992	Distribution of the enzyme monoamine oxidase B (MAO-B) and the peripheral benzodiazepine binding site (omega 3 site) was studied by quantitative autoradiography using [3H]L-deprenyl and [3H]PK 11195, two tentative glial markers, as ligands.	Tritium	187-189	monoamine oxidase B	Homo sapiens	27-46
1434048-11	1992	Recently selective monoamine oxidase (MAO) B inhibitors have been used in order to slow clinical progression of the disease, in addition to an attempt to increase the potential of dopamine through inhibition of MAO.	Dopamine	180-188	monoamine oxidase B	Homo sapiens	19-44
1614586-4	1992	The study demonstrated high binding of [11C]-L-deprenyl to monoamine oxidase B in pituitary adenomas, whereas the binding in meningiomas was very low.	Carbon-11	40-43	monoamine oxidase B	Homo sapiens	59-78
1610807-3	1992	The insertion of a methylene bridge between the phenyl and tetrahydropyridine moieties of MPTP to yield N-methyl-4-benzyl-1,2,3,6-tetrahydropyridine, rendering the molecule more flexible, greatly enhances reactivity with MAO B, but not with MAO A, as compared with MPTP itself, in accord with data in the literature (Youngster et al., 1989a).	acetophenone	48-54	monoamine oxidase B	Homo sapiens	221-226
1610807-3	1992	The insertion of a methylene bridge between the phenyl and tetrahydropyridine moieties of MPTP to yield N-methyl-4-benzyl-1,2,3,6-tetrahydropyridine, rendering the molecule more flexible, greatly enhances reactivity with MAO B, but not with MAO A, as compared with MPTP itself, in accord with data in the literature (Youngster et al., 1989a).	Pyrrolidines	59-77	monoamine oxidase B	Homo sapiens	221-226
1610807-3	1992	The insertion of a methylene bridge between the phenyl and tetrahydropyridine moieties of MPTP to yield N-methyl-4-benzyl-1,2,3,6-tetrahydropyridine, rendering the molecule more flexible, greatly enhances reactivity with MAO B, but not with MAO A, as compared with MPTP itself, in accord with data in the literature (Youngster et al., 1989a).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	90-94	monoamine oxidase B	Homo sapiens	221-226
1610807-3	1992	The insertion of a methylene bridge between the phenyl and tetrahydropyridine moieties of MPTP to yield N-methyl-4-benzyl-1,2,3,6-tetrahydropyridine, rendering the molecule more flexible, greatly enhances reactivity with MAO B, but not with MAO A, as compared with MPTP itself, in accord with data in the literature (Youngster et al., 1989a).	n-methyl-4-benzyl-1,2,3,6-tetrahydropyridine	104-148	monoamine oxidase B	Homo sapiens	221-226
1610807-3	1992	The insertion of a methylene bridge between the phenyl and tetrahydropyridine moieties of MPTP to yield N-methyl-4-benzyl-1,2,3,6-tetrahydropyridine, rendering the molecule more flexible, greatly enhances reactivity with MAO B, but not with MAO A, as compared with MPTP itself, in accord with data in the literature (Youngster et al., 1989a).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	265-269	monoamine oxidase B	Homo sapiens	221-226
1639115-1	1992	L-Deprenyl, the selective inhibitor of monoamine oxidase type B (MAO-B), has gained wide acceptance as a useful form of adjunct therapeutic drug in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	39-63
1639115-1	1992	L-Deprenyl, the selective inhibitor of monoamine oxidase type B (MAO-B), has gained wide acceptance as a useful form of adjunct therapeutic drug in the treatment of Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	65-70
1639115-7	1992	The observed in vitro selectivity of L-deprenyl for MAO-B may be accounted for by differences in the affinities of the two MAO subtypes for reversible interaction with L-deprenyl, differences in the rates of reaction within the noncovalent complexes to form the irreversibly inhibited adduct, or a combination of both these factors.	Selegiline	37-47	monoamine oxidase B	Homo sapiens	52-57
1639115-7	1992	The observed in vitro selectivity of L-deprenyl for MAO-B may be accounted for by differences in the affinities of the two MAO subtypes for reversible interaction with L-deprenyl, differences in the rates of reaction within the noncovalent complexes to form the irreversibly inhibited adduct, or a combination of both these factors.	Selegiline	168-178	monoamine oxidase B	Homo sapiens	52-57
1609337-6	1992	The reversible inhibitors of monoamine oxidase A (RIMAs) are a group of drugs that, by producing inhibition selectively of monoamine oxidase A (MOA-A), still allow metabolism of tyramine by MAO-B.	Tyramine	178-186	monoamine oxidase B	Homo sapiens	190-195
1303171-1	1992	It has been shown from pulsed-field gel electrophoresis (PFGE) that the monoamine oxidase genes A and B (MAOA &amp; MAOB) and DXS7 loci are physically very close.	Adenosine Monophosphate	111-114	monoamine oxidase B	Homo sapiens	116-120
1614586-6	1992	Operative samples from 10 patients with meningioma and from 5 patients with pituitary adenoma were analyzed biochemically for activity of monoamine oxidase B, using [14C]-phenyl-ethylamine as substrate.	[14c]-phenyl-ethylamine	165-188	monoamine oxidase B	Homo sapiens	138-157
1504260-3	1992	A quantitative structure-metabolism relationship (QSMR) study of MPTP and analogues based on literature data was undertaken in order to determine the key features eliciting MAO-A and MAO-B reactivity and selectivity and influencing toxication.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	65-69	monoamine oxidase B	Homo sapiens	183-188
1504260-4	1992	Multiple regression analysis (MRA) and comparative molecular field analysis (CoMFA) showed that MAO-B activity is nonlinearly (parabolically or bilinearly) correlated to the lipophilicity of MPTP analogues and influenced negatively by steric effects exerted by bulky substituents in the ortho position.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	191-195	monoamine oxidase B	Homo sapiens	96-101
1350053-6	1992	The rational for starting treatment with selegiline at this time is discussed in the context of the role that increased MAO-B activity plays in the progression of Parkinson"s disease.	Selegiline	41-51	monoamine oxidase B	Homo sapiens	120-125
1600360-1	1992	Selegiline (10 mg per day) selectively inhibits monoamine oxidase type B and thus thwarts the metabolism of dopamine by this enzyme.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	48-72
1600360-6	1992	It decreases oxidative stress resulting from the metabolism of dopamine via MAO-B.	Dopamine	63-71	monoamine oxidase B	Homo sapiens	76-81
1634705-1	1992	OBJECTIVE: Milacemide, a MAO-B inhibitor that is also a prodrug for glycine, was tested as a treatment for senile dementia of the Alzheimer type (SDAT) because of its potential for enhancing cognition in animal models of impaired learning and memory.	milacemide	11-21	monoamine oxidase B	Homo sapiens	25-30
1349639-10	1992	By using the MAOA-specific inhibitor clorgyline and the MAOB-specific inhibitor deprenyl we were able to confirm that the MAOA form of the enzyme is involved in DA metabolism in this preparation.	Selegiline	80-88	monoamine oxidase B	Homo sapiens	56-60
1349639-10	1992	By using the MAOA-specific inhibitor clorgyline and the MAOB-specific inhibitor deprenyl we were able to confirm that the MAOA form of the enzyme is involved in DA metabolism in this preparation.	Dopamine	161-163	monoamine oxidase B	Homo sapiens	56-60
1301161-8	1992	The apparent order of these loci is telomere ... DXS7-MAOA-MAOB-NDP-dc12-YMAO.AluR ... centromere.	dc12-ymao	68-77	monoamine oxidase B	Homo sapiens	59-63
1284959-0	1992	4-(Aminomethyl)-1-aryl-2-pyrrolidinones, a new class of monoamine oxidase B inactivators.	4-(aminomethyl)-1-aryl-2-pyrrolidinones	0-39	monoamine oxidase B	Homo sapiens	56-75
1584187-7	1992	Another approach is the use of selegiline (deprenyl), MAO-B inhibitor slowing the breakdown of dopamine and thereby extending the duration of levodopa effect.	Selegiline	31-41	monoamine oxidase B	Homo sapiens	54-59
1584187-7	1992	Another approach is the use of selegiline (deprenyl), MAO-B inhibitor slowing the breakdown of dopamine and thereby extending the duration of levodopa effect.	Dopamine	95-103	monoamine oxidase B	Homo sapiens	54-59
1584187-7	1992	Another approach is the use of selegiline (deprenyl), MAO-B inhibitor slowing the breakdown of dopamine and thereby extending the duration of levodopa effect.	Levodopa	142-150	monoamine oxidase B	Homo sapiens	54-59
1413647-3	1992	In the growing placenta activity of MAO-B with benzylamine as a substrate reached 365% of the MAO-B activity in the mature placenta.	benzylamine	47-58	monoamine oxidase B	Homo sapiens	36-41
1413647-5	1992	At the early periods of pregnancy the rate of placental MAO-B oxidative deamination of benzylamine was distinctly higher as compared with that during the delivery act.	benzylamine	87-98	monoamine oxidase B	Homo sapiens	56-61
1413647-7	1992	Possible biological significance of alterations in the amine oxidases ratio in the growing placenta is discussed considering the known property of the MAO-B inhibitor pargyline to cause abortion within early periods of pregnancy.	Pargyline	167-176	monoamine oxidase B	Homo sapiens	151-156
1350073-1	1992	Studies indicate that selegiline, a monoamine oxidase type B inhibitor, slows progression of Parkinson"s disease (PD) and delays the need for levodopa.	Selegiline	22-32	monoamine oxidase B	Homo sapiens	36-60
1350073-1	1992	Studies indicate that selegiline, a monoamine oxidase type B inhibitor, slows progression of Parkinson"s disease (PD) and delays the need for levodopa.	Levodopa	142-150	monoamine oxidase B	Homo sapiens	36-60
1548678-0	1992	5-(Aminomethyl)-3-aryldihydrofuran-2(3H)-ones, a new class of monoamine oxidase-B inactivators.	5-(aminomethyl)-3-aryldihydrofuran-2(3h)-ones	0-45	monoamine oxidase B	Homo sapiens	62-81
1592575-1	1992	In a double blind randomized crossover trial lasting 6 months selegiline, a selective MAO-B inhibitor, was tested against placebo for activity on verbal memory performances in Alzheimer-type dementia (DAT).	Selegiline	62-72	monoamine oxidase B	Homo sapiens	86-91
1542591-0	1992	Dinucleotide repeat (TG)23 polymorphism in the MAOB gene.	Dinucleoside Phosphates	0-12	monoamine oxidase B	Homo sapiens	47-51
1542591-0	1992	Dinucleotide repeat (TG)23 polymorphism in the MAOB gene.	Thioguanine	21-23	monoamine oxidase B	Homo sapiens	47-51
1571860-1	1992	Deprenyl is a synthetic, selective inhibitor of the monoamine oxidase-B enzyme system.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	52-71
1482291-1	1992	Selegiline (R(-)-N-methyl-N-(1-phenyl-2-propyl)-2-propinylamine), a selective MAO-B inhibitor used as an antiparkinsonian, is excreted in urine as N-desmethyl selegiline (norselegiline), R(-)-methamphetamine (R(-)-MA), R(-)-amphetamine (R(-)-AM) and their conjugated p-hydroxy derivatives.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	78-83
1482291-1	1992	Selegiline (R(-)-N-methyl-N-(1-phenyl-2-propyl)-2-propinylamine), a selective MAO-B inhibitor used as an antiparkinsonian, is excreted in urine as N-desmethyl selegiline (norselegiline), R(-)-methamphetamine (R(-)-MA), R(-)-amphetamine (R(-)-AM) and their conjugated p-hydroxy derivatives.	r(-)-N-methyl-N-(1-phenyl-2-propyl)-2-propinylamine	12-63	monoamine oxidase B	Homo sapiens	78-83
1729144-5	1992	The monoamine oxidase type B inhibitor selegiline is also being used by many physicians to delay the onset of disability.	Selegiline	39-49	monoamine oxidase B	Homo sapiens	4-28
1288668-3	1992	Based on earlier positive findings in Alzheimer patients with the monoamine oxidase B inhibitor, 1-deprenyl, the authors speculate that a combination of physostigmine, the short-acting cholinesterase inhibitor, and 1-deprenyl might be more beneficial than either agent alone.	Physostigmine	153-166	monoamine oxidase B	Homo sapiens	66-85
1288668-3	1992	Based on earlier positive findings in Alzheimer patients with the monoamine oxidase B inhibitor, 1-deprenyl, the authors speculate that a combination of physostigmine, the short-acting cholinesterase inhibitor, and 1-deprenyl might be more beneficial than either agent alone.	1-deprenyl	215-225	monoamine oxidase B	Homo sapiens	66-85
1546134-3	1992	In the substantia nigra, MAO-B was more abundant than MAO-A; the former was localized in the reticular zone and the latter in the compact zone (where melanin-containing dopaminergic neurons are found).	Melanins	150-157	monoamine oxidase B	Homo sapiens	25-30
1418862-2	1992	L-deprenyl binds irreversibly and quantitatively to the B-form of monoamine oxidase, MAO, and is an ideal 3H-ligand to measure the MAO-B enzyme protein in tissues by means of in vitro autoradiography.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	131-136
1418862-6	1992	There was a high correlation between glial cell count and 3H-L-deprenyl binding with a relation indicating enhanced MAO-B protein in glial cells within areas of neurodegeneration.	Tritium	58-60	monoamine oxidase B	Homo sapiens	116-121
1418862-6	1992	There was a high correlation between glial cell count and 3H-L-deprenyl binding with a relation indicating enhanced MAO-B protein in glial cells within areas of neurodegeneration.	Selegiline	61-71	monoamine oxidase B	Homo sapiens	116-121
1418864-0	1992	Effect of the selective MAO-A inhibitors brofaromine, clorgyline and moclobemide on human platelet MAO-B activity.	brofaromine	41-52	monoamine oxidase B	Homo sapiens	99-104
1418864-0	1992	Effect of the selective MAO-A inhibitors brofaromine, clorgyline and moclobemide on human platelet MAO-B activity.	Clorgyline	54-64	monoamine oxidase B	Homo sapiens	99-104
1418864-0	1992	Effect of the selective MAO-A inhibitors brofaromine, clorgyline and moclobemide on human platelet MAO-B activity.	Moclobemide	69-80	monoamine oxidase B	Homo sapiens	99-104
1418864-6	1992	Following moclobemide treatment, MAO-B activity was reduced by 32% (p less than 0.05).	Moclobemide	10-21	monoamine oxidase B	Homo sapiens	33-38
1418864-9	1992	The explanation for this finding may be that metabolites of moclobemide are active inhibitors of MAO-B.	Moclobemide	60-71	monoamine oxidase B	Homo sapiens	97-102
1557063-5	1992	Treatment with deprenyl, an inhibitor of monoamine oxidase type B, partially prevented levodopa neurotoxicity, suggesting that the mechanism of toxicity was, at least in part, related to an increase in the metabolism of dopamine catalyzed by monoamine oxidase.	Selegiline	15-23	monoamine oxidase B	Homo sapiens	41-65
1557063-5	1992	Treatment with deprenyl, an inhibitor of monoamine oxidase type B, partially prevented levodopa neurotoxicity, suggesting that the mechanism of toxicity was, at least in part, related to an increase in the metabolism of dopamine catalyzed by monoamine oxidase.	Levodopa	87-95	monoamine oxidase B	Homo sapiens	41-65
1557063-5	1992	Treatment with deprenyl, an inhibitor of monoamine oxidase type B, partially prevented levodopa neurotoxicity, suggesting that the mechanism of toxicity was, at least in part, related to an increase in the metabolism of dopamine catalyzed by monoamine oxidase.	Dopamine	220-228	monoamine oxidase B	Homo sapiens	41-65
1388699-3	1992	As anticipated, MAO-B was lowest in PD cases on selegiline (L-deprenyl) therapy (mean 1.10).	Selegiline	48-58	monoamine oxidase B	Homo sapiens	16-21
1388699-3	1992	As anticipated, MAO-B was lowest in PD cases on selegiline (L-deprenyl) therapy (mean 1.10).	Selegiline	60-70	monoamine oxidase B	Homo sapiens	16-21
1388699-4	1992	There was a slight deficit of MAO-B among male cases not taking selegiline compared to controls (3.78 vs. 4.15), but the opposite trend was observed for females (6.18 vs. 4.16).	Selegiline	64-74	monoamine oxidase B	Homo sapiens	30-35
1609114-5	1992	In the central nervous system of man MAO-A seems to be mainly involved in the metabolism of 5 HT and noradrenaline, whereas 2-phenylethylamine and probably dopamine are predominantly deaminated by MAO-B.	phenethylamine	124-142	monoamine oxidase B	Homo sapiens	197-202
1609114-5	1992	In the central nervous system of man MAO-A seems to be mainly involved in the metabolism of 5 HT and noradrenaline, whereas 2-phenylethylamine and probably dopamine are predominantly deaminated by MAO-B.	Dopamine	156-164	monoamine oxidase B	Homo sapiens	197-202
1609114-16	1992	In subjects with Parkinson"s disease the MAO-B inhibitor L-deprenyl exerts a L-dopa-sparing effect, prolongs L-dopa action and seems to have a favorable influence regarding on-off disabilities.	Selegiline	57-67	monoamine oxidase B	Homo sapiens	41-46
1609114-16	1992	In subjects with Parkinson"s disease the MAO-B inhibitor L-deprenyl exerts a L-dopa-sparing effect, prolongs L-dopa action and seems to have a favorable influence regarding on-off disabilities.	Levodopa	77-83	monoamine oxidase B	Homo sapiens	41-46
1609114-16	1992	In subjects with Parkinson"s disease the MAO-B inhibitor L-deprenyl exerts a L-dopa-sparing effect, prolongs L-dopa action and seems to have a favorable influence regarding on-off disabilities.	Levodopa	109-115	monoamine oxidase B	Homo sapiens	41-46
1776388-1	1991	Eighteen patients with Parkinson"s disease were treated with placebo for 4 weeks and with the MAO-B inhibitor selegiline for 8 weeks without levodopa in a randomized double-blind clinical study.	Selegiline	110-120	monoamine oxidase B	Homo sapiens	94-99
1815982-5	1991	Major steps in the expression of neurotoxicity involve the conversion of MPTP to the toxic agent 1-methyl-4-phenylpyridinium ion (MPP+) by type B monoamine oxidase (MAO-B) in the glia, specific uptake of MPP+ into the nigro-striatal dopaminergic neurones, the intraneuronal accumulation of MPP+, and the neurotoxic action of MPP+.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	73-77	monoamine oxidase B	Homo sapiens	165-170
1815982-5	1991	Major steps in the expression of neurotoxicity involve the conversion of MPTP to the toxic agent 1-methyl-4-phenylpyridinium ion (MPP+) by type B monoamine oxidase (MAO-B) in the glia, specific uptake of MPP+ into the nigro-striatal dopaminergic neurones, the intraneuronal accumulation of MPP+, and the neurotoxic action of MPP+.	1-Methyl-4-phenylpyridinium	97-128	monoamine oxidase B	Homo sapiens	165-170
1815982-5	1991	Major steps in the expression of neurotoxicity involve the conversion of MPTP to the toxic agent 1-methyl-4-phenylpyridinium ion (MPP+) by type B monoamine oxidase (MAO-B) in the glia, specific uptake of MPP+ into the nigro-striatal dopaminergic neurones, the intraneuronal accumulation of MPP+, and the neurotoxic action of MPP+.	mangion-purified polysaccharide (Candida albicans)	130-134	monoamine oxidase B	Homo sapiens	165-170
1815982-5	1991	Major steps in the expression of neurotoxicity involve the conversion of MPTP to the toxic agent 1-methyl-4-phenylpyridinium ion (MPP+) by type B monoamine oxidase (MAO-B) in the glia, specific uptake of MPP+ into the nigro-striatal dopaminergic neurones, the intraneuronal accumulation of MPP+, and the neurotoxic action of MPP+.	mangion-purified polysaccharide (Candida albicans)	204-208	monoamine oxidase B	Homo sapiens	165-170
1815982-5	1991	Major steps in the expression of neurotoxicity involve the conversion of MPTP to the toxic agent 1-methyl-4-phenylpyridinium ion (MPP+) by type B monoamine oxidase (MAO-B) in the glia, specific uptake of MPP+ into the nigro-striatal dopaminergic neurones, the intraneuronal accumulation of MPP+, and the neurotoxic action of MPP+.	mangion-purified polysaccharide (Candida albicans)	204-208	monoamine oxidase B	Homo sapiens	165-170
1815982-5	1991	Major steps in the expression of neurotoxicity involve the conversion of MPTP to the toxic agent 1-methyl-4-phenylpyridinium ion (MPP+) by type B monoamine oxidase (MAO-B) in the glia, specific uptake of MPP+ into the nigro-striatal dopaminergic neurones, the intraneuronal accumulation of MPP+, and the neurotoxic action of MPP+.	mangion-purified polysaccharide (Candida albicans)	204-208	monoamine oxidase B	Homo sapiens	165-170
1773423-8	1991	We suggest that L-deprenyl, through selective inhibition of MAO-B and by increasing the activity of the catecholaminergic systems, positively influences cognitive functions and behaviour founded on memory efficiency.	Selegiline	16-26	monoamine oxidase B	Homo sapiens	60-65
1886775-7	1991	Exon 12 (bearing the codon for cysteine, which carries the covalently bound FAD cofactor) and exon 13 are highly conserved between human MAOA and MAOB genes (92% at the amino acid level).	Cysteine	31-39	monoamine oxidase B	Homo sapiens	146-150
1658311-0	1991	Deprenyl (selegiline), a selective MAO-B inhibitor with active metabolites; effects on locomotor activity, dopaminergic neurotransmission and firing rate of nigral dopamine neurons.	Selegiline	0-8	monoamine oxidase B	Homo sapiens	35-40
1658311-1	1991	Utilizing behavioral, biochemical and electrophysiological methods, central effects of the monoamine oxidase-B inhibitor deprenyl (selegiline) were analyzed.	Selegiline	121-129	monoamine oxidase B	Homo sapiens	91-110
1741773-8	1991	The ratio, MAO A molecular activity:MAO B molecular activity decreased in the order: serotonin (35:1) greater than tryptamine (12:1) greater than tyramine (3.3:1) greater than dopamine (2.4:1) greater than benzylamine (1:23).	Serotonin	85-94	monoamine oxidase B	Homo sapiens	36-41
1741773-8	1991	The ratio, MAO A molecular activity:MAO B molecular activity decreased in the order: serotonin (35:1) greater than tryptamine (12:1) greater than tyramine (3.3:1) greater than dopamine (2.4:1) greater than benzylamine (1:23).	tryptamine	115-125	monoamine oxidase B	Homo sapiens	36-41
1741773-8	1991	The ratio, MAO A molecular activity:MAO B molecular activity decreased in the order: serotonin (35:1) greater than tryptamine (12:1) greater than tyramine (3.3:1) greater than dopamine (2.4:1) greater than benzylamine (1:23).	Tyramine	146-154	monoamine oxidase B	Homo sapiens	36-41
1741773-8	1991	The ratio, MAO A molecular activity:MAO B molecular activity decreased in the order: serotonin (35:1) greater than tryptamine (12:1) greater than tyramine (3.3:1) greater than dopamine (2.4:1) greater than benzylamine (1:23).	Dopamine	176-184	monoamine oxidase B	Homo sapiens	36-41
1776993-4	1991	The cells could be protected against the reduced toxins, but not MPP+, by either the MAO A selective inhibitor, clorgyline or the MAO B selective inhibitor, deprenyl.	Selegiline	157-165	monoamine oxidase B	Homo sapiens	130-135
1759390-3	1991	Pretreatment of the organelles with a mixture containing chlorgyline and deprenyl completely inhibited monoamine oxidase (MAO) activity and prevented the effects of all the amines studied on mitochondrial enzymes.	Clorgyline	57-68	monoamine oxidase B	Homo sapiens	122-125
1759390-3	1991	Pretreatment of the organelles with a mixture containing chlorgyline and deprenyl completely inhibited monoamine oxidase (MAO) activity and prevented the effects of all the amines studied on mitochondrial enzymes.	Selegiline	73-81	monoamine oxidase B	Homo sapiens	122-125
1759390-4	1991	MAO-dependent effects of 5-methoxytryptamine were fully reproduced by 5-methoxyindolyl-3-acetaldehyde (one of probable products of 5-methoxytryptamine deamination).	5-Methoxytryptamine	25-44	monoamine oxidase B	Homo sapiens	0-3
1759390-4	1991	MAO-dependent effects of 5-methoxytryptamine were fully reproduced by 5-methoxyindolyl-3-acetaldehyde (one of probable products of 5-methoxytryptamine deamination).	5-methoxyindolyl-3-acetaldehyde	70-101	monoamine oxidase B	Homo sapiens	0-3
1759390-4	1991	MAO-dependent effects of 5-methoxytryptamine were fully reproduced by 5-methoxyindolyl-3-acetaldehyde (one of probable products of 5-methoxytryptamine deamination).	5-Methoxytryptamine	131-150	monoamine oxidase B	Homo sapiens	0-3
1686901-0	1991	Synthesis, biological evaluation and quantitative structure activity relationship analysis of nuclear-substituted pargylines as competitive inhibitors of MAO-A and MAO-B.	Pargyline	114-124	monoamine oxidase B	Homo sapiens	164-169
1759390-6	1991	After selective inhibition of MAO-A by chlorgyline the order of MAO-B-dependent effects of biogenic amines on mitochondrial enzymes studied was as follows: tyramine greater than or equal to 2-phenylethylamine much greater than serotonin.	Clorgyline	39-50	monoamine oxidase B	Homo sapiens	64-69
1759390-6	1991	After selective inhibition of MAO-A by chlorgyline the order of MAO-B-dependent effects of biogenic amines on mitochondrial enzymes studied was as follows: tyramine greater than or equal to 2-phenylethylamine much greater than serotonin.	Tyramine	156-164	monoamine oxidase B	Homo sapiens	64-69
1759390-6	1991	After selective inhibition of MAO-A by chlorgyline the order of MAO-B-dependent effects of biogenic amines on mitochondrial enzymes studied was as follows: tyramine greater than or equal to 2-phenylethylamine much greater than serotonin.	phenethylamine	190-208	monoamine oxidase B	Homo sapiens	64-69
1759390-6	1991	After selective inhibition of MAO-A by chlorgyline the order of MAO-B-dependent effects of biogenic amines on mitochondrial enzymes studied was as follows: tyramine greater than or equal to 2-phenylethylamine much greater than serotonin.	Serotonin	227-236	monoamine oxidase B	Homo sapiens	64-69
1759390-8	1991	The data obtained suggest that the product(s) of oxidative deamination of biogenic amines (probably the aldehydes) catalyzed by both types of MAO (MAO-A and MAO-B) are able to regulate the energy functions of mitochondria.	Amines	83-89	monoamine oxidase B	Homo sapiens	142-145
1759390-8	1991	The data obtained suggest that the product(s) of oxidative deamination of biogenic amines (probably the aldehydes) catalyzed by both types of MAO (MAO-A and MAO-B) are able to regulate the energy functions of mitochondria.	Amines	83-89	monoamine oxidase B	Homo sapiens	157-162
1759390-8	1991	The data obtained suggest that the product(s) of oxidative deamination of biogenic amines (probably the aldehydes) catalyzed by both types of MAO (MAO-A and MAO-B) are able to regulate the energy functions of mitochondria.	Aldehydes	104-113	monoamine oxidase B	Homo sapiens	142-145
1759390-8	1991	The data obtained suggest that the product(s) of oxidative deamination of biogenic amines (probably the aldehydes) catalyzed by both types of MAO (MAO-A and MAO-B) are able to regulate the energy functions of mitochondria.	Aldehydes	104-113	monoamine oxidase B	Homo sapiens	157-162
1907217-0	1991	Quantitative localization of human brain monoamine oxidase B by large section autoradiography using L-[3H]deprenyl.	l-[3h]deprenyl	100-114	monoamine oxidase B	Homo sapiens	41-60
1922929-3	1991	An MAO-B inhibitor, deprenyl also decreased the neuronal necrosis, but it inhibited only the changes in 3,4-dihydroxyphenylacetic acid (DOPAC) content after reperfusion.	Selegiline	20-28	monoamine oxidase B	Homo sapiens	3-8
1922929-4	1991	The results suggest that the activation of dopamine metabolism after transient ischemia was mainly mediated by MAO-A and partly by MAO-B and suggest a possible role of dopamine deamination by MAO in the development of ischemic neuronal necrosis.	Dopamine	43-51	monoamine oxidase B	Homo sapiens	131-136
1794016-2	1991	Selegiline (deprenyl) is a selective inhibitor of cerebral monoamine oxidase type B at the dosage (10 mg/day) used in patients with Parkinson"s disease.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	59-83
1794016-2	1991	Selegiline (deprenyl) is a selective inhibitor of cerebral monoamine oxidase type B at the dosage (10 mg/day) used in patients with Parkinson"s disease.	Selegiline	12-20	monoamine oxidase B	Homo sapiens	59-83
2041591-2	1991	Platelet monoamine oxidase-B activity is increased by the use of phenylethylamine but decreased by the use of dopamine as substrate.	Phenethylamines	65-81	monoamine oxidase B	Homo sapiens	9-28
2041591-2	1991	Platelet monoamine oxidase-B activity is increased by the use of phenylethylamine but decreased by the use of dopamine as substrate.	Dopamine	110-118	monoamine oxidase B	Homo sapiens	9-28
2023912-1	1991	Monoamine oxidases A and B [MAOA and MAOB; amine:oxygen oxidoreductase (deaminating) (flavin-containing), EC 1.4.3.4] play important roles in the metabolism of neuroactive, vasoactive amines and the Parkinsonism-producing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	279-283	monoamine oxidase B	Homo sapiens	37-41
2023912-3	1991	Exon 12 codes for the covalent FAD-binding-site and is the most conserved exon; the MAOA and MAOB exon 12 products share 93.9% peptide identity.	Flavin-Adenine Dinucleotide	31-34	monoamine oxidase B	Homo sapiens	93-97
1904879-0	1991	Measurement of cerebral monoamine oxidase B activity using L-[11C]deprenyl and dynamic positron emission tomography.	l-[11c]deprenyl	59-74	monoamine oxidase B	Homo sapiens	24-43
1904879-1	1991	A tracer kinetic procedure was developed for the measurement of monoamine oxidase type B (MAO-B) activity using L-[11C]deprenyl and positron emission tomography (PET).	l-[11c]deprenyl	112-127	monoamine oxidase B	Homo sapiens	64-88
1904879-1	1991	A tracer kinetic procedure was developed for the measurement of monoamine oxidase type B (MAO-B) activity using L-[11C]deprenyl and positron emission tomography (PET).	l-[11c]deprenyl	112-127	monoamine oxidase B	Homo sapiens	90-95
1904879-5	1991	The method was applied to the measurement of the dose-response curve of a reversible MAO-B inhibitor (Ro 19-6327).	lazabemide	102-112	monoamine oxidase B	Homo sapiens	85-90
1909485-1	1991	We treated 20 early Parkinson"s disease subjects with the dopamine agonist lisuride in combination with the MAO-B inhibitor selegiline (L-deprenyl).	Selegiline	124-134	monoamine oxidase B	Homo sapiens	108-113
21229030-3	1991	Research suggests that monoamine oxidase B inhibitors, such as selegiline, should benefit Parkinson"s patients.	Selegiline	63-73	monoamine oxidase B	Homo sapiens	23-42
2023912-1	1991	Monoamine oxidases A and B [MAOA and MAOB; amine:oxygen oxidoreductase (deaminating) (flavin-containing), EC 1.4.3.4] play important roles in the metabolism of neuroactive, vasoactive amines and the Parkinsonism-producing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	4,6-dinitro-o-cresol	86-92	monoamine oxidase B	Homo sapiens	37-41
2023912-1	1991	Monoamine oxidases A and B [MAOA and MAOB; amine:oxygen oxidoreductase (deaminating) (flavin-containing), EC 1.4.3.4] play important roles in the metabolism of neuroactive, vasoactive amines and the Parkinsonism-producing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	Amines	184-190	monoamine oxidase B	Homo sapiens	37-41
2023912-1	1991	Monoamine oxidases A and B [MAOA and MAOB; amine:oxygen oxidoreductase (deaminating) (flavin-containing), EC 1.4.3.4] play important roles in the metabolism of neuroactive, vasoactive amines and the Parkinsonism-producing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	233-277	monoamine oxidase B	Homo sapiens	37-41
1907217-1	1991	The distribution of monoamine oxidase B (MAO-B) in the human brain was studied by quantitative autoradiography using L-[3H]deprenyl as a ligand.	l-[3h]deprenyl	117-131	monoamine oxidase B	Homo sapiens	20-39
1907217-1	1991	The distribution of monoamine oxidase B (MAO-B) in the human brain was studied by quantitative autoradiography using L-[3H]deprenyl as a ligand.	l-[3h]deprenyl	117-131	monoamine oxidase B	Homo sapiens	41-46
1907217-10	1991	When the specific binding of L-[3H]deprenyl was plotted against the MAO-B activities estimated biochemically in punches from the same areas, a high positive correlation was found.	l-[3h]deprenyl	29-43	monoamine oxidase B	Homo sapiens	68-73
1989626-3	1991	These recent developments have provided new therapeutic perspectives for the management of Parkinson"s disease and seizure disorders via the use of selective inhibitors and amino acid amine prodrug substrates of MAO-B.	amino acid amine	173-189	monoamine oxidase B	Homo sapiens	212-217
1905757-3	1991	Both molecular forms of MAO, MAO A and MAO B, were found using specific inhibitors clorgyline and deprenyl.	Clorgyline	83-93	monoamine oxidase B	Homo sapiens	39-44
1905757-3	1991	Both molecular forms of MAO, MAO A and MAO B, were found using specific inhibitors clorgyline and deprenyl.	Selegiline	98-106	monoamine oxidase B	Homo sapiens	39-44
1906004-0	1991	Measurement of human cerebral monoamine oxidase type B (MAO-B) activity with positron emission tomography (PET): a dose ranging study with the reversible inhibitor Ro 19-6327.	lazabemide	164-174	monoamine oxidase B	Homo sapiens	56-61
1686954-2	1991	Because in the human brain, dopamine is metabolised mainly by MAO-B, selegiline increases dopamine content in the central nervous system.	Dopamine	28-36	monoamine oxidase B	Homo sapiens	62-67
1686954-2	1991	Because in the human brain, dopamine is metabolised mainly by MAO-B, selegiline increases dopamine content in the central nervous system.	Selegiline	69-79	monoamine oxidase B	Homo sapiens	62-67
1686954-3	1991	Besides the inhibition of MAO-B, selegiline also inhibits the uptake of dopamine and noradrenaline into presynaptic nerve and increases the turnover of dopamine.	Selegiline	33-43	monoamine oxidase B	Homo sapiens	26-31
2029154-2	1991	Experimental 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine induced parkinsonism can be prevented by monoamine oxidase B inhibitors.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	13-57	monoamine oxidase B	Homo sapiens	99-118
1801535-6	1991	11C-selegiline have been used to demonstrate the intracerebral MAO-B inhibition by therapeutic doses of this drug.	11c-selegiline	0-14	monoamine oxidase B	Homo sapiens	63-68
1801538-2	1991	1.4.3.4) are of obvious interest in relation to Parkinson"s disease and its treatment with the irreversible and selective MAO-B inhibitor L-deprenyl and are discussed in this review: 1) To what extent the two forms of MAO are of importance for the deamination of dopamine and to what degree MAO localised inside and outside of dopaminergic nerve terminals contributes 2) The kinetics of the MAO-protein, i.e. the rate of recovery of MAO after irreversible inhibition.	Selegiline	138-148	monoamine oxidase B	Homo sapiens	122-127
1801542-10	1991	Monoamine oxidase type-B (MAO-B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron.	Dopamine	47-55	monoamine oxidase B	Homo sapiens	0-24
1801542-10	1991	Monoamine oxidase type-B (MAO-B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron.	Dopamine	47-55	monoamine oxidase B	Homo sapiens	26-31
1801542-10	1991	Monoamine oxidase type-B (MAO-B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron.	Hydrogen Peroxide	66-83	monoamine oxidase B	Homo sapiens	0-24
1801542-10	1991	Monoamine oxidase type-B (MAO-B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron.	Hydrogen Peroxide	66-83	monoamine oxidase B	Homo sapiens	26-31
1801542-11	1991	The inhibition of MAO-B by DP may have been the means by which progression of Parkinsonism was attenuated, although other mechanisms are also tenable.	Selegiline	27-29	monoamine oxidase B	Homo sapiens	18-23
1901185-3	1991	Selegiline (also known as deprenyl), is a selective irreversible monoamine oxidase type B inhibitor virtually devoid of the tyramine reaction at the recommended dosage of 10 mg/d.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	65-89
1901185-3	1991	Selegiline (also known as deprenyl), is a selective irreversible monoamine oxidase type B inhibitor virtually devoid of the tyramine reaction at the recommended dosage of 10 mg/d.	Selegiline	26-34	monoamine oxidase B	Homo sapiens	65-89
1906004-4	1991	Data analysis was modelled for two tissue compartments and using an iterative curve fitting technique the value of the rate constant for irreversible binding of L-[11C] deprenyl to MAO-B (k3) in whole brain was obtained for each subject.	l-[11c] deprenyl	161-177	monoamine oxidase B	Homo sapiens	181-186
2018626-2	1991	This abnormality was associated with almost total (90%) reductions in the oxidatively deaminated urinary metabolites of the MAO-A substrate, norepinephrine, and with marked (100-fold) increases in an MAO-B substrate, phenylethylamine, confirming systemic functional consequences of the genetic enzyme deficiency.	Phenethylamines	217-233	monoamine oxidase B	Homo sapiens	200-205
1712206-3	1991	L-deprenyl (LD), a selective and irreversible MAO-B inhibitor, has recently been proposed for the treatment of AD.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	46-51
1712206-3	1991	L-deprenyl (LD), a selective and irreversible MAO-B inhibitor, has recently been proposed for the treatment of AD.	Selegiline	12-14	monoamine oxidase B	Homo sapiens	46-51
1958292-2	1991	The inhibition of dopa decarboxylase and monoamine oxidase B resulting from this combination suggests that there may be a counter-regulatory increase in the activity of the third main enzyme in the catabolism of levodopa, i.e. catecholamine-O-methyl transferase (COMT).	Levodopa	212-220	monoamine oxidase B	Homo sapiens	41-60
2018626-4	1991	To investigate other deaminating systems besides MAO-A and MAO-B that might produce these metabolites of dopamine and 5-HT, we examined plasma amine oxidase (AO) activity in these two patients and two additional patients with the same X-chromosomal deletion.	Dopamine	105-113	monoamine oxidase B	Homo sapiens	59-64
2064731-4	1991	While MAO-B inhibitors, like L-Deprenyl, are thought to protect dopaminergic neurons from MPTP-induced cell death by preventing the conversion of MPTP to its toxic metabolite MPP+, ALC is not known to have MAO-B affinity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	90-94	monoamine oxidase B	Homo sapiens	6-11
2064731-4	1991	While MAO-B inhibitors, like L-Deprenyl, are thought to protect dopaminergic neurons from MPTP-induced cell death by preventing the conversion of MPTP to its toxic metabolite MPP+, ALC is not known to have MAO-B affinity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	146-150	monoamine oxidase B	Homo sapiens	6-11
2362262-0	1990	Vinblastine and vincristine are inhibitors of monoamine oxidase B.	Vinblastine	0-11	monoamine oxidase B	Homo sapiens	46-65
2253761-3	1990	The initial biochemical event is a two-step oxidation by monoamine oxidase B in glial cells to MPP+ (1-methyl-4-phenylpyridinium).	mangion-purified polysaccharide (Candida albicans)	95-99	monoamine oxidase B	Homo sapiens	57-76
2253761-3	1990	The initial biochemical event is a two-step oxidation by monoamine oxidase B in glial cells to MPP+ (1-methyl-4-phenylpyridinium).	1-Methyl-4-phenylpyridinium	101-128	monoamine oxidase B	Homo sapiens	57-76
2246119-2	1990	Recent studies have demonstrated that in humans the hypothalamus has the highest binding density for (3H) MPTP, which corresponds to monoamine oxidase type B (MAO-B).	(3h) mptp	101-110	monoamine oxidase B	Homo sapiens	133-157
2246119-2	1990	Recent studies have demonstrated that in humans the hypothalamus has the highest binding density for (3H) MPTP, which corresponds to monoamine oxidase type B (MAO-B).	(3h) mptp	101-110	monoamine oxidase B	Homo sapiens	159-164
2246119-7	1990	It is suggested that consideration of hypothalamic involvement in MPTP-induced parkinsonism may provide a broader understanding of the pathophysiology of parkinsonism and may, in addition, account for the preliminary observations that MAO-B inhibitors retard the progression of Parkinson disease and possibly prolong life expectancy.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	66-70	monoamine oxidase B	Homo sapiens	235-240
22282124-7	1991	The MAO-B inhibitor, selegiline (5 mg once daily), also lowered the oral tyramine threshold significantly.	Selegiline	21-31	monoamine oxidase B	Homo sapiens	4-9
22282124-7	1991	The MAO-B inhibitor, selegiline (5 mg once daily), also lowered the oral tyramine threshold significantly.	Tyramine	73-81	monoamine oxidase B	Homo sapiens	4-9
1754059-1	1991	In vitro quantitative autoradiography using [3H]L-deprenyl, an irreversible and preferential inhibitor of monoamine oxidase B, was performed to investigate the localization of the enzyme in brains from senile dementia of Alzheimer type and control cases.	[3h]l-deprenyl	44-58	monoamine oxidase B	Homo sapiens	106-125
1754059-8	1991	A high correlation coefficient (r approximately 0.9) was obtained between [3H]L-deprenyl binding and monoamine oxidase-B activity, both in the senile dementia of Alzheimer type and in the control brains.	Selegiline	78-88	monoamine oxidase B	Homo sapiens	101-120
1651528-4	1991	It is synthesised from phenylalanine by L-AADC and oxidatively deaminated by MAO-B.	Phenylalanine	23-36	monoamine oxidase B	Homo sapiens	77-82
2244915-1	1990	It is well established that 1-methyl-4-phenylpyridinium (MPP), the neurotoxic bioactivation product of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and most of its analogs are good competitive inhibitors of monoamine oxidase A, with Ki values in the micromolar range, but they inhibit monoamine oxidase B only at much higher concentrations.	1-Methyl-4-phenylpyridinium	28-55	monoamine oxidase B	Homo sapiens	292-311
2244915-1	1990	It is well established that 1-methyl-4-phenylpyridinium (MPP), the neurotoxic bioactivation product of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and most of its analogs are good competitive inhibitors of monoamine oxidase A, with Ki values in the micromolar range, but they inhibit monoamine oxidase B only at much higher concentrations.	1-Methyl-4-phenylpyridinium	57-60	monoamine oxidase B	Homo sapiens	292-311
2244915-1	1990	It is well established that 1-methyl-4-phenylpyridinium (MPP), the neurotoxic bioactivation product of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and most of its analogs are good competitive inhibitors of monoamine oxidase A, with Ki values in the micromolar range, but they inhibit monoamine oxidase B only at much higher concentrations.	methyl radical	29-37	monoamine oxidase B	Homo sapiens	292-311
2244915-1	1990	It is well established that 1-methyl-4-phenylpyridinium (MPP), the neurotoxic bioactivation product of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and most of its analogs are good competitive inhibitors of monoamine oxidase A, with Ki values in the micromolar range, but they inhibit monoamine oxidase B only at much higher concentrations.	3,6-tetrahydropyridine	125-147	monoamine oxidase B	Homo sapiens	292-311
2266365-1	1990	Monoamine oxidase B (MAO B) plays a pivotal role in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced Parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	52-96	monoamine oxidase B	Homo sapiens	0-19
2266365-1	1990	Monoamine oxidase B (MAO B) plays a pivotal role in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced Parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	52-96	monoamine oxidase B	Homo sapiens	21-26
2266365-1	1990	Monoamine oxidase B (MAO B) plays a pivotal role in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced Parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	monoamine oxidase B	Homo sapiens	0-19
2266365-1	1990	Monoamine oxidase B (MAO B) plays a pivotal role in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced Parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	monoamine oxidase B	Homo sapiens	21-26
2125242-1	1990	The efficacy and tolerability of the monoamine oxidase B inhibitor selegiline and of the nootropic agent oxiracetam were compared in a single-blind, controlled, parallel study.	Selegiline	67-77	monoamine oxidase B	Homo sapiens	37-56
2121360-1	1990	Selegiline, an inhibitor of monoamine oxidase B, was tested on patients with mild to moderate dementia of the Alzheimer type.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	28-47
2362262-0	1990	Vinblastine and vincristine are inhibitors of monoamine oxidase B.	Vincristine	16-27	monoamine oxidase B	Homo sapiens	46-65
2344359-5	1990	For monoamine oxidase B, the dihydropyridiniums were more effective inactivators than the tetrahydropyridines.	dihydropyridiniums	29-47	monoamine oxidase B	Homo sapiens	4-23
2143389-3	1990	Inhibition of MAO-A increased the accumulation of newly-formed DA and reduced DOPAC formation; by contrast, the inhibition of monoamine oxidase, MAO-B, only resulted in a decrease in DOPAC formation.	3,4-Dihydroxyphenylacetic Acid	183-188	monoamine oxidase B	Homo sapiens	145-150
2380287-0	1990	Determination of the monoamine oxidase B inhibitor Ro 19-6327 in plasma by high-performance liquid chromatography using precolumn derivatization with fluorescamine and fluorescence detection.	lazabemide	51-61	monoamine oxidase B	Homo sapiens	21-40
2380287-0	1990	Determination of the monoamine oxidase B inhibitor Ro 19-6327 in plasma by high-performance liquid chromatography using precolumn derivatization with fluorescamine and fluorescence detection.	Fluorescamine	150-163	monoamine oxidase B	Homo sapiens	21-40
2380287-1	1990	A specific high-performance liquid chromatographic (HPLC) method using precolumn derivatization and fluorescence detection was developed for the determination of the monoamine oxidase B inhibitor Ro 19-6327 in human plasma.	lazabemide	196-206	monoamine oxidase B	Homo sapiens	166-185
2344359-5	1990	For monoamine oxidase B, the dihydropyridiniums were more effective inactivators than the tetrahydropyridines.	Pyrrolidines	90-109	monoamine oxidase B	Homo sapiens	4-23
2196964-5	1990	The same depressant effect was observed in animals pretreated with the monoamine oxidase B inhibitor (IMAO-B) deprenyl which is known to reduce milacemide metabolism into glycinamide and glycine.	Selegiline	110-118	monoamine oxidase B	Homo sapiens	71-90
2196964-5	1990	The same depressant effect was observed in animals pretreated with the monoamine oxidase B inhibitor (IMAO-B) deprenyl which is known to reduce milacemide metabolism into glycinamide and glycine.	milacemide	144-154	monoamine oxidase B	Homo sapiens	71-90
2196964-5	1990	The same depressant effect was observed in animals pretreated with the monoamine oxidase B inhibitor (IMAO-B) deprenyl which is known to reduce milacemide metabolism into glycinamide and glycine.	glycine amide	171-182	monoamine oxidase B	Homo sapiens	71-90
2196964-5	1990	The same depressant effect was observed in animals pretreated with the monoamine oxidase B inhibitor (IMAO-B) deprenyl which is known to reduce milacemide metabolism into glycinamide and glycine.	Glycine	187-194	monoamine oxidase B	Homo sapiens	71-90
2248084-5	1990	Moclobemide and clorgyline were found to be the most highly selective MAO-A inhibitors, although both also inhibited 30% of platelet MAO-B activity.	Clorgyline	16-26	monoamine oxidase B	Homo sapiens	133-138
2109658-3	1990	Twenty patients with a clinical diagnosis of DAT and with a slight-moderate mental deterioration were treated with 10 mg/day of L-deprenyl, a selective MAO-B inhibitor, according to a double-blind crossover design vs. placebo.	Selegiline	128-138	monoamine oxidase B	Homo sapiens	152-157
2314388-1	1990	The novel reversible and selective inhibitor of monoamine oxidase-A (MAO-A) Ro 41-1049 [N-(2-aminoethyl)-5-(m-fluorophenyl)-4-thiazole carboxamide HCl] shows inhibition characteristics similar to those of the structurally related reversible MAO-B inhibitors Ro 16-6491 and Ro 19-6327.	Ro 41-1049	76-86	monoamine oxidase B	Homo sapiens	241-246
2314388-1	1990	The novel reversible and selective inhibitor of monoamine oxidase-A (MAO-A) Ro 41-1049 [N-(2-aminoethyl)-5-(m-fluorophenyl)-4-thiazole carboxamide HCl] shows inhibition characteristics similar to those of the structurally related reversible MAO-B inhibitors Ro 16-6491 and Ro 19-6327.	n-(2-aminoethyl)-5-(m-fluorophenyl)-4-thiazole carboxamide hcl	88-150	monoamine oxidase B	Homo sapiens	241-246
2314388-10	1990	As previously reported for the MAO-B ligands [3H]Ro 16-6491 and [3H]Ro 19-6327, the analysis of the membrane-bound radioactivity showed that [3H]Ro 41-1049 was entirely recovered in the form of its aldehyde derivative, indicating that Ro 41-1049 was deaminated by MAO-A.	Tritium	46-48	monoamine oxidase B	Homo sapiens	31-36
2314388-10	1990	As previously reported for the MAO-B ligands [3H]Ro 16-6491 and [3H]Ro 19-6327, the analysis of the membrane-bound radioactivity showed that [3H]Ro 41-1049 was entirely recovered in the form of its aldehyde derivative, indicating that Ro 41-1049 was deaminated by MAO-A.	Tritium	65-67	monoamine oxidase B	Homo sapiens	31-36
2314388-10	1990	As previously reported for the MAO-B ligands [3H]Ro 16-6491 and [3H]Ro 19-6327, the analysis of the membrane-bound radioactivity showed that [3H]Ro 41-1049 was entirely recovered in the form of its aldehyde derivative, indicating that Ro 41-1049 was deaminated by MAO-A.	Tritium	65-67	monoamine oxidase B	Homo sapiens	31-36
2248084-3	1990	Toloxatone and low doses of deprenyl (a MAO-B inhibitor) caused 20% and 17% inhibition respectively; higher doses of deprenyl, however, strongly inhibited MAO-A.	toloxatone	0-10	monoamine oxidase B	Homo sapiens	40-45
2248084-3	1990	Toloxatone and low doses of deprenyl (a MAO-B inhibitor) caused 20% and 17% inhibition respectively; higher doses of deprenyl, however, strongly inhibited MAO-A.	Selegiline	28-36	monoamine oxidase B	Homo sapiens	40-45
2113756-1	1990	Twenty patients with Parkinson"s disease were treated with the MAO-B inhibitor selegiline (l-deprenyl) and placebo without levodopa (L-dopa) in a randomized double-blind clinical cross-over study to analyze relative importances of dopamine (DA) synthesis and metabolism.	Selegiline	79-89	monoamine oxidase B	Homo sapiens	63-68
2113756-1	1990	Twenty patients with Parkinson"s disease were treated with the MAO-B inhibitor selegiline (l-deprenyl) and placebo without levodopa (L-dopa) in a randomized double-blind clinical cross-over study to analyze relative importances of dopamine (DA) synthesis and metabolism.	Selegiline	91-101	monoamine oxidase B	Homo sapiens	63-68
2239154-6	1990	The present results clearly indicate that MAO-B activity is expressed in fibrillary astrocytes in or around senile plaques, suggesting that these astrocytes metabolize exogenous amines in senile plaques.	Amines	178-184	monoamine oxidase B	Homo sapiens	42-47
2297358-0	1990	Characterization of [3H]Ro 16-6491 binding to digitonin solubilized monoamine oxidase-B and purification of the enzyme from human platelets by affinity chromatography.	Tritium	21-23	monoamine oxidase B	Homo sapiens	68-87
2122649-0	1990	L-deprenyl, a MAO-B inhibitor, as an adjunct to conventional L-dopa therapy in Parkinson"s disease: experience in 200 patients.	Selegiline	0-10	monoamine oxidase B	Homo sapiens	14-19
2122653-0	1990	Ro 19-6327, a reversible and highly selective monoamine, oxidase B inhibitor: a novel tool to explore the MAO-B function in humans.	lazabemide	0-10	monoamine oxidase B	Homo sapiens	106-111
2297358-0	1990	Characterization of [3H]Ro 16-6491 binding to digitonin solubilized monoamine oxidase-B and purification of the enzyme from human platelets by affinity chromatography.	Digitonin	46-55	monoamine oxidase B	Homo sapiens	68-87
2089094-4	1990	In addition to the description of the neuroprotective mechanism of the MAO-B-inhibitor L-deprenyl a new aspect focuses the role of the endogenous MAO-B substrates "polyamines" which occur both in neurons and glia.	Polyamines	164-174	monoamine oxidase B	Homo sapiens	146-151
2089092-1	1990	MDL 72.974A [(E) 4-fluoro-beta-fluorethylene benzene butanamine] has been shown in animal studies, both in vitro and in vivo, to be a potent, selective, enzyme-activated irreversible inhibitor of MAO-B (Zreika et al., 1989).	4-fluoro-beta-fluorethylene benzene butanamine	17-63	monoamine oxidase B	Homo sapiens	196-201
2153484-1	1990	In this rapid, simple, and convenient enzymatic method for measurement of tyrosine in plasma, tyrosine is converted to tyramine by action of tyrosine decarboxylase (EC 4.1.1.25) and the tyramine produced is oxidized to p-hydroxybenzyl aldehyde and hydrogen peroxide by action of tyramine oxidase (EC 1.4.3.9).	Tyrosine	74-82	monoamine oxidase B	Homo sapiens	279-295
2153484-1	1990	In this rapid, simple, and convenient enzymatic method for measurement of tyrosine in plasma, tyrosine is converted to tyramine by action of tyrosine decarboxylase (EC 4.1.1.25) and the tyramine produced is oxidized to p-hydroxybenzyl aldehyde and hydrogen peroxide by action of tyramine oxidase (EC 1.4.3.9).	Tyrosine	94-102	monoamine oxidase B	Homo sapiens	279-295
2153484-1	1990	In this rapid, simple, and convenient enzymatic method for measurement of tyrosine in plasma, tyrosine is converted to tyramine by action of tyrosine decarboxylase (EC 4.1.1.25) and the tyramine produced is oxidized to p-hydroxybenzyl aldehyde and hydrogen peroxide by action of tyramine oxidase (EC 1.4.3.9).	Tyramine	119-127	monoamine oxidase B	Homo sapiens	279-295
2153484-1	1990	In this rapid, simple, and convenient enzymatic method for measurement of tyrosine in plasma, tyrosine is converted to tyramine by action of tyrosine decarboxylase (EC 4.1.1.25) and the tyramine produced is oxidized to p-hydroxybenzyl aldehyde and hydrogen peroxide by action of tyramine oxidase (EC 1.4.3.9).	Tyramine	186-194	monoamine oxidase B	Homo sapiens	279-295
2089094-4	1990	In addition to the description of the neuroprotective mechanism of the MAO-B-inhibitor L-deprenyl a new aspect focuses the role of the endogenous MAO-B substrates "polyamines" which occur both in neurons and glia.	Selegiline	87-97	monoamine oxidase B	Homo sapiens	71-76
2193105-3	1990	In the presence of MAO-B inhibitors treatment with reserpine causes reciprocal changes to PE and DA suggesting a functional relationship between them and after unilateral lesions of the substantia nigra an ipsilateral reduction in striatal PE is seen suggesting again a co-relationship with DA.	Reserpine	51-60	monoamine oxidase B	Homo sapiens	19-24
2128498-1	1990	The DATATOP study is a clinical trial in which deprenyl, a selective inhibitor of monoamine oxidase-B (MAO-B), is being given to newly diagnosed Parkinsonian patients in an attempt to halt the progression of their disorder.	Selegiline	47-55	monoamine oxidase B	Homo sapiens	82-101
2128498-1	1990	The DATATOP study is a clinical trial in which deprenyl, a selective inhibitor of monoamine oxidase-B (MAO-B), is being given to newly diagnosed Parkinsonian patients in an attempt to halt the progression of their disorder.	Selegiline	47-55	monoamine oxidase B	Homo sapiens	103-108
2128498-3	1990	In the present study we point out that several analogs of MPTP are good substrates not only for MAO-B but also for MAO-A.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	58-62	monoamine oxidase B	Homo sapiens	96-101
2128498-4	1990	In addition, we point out that with long-term administration to rodents, deprenyl loses its selectivity as an inhibitor of MAO-B and also inhibits MAO-A.	Selegiline	73-81	monoamine oxidase B	Homo sapiens	123-128
2193111-0	1990	From moclobemide to Ro 19-6327 and Ro 41-1049: the development of a new class of reversible, selective MAO-A and MAO-B inhibitors.	Moclobemide	5-16	monoamine oxidase B	Homo sapiens	113-118
2358804-2	1990	The desmethyl derivative, 4-phenyl-1,2,3,6-tetrahydropyridine (PTP), was oxidised by MAO-B to form the corresponding dihydropyridine.	4-phenyl-1,2,3,6-tetrahydropyridine	26-61	monoamine oxidase B	Homo sapiens	85-90
2358804-2	1990	The desmethyl derivative, 4-phenyl-1,2,3,6-tetrahydropyridine (PTP), was oxidised by MAO-B to form the corresponding dihydropyridine.	4-phenyl-1,2,3,6-tetrahydropyridine	63-66	monoamine oxidase B	Homo sapiens	85-90
2193111-4	1990	The study of the MAO inhibitory characteristics of several known and putative moclobemide metabolites did not allow the identification of a potent MAO-A inhibitor but led to the discovery of Ro 16-6491, a potent MAO-B inhibitor of novel chemical structure.	Ro 16-6491	191-201	monoamine oxidase B	Homo sapiens	212-217
2358804-2	1990	The desmethyl derivative, 4-phenyl-1,2,3,6-tetrahydropyridine (PTP), was oxidised by MAO-B to form the corresponding dihydropyridine.	1,4-dihydropyridine	117-132	monoamine oxidase B	Homo sapiens	85-90
2358804-5	1990	Substitution of a methyl group at the 6-position of the heterocyclic ring of MPTP prevented it from acting as a substrate for MAO-B and greatly decreased its potency as an inhibitor of that form of MAO, although it remained a good competitive inhibitor of MAO-A.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	77-81	monoamine oxidase B	Homo sapiens	126-131
2293615-2	1990	Marked (four-to 100-fold) elevations in levels of urinary phenylethylamine, o-tyramine, and m-tyramine (which are preferential substrates for MAO-B) and marked reductions (90%) in levels of 3-methoxy-4-hydroxyphenylglycol (a deaminated metabolite of norepinephrine, a preferential substrate for MAO-A) in urine and plasma confirmed the presence of a systemic, functionally significant reduction in the activities of both MAO isozymes.	3-tyramine	92-102	monoamine oxidase B	Homo sapiens	142-147
2358804-6	1990	Replacement of the tetrahydropyridine ring of PTP by piperidine apparently abolished the ability to act as a substrate for MAO-B.	Pyrrolidines	19-37	monoamine oxidase B	Homo sapiens	123-128
2358804-6	1990	Replacement of the tetrahydropyridine ring of PTP by piperidine apparently abolished the ability to act as a substrate for MAO-B.	piperidine	53-63	monoamine oxidase B	Homo sapiens	123-128
20504633-6	1990	Thus, although DA is a substrate for both enzyme forms in monkey brain, similar to what has been reported in human brain, its inactivation is primarily dependent on MAO-B activity.	Dopamine	15-17	monoamine oxidase B	Homo sapiens	165-170
1691454-1	1990	Isatin (Tribulin) produced a dose-dependent inhibition of both MAO A and MAO B in broken cell preparations from rat brain and pineal.	Isatin	0-6	monoamine oxidase B	Homo sapiens	73-78
33775841-1	2021	Tranylcypromine (TCP)-based structural modifications lead to the discovery of new LSD1 inhibitors, of which compounds 26b and 29b effectively inhibit LSD1 with the IC50 values of 17 and 11 nM, respectively and also show good selectivity over MAO-B.	Tranylcypromine	0-15	monoamine oxidase B	Homo sapiens	242-247
2300680-3	1990	The investigation was later continued in an open fashion by giving a single 10 mg dose of the MAO-B inhibitor deprenyl to the same subjects.	Selegiline	110-118	monoamine oxidase B	Homo sapiens	94-99
2222781-2	1990	With this in mind we studied platelet monoamine oxidase B (MAO B) activity and 3H-imipramine (IMI) binding in both AD patients and healthy subjects and found a significantly higher level of platelet MAO B activity and 3H-IMI Bmax values in the AD patients.	Tritium	79-81	monoamine oxidase B	Homo sapiens	199-204
2222781-3	1990	In view of the part that MAO B plays in metabolizing serotonin (5HT) and of the relationship which exists between 3H-IMI binding and 5HT uptake, our results would suggest that with AD there occurs a complex dysfunction in the 5HT system, at least at a peripheral level.	Serotonin	53-62	monoamine oxidase B	Homo sapiens	25-30
2222781-3	1990	In view of the part that MAO B plays in metabolizing serotonin (5HT) and of the relationship which exists between 3H-IMI binding and 5HT uptake, our results would suggest that with AD there occurs a complex dysfunction in the 5HT system, at least at a peripheral level.	Serotonin	64-67	monoamine oxidase B	Homo sapiens	25-30
2111588-7	1990	Selective accumulation of [125I]MHTP-derived radioactivity within these structures was blocked by pretreatment with pargyline, suggesting that monoamine oxidase B is involved in the bioactivation of radioiodinated MHTP.	7-mercaptoheptanoylthreonine phosphate	32-36	monoamine oxidase B	Homo sapiens	143-162
2111588-7	1990	Selective accumulation of [125I]MHTP-derived radioactivity within these structures was blocked by pretreatment with pargyline, suggesting that monoamine oxidase B is involved in the bioactivation of radioiodinated MHTP.	Pargyline	116-125	monoamine oxidase B	Homo sapiens	143-162
2111588-7	1990	Selective accumulation of [125I]MHTP-derived radioactivity within these structures was blocked by pretreatment with pargyline, suggesting that monoamine oxidase B is involved in the bioactivation of radioiodinated MHTP.	7-mercaptoheptanoylthreonine phosphate	214-218	monoamine oxidase B	Homo sapiens	143-162
33775841-1	2021	Tranylcypromine (TCP)-based structural modifications lead to the discovery of new LSD1 inhibitors, of which compounds 26b and 29b effectively inhibit LSD1 with the IC50 values of 17 and 11 nM, respectively and also show good selectivity over MAO-B.	Tranylcypromine	17-20	monoamine oxidase B	Homo sapiens	242-247
33237524-5	2021	Out of the three best selected natural products, cardamomin showed excellently predicted drug-like properties, superior pharmacological profile, and specific interactions with MAO-B active site, indicating a potential selectivity over MAO-B.	cardamonin	49-59	monoamine oxidase B	Homo sapiens	176-181
33033175-2	2020	The mitochondrial enzyme monoamine oxidase B (MAOB) is highly expressed in GBM and oxidizes an uncharged methyl-tetrahydropyridine (MP-) moiety into the mitochondrially-targeted cationic form, methyl-pyridinium (P+-).	methyl-tetrahydropyridine	105-130	monoamine oxidase B	Homo sapiens	25-44
33033175-2	2020	The mitochondrial enzyme monoamine oxidase B (MAOB) is highly expressed in GBM and oxidizes an uncharged methyl-tetrahydropyridine (MP-) moiety into the mitochondrially-targeted cationic form, methyl-pyridinium (P+-).	methyl-tetrahydropyridine	105-130	monoamine oxidase B	Homo sapiens	46-50
33033175-2	2020	The mitochondrial enzyme monoamine oxidase B (MAOB) is highly expressed in GBM and oxidizes an uncharged methyl-tetrahydropyridine (MP-) moiety into the mitochondrially-targeted cationic form, methyl-pyridinium (P+-).	6-trimethylsilylthio-9-trimethylsilylpurine	132-135	monoamine oxidase B	Homo sapiens	25-44
33033175-2	2020	The mitochondrial enzyme monoamine oxidase B (MAOB) is highly expressed in GBM and oxidizes an uncharged methyl-tetrahydropyridine (MP-) moiety into the mitochondrially-targeted cationic form, methyl-pyridinium (P+-).	6-trimethylsilylthio-9-trimethylsilylpurine	132-135	monoamine oxidase B	Homo sapiens	46-50
33033175-2	2020	The mitochondrial enzyme monoamine oxidase B (MAOB) is highly expressed in GBM and oxidizes an uncharged methyl-tetrahydropyridine (MP-) moiety into the mitochondrially-targeted cationic form, methyl-pyridinium (P+-).	methyl-pyridinium	193-210	monoamine oxidase B	Homo sapiens	25-44
33033175-2	2020	The mitochondrial enzyme monoamine oxidase B (MAOB) is highly expressed in GBM and oxidizes an uncharged methyl-tetrahydropyridine (MP-) moiety into the mitochondrially-targeted cationic form, methyl-pyridinium (P+-).	methyl-pyridinium	193-210	monoamine oxidase B	Homo sapiens	46-50
33033175-3	2020	Coupling this MAOB-sensitive group to a nitrogen mustard produced a prodrug that damaged GBM mitochondria and killed GBM cells.	Nitrogen	40-48	monoamine oxidase B	Homo sapiens	14-18
33033175-9	2020	Our studies demonstrate that MP-Pt(IV) is selectively activated by MAOB.	mp-pt	29-34	monoamine oxidase B	Homo sapiens	67-71
33033175-12	2020	In in vitro studies, sub-lethal MP-Pt(IV) doses elevated mitochondrial MAOB levels in surviving GBM cells.	mp-pt	32-37	monoamine oxidase B	Homo sapiens	71-75
33237524-5	2021	Out of the three best selected natural products, cardamomin showed excellently predicted drug-like properties, superior pharmacological profile, and specific interactions with MAO-B active site, indicating a potential selectivity over MAO-B.	cardamonin	49-59	monoamine oxidase B	Homo sapiens	235-240
34990933-0	2022	Indoles and 1-(3-(benzyloxy)benzyl)piperazines: Reversible and selective monoamine oxidase B inhibitors identified by screening an in-house compound library.	Indoles	0-7	monoamine oxidase B	Homo sapiens	73-92
32920430-0	2020	Chalcones: Unearthing their therapeutic possibility as monoamine oxidase B inhibitors.	Chalcones	0-9	monoamine oxidase B	Homo sapiens	55-74
29432286-10	2018	For patients on oral LD regimens and taking a dopaminergic agonist, and/or a MAO-B inhibitor, changing from an IR to an ER CD-LD formulation provides approximately an additional hour of "good" on time.	carbidopa, levodopa drug combination	123-128	monoamine oxidase B	Homo sapiens	77-82
24165688-2	2013	Dopamine agonists, the next most effective class of drugs, can be used alone before the introduction of levodopa or as an adjunct to levodopa.Addition of a peripherally-acting COMT inhibitor or an MAO-B inhibitor to levodopa can reduce motor fluctuations in patients with advanced disease.Amantadine may have mild symptomatic benefit and can decrease levodopa-induced dyskinesias.Anticholinergics are rarely used because of their adverse effects, but can be a useful addition to levodopa for control of tremor and drooling.Subcutaneous apomorphine should be available for rescue use in patients with "off" episodes.	Dopamine	0-8	monoamine oxidase B	Homo sapiens	197-202
20029636-4	2009	However, forcing central dopamine metabolism further down the methylation path by central blocking of COMT and MAO-B may reduce oxidative stress and homocysteine levels.	Dopamine	25-33	monoamine oxidase B	Homo sapiens	111-116
20029636-4	2009	However, forcing central dopamine metabolism further down the methylation path by central blocking of COMT and MAO-B may reduce oxidative stress and homocysteine levels.	Homocysteine	149-161	monoamine oxidase B	Homo sapiens	111-116
1447747-1	1992	The exceptionally good MAO-B substrate properties of several 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) derivatives have prompted studies to evaluate the corresponding properties of tetrahydropyridines bearing heteroatom-linked groups at C-4.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	107-111	monoamine oxidase B	Homo sapiens	23-28
1447747-2	1992	The 1-methyl-4-phenoxy-1,2,3,6-tetrahydropyridine analog proved to be an excellent MAO-B substrate.	1-methyl-4-phenoxy-1,2,3,6-tetrahydropyridine	4-49	monoamine oxidase B	Homo sapiens	83-88
34990933-0	2022	Indoles and 1-(3-(benzyloxy)benzyl)piperazines: Reversible and selective monoamine oxidase B inhibitors identified by screening an in-house compound library.	1-(3-(benzyloxy)benzyl)piperazines	12-46	monoamine oxidase B	Homo sapiens	73-92
34990933-3	2022	Two series of indole (23 analogues) and 3-(benzyloxy)benzyl)piperazine (16 analogues) MAO-B inhibitors were derived from hits, and screened for their structure-activity relationships.	3-(benzyloxy)benzyl)piperazine	40-70	monoamine oxidase B	Homo sapiens	86-91
34990933-4	2022	Both series yielded low micromolar selective inhibitors of human MAO-B, namely indole 2 (IC50 = 12.63 +- 1.21 microM) and piperazine 39 (IC50 = 19.25 +- 4.89 microM), which is comparable to selective MAO-B inhibitor isatin (IC50 = 6.10 +- 2.81 microM), yet less potent in comparison to safinamide (IC50 = 0.029 +- 0.002 microM).	indole 2	79-87	monoamine oxidase B	Homo sapiens	65-70
34990933-4	2022	Both series yielded low micromolar selective inhibitors of human MAO-B, namely indole 2 (IC50 = 12.63 +- 1.21 microM) and piperazine 39 (IC50 = 19.25 +- 4.89 microM), which is comparable to selective MAO-B inhibitor isatin (IC50 = 6.10 +- 2.81 microM), yet less potent in comparison to safinamide (IC50 = 0.029 +- 0.002 microM).	Piperazine	122-132	monoamine oxidase B	Homo sapiens	65-70
34990933-4	2022	Both series yielded low micromolar selective inhibitors of human MAO-B, namely indole 2 (IC50 = 12.63 +- 1.21 microM) and piperazine 39 (IC50 = 19.25 +- 4.89 microM), which is comparable to selective MAO-B inhibitor isatin (IC50 = 6.10 +- 2.81 microM), yet less potent in comparison to safinamide (IC50 = 0.029 +- 0.002 microM).	Isatin	216-222	monoamine oxidase B	Homo sapiens	65-70
34990933-4	2022	Both series yielded low micromolar selective inhibitors of human MAO-B, namely indole 2 (IC50 = 12.63 +- 1.21 microM) and piperazine 39 (IC50 = 19.25 +- 4.89 microM), which is comparable to selective MAO-B inhibitor isatin (IC50 = 6.10 +- 2.81 microM), yet less potent in comparison to safinamide (IC50 = 0.029 +- 0.002 microM).	Isatin	216-222	monoamine oxidase B	Homo sapiens	200-205
34990933-4	2022	Both series yielded low micromolar selective inhibitors of human MAO-B, namely indole 2 (IC50 = 12.63 +- 1.21 microM) and piperazine 39 (IC50 = 19.25 +- 4.89 microM), which is comparable to selective MAO-B inhibitor isatin (IC50 = 6.10 +- 2.81 microM), yet less potent in comparison to safinamide (IC50 = 0.029 +- 0.002 microM).	safinamide	286-296	monoamine oxidase B	Homo sapiens	65-70
34814086-5	2022	The compound 42e and 42h displayed the highest inhibitory activity against hMAO-B with IC50 values of 2.51 and 2.81 microM, respectively, and more than 25-fold selectivity towards inhibition of hMAO-B.	1-Oleoylglycerophosphocholine	21-24	monoamine oxidase B	Homo sapiens	194-200
34713936-4	2022	Here, we investigate the role of MAO-B, a GABA-producing enzyme, in reactive astrogliosis in STAB.	gamma-Aminobutyric Acid	42-46	monoamine oxidase B	Homo sapiens	33-38
34713936-5	2022	We observed that the genetic removal of MAO-B significantly reduced the hypertrophy, scar formation, and GABA production of reactive astrocytes, whereas the MAO-B overexpression under glial fibrillary acidic protein (GFAP) promoter enhanced the levels of GFAP and GABA.	gamma-Aminobutyric Acid	105-109	monoamine oxidase B	Homo sapiens	40-45
34713936-5	2022	We observed that the genetic removal of MAO-B significantly reduced the hypertrophy, scar formation, and GABA production of reactive astrocytes, whereas the MAO-B overexpression under glial fibrillary acidic protein (GFAP) promoter enhanced the levels of GFAP and GABA.	gamma-Aminobutyric Acid	264-268	monoamine oxidase B	Homo sapiens	157-162
34713936-6	2022	Furthermore, we found that one of the by-products of the MAO-B action, H2 O2 , but not GABA, was sufficient and necessary for the hypertrophy of reactive astrocytes.	Hydrogen Peroxide	71-76	monoamine oxidase B	Homo sapiens	57-62
34713936-7	2022	Notably, we identified two potent pharmacological tools to attenuate scar-forming astrogliosis-the recently developed reversible MAO-B inhibitor, KDS2010, and an H2 O2 scavenger, crisdesalazine (AAD-2004).	kds2010	146-153	monoamine oxidase B	Homo sapiens	129-134
34713936-8	2022	Our results implicate that inhibiting MAO-B activity has dual beneficial effects in preventing astrogliosis and scar-formation under brain injury, and that the MAO-B/H2 O2 pathway can be a useful therapeutic target with a high clinical potential.	Deuterium	166-168	monoamine oxidase B	Homo sapiens	38-43
34713936-8	2022	Our results implicate that inhibiting MAO-B activity has dual beneficial effects in preventing astrogliosis and scar-formation under brain injury, and that the MAO-B/H2 O2 pathway can be a useful therapeutic target with a high clinical potential.	Deuterium	166-168	monoamine oxidase B	Homo sapiens	160-165
34713936-8	2022	Our results implicate that inhibiting MAO-B activity has dual beneficial effects in preventing astrogliosis and scar-formation under brain injury, and that the MAO-B/H2 O2 pathway can be a useful therapeutic target with a high clinical potential.	Oxygen	169-171	monoamine oxidase B	Homo sapiens	38-43
34713936-8	2022	Our results implicate that inhibiting MAO-B activity has dual beneficial effects in preventing astrogliosis and scar-formation under brain injury, and that the MAO-B/H2 O2 pathway can be a useful therapeutic target with a high clinical potential.	Oxygen	169-171	monoamine oxidase B	Homo sapiens	160-165
34814086-5	2022	The compound 42e and 42h displayed the highest inhibitory activity against hMAO-B with IC50 values of 2.51 and 2.81 microM, respectively, and more than 25-fold selectivity towards inhibition of hMAO-B.	3TC-MP	13-16	monoamine oxidase B	Homo sapiens	75-81
34814086-5	2022	The compound 42e and 42h displayed the highest inhibitory activity against hMAO-B with IC50 values of 2.51 and 2.81 microM, respectively, and more than 25-fold selectivity towards inhibition of hMAO-B.	3TC-MP	13-16	monoamine oxidase B	Homo sapiens	194-200
34814086-5	2022	The compound 42e and 42h displayed the highest inhibitory activity against hMAO-B with IC50 values of 2.51 and 2.81 microM, respectively, and more than 25-fold selectivity towards inhibition of hMAO-B.	1-Oleoylglycerophosphocholine	21-24	monoamine oxidase B	Homo sapiens	75-81
34597253-2	2022	AREAS COVERED: : Safinamide is a highly selective and reversible monoamine oxidase B inhibitor introduced in the European Union, Japan, and the United States as an adjunctive agent to levodopa in PD patients with motor fluctuation.	safinamide	17-27	monoamine oxidase B	Homo sapiens	65-84
34915314-3	2022	In an attempt to discover novel MAO inhibitors, 30 phenothiazine, anthraquinone and related tricyclic derivatives were selected and evaluated as potential inhibitors of human MAO-A and MAO-B.	phenothiazine	51-64	monoamine oxidase B	Homo sapiens	185-190
34814086-7	2022	According to our findings the (1,2,4)triazolo(3,4-b)(1,3,4)thiadiazole emerged as a promising scaffold for the development of novel and selective hMAO-B inhibitors.	1,2,4-triazolo-(3,4-b)-1,3,4-thiadiazoles	30-70	monoamine oxidase B	Homo sapiens	146-152
34823038-2	2022	We previously showed that short-term treatment with safinamide, a monoamine oxidase type-B inhibitor with anti-glutamatergic properties, improves abnormally enhanced short-interval intracortical facilitation (SICF) in PD patients.	safinamide	52-62	monoamine oxidase B	Homo sapiens	66-90
34931332-0	2022	Design, synthesis, biological activity, molecular docking, and molecular dynamics of novel benzimidazole derivatives as potential AChE/MAO-B dual inhibitors.	benzimidazole	91-104	monoamine oxidase B	Homo sapiens	135-140
34931332-1	2022	To develop new acetylcholinesterase (AChE)-monoamine oxidase-B (MAO-B) dual inhibitors against Alzheimer"s disease, the benzimidazole ring, which has a propargyl side chain with previously proven selective MAO-B inhibitory activity, was used as the main structure.	benzimidazole	120-133	monoamine oxidase B	Homo sapiens	43-62
34931332-1	2022	To develop new acetylcholinesterase (AChE)-monoamine oxidase-B (MAO-B) dual inhibitors against Alzheimer"s disease, the benzimidazole ring, which has a propargyl side chain with previously proven selective MAO-B inhibitory activity, was used as the main structure.	benzimidazole	120-133	monoamine oxidase B	Homo sapiens	64-69
34931332-1	2022	To develop new acetylcholinesterase (AChE)-monoamine oxidase-B (MAO-B) dual inhibitors against Alzheimer"s disease, the benzimidazole ring, which has a propargyl side chain with previously proven selective MAO-B inhibitory activity, was used as the main structure.	benzimidazole	120-133	monoamine oxidase B	Homo sapiens	206-211
34977548-3	2022	Some monoamine oxidase (MAO)-B inhibitors have a sympathomimetic amine, which can be attributed to OH.	Amines	65-70	monoamine oxidase B	Homo sapiens	5-30
34977548-4	2022	Therefore, we determined whether rasagiline, a common MAO-B inhibitor used in PD treatment, can contribute to cardiovascular autonomic BP dysregulation in patients with early or mild PD.	rasagiline	33-43	monoamine oxidase B	Homo sapiens	54-59
34281458-6	2021	The overall results demonstrated that substitution of the phenylethyloxy moiety at the 7-position imparted superior general activity to the derivatives, with the propargylamine substitution at the 3-position, in particular, displaying the best MAO-B selectivity and neuroprotection.	propargylamine	162-176	monoamine oxidase B	Homo sapiens	244-249
34666128-8	2021	Besides, baicalein improved the neurotoxicity induced by MPTP as seen by a significant raise of tyrosine hydroxylase (TH) and simultaneous decrease of monoamine-oxidase-B (MAO-B).	baicalein	9-18	monoamine oxidase B	Homo sapiens	151-170
34666128-8	2021	Besides, baicalein improved the neurotoxicity induced by MPTP as seen by a significant raise of tyrosine hydroxylase (TH) and simultaneous decrease of monoamine-oxidase-B (MAO-B).	baicalein	9-18	monoamine oxidase B	Homo sapiens	172-177
34666128-8	2021	Besides, baicalein improved the neurotoxicity induced by MPTP as seen by a significant raise of tyrosine hydroxylase (TH) and simultaneous decrease of monoamine-oxidase-B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	57-61	monoamine oxidase B	Homo sapiens	151-170
34666128-8	2021	Besides, baicalein improved the neurotoxicity induced by MPTP as seen by a significant raise of tyrosine hydroxylase (TH) and simultaneous decrease of monoamine-oxidase-B (MAO-B).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	57-61	monoamine oxidase B	Homo sapiens	172-177
34773851-0	2022	Imaging of astrocytes in posttraumatic stress disorder: A PET study with the monoamine oxidase B radioligand (11C)SL25.1188.	Carbon-11	110-113	monoamine oxidase B	Homo sapiens	77-96
34970960-3	2021	Inhibitors of MAO-B are used to alleviate symptoms by reducing monoamine oxidase-catalysed degradation of dopamine; hence, preserving functional levels of dopamine.	Dopamine	106-114	monoamine oxidase B	Homo sapiens	14-19
34970960-3	2021	Inhibitors of MAO-B are used to alleviate symptoms by reducing monoamine oxidase-catalysed degradation of dopamine; hence, preserving functional levels of dopamine.	Dopamine	155-163	monoamine oxidase B	Homo sapiens	14-19
34970960-4	2021	The very first MAO-B used therapeutically was selegiline, followed by rasagiline, its indane derivative which has superior efficacy and selectivity.	Selegiline	46-56	monoamine oxidase B	Homo sapiens	15-20
34970960-6	2021	Safinamide, a reversible MAO-B inhibitor that utilises both dopaminergic and non-dopaminergic mechanisms, was recently approved by the European Medicines Agency (EMA) (2015) and U.S. FDA (2017) as an add-on therapy for patients with mid- or late-stage Parkinson"s disease.	safinamide	0-10	monoamine oxidase B	Homo sapiens	25-30
34962574-3	2022	Objective: To compare the long-term effects on patient-rated quality of life of adding a dopamine agonist vs a dopamine reuptake inhibitor (DRI), either a monoamine oxidase type B (MAO-B) inhibitor or a catechol-O-methyltransferase (COMT) inhibitor, to levodopa therapy for the treatment of patients with motor complications of PD.	Levodopa	253-261	monoamine oxidase B	Homo sapiens	155-179
34962574-3	2022	Objective: To compare the long-term effects on patient-rated quality of life of adding a dopamine agonist vs a dopamine reuptake inhibitor (DRI), either a monoamine oxidase type B (MAO-B) inhibitor or a catechol-O-methyltransferase (COMT) inhibitor, to levodopa therapy for the treatment of patients with motor complications of PD.	Levodopa	253-261	monoamine oxidase B	Homo sapiens	181-186
34653442-7	2021	Molecular modelling rationalised the binding mode of 2"-hydroxychalcones in the active site of hMAO-B.	2'-hydroxychalcone	53-72	monoamine oxidase B	Homo sapiens	95-101
34912209-1	2021	Introduction: We aimed to determine whether in vivo tau deposits and monoamine oxidase B (MAO-B) detection using 18F-THK5351 positron emission tomography (PET) can assist in the differential distribution in patients with corticobasal syndrome (CBS), progressive supranuclear palsy (PSP), and Alzheimer"s disease (AD) and whether 18F-THK5351 retention of lesion sites in CBS and PSP can correlate with clinical parameters.	THK5351	117-124	monoamine oxidase B	Homo sapiens	69-88
34912209-1	2021	Introduction: We aimed to determine whether in vivo tau deposits and monoamine oxidase B (MAO-B) detection using 18F-THK5351 positron emission tomography (PET) can assist in the differential distribution in patients with corticobasal syndrome (CBS), progressive supranuclear palsy (PSP), and Alzheimer"s disease (AD) and whether 18F-THK5351 retention of lesion sites in CBS and PSP can correlate with clinical parameters.	THK5351	117-124	monoamine oxidase B	Homo sapiens	90-95
34912209-1	2021	Introduction: We aimed to determine whether in vivo tau deposits and monoamine oxidase B (MAO-B) detection using 18F-THK5351 positron emission tomography (PET) can assist in the differential distribution in patients with corticobasal syndrome (CBS), progressive supranuclear palsy (PSP), and Alzheimer"s disease (AD) and whether 18F-THK5351 retention of lesion sites in CBS and PSP can correlate with clinical parameters.	THK5351	333-340	monoamine oxidase B	Homo sapiens	69-88
34912209-1	2021	Introduction: We aimed to determine whether in vivo tau deposits and monoamine oxidase B (MAO-B) detection using 18F-THK5351 positron emission tomography (PET) can assist in the differential distribution in patients with corticobasal syndrome (CBS), progressive supranuclear palsy (PSP), and Alzheimer"s disease (AD) and whether 18F-THK5351 retention of lesion sites in CBS and PSP can correlate with clinical parameters.	THK5351	333-340	monoamine oxidase B	Homo sapiens	90-95
34503991-3	2021	Catecholamines are metabolized by two isoforms of monoamine oxidase, MAO-A and MAO-B; and although the anatomic localization of MAO-A and MAO-B and substrate specificities of enzyme inhibitors are well characterized, relative susceptibilities of the endogenous catecholamines to enzymatic oxidation by MAO-A and MAO-B have not been studied systematically.	Catecholamines	261-275	monoamine oxidase B	Homo sapiens	312-317
34867348-0	2021	Monoamine Oxidase-B Inhibitor Reduction in Pro-Inflammatory Cytokines Mediated by Inhibition of cAMP-PKA/EPAC Signaling.	Cyclic AMP	96-100	monoamine oxidase B	Homo sapiens	0-19
34867348-4	2021	We tested the anti-inflammatory therapeutic potential of a recently developed reversible MAO-B inhibitor (RG0216) with reduced transport across the blood-brain barrier.	rg0216	106-112	monoamine oxidase B	Homo sapiens	89-94
34867348-5	2021	In an epithelial cell culture model, RG0216 significantly decreased LPS-induced interleukin (IL)-6 and IL-1beta gene and protein expression and was as effective as equimolar concentrations of deprenyl (an existing irreversible MAO-B inhibitor).	rg0216	37-43	monoamine oxidase B	Homo sapiens	227-232
34867348-5	2021	In an epithelial cell culture model, RG0216 significantly decreased LPS-induced interleukin (IL)-6 and IL-1beta gene and protein expression and was as effective as equimolar concentrations of deprenyl (an existing irreversible MAO-B inhibitor).	Selegiline	192-200	monoamine oxidase B	Homo sapiens	227-232
34784871-11	2021	Of monoamine oxidase B inhibitors, safinamide is the least susceptible for interaction with the tyramine-rich food, whereas selegiline and rasagiline may lose selectivity to monoamine oxidase B when administered in supratherapeutic doses.	safinamide	35-45	monoamine oxidase B	Homo sapiens	3-22
34784871-11	2021	Of monoamine oxidase B inhibitors, safinamide is the least susceptible for interaction with the tyramine-rich food, whereas selegiline and rasagiline may lose selectivity to monoamine oxidase B when administered in supratherapeutic doses.	Tyramine	96-104	monoamine oxidase B	Homo sapiens	3-22
34784871-11	2021	Of monoamine oxidase B inhibitors, safinamide is the least susceptible for interaction with the tyramine-rich food, whereas selegiline and rasagiline may lose selectivity to monoamine oxidase B when administered in supratherapeutic doses.	Selegiline	124-134	monoamine oxidase B	Homo sapiens	174-193
34784871-11	2021	Of monoamine oxidase B inhibitors, safinamide is the least susceptible for interaction with the tyramine-rich food, whereas selegiline and rasagiline may lose selectivity to monoamine oxidase B when administered in supratherapeutic doses.	rasagiline	139-149	monoamine oxidase B	Homo sapiens	174-193
34771054-0	2021	Novel Thiosemicarbazone Derivatives: In Vitro and In Silico Evaluation as Potential MAO-B Inhibitors.	Thiosemicarbazones	6-23	monoamine oxidase B	Homo sapiens	84-89
34771054-5	2021	Based on this view, new benzofuran/benzothiophene and thiosemicarbazone hybrid compounds were synthesized, characterized and screened for their hMAO-A and hMAO-B inhibitory activity by an in vitro fluorometric method.	benzofuran	24-34	monoamine oxidase B	Homo sapiens	155-161
34771054-5	2021	Based on this view, new benzofuran/benzothiophene and thiosemicarbazone hybrid compounds were synthesized, characterized and screened for their hMAO-A and hMAO-B inhibitory activity by an in vitro fluorometric method.	Thiosemicarbazones	54-71	monoamine oxidase B	Homo sapiens	155-161
34771054-7	2021	The mechanism of hMAO-B inhibition of compounds 2b and 2h was investigated by Lineweaver-Burk graphics.	Deuterium	55-57	monoamine oxidase B	Homo sapiens	17-23
34771054-10	2021	The docking study of compound 2b and 2h revealed that there is a strong interaction between the active sites of hMAO-B and analyzed compound.	Deuterium	37-39	monoamine oxidase B	Homo sapiens	112-118
34562673-0	2021	Discovery of 3,4-dichloro-N-(1H-indol-5-yl)benzamide: A highly potent, selective, and competitive hMAO-B inhibitor with high BBB permeability profile and neuroprotective action.	AKOS008253825	13-52	monoamine oxidase B	Homo sapiens	98-104
34562673-2	2021	Herein, we report the design, synthesis, and full characterization of new twenty-six indole derivatives as potential human MAO-B (hMAO-B) selective inhibitors.	indole	85-91	monoamine oxidase B	Homo sapiens	123-128
34562673-2	2021	Herein, we report the design, synthesis, and full characterization of new twenty-six indole derivatives as potential human MAO-B (hMAO-B) selective inhibitors.	indole	85-91	monoamine oxidase B	Homo sapiens	130-136
34562673-3	2021	Six compounds (2i, 3b-e, and 5) exhibited low micromolar to nanomolar inhibitory activities over hMAO-B; compared to our recently reported N-substituted indole-based lead compound VIII (hMAO-B IC50 = 777 nM), compound 5 (3,4-dichloro-N-(1H-indol-5-yl)benzamide) exhibited 18-fold increase in potency (IC50 = 42 nM).	n-substituted indole-based lead	139-170	monoamine oxidase B	Homo sapiens	97-103
34562673-3	2021	Six compounds (2i, 3b-e, and 5) exhibited low micromolar to nanomolar inhibitory activities over hMAO-B; compared to our recently reported N-substituted indole-based lead compound VIII (hMAO-B IC50 = 777 nM), compound 5 (3,4-dichloro-N-(1H-indol-5-yl)benzamide) exhibited 18-fold increase in potency (IC50 = 42 nM).	n-substituted indole-based lead	139-170	monoamine oxidase B	Homo sapiens	186-192
34562673-3	2021	Six compounds (2i, 3b-e, and 5) exhibited low micromolar to nanomolar inhibitory activities over hMAO-B; compared to our recently reported N-substituted indole-based lead compound VIII (hMAO-B IC50 = 777 nM), compound 5 (3,4-dichloro-N-(1H-indol-5-yl)benzamide) exhibited 18-fold increase in potency (IC50 = 42 nM).	AKOS008253825	221-260	monoamine oxidase B	Homo sapiens	97-103
34562673-4	2021	A selectivity study over hMAO-A revealed an excellent selectivity index of compound 5 (SI > 2375) with a 47-fold increase compared to rasagiline (II, a well-known MAO-B inhibitor, SI > 50).	rasagiline	134-144	monoamine oxidase B	Homo sapiens	163-168
34492558-7	2021	4-Bromo-2-((prop-2-yn-1-ylimino)methyl)phenol 4a was the most potent inhibitor of MAOs (IC50 of 3.95 and  10 microM for MAO-B and MAO-A, respectively) along with a balanced inhibition of both cholinesterases being a real MTDL.	4-bromo-2-((prop-2-yn-1-ylimino)methyl)phenol	0-45	monoamine oxidase B	Homo sapiens	120-125
34503991-3	2021	Catecholamines are metabolized by two isoforms of monoamine oxidase, MAO-A and MAO-B; and although the anatomic localization of MAO-A and MAO-B and substrate specificities of enzyme inhibitors are well characterized, relative susceptibilities of the endogenous catecholamines to enzymatic oxidation by MAO-A and MAO-B have not been studied systematically.	Catecholamines	0-14	monoamine oxidase B	Homo sapiens	79-84
34503991-3	2021	Catecholamines are metabolized by two isoforms of monoamine oxidase, MAO-A and MAO-B; and although the anatomic localization of MAO-A and MAO-B and substrate specificities of enzyme inhibitors are well characterized, relative susceptibilities of the endogenous catecholamines to enzymatic oxidation by MAO-A and MAO-B have not been studied systematically.	Catecholamines	0-14	monoamine oxidase B	Homo sapiens	138-143
34503991-3	2021	Catecholamines are metabolized by two isoforms of monoamine oxidase, MAO-A and MAO-B; and although the anatomic localization of MAO-A and MAO-B and substrate specificities of enzyme inhibitors are well characterized, relative susceptibilities of the endogenous catecholamines to enzymatic oxidation by MAO-A and MAO-B have not been studied systematically.	Catecholamines	0-14	monoamine oxidase B	Homo sapiens	312-317
34503991-5	2021	In this study we exploited the technical ability to assay DOPAL and DOPEGAL simultaneously with the substrate catecholamines to compare DA, NE, and EPI in their metabolism by MAO-A and MAO-B.	Dopamine	136-138	monoamine oxidase B	Homo sapiens	185-190
34503991-5	2021	In this study we exploited the technical ability to assay DOPAL and DOPEGAL simultaneously with the substrate catecholamines to compare DA, NE, and EPI in their metabolism by MAO-A and MAO-B.	Epinephrine	148-151	monoamine oxidase B	Homo sapiens	185-190
34503991-7	2021	Since catecholaminergic neurons express mainly MAO-A, the finding that MAO-A is more efficient than MAO-B in metabolizing endogenous catecholamines reinforces the view that the predominant route of intra-neuronal enzymatic oxidation of catecholamines is via MAO-A.	Catecholamines	133-147	monoamine oxidase B	Homo sapiens	100-105
34503991-7	2021	Since catecholaminergic neurons express mainly MAO-A, the finding that MAO-A is more efficient than MAO-B in metabolizing endogenous catecholamines reinforces the view that the predominant route of intra-neuronal enzymatic oxidation of catecholamines is via MAO-A.	Catecholamines	236-250	monoamine oxidase B	Homo sapiens	100-105
34503991-11	2021	Based on measurements of DOPAL and DOPEGAL production, DA is a better substrate than NE or EPI for both MAO isoforms, and MAO-A is more efficient than MAO-B in metabolizing DA, NE, and EPI.	Dopamine	173-175	monoamine oxidase B	Homo sapiens	151-156
33818516-9	2021	All the tested compounds were capable to inhibit human monoamine oxidase-B enzyme to a significant extent, however, compound 7 exerted the most prominent inhibitory activity, similar to selegiline and rasagiline.	Selegiline	186-196	monoamine oxidase B	Homo sapiens	55-74
33818516-9	2021	All the tested compounds were capable to inhibit human monoamine oxidase-B enzyme to a significant extent, however, compound 7 exerted the most prominent inhibitory activity, similar to selegiline and rasagiline.	rasagiline	201-211	monoamine oxidase B	Homo sapiens	55-74
34142645-1	2021	Besides the inhibition of monoamine-oxidase-B, high-dose safinamide (100 mg) also blocks voltage-gated Na+ and Ca++ channels and inhibits glutamate release at overactive synapses.	safinamide	57-67	monoamine oxidase B	Homo sapiens	26-45
34311047-4	2021	At very high concentrations of RDV, there was partial inhibition of complex I- (IC50 675 micromol/L, residual activity 39.4 %) and complex II-linked (IC50 81.8 micromol/L, residual activity 40.7 %) respiration, without inhibition of complex IV-linked respiration, and partial inhibition both of MAO-A (IC50 26.6 micromol/L, residual activity 35.2 %) and MAO-B (IC50 89.8 micromol/L, residual activity 34.0 %) activity.	remdesivir	31-34	monoamine oxidase B	Homo sapiens	354-359
34674410-7	2022	Based on this view, new thiazolyl-hydrazone compounds were synthesized, characterized, and screened for their hMAO-A and hMAO-B inhibitory activity by an in vitro fluorometric method.	thiazolyl-hydrazone	24-43	monoamine oxidase B	Homo sapiens	121-127
34090156-7	2021	Last, the antimicrobial activity and the performance of the MAOI-like AuNCs in the human blood sample were explored and suggested that MAOI-like AuNCs do not possess strong antimicrobial activity and have no visualized side effect on blood cells, although the by-product peroxide of MAO reaction may reshape the white blood cells.	Peroxides	271-279	monoamine oxidase B	Homo sapiens	283-286
34553601-0	2021	Identification of a Chlorogenic Ester as a Monoamine Oxidase (MAO-B) Inhibitor by Integrating "Traditional and Machine Learning" Virtual Screening and In Vitro as well as In Vivo Validation: A Lead against Neurodegenerative Disorders?	chlorogenic ester	20-37	monoamine oxidase B	Homo sapiens	62-67
34553601-3	2021	Expression of MAO-B has been found to be elevated in PD patients for increased uptake of dopamine, producing hydrogen peroxide and finally causing neuronal injury.	Dopamine	89-97	monoamine oxidase B	Homo sapiens	14-19
34553601-3	2021	Expression of MAO-B has been found to be elevated in PD patients for increased uptake of dopamine, producing hydrogen peroxide and finally causing neuronal injury.	Hydrogen Peroxide	109-126	monoamine oxidase B	Homo sapiens	14-19
34553601-5	2021	From the Protein Data Bank, MAO-B protein structures complexed with selegiline, 6-hydroxy-N-propargyl-1(R)-aminoindan, or a chromen derivative have been selected as templates for shape-based virtual screening (SB-VS) against the Traditional Chinese Medicinal (TCM) natural database.	Selegiline	68-78	monoamine oxidase B	Homo sapiens	28-33
34553601-5	2021	From the Protein Data Bank, MAO-B protein structures complexed with selegiline, 6-hydroxy-N-propargyl-1(R)-aminoindan, or a chromen derivative have been selected as templates for shape-based virtual screening (SB-VS) against the Traditional Chinese Medicinal (TCM) natural database.	5-HYDROXY-N-PROPARGYL-1(R)-AMINOINDAN	80-117	monoamine oxidase B	Homo sapiens	28-33
34641548-0	2021	Selected Class of Enamides Bearing Nitro Functionality as Dual-Acting with Highly Selective Monoamine Oxidase-B and BACE1 Inhibitors.	enamides	18-26	monoamine oxidase B	Homo sapiens	92-111
34641548-2	2021	Compounds NEA3 and NEA1 exhibited a more potent MAO-B inhibition (IC50 value = 0.0092 and 0.016 microM, respectively) than the standards (IC50 value = 0.11 and 0.14 microM, respectively, for lazabemide and pargyline).	lazabemide	191-201	monoamine oxidase B	Homo sapiens	48-53
34641548-2	2021	Compounds NEA3 and NEA1 exhibited a more potent MAO-B inhibition (IC50 value = 0.0092 and 0.016 microM, respectively) than the standards (IC50 value = 0.11 and 0.14 microM, respectively, for lazabemide and pargyline).	Pargyline	206-215	monoamine oxidase B	Homo sapiens	48-53
34390968-0	2021	Discovery of novel and potent safinamide-based derivatives as highly selective hMAO-B inhibitors for treatment of Parkinson"s disease (PD): Design, synthesis, in vitro, in vivo and in silico biological studies.	safinamide	30-40	monoamine oxidase B	Homo sapiens	79-85
34371375-0	2021	Pyridazinones containing dithiocarbamoyl moieties as a new class of selective MAO-B inhibitors.	pyridazinones	0-13	monoamine oxidase B	Homo sapiens	78-83
34371375-0	2021	Pyridazinones containing dithiocarbamoyl moieties as a new class of selective MAO-B inhibitors.	dithiocarbamoyl	25-40	monoamine oxidase B	Homo sapiens	78-83
34371375-1	2021	A novel class of potential MAO-B inhibitors was designed and synthesized in good yield by combining the pyridazinone moiety with the dithiocarbamate framework, two relevant pharmacophores for drug discovery.	2-phenyl-3(2H)-pyridazinone	104-116	monoamine oxidase B	Homo sapiens	27-32
34352710-3	2021	Compound 20 exhibited the best activity and selectivity towards hMAO-B with IC50 value of 53 nM and selectivity index of 1122 folds over MAO-A, compared to the reference drugs rasagiline (IC50 = 66 nM) and selegiline (IC50 = 40 nM).	rasagiline	176-186	monoamine oxidase B	Homo sapiens	64-70
34352710-3	2021	Compound 20 exhibited the best activity and selectivity towards hMAO-B with IC50 value of 53 nM and selectivity index of 1122 folds over MAO-A, compared to the reference drugs rasagiline (IC50 = 66 nM) and selegiline (IC50 = 40 nM).	Selegiline	206-216	monoamine oxidase B	Homo sapiens	64-70
34390968-3	2021	Herein, a structural optimization strategy for safinamide (a well-known second generation hMAO-B inhibitor) afforded a series of thirty-six safinamide-derived new analogs (4aa-bj).	safinamide	47-57	monoamine oxidase B	Homo sapiens	90-96
34371375-1	2021	A novel class of potential MAO-B inhibitors was designed and synthesized in good yield by combining the pyridazinone moiety with the dithiocarbamate framework, two relevant pharmacophores for drug discovery.	Dithiocarbamate	133-148	monoamine oxidase B	Homo sapiens	27-32
34371375-2	2021	The biological results obtained for the different pyridazinone/dithiocarbamate hybrids (compounds 8-14) indicated that most of them reversibly and selectively inhibit the hMAO-B in vitro with IC50 values in the microM range and exhibit not significant cellular toxicity.	2-phenyl-3(2H)-pyridazinone	50-62	monoamine oxidase B	Homo sapiens	171-177
34371375-2	2021	The biological results obtained for the different pyridazinone/dithiocarbamate hybrids (compounds 8-14) indicated that most of them reversibly and selectively inhibit the hMAO-B in vitro with IC50 values in the microM range and exhibit not significant cellular toxicity.	Dithiocarbamate	63-78	monoamine oxidase B	Homo sapiens	171-177
34390968-3	2021	Herein, a structural optimization strategy for safinamide (a well-known second generation hMAO-B inhibitor) afforded a series of thirty-six safinamide-derived new analogs (4aa-bj).	safinamide	140-150	monoamine oxidase B	Homo sapiens	90-96
34390968-9	2021	Accordingly, we present compound 4bf as a novel, highly potent, and selective hMAO-B inhibitor with an effective therapeutic profile for relieving PD.	4-BROMO-L-PHENYLALANINE	33-36	monoamine oxidase B	Homo sapiens	78-84
34679329-1	2021	Genetic analysis of the association between alcohol, cocaine, and opiate addiction and variable number tandem repeat (VNTR) polymorphisms in monoamine oxidase B (MAOB) and serotonergic 5-hydroxytryptamine (serotonin) receptor 1B and 2C (HTR1B 21 and HTR2C) pathway genes was performed in a sample of 302 polyconsumers.	Alcohols	44-51	monoamine oxidase B	Homo sapiens	141-160
34346015-0	2021	Association of COMT rs4680 and MAO-B rs1799836 polymorphisms with levodopa-induced dyskinesia in Parkinson"s disease-a meta-analysis.	Levodopa	66-74	monoamine oxidase B	Homo sapiens	31-36
34346015-3	2021	Thus, we performed a meta-analysis to assess whether COMT and MAO-B genetic variants are associated with an increased incidence of levodopa-induced dyskinesia (LID) in PD patients.	Levodopa	131-139	monoamine oxidase B	Homo sapiens	62-67
34679329-1	2021	Genetic analysis of the association between alcohol, cocaine, and opiate addiction and variable number tandem repeat (VNTR) polymorphisms in monoamine oxidase B (MAOB) and serotonergic 5-hydroxytryptamine (serotonin) receptor 1B and 2C (HTR1B 21 and HTR2C) pathway genes was performed in a sample of 302 polyconsumers.	Alcohols	44-51	monoamine oxidase B	Homo sapiens	162-166
34679329-1	2021	Genetic analysis of the association between alcohol, cocaine, and opiate addiction and variable number tandem repeat (VNTR) polymorphisms in monoamine oxidase B (MAOB) and serotonergic 5-hydroxytryptamine (serotonin) receptor 1B and 2C (HTR1B 21 and HTR2C) pathway genes was performed in a sample of 302 polyconsumers.	Cocaine	53-60	monoamine oxidase B	Homo sapiens	141-160
34679329-1	2021	Genetic analysis of the association between alcohol, cocaine, and opiate addiction and variable number tandem repeat (VNTR) polymorphisms in monoamine oxidase B (MAOB) and serotonergic 5-hydroxytryptamine (serotonin) receptor 1B and 2C (HTR1B 21 and HTR2C) pathway genes was performed in a sample of 302 polyconsumers.	Cocaine	53-60	monoamine oxidase B	Homo sapiens	162-166
34679329-2	2021	Our genetic association analysis revealed a significant association between a 184 base pair (bp) VNTR polymorphism in the MAOB gene and addiction to cocaine and opiates.	Cocaine	149-156	monoamine oxidase B	Homo sapiens	122-126
34397324-0	2021	Development of 2D, 3D-QSAR and Pharmacophore Modeling of Chalcones for the Inhibition of Monoamine Oxidase B.	Chalcones	57-66	monoamine oxidase B	Homo sapiens	89-108
34225162-3	2021	Inhibitors of the MAO-B isoform, in turn, are used as monotherapy or in conjunction with levodopa in PD, and function by reducing the central degradation of dopamine.	Levodopa	89-97	monoamine oxidase B	Homo sapiens	18-23
34225162-3	2021	Inhibitors of the MAO-B isoform, in turn, are used as monotherapy or in conjunction with levodopa in PD, and function by reducing the central degradation of dopamine.	Dopamine	157-165	monoamine oxidase B	Homo sapiens	18-23
34225162-4	2021	It has been reported that 1-tetralone and 1-indanone derivatives are potent and specific inhibitors of MAO-B, while compounds containing the nitrocatechol moiety (e.g. tolcapone and entacapone) are often potent COMT inhibitors.	Tetralones	26-37	monoamine oxidase B	Homo sapiens	103-108
34225162-4	2021	It has been reported that 1-tetralone and 1-indanone derivatives are potent and specific inhibitors of MAO-B, while compounds containing the nitrocatechol moiety (e.g. tolcapone and entacapone) are often potent COMT inhibitors.	indacrinone	42-52	monoamine oxidase B	Homo sapiens	103-108
34225162-5	2021	The present study attempted to discover compounds that exhibit dual COMT and MAO-B inhibition by synthesizing series of 1-tetralone, 1-indanone and related derivatives substituted with the nitrocatechol moiety.	nitrocatechol	189-202	monoamine oxidase B	Homo sapiens	77-82
34225162-7	2021	The results show that 4-chromanone derivative (7) is the most promising dual inhibitor with IC50 values of 0.57 and 7.26 muM for COMT and MAO-B, respectively, followed by 1-tetralone derivative (4d) with IC50 values of 0.42 and 7.83 muM for COMT and MAO-B, respectively.	4-chromanone	22-34	monoamine oxidase B	Homo sapiens	138-143
34174267-4	2021	A docking study of gamma-decanolactone has been carried out with the molecular targets of MAO-A and MAO-B isoforms.	decan-4-olide	19-38	monoamine oxidase B	Homo sapiens	100-105
34174267-8	2021	Gamma-decanolactone inhibited preferentially the MAO-B in a reversible manner, with an inhibitory concentration of 50% (IC50) 55.95 +- 9.06 muM.	decan-4-olide	0-19	monoamine oxidase B	Homo sapiens	49-54
34174267-11	2021	The molecular docking study show that the gamma-decanolactone ligand adopts a relatively compact conformation in the active site of hMAO-B, while we note an extended conformation of gamma-decanolactone ligand in the hMAO-A isoform.	decan-4-olide	42-61	monoamine oxidase B	Homo sapiens	132-138
34126574-3	2021	The curiosity in MAO inhibitors is reviving, and novel MAO-B inhibitors recently developed with ancillary activities (e.g., Abeta aggregation and AChE inhibition, anti-ROS and chelating activities) have been proposed as multitarget drugs foreshadowing a positive outlook for the treatment of AD.	ros	168-171	monoamine oxidase B	Homo sapiens	55-60
34290084-5	2021	Both inhibition of MAO-B by selegiline or rasagiline and siRNA-mediated knockdown of MAO-B facilitated alpha-syn secretion.	Selegiline	28-38	monoamine oxidase B	Homo sapiens	19-24
34290084-5	2021	Both inhibition of MAO-B by selegiline or rasagiline and siRNA-mediated knockdown of MAO-B facilitated alpha-syn secretion.	rasagiline	42-52	monoamine oxidase B	Homo sapiens	19-24
34290084-7	2021	Additionally, the MAO-B inhibition-induced increase in alpha-syn secretion was unaffected by brefeldin A, which inhibits endoplasmic reticulum/Golgi transport, but was blocked by probenecid and glyburide, which inhibit ATP-binding cassette (ABC) transporter function.	Probenecid	179-189	monoamine oxidase B	Homo sapiens	18-23
34290084-7	2021	Additionally, the MAO-B inhibition-induced increase in alpha-syn secretion was unaffected by brefeldin A, which inhibits endoplasmic reticulum/Golgi transport, but was blocked by probenecid and glyburide, which inhibit ATP-binding cassette (ABC) transporter function.	Glyburide	194-203	monoamine oxidase B	Homo sapiens	18-23
34290084-8	2021	MAO-B inhibition preferentially facilitated the secretion of detergent-insoluble alpha-syn protein and decreased its intracellular accumulation under chloroquine-induced lysosomal dysfunction.	Chloroquine	150-161	monoamine oxidase B	Homo sapiens	0-5
34290084-14	2021	MAO-B inhibition preferentially facilitated secretion of detergent-insoluble alpha-synuclein protein and reduced its intracellular accumulation under chloroquine-induced lysosomal dysfunction.	Chloroquine	150-161	monoamine oxidase B	Homo sapiens	0-5
34397324-2	2021	Several functionalized chalcone derivatives were shown to have potential reversible MAO-B inhibitory activity, which have recently been reported from our laboratory.	Chalcone	23-31	monoamine oxidase B	Homo sapiens	84-89
34397324-3	2021	METHODS: With the experimental results of about 70 chalcone derivatives, we further developed a pharmacophore modelling, and 2D and 3D- QSAR analyses of these reported chalcones for MAO-B inhibition.	Chalcone	51-59	monoamine oxidase B	Homo sapiens	182-187
34397324-3	2021	METHODS: With the experimental results of about 70 chalcone derivatives, we further developed a pharmacophore modelling, and 2D and 3D- QSAR analyses of these reported chalcones for MAO-B inhibition.	Chalcones	168-177	monoamine oxidase B	Homo sapiens	182-187
34119696-0	2021	Synthesis and biological evaluation of 3-styrylchromone derivatives as selective monoamine oxidase B inhibitors.	3-styrylchromone	39-55	monoamine oxidase B	Homo sapiens	81-100
34269579-1	2021	Chromone-3-phenylcarboxamides (Crom-1 and Crom-2) were identified as potent, selective, and reversible inhibitors of human monoamine oxidase B (hMAO-B).	chromone-3-phenylcarboxamides	0-29	monoamine oxidase B	Homo sapiens	123-142
34269579-1	2021	Chromone-3-phenylcarboxamides (Crom-1 and Crom-2) were identified as potent, selective, and reversible inhibitors of human monoamine oxidase B (hMAO-B).	chromone-3-phenylcarboxamides	0-29	monoamine oxidase B	Homo sapiens	144-150
34269579-3	2021	Structure-activity relationship data, supported by molecular docking studies, provided a rationale for the contribution of the heterocycle"s rigidity, the carbonyl group, and the benzopyran heteroatom for hMAO-B inhibitory activity.	Benzopyrans	179-189	monoamine oxidase B	Homo sapiens	205-211
34269579-4	2021	From the study, N-(3-chlorophenyl)-4H-thiochromone-3-carboxamide (31) (hMAO-B IC50 = 1.52 +- 0.15 nM) emerged as a reversible tight binding inhibitor with an improved pharmacological profile.	n-(3-chlorophenyl)-4h-thiochromone-3-carboxamide	16-64	monoamine oxidase B	Homo sapiens	71-77
34119696-3	2021	Compound 19, which had a methoxy group at R2 on the chromone ring and chlorine at R4 on phenyl ring, potently inhibited MAO-B, with an IC50 value of 2.2 nM.	Chromones	52-60	monoamine oxidase B	Homo sapiens	120-125
34119696-3	2021	Compound 19, which had a methoxy group at R2 on the chromone ring and chlorine at R4 on phenyl ring, potently inhibited MAO-B, with an IC50 value of 2.2 nM.	Chlorine	70-78	monoamine oxidase B	Homo sapiens	120-125
34305778-8	2021	Moreover, 18F-THK5351 accumulated in the bilateral globus pallidum, amygdala, caudate nuclei, and the substantia nigra of the midbrain, which were probably off-target reaction, by binding to monoamine oxidase B (MAO-B).	THK5351	14-21	monoamine oxidase B	Homo sapiens	191-210
34287249-3	2021	Catechol-O-methyltransferase (COMT) and monoamine oxidase type B (MAO-B) degrade dopamine and affect its neurotransmission.	Dopamine	81-89	monoamine oxidase B	Homo sapiens	40-64
34287249-3	2021	Catechol-O-methyltransferase (COMT) and monoamine oxidase type B (MAO-B) degrade dopamine and affect its neurotransmission.	Dopamine	81-89	monoamine oxidase B	Homo sapiens	66-71
34287249-8	2021	These findings suggest that higher dopamine degradation, associated with COMT and MAO-B genetic variants, is associated with a sex-specific increase in the severity of negative symptoms in schizophrenia patients.	Dopamine	35-43	monoamine oxidase B	Homo sapiens	82-87
34305778-8	2021	Moreover, 18F-THK5351 accumulated in the bilateral globus pallidum, amygdala, caudate nuclei, and the substantia nigra of the midbrain, which were probably off-target reaction, by binding to monoamine oxidase B (MAO-B).	THK5351	14-21	monoamine oxidase B	Homo sapiens	212-217
34306611-2	2021	Our primary endpoint was time until need for levodopa among new monotherapy users of dopamine agonists and MAO-B inhibitors.	Levodopa	45-53	monoamine oxidase B	Homo sapiens	107-112
34162132-5	2021	Safinamide is a selective and reversible monoamine oxidase B (MAOB) inhibitor that has been used for the treatment of Parkinson"s disease.	safinamide	0-10	monoamine oxidase B	Homo sapiens	41-60
34162132-5	2021	Safinamide is a selective and reversible monoamine oxidase B (MAOB) inhibitor that has been used for the treatment of Parkinson"s disease.	safinamide	0-10	monoamine oxidase B	Homo sapiens	62-66
34306611-0	2021	Time until Need for Levodopa among New Users of Dopamine Agonists or MAO-B Inhibitors.	Levodopa	20-28	monoamine oxidase B	Homo sapiens	69-74
34299393-0	2021	4-Phenethyl-1-Propargylpiperidine-Derived Dual Inhibitors of Butyrylcholinesterase and Monoamine Oxidase B.	4-phenethyl-1-propargylpiperidine	0-33	monoamine oxidase B	Homo sapiens	87-106
34299393-2	2021	Based on the structure of an in-house irreversible monoamine oxidase B (MAO-B) inhibitor, we aimed to introduce a carbamate moiety on the aromatic ring to impart cholinesterase (ChE) inhibition, and to furnish multifunctional ligands targeting two enzymes that are intricately involved in AD pathobiology.	Carbamates	114-123	monoamine oxidase B	Homo sapiens	51-70
34299393-2	2021	Based on the structure of an in-house irreversible monoamine oxidase B (MAO-B) inhibitor, we aimed to introduce a carbamate moiety on the aromatic ring to impart cholinesterase (ChE) inhibition, and to furnish multifunctional ligands targeting two enzymes that are intricately involved in AD pathobiology.	Carbamates	114-123	monoamine oxidase B	Homo sapiens	72-77
34611843-0	2021	KDS2010, a Newly Developed Reversible MAO-B Inhibitor, as an Effective Therapeutic Candidate for Parkinson"s Disease.	kds2010	0-7	monoamine oxidase B	Homo sapiens	38-43
34306611-9	2021	The mean number of days until the first prescription of levodopa was dispensed was higher among the dopamine agonist users (621 days) compared to the MAO-B inhibitor users (352 days).	Levodopa	56-64	monoamine oxidase B	Homo sapiens	150-155
34201128-4	2021	Compound CH5 most potently inhibited MAO-B, with an IC50 value of 0.46 microM, followed by CH4 (IC50 = 0.84 microM).	2-(((R)-2,3-DIHYDROXYPROPYL)PHOSPHORYLOXY)-N,N,N-TRIMETHYLETHANAMINIUM	9-12	monoamine oxidase B	Homo sapiens	37-42
34262643-0	2021	Promising Non-cytotoxic Monosubstituted Chalcones to Target Monoamine Oxidase-B.	Chalcones	40-49	monoamine oxidase B	Homo sapiens	60-79
34262643-7	2021	The main conclusion of this cell biology, biochemistry, and structural study is to highlights 13 as a chalcone derivative that is worth consideration for the development of novel MAO-B-selective inhibitors for the treatment of neurodegenerative diseases.	Chalcone	102-110	monoamine oxidase B	Homo sapiens	179-184
34201128-0	2021	Trimethoxylated Halogenated Chalcones as Dual Inhibitors of MAO-B and BACE-1 for the Treatment of Neurodegenerative Disorders.	trimethoxylated halogenated chalcones	0-37	monoamine oxidase B	Homo sapiens	60-65
34879800-9	2021	Coumarin scaffolds have shown the excellent potential of ACh esterase inhibition, MAO-B inhibition, and anti-Abeta aggregation.	coumarin	0-8	monoamine oxidase B	Homo sapiens	82-87
34201128-3	2021	Six compounds inhibited MAO-B more effectively than MAO-A, and the 2",3",4"-methoxy moiety in CH4-CH6 was more effective for MAO-B inhibition than the 2",4",6"-methoxy moiety in CH1-CH3.	2",3",4"-methoxy	67-83	monoamine oxidase B	Homo sapiens	24-29
34201128-3	2021	Six compounds inhibited MAO-B more effectively than MAO-A, and the 2",3",4"-methoxy moiety in CH4-CH6 was more effective for MAO-B inhibition than the 2",4",6"-methoxy moiety in CH1-CH3.	2",3",4"-methoxy	67-83	monoamine oxidase B	Homo sapiens	125-130
34201128-3	2021	Six compounds inhibited MAO-B more effectively than MAO-A, and the 2",3",4"-methoxy moiety in CH4-CH6 was more effective for MAO-B inhibition than the 2",4",6"-methoxy moiety in CH1-CH3.	ch4-ch6	94-101	monoamine oxidase B	Homo sapiens	24-29
34201128-3	2021	Six compounds inhibited MAO-B more effectively than MAO-A, and the 2",3",4"-methoxy moiety in CH4-CH6 was more effective for MAO-B inhibition than the 2",4",6"-methoxy moiety in CH1-CH3.	ch4-ch6	94-101	monoamine oxidase B	Homo sapiens	125-130
34201128-3	2021	Six compounds inhibited MAO-B more effectively than MAO-A, and the 2",3",4"-methoxy moiety in CH4-CH6 was more effective for MAO-B inhibition than the 2",4",6"-methoxy moiety in CH1-CH3.	2",4",6"-methoxy	151-167	monoamine oxidase B	Homo sapiens	24-29
34082669-6	2021	Compound (2E)-3-(4-bromophenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one (TMh) showed good MAO-B inhibition, with an inhibition constant of 0.46+-0.009 muM.	(2e)-3-(4-bromophenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one	9-73	monoamine oxidase B	Homo sapiens	92-97
34082669-6	2021	Compound (2E)-3-(4-bromophenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one (TMh) showed good MAO-B inhibition, with an inhibition constant of 0.46+-0.009 muM.	tmh	75-78	monoamine oxidase B	Homo sapiens	92-97
34082669-10	2021	To shed light on the molecular interactions of TMf and TMh towards MAO-A and MAO-B, molecular docking simulations and MM/GBSA calculations have been carried out.	TMF protocol	47-50	monoamine oxidase B	Homo sapiens	77-82
34082669-10	2021	To shed light on the molecular interactions of TMf and TMh towards MAO-A and MAO-B, molecular docking simulations and MM/GBSA calculations have been carried out.	tmh	55-58	monoamine oxidase B	Homo sapiens	77-82
34071665-0	2021	Development of Halogenated Pyrazolines as Selective Monoamine Oxidase-B Inhibitors: Deciphering via Molecular Dynamics Approach.	halogenated pyrazolines	15-38	monoamine oxidase B	Homo sapiens	52-71
34071665-3	2021	Halogen substitutions on the phenyl ring located at the fifth position of pyrazoline showed potent MAO-B inhibition.	pyrazoline	74-84	monoamine oxidase B	Homo sapiens	99-104
34071665-4	2021	Compound 3-(4-ethoxyphenyl)-5-(4-fluorophenyl)-4,5-dihydro-1H-pyrazole (EH7) showed the highest potency against MAO-B with an IC50 value of 0.063 microM.	3-(4-ethoxyphenyl)-5-(4-fluorophenyl)-4,5-dihydro-1h-pyrazole	9-70	monoamine oxidase B	Homo sapiens	112-117
34071665-4	2021	Compound 3-(4-ethoxyphenyl)-5-(4-fluorophenyl)-4,5-dihydro-1H-pyrazole (EH7) showed the highest potency against MAO-B with an IC50 value of 0.063 microM.	eh7	72-75	monoamine oxidase B	Homo sapiens	112-117
34223165-3	2021	6-(4-(Piperidin-1-yl)butoxy)-4H-chromen-4-one (7), a previously identified MSM with potent dual-target activities against acetylcholinesterase and monoamine oxidase B, also exhibited sigma1/sigma2 affinity.	6-(4-(piperidin-1-yl)butoxy)-4h-chromen-4-one	0-45	monoamine oxidase B	Homo sapiens	147-166
34533445-2	2021	The activity of monoamine oxidase B (MAOB), the enzyme involved in the degradation of dopamine, is increased during AD.	Dopamine	86-94	monoamine oxidase B	Homo sapiens	16-35
34533445-2	2021	The activity of monoamine oxidase B (MAOB), the enzyme involved in the degradation of dopamine, is increased during AD.	Dopamine	86-94	monoamine oxidase B	Homo sapiens	37-41
35472505-1	2022	Monoamine oxidases A and B (MAO-A and MAO-B) play important roles in biogenic amine metabolism, oxidative stress, and chronic inflammation.	Amines	78-83	monoamine oxidase B	Homo sapiens	38-43
34477522-8	2021	Chalcones, generally, are potential and more selective towards MAO-B inhibitions whereas pyrazolines derived from chalcones turned into selective towards MAO-A inhibitions due to maybe the presence of two nitrogen heteroatoms.	Chalcones	0-9	monoamine oxidase B	Homo sapiens	63-68
35472505-4	2022	Structure-activity relationships were investigated, and all of the compounds with (R)-3-hydroxy pyrrolidine moiety on the 6-position displayed preferable inhibition toward the MAO-B isoform.	(r)-3-hydroxy pyrrolidine	82-107	monoamine oxidase B	Homo sapiens	176-181
35447344-1	2022	Monoamine oxidase B (MAO-B) inhibitors are established therapy for Parkinson"s disease and act, in part, by blocking the MAO-catalysed metabolism of dopamine in the brain.	Dopamine	149-157	monoamine oxidase B	Homo sapiens	0-19
35447344-1	2022	Monoamine oxidase B (MAO-B) inhibitors are established therapy for Parkinson"s disease and act, in part, by blocking the MAO-catalysed metabolism of dopamine in the brain.	Dopamine	149-157	monoamine oxidase B	Homo sapiens	21-26
35447344-2	2022	Two propargylamine-containing MAO-B inhibitors, selegiline ((R)-deprenyl) and rasagiline, are currently used in the clinic for this purpose.	propargylamine	4-18	monoamine oxidase B	Homo sapiens	30-35
35447344-4	2022	An important consideration is that selegiline and rasagiline display specificity for MAO-B over the MAO-A isoform thus reducing the risk of tyramine-induced changes in blood-pressure.	Selegiline	35-45	monoamine oxidase B	Homo sapiens	85-90
35447344-4	2022	An important consideration is that selegiline and rasagiline display specificity for MAO-B over the MAO-A isoform thus reducing the risk of tyramine-induced changes in blood-pressure.	rasagiline	50-60	monoamine oxidase B	Homo sapiens	85-90
35447344-7	2022	Interestingly, dialysis studies found that 2-PAT is a reversible MAO-A inhibitor, while acting as an inactivator of MAO-B.	2-PAT	43-48	monoamine oxidase B	Homo sapiens	116-121
35447344-2	2022	Two propargylamine-containing MAO-B inhibitors, selegiline ((R)-deprenyl) and rasagiline, are currently used in the clinic for this purpose.	Selegiline	48-58	monoamine oxidase B	Homo sapiens	30-35
35472505-5	2022	Among them, compounds 6c with a 4"-fluorobenzyl ring and 6m bearing a 3",4"-difluorobenzyl ring on the 3-position were the most potent MAO-B inhibitors with IC50 values of 0.35 muM and 0.32 muM, respectively.	4"-fluorobenzyl	32-47	monoamine oxidase B	Homo sapiens	135-140
35472505-5	2022	Among them, compounds 6c with a 4"-fluorobenzyl ring and 6m bearing a 3",4"-difluorobenzyl ring on the 3-position were the most potent MAO-B inhibitors with IC50 values of 0.35 muM and 0.32 muM, respectively.	3",4"-difluorobenzyl	70-90	monoamine oxidase B	Homo sapiens	135-140
35472505-6	2022	The binding mode of compound 6m in MAO-B was predicted by CDOCKER program, revealing that (R)-3-hydroxypyrrolidine moiety is a critical structural feature for this series of MAO-B inhibitors.	(R)-3-Hydroxypyrrolidine	90-114	monoamine oxidase B	Homo sapiens	35-40
35447344-2	2022	Two propargylamine-containing MAO-B inhibitors, selegiline ((R)-deprenyl) and rasagiline, are currently used in the clinic for this purpose.	(r)-deprenyl	60-72	monoamine oxidase B	Homo sapiens	30-35
35447344-2	2022	Two propargylamine-containing MAO-B inhibitors, selegiline ((R)-deprenyl) and rasagiline, are currently used in the clinic for this purpose.	rasagiline	78-88	monoamine oxidase B	Homo sapiens	30-35
35472505-6	2022	The binding mode of compound 6m in MAO-B was predicted by CDOCKER program, revealing that (R)-3-hydroxypyrrolidine moiety is a critical structural feature for this series of MAO-B inhibitors.	(R)-3-Hydroxypyrrolidine	90-114	monoamine oxidase B	Homo sapiens	174-179
35587267-1	2022	Inhibitors for monoamine oxidase-B (MAO-B) were screened from an FV library with a randomized complementarity-determining region 3 (CDR3) region using a monoclonal antibody against dopamine.	Dopamine	181-189	monoamine oxidase B	Homo sapiens	15-34
35587267-1	2022	Inhibitors for monoamine oxidase-B (MAO-B) were screened from an FV library with a randomized complementarity-determining region 3 (CDR3) region using a monoclonal antibody against dopamine.	Dopamine	181-189	monoamine oxidase B	Homo sapiens	36-41
35587267-6	2022	The inhibitory activity of two mimotopes against MAO-B was analyzed using HeLa cells overexpressing MAO-B, as well as using activated human astrocytes; their inhibitory activity was compared to that of a commercial inhibitor of MAO-B, selegiline.	Selegiline	235-245	monoamine oxidase B	Homo sapiens	49-54
35624406-2	2022	Following introduction of the monoamine oxidase type B inhibitor selegiline for the treatment of Parkinson"s disease (PD), discovery of the action mechanism of Alzheimer"s disease-modifying agent memantine, the role of iron in PD, and the loss of electron transport chain complex I in PD, and development of the concept of clinical neuroprotection, Peter Riederer launched one of the most challenging research project neurodevelopmental aspects of neuropsychiatric disorders.	Selegiline	65-75	monoamine oxidase B	Homo sapiens	30-54
35107654-4	2022	For the MAO-B inhibitor safinamide, recently introduced to the market, an additional inhibition of pathological release of glutamate has been postulated.	safinamide	24-34	monoamine oxidase B	Homo sapiens	8-13
35624746-0	2022	Study on the Neuroprotective, Radical-Scavenging and MAO-B Inhibiting Properties of New Benzimidazole Arylhydrazones as Potential Multi-Target Drugs for the Treatment of Parkinson"s Disease.	benzimidazole	88-101	monoamine oxidase B	Homo sapiens	53-58
35107654-4	2022	For the MAO-B inhibitor safinamide, recently introduced to the market, an additional inhibition of pathological release of glutamate has been postulated.	Glutamic Acid	123-132	monoamine oxidase B	Homo sapiens	8-13
35596745-2	2022	Due to structural similarities of flortaucipir with some monoamine oxidase A (MAO-A) inhibitors, this study aimed to evaluate flortaucipir binding to MAO-A and MAO-B and any potential impact on PET interpretation.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	126-138	monoamine oxidase B	Homo sapiens	160-165
35596745-8	2022	Direct binding of flortaucipir to human MAO-B was not detected in a microsomal preparation.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	18-30	monoamine oxidase B	Homo sapiens	40-45
35596745-9	2022	A high concentration of flortaucipir (IC50 of 1.3 muM) was found to block binding of the MAO-B ligand safinamide to MAO-B on microsomes suggesting that, at micromolar concentrations, flortaucipir weakly binds to MAO-B in vitro.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	24-36	monoamine oxidase B	Homo sapiens	89-94
35596745-9	2022	A high concentration of flortaucipir (IC50 of 1.3 muM) was found to block binding of the MAO-B ligand safinamide to MAO-B on microsomes suggesting that, at micromolar concentrations, flortaucipir weakly binds to MAO-B in vitro.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	24-36	monoamine oxidase B	Homo sapiens	116-121
35596745-9	2022	A high concentration of flortaucipir (IC50 of 1.3 muM) was found to block binding of the MAO-B ligand safinamide to MAO-B on microsomes suggesting that, at micromolar concentrations, flortaucipir weakly binds to MAO-B in vitro.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	24-36	monoamine oxidase B	Homo sapiens	212-217
35596745-9	2022	A high concentration of flortaucipir (IC50 of 1.3 muM) was found to block binding of the MAO-B ligand safinamide to MAO-B on microsomes suggesting that, at micromolar concentrations, flortaucipir weakly binds to MAO-B in vitro.	safinamide	102-112	monoamine oxidase B	Homo sapiens	89-94
35596745-9	2022	A high concentration of flortaucipir (IC50 of 1.3 muM) was found to block binding of the MAO-B ligand safinamide to MAO-B on microsomes suggesting that, at micromolar concentrations, flortaucipir weakly binds to MAO-B in vitro.	safinamide	102-112	monoamine oxidase B	Homo sapiens	116-121
35596745-9	2022	A high concentration of flortaucipir (IC50 of 1.3 muM) was found to block binding of the MAO-B ligand safinamide to MAO-B on microsomes suggesting that, at micromolar concentrations, flortaucipir weakly binds to MAO-B in vitro.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	183-195	monoamine oxidase B	Homo sapiens	89-94
35596745-9	2022	A high concentration of flortaucipir (IC50 of 1.3 muM) was found to block binding of the MAO-B ligand safinamide to MAO-B on microsomes suggesting that, at micromolar concentrations, flortaucipir weakly binds to MAO-B in vitro.	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole	183-195	monoamine oxidase B	Homo sapiens	116-121
35601305-3	2022	Isatin is an endogenous small fragment, reversible inhibitor for MAO enzymes and is more selective for MAO-B than -A.	Isatin	0-6	monoamine oxidase B	Homo sapiens	103-108
35601305-6	2022	Isatin has a polypharmacological profile in medicinal chemistry, is a reversible inhibitor for both the MAOs, and shows high selectivity potent inhibition for MAO-B.	Isatin	0-6	monoamine oxidase B	Homo sapiens	159-164
35510607-1	2022	Unsaturated ketone derivatives are known as inhibitors of monoamine oxidase B (MAO-B), a potential drug target of Parkinson"s disease.	unsaturated ketone	0-18	monoamine oxidase B	Homo sapiens	58-77
35510607-1	2022	Unsaturated ketone derivatives are known as inhibitors of monoamine oxidase B (MAO-B), a potential drug target of Parkinson"s disease.	unsaturated ketone	0-18	monoamine oxidase B	Homo sapiens	79-84
35624746-0	2022	Study on the Neuroprotective, Radical-Scavenging and MAO-B Inhibiting Properties of New Benzimidazole Arylhydrazones as Potential Multi-Target Drugs for the Treatment of Parkinson"s Disease.	arylhydrazones	102-116	monoamine oxidase B	Homo sapiens	53-58
35624746-2	2022	The inhibition of MAO-B affords higher dopamine bioavailability and stops ROS formation.	Dopamine	39-47	monoamine oxidase B	Homo sapiens	18-23
35624746-2	2022	The inhibition of MAO-B affords higher dopamine bioavailability and stops ROS formation.	ros	74-77	monoamine oxidase B	Homo sapiens	18-23
35624746-6	2022	Statistically significant MAO-B inhibitory effects were exerted by some of the compounds where again the catecholic compound 3h was the most potent inhibitor similar to selegiline and rasagiline.	Tritium	125-127	monoamine oxidase B	Homo sapiens	26-31
35626478-6	2022	Docking interaction analysis revealed that Soyasapogenol B bound effectively to all of the targeted proteins (AChE, BuChE MAO-A, MAO-B, GSK3beta, and NMDA), in contrast to other screened abrineurin natural inducers and inhibitors.	soyasapogenol B	43-58	monoamine oxidase B	Homo sapiens	129-134
35298568-4	2022	Furthermore, we aimed to characterize the possible MAO-B inhibiting features of Ononis isoflavonoids in silico.	ononis isoflavonoids	80-100	monoamine oxidase B	Homo sapiens	51-56
35457272-3	2022	Instead, MAOB mediates the aberrant synthesis of GABA and hydrogen peroxide (H2O2) in reactive astrocytes of Parkinson"s disease (PD).	gamma-Aminobutyric Acid	49-53	monoamine oxidase B	Homo sapiens	9-13
35457272-3	2022	Instead, MAOB mediates the aberrant synthesis of GABA and hydrogen peroxide (H2O2) in reactive astrocytes of Parkinson"s disease (PD).	Hydrogen Peroxide	58-75	monoamine oxidase B	Homo sapiens	9-13
35457272-3	2022	Instead, MAOB mediates the aberrant synthesis of GABA and hydrogen peroxide (H2O2) in reactive astrocytes of Parkinson"s disease (PD).	Hydrogen Peroxide	77-81	monoamine oxidase B	Homo sapiens	9-13
35457272-6	2022	In this perspective, we redefine the role of MAOB for the aberrant suppression and deterioration of dopaminergic neurons through excessive GABA and H2O2 synthesis of reactive astrocytes in PD.	gamma-Aminobutyric Acid	139-143	monoamine oxidase B	Homo sapiens	45-49
35457272-6	2022	In this perspective, we redefine the role of MAOB for the aberrant suppression and deterioration of dopaminergic neurons through excessive GABA and H2O2 synthesis of reactive astrocytes in PD.	Hydrogen Peroxide	148-152	monoamine oxidase B	Homo sapiens	45-49
35458667-7	2022	Among the screened compounds, Bergamottin, a furocoumarin, showed selective hMAO-B inhibitory activity, fitting its active site well.	bergamottin	30-41	monoamine oxidase B	Homo sapiens	76-82
35458667-7	2022	Among the screened compounds, Bergamottin, a furocoumarin, showed selective hMAO-B inhibitory activity, fitting its active site well.	Furocoumarins	45-57	monoamine oxidase B	Homo sapiens	76-82
35457272-1	2022	Monoamine oxidase-B (MAOB) has been believed to mediate the degradation of monoamine neurotransmitters such as dopamine.	Dopamine	111-119	monoamine oxidase B	Homo sapiens	0-19
35457272-1	2022	Monoamine oxidase-B (MAOB) has been believed to mediate the degradation of monoamine neurotransmitters such as dopamine.	Dopamine	111-119	monoamine oxidase B	Homo sapiens	21-25
35457272-2	2022	However, this traditional belief has been challenged by demonstrating that it is not MAOB but MAOA which mediates dopamine degradation.	Dopamine	114-122	monoamine oxidase B	Homo sapiens	85-89
35298568-14	2022	Our finding reflects that Ononis isoflavonoid aglycones show an excellent fit with the suggested parameters for BBB permeability and this is the first study to confirm the highly favorable position of these natural products for MAO-B inhibition.	ononis isoflavonoid aglycones	26-55	monoamine oxidase B	Homo sapiens	228-233
35280341-7	2021	Subsequently, (11C)SL25.1188, a reversible binding MAO-B radioligand with outstanding properties including high specific binding and excellent reversibility was developed.	Carbon-11	15-18	monoamine oxidase B	Homo sapiens	51-56
35195417-1	2022	Bioisosteric H/F or CH2OH/CF2H replacement was introduced in coumarin derivatives previously characterized as dual AChE-MAO B inhibitors to probe the effects on both inhibitory potency and drug-likeness.	coumarin	61-69	monoamine oxidase B	Homo sapiens	120-125
35270118-8	2022	A study of molecular docking and molecular dynamic (MD) simulation of IR3G and its aglycone isorhamnetin (IR) against human acetylcholine esterase (AChE), monoamine oxidase B (MAO-B), and Polo-like kinase-2 (PLK2) was performed and further outlined a putative mechanism in modulating neurodegenerative diseases such as PD.	3-methylquercetin	92-104	monoamine oxidase B	Homo sapiens	155-174
35270118-8	2022	A study of molecular docking and molecular dynamic (MD) simulation of IR3G and its aglycone isorhamnetin (IR) against human acetylcholine esterase (AChE), monoamine oxidase B (MAO-B), and Polo-like kinase-2 (PLK2) was performed and further outlined a putative mechanism in modulating neurodegenerative diseases such as PD.	3-methylquercetin	92-104	monoamine oxidase B	Homo sapiens	176-181
35156567-0	2022	Extended double bond conjugation in the chalcone framework favours MAO-B inhibition: A structural perspective on molecular dynamics.	Chalcone	40-48	monoamine oxidase B	Homo sapiens	67-72
35190544-1	2022	Safinamide is a highly selective, reversible MAO B-inhibitor recently marketed in European and North American countries.	safinamide	0-10	monoamine oxidase B	Homo sapiens	45-50
35300078-0	2022	Dual Reversible Coumarin Inhibitors Mutually Bound to Monoamine Oxidase B and Acetylcholinesterase Crystal Structures.	coumarin	16-24	monoamine oxidase B	Homo sapiens	54-73
35300078-3	2022	Among previously reported micromolar or sub-micromolar coumarin-bearing dual inhibitors, compound 1 returned a tight-binding inhibition of MAO B (K i = 4.5 muM) and a +5.5  C increase in the enzyme T m value.	coumarin	55-63	monoamine oxidase B	Homo sapiens	139-144
35168478-0	2022	Structural exploration of selected C6 and C7-substituted coumarin isomers as selective MAO-B inhibitors.	coumarin	57-65	monoamine oxidase B	Homo sapiens	87-92
35168478-3	2022	A recent study has shown that coumarins tend to be more selective towards MAO-B than MAO-A when connected to a hex-5-ynyloxy chain at position 6 in contrast to their C7-isomers.	Coumarins	30-39	monoamine oxidase B	Homo sapiens	74-79
35168478-4	2022	The present study describes the mode of interaction of the C6 and C7-substituted coumarin isomers characterized by their difference in selectivity towards MAO-B through molecular docking and molecular dynamics simulations in an effort to elucidate the structural components and molecular interactions that may be responsible for MAO-B selectivity.	coumarin	81-89	monoamine oxidase B	Homo sapiens	155-160
35168478-4	2022	The present study describes the mode of interaction of the C6 and C7-substituted coumarin isomers characterized by their difference in selectivity towards MAO-B through molecular docking and molecular dynamics simulations in an effort to elucidate the structural components and molecular interactions that may be responsible for MAO-B selectivity.	coumarin	81-89	monoamine oxidase B	Homo sapiens	329-334
35168478-7	2022	Resulting complexes of one isomeric coumarin pair that displayed the highest selectivity shift towards MAO-B were subject to 100 ns molecular dynamics simulations study to analyze the stability of the docked complexes.	coumarin	36-44	monoamine oxidase B	Homo sapiens	103-108
35156567-2	2022	The design of recent inhibitor therapeutic agents of MAO-B involves conjugation and modification of a chalcone scaffold comprising two aryl or heteroaryl rings connected via a short spacer unit with rotatable bonds.	Chalcone	102-110	monoamine oxidase B	Homo sapiens	53-58
35156567-8	2022	CONCLUSION: These insights present useful structural perspectives of the extended double bond conjugation associated with the experimentally reported enhanced inhibitory activity of F1 and MO10 against MAO-B.	Deoxyguanosine	182-184	monoamine oxidase B	Homo sapiens	202-207
35156567-8	2022	CONCLUSION: These insights present useful structural perspectives of the extended double bond conjugation associated with the experimentally reported enhanced inhibitory activity of F1 and MO10 against MAO-B.	mo10	189-193	monoamine oxidase B	Homo sapiens	202-207
35163835-0	2022	Why Monoamine Oxidase B Preferably Metabolizes N-Methylhistamine over Histamine: Evidence from the Multiscale Simulation of the Rate-Limiting Step.	N-methylhistamine	47-64	monoamine oxidase B	Homo sapiens	4-23
35210989-7	2022	(18F)THK-5351, which was originally designed to target tau aggregates in AD, showed high affinity for MAO-B and clearly visualized reactive astrocytes in progressive supranuclear palsy (PSP).	thk	5-8	monoamine oxidase B	Homo sapiens	102-107
35163835-2	2022	In the first step, histamine is enzymatically methylated at its imidazole Ntau atom, and the produced N-methylhistamine undergoes an oxidative deamination catalyzed by monoamine oxidase B (MAO-B), as is common with other monoaminergic neurotransmitters and neuromodulators of the central nervous system.	Histamine	19-28	monoamine oxidase B	Homo sapiens	168-187
35210989-8	2022	However, the lack of selectivity of (18F)THK-5351 binding to both MAO-B and tau, severely limits its clinical utility as a biomarker.	THK5351	41-49	monoamine oxidase B	Homo sapiens	66-71
35163835-2	2022	In the first step, histamine is enzymatically methylated at its imidazole Ntau atom, and the produced N-methylhistamine undergoes an oxidative deamination catalyzed by monoamine oxidase B (MAO-B), as is common with other monoaminergic neurotransmitters and neuromodulators of the central nervous system.	Histamine	19-28	monoamine oxidase B	Homo sapiens	189-194
35163835-2	2022	In the first step, histamine is enzymatically methylated at its imidazole Ntau atom, and the produced N-methylhistamine undergoes an oxidative deamination catalyzed by monoamine oxidase B (MAO-B), as is common with other monoaminergic neurotransmitters and neuromodulators of the central nervous system.	imidazole	64-73	monoamine oxidase B	Homo sapiens	168-187
35163835-2	2022	In the first step, histamine is enzymatically methylated at its imidazole Ntau atom, and the produced N-methylhistamine undergoes an oxidative deamination catalyzed by monoamine oxidase B (MAO-B), as is common with other monoaminergic neurotransmitters and neuromodulators of the central nervous system.	imidazole	64-73	monoamine oxidase B	Homo sapiens	189-194
35163835-2	2022	In the first step, histamine is enzymatically methylated at its imidazole Ntau atom, and the produced N-methylhistamine undergoes an oxidative deamination catalyzed by monoamine oxidase B (MAO-B), as is common with other monoaminergic neurotransmitters and neuromodulators of the central nervous system.	N-methylhistamine	102-119	monoamine oxidase B	Homo sapiens	168-187
35163835-2	2022	In the first step, histamine is enzymatically methylated at its imidazole Ntau atom, and the produced N-methylhistamine undergoes an oxidative deamination catalyzed by monoamine oxidase B (MAO-B), as is common with other monoaminergic neurotransmitters and neuromodulators of the central nervous system.	N-methylhistamine	102-119	monoamine oxidase B	Homo sapiens	189-194
35163835-3	2022	The fact that histamine requires such a conversion prior to oxidative deamination is intriguing since MAO-B is known to be relatively promiscuous towards monoaminergic substrates; its in-vitro oxidation of N-methylhistamine is about 10 times faster than that for histamine, yet this rather subtle difference appears to be governing the decomposition pathway.	Histamine	14-23	monoamine oxidase B	Homo sapiens	102-107
35163835-3	2022	The fact that histamine requires such a conversion prior to oxidative deamination is intriguing since MAO-B is known to be relatively promiscuous towards monoaminergic substrates; its in-vitro oxidation of N-methylhistamine is about 10 times faster than that for histamine, yet this rather subtle difference appears to be governing the decomposition pathway.	N-methylhistamine	206-223	monoamine oxidase B	Homo sapiens	102-107
35163835-3	2022	The fact that histamine requires such a conversion prior to oxidative deamination is intriguing since MAO-B is known to be relatively promiscuous towards monoaminergic substrates; its in-vitro oxidation of N-methylhistamine is about 10 times faster than that for histamine, yet this rather subtle difference appears to be governing the decomposition pathway.	Histamine	263-272	monoamine oxidase B	Homo sapiens	102-107
35163835-4	2022	This work clarifies the MAO-B selectivity toward histamine and N-methylhistamine by multiscale simulations of the rate-limiting hydride abstraction step for both compounds in the gas phase, in aqueous solution, and in the enzyme, using the established empirical valence bond methodology, assisted by gas-phase density functional theory (DFT) calculations.	Histamine	49-58	monoamine oxidase B	Homo sapiens	24-29
35163835-4	2022	This work clarifies the MAO-B selectivity toward histamine and N-methylhistamine by multiscale simulations of the rate-limiting hydride abstraction step for both compounds in the gas phase, in aqueous solution, and in the enzyme, using the established empirical valence bond methodology, assisted by gas-phase density functional theory (DFT) calculations.	N-methylhistamine	63-80	monoamine oxidase B	Homo sapiens	24-29
35049267-1	2022	(S)-(2-Methylpyrid-5-yl)-6-((3-(18F)fluoro-2-hydroxy)propoxy)quinoline ((18F)SMBT-1) was recently developed as a novel class of selective and reversible monoamine oxidase-B (MAO-B) tracers for in vivo imaging of reactive astrogliosis via positron emission tomography.	(s)-(2-methylpyrid-5-yl)-6-((3-(18f)fluoro-2-hydroxy)propoxy)quinoline	0-70	monoamine oxidase B	Homo sapiens	153-172
35203982-4	2022	To date, no DRT-related withdrawal syndrome has been described in PD patients who discontinue rasagiline, an irreversible inhibitor of monoamine oxidase-B (MAO-B).	rasagiline	94-104	monoamine oxidase B	Homo sapiens	135-154
35203982-4	2022	To date, no DRT-related withdrawal syndrome has been described in PD patients who discontinue rasagiline, an irreversible inhibitor of monoamine oxidase-B (MAO-B).	rasagiline	94-104	monoamine oxidase B	Homo sapiens	156-161
35208214-0	2022	Hepatic CYP3A4 Enzyme Compensatively Maintains Endogenous Geranylgeranoic Acid Levels in MAOB-Knockout Human Hepatoma Cells.	geranylgeranic acid	58-78	monoamine oxidase B	Homo sapiens	89-93
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	geranylgeraniol	78-93	monoamine oxidase B	Homo sapiens	24-43
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	geranylgeraniol	78-93	monoamine oxidase B	Homo sapiens	45-49
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	geranylgeraniol	78-93	monoamine oxidase B	Homo sapiens	254-258
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	ggoh	95-99	monoamine oxidase B	Homo sapiens	24-43
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	ggoh	95-99	monoamine oxidase B	Homo sapiens	45-49
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	ggoh	95-99	monoamine oxidase B	Homo sapiens	254-258
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	Tranylcypromine	198-213	monoamine oxidase B	Homo sapiens	24-43
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	Tranylcypromine	198-213	monoamine oxidase B	Homo sapiens	45-49
35208214-2	2022	Recently, we found that monoamine oxidase B (MAOB) catalyzed the oxidation of geranylgeraniol (GGOH) to produce geranylgeranial (GGal), a direct precursor of endogenous GGA in hepatoma cells, using tranylcypromine, an inhibitor of MAOs, and knockdown by MAOB siRNA.	Tranylcypromine	198-213	monoamine oxidase B	Homo sapiens	254-258
35208214-6	2022	Second, among the eight members of cytochrome P450 superfamily that have been suggested to be involved in the oxidation of isoprenols and/or retinol in previous studies, only the CYP3A4 gene significantly upregulated its cellular mRNA level in Hep3B/MAOB-KO cells.	3-methyl-3-buten-1-ol	123-133	monoamine oxidase B	Homo sapiens	250-254
35208214-6	2022	Second, among the eight members of cytochrome P450 superfamily that have been suggested to be involved in the oxidation of isoprenols and/or retinol in previous studies, only the CYP3A4 gene significantly upregulated its cellular mRNA level in Hep3B/MAOB-KO cells.	Vitamin A	141-148	monoamine oxidase B	Homo sapiens	250-254
35208214-7	2022	Third, a commercially available recombinant human CYP3A4 enzyme was able to oxidize GGOH to GGal, and fourth, the knockdown of CYP3A4 by siRNA significantly reduced the amount of endogenous GGA in Hep3B/MAOB-KO cells.	ggoh	84-88	monoamine oxidase B	Homo sapiens	203-207
35198978-9	2022	(3H)L-deprenyl quantified a monoamine oxidase-B target density of 304.23 +- 115.93 nM (n = 8 cases; mean +- standard deviation) in healthy control tissue and is similar to the target density in chronic traumatic encephalopathy tissues (365.80 +- 128.55 nM; n = 12 cases; mean +- standard deviation).	Selegiline	4-14	monoamine oxidase B	Homo sapiens	28-47
35049267-3	2022	(S)-6 showed higher binding affinity to MAO-B and lower binding affinity to MAO-A than (R)-6, demonstrating a higher selectivity ratio (MAO-B/MAO-A).	(r)-6	87-92	monoamine oxidase B	Homo sapiens	136-141
35049267-10	2022	In conclusion, (S)-(18F)6 had a more favorable binding affinity and binding selectivity for MAO-B than (R)-(18F)6.	(s)-(18f)6	15-25	monoamine oxidase B	Homo sapiens	92-97
35049267-1	2022	(S)-(2-Methylpyrid-5-yl)-6-((3-(18F)fluoro-2-hydroxy)propoxy)quinoline ((18F)SMBT-1) was recently developed as a novel class of selective and reversible monoamine oxidase-B (MAO-B) tracers for in vivo imaging of reactive astrogliosis via positron emission tomography.	(s)-(2-methylpyrid-5-yl)-6-((3-(18f)fluoro-2-hydroxy)propoxy)quinoline	0-70	monoamine oxidase B	Homo sapiens	174-179
35049267-12	2022	These results suggest that (S)-(18F)6 ((18F)SMBT-1) is a promising candidate for application in the imaging of MAO-B in vivo.	(s)-(18f)6 (	27-39	monoamine oxidase B	Homo sapiens	111-116
35049267-1	2022	(S)-(2-Methylpyrid-5-yl)-6-((3-(18F)fluoro-2-hydroxy)propoxy)quinoline ((18F)SMBT-1) was recently developed as a novel class of selective and reversible monoamine oxidase-B (MAO-B) tracers for in vivo imaging of reactive astrogliosis via positron emission tomography.	SMBT-1 F-18	72-83	monoamine oxidase B	Homo sapiens	153-172
35049267-1	2022	(S)-(2-Methylpyrid-5-yl)-6-((3-(18F)fluoro-2-hydroxy)propoxy)quinoline ((18F)SMBT-1) was recently developed as a novel class of selective and reversible monoamine oxidase-B (MAO-B) tracers for in vivo imaging of reactive astrogliosis via positron emission tomography.	SMBT-1 F-18	72-83	monoamine oxidase B	Homo sapiens	174-179
35049267-3	2022	(S)-6 showed higher binding affinity to MAO-B and lower binding affinity to MAO-A than (R)-6, demonstrating a higher selectivity ratio (MAO-B/MAO-A).	(s)-6	0-5	monoamine oxidase B	Homo sapiens	40-45
35049267-3	2022	(S)-6 showed higher binding affinity to MAO-B and lower binding affinity to MAO-A than (R)-6, demonstrating a higher selectivity ratio (MAO-B/MAO-A).	(s)-6	0-5	monoamine oxidase B	Homo sapiens	136-141
35164192-7	2022	Both molecules proved to inhibit MAO-B, with trans-6-styrylcoumarin being 107 times more active than 3-phenylcoumarin, and 267 times more active than trans-resveratrol.	trans-6-styrylcoumarin	45-67	monoamine oxidase B	Homo sapiens	33-38
35164192-7	2022	Both molecules proved to inhibit MAO-B, with trans-6-styrylcoumarin being 107 times more active than 3-phenylcoumarin, and 267 times more active than trans-resveratrol.	3-Phenylcoumarin	101-117	monoamine oxidase B	Homo sapiens	33-38
35164192-7	2022	Both molecules proved to inhibit MAO-B, with trans-6-styrylcoumarin being 107 times more active than 3-phenylcoumarin, and 267 times more active than trans-resveratrol.	Resveratrol	150-167	monoamine oxidase B	Homo sapiens	33-38
35203483-8	2022	The hopeaphenol, vitisin A, and vitisin B, showed AChE and monoamine oxidase-B inhibitions in a dose-dependent manner, among which vitisin B and vitisin A exhibited much better activities than those of resveratrol, and had neuroprotective activities against methylglyoxal-induced SH-SY5Y cell deaths.	hopeaphenol	4-15	monoamine oxidase B	Homo sapiens	59-78
35086898-14	2022	Conclusion: 18F-SMBT-1 is a highly selective MAO-B tracer, with low non-specific binding, high entry into the brain and displaying reversible kinetics.	-smbt-	15-21	monoamine oxidase B	Homo sapiens	45-50
35203483-8	2022	The hopeaphenol, vitisin A, and vitisin B, showed AChE and monoamine oxidase-B inhibitions in a dose-dependent manner, among which vitisin B and vitisin A exhibited much better activities than those of resveratrol, and had neuroprotective activities against methylglyoxal-induced SH-SY5Y cell deaths.	vitisin A	17-26	monoamine oxidase B	Homo sapiens	59-78
35203483-8	2022	The hopeaphenol, vitisin A, and vitisin B, showed AChE and monoamine oxidase-B inhibitions in a dose-dependent manner, among which vitisin B and vitisin A exhibited much better activities than those of resveratrol, and had neuroprotective activities against methylglyoxal-induced SH-SY5Y cell deaths.	malvidin-3-O-glucoside-4 vinyl	32-41	monoamine oxidase B	Homo sapiens	59-78
35203483-8	2022	The hopeaphenol, vitisin A, and vitisin B, showed AChE and monoamine oxidase-B inhibitions in a dose-dependent manner, among which vitisin B and vitisin A exhibited much better activities than those of resveratrol, and had neuroprotective activities against methylglyoxal-induced SH-SY5Y cell deaths.	malvidin-3-O-glucoside-4 vinyl	131-140	monoamine oxidase B	Homo sapiens	59-78
35203483-8	2022	The hopeaphenol, vitisin A, and vitisin B, showed AChE and monoamine oxidase-B inhibitions in a dose-dependent manner, among which vitisin B and vitisin A exhibited much better activities than those of resveratrol, and had neuroprotective activities against methylglyoxal-induced SH-SY5Y cell deaths.	vitisin A	145-154	monoamine oxidase B	Homo sapiens	59-78
35203483-8	2022	The hopeaphenol, vitisin A, and vitisin B, showed AChE and monoamine oxidase-B inhibitions in a dose-dependent manner, among which vitisin B and vitisin A exhibited much better activities than those of resveratrol, and had neuroprotective activities against methylglyoxal-induced SH-SY5Y cell deaths.	Resveratrol	202-213	monoamine oxidase B	Homo sapiens	59-78
34776443-2	2022	OBJECTIVE: Using 18F-THK5351 as a tracer that binds to both tau and MAO-B, we investigated the changes in 18F-THK5351 accumulation patterns in AD continuum individuals with positive amyloid PET consisting of cognitively normal individuals (CNp), amnestic mild cognitive impairment (aMCI), and AD and cognitively normal individuals (CNn) with negative amyloid PET.	THK5351	21-28	monoamine oxidase B	Homo sapiens	68-73
35116210-9	2022	Istradefylline is an alternative option to dopaminergic drugs such as dopamine agonists, monoamine oxidase B inhibitors, and catechol-O-methyltransferase inhibitors as an adjunct to L/C in patients with motor fluctuations, but clinical use will further define its role in treatment of PD.	istradefylline	0-14	monoamine oxidase B	Homo sapiens	89-108
35001806-2	2022	Safinamide is one of the clinically prescribed monoamine oxidase B (MAOB) inhibitors.	safinamide	0-10	monoamine oxidase B	Homo sapiens	47-66
35001806-2	2022	Safinamide is one of the clinically prescribed monoamine oxidase B (MAOB) inhibitors.	safinamide	0-10	monoamine oxidase B	Homo sapiens	68-72
34776443-2	2022	OBJECTIVE: Using 18F-THK5351 as a tracer that binds to both tau and MAO-B, we investigated the changes in 18F-THK5351 accumulation patterns in AD continuum individuals with positive amyloid PET consisting of cognitively normal individuals (CNp), amnestic mild cognitive impairment (aMCI), and AD and cognitively normal individuals (CNn) with negative amyloid PET.	THK5351	110-117	monoamine oxidase B	Homo sapiens	68-73