PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
3149290-1	1988	Two patients with congenital dopamine beta-hydroxylase (DBH) deficiency were treated with d,l-threo-3,4-dihydroxyphenylserine (DOPS), 500 mg twice daily.	Droxidopa	127-131	dopamine beta-hydroxylase	Homo sapiens	29-54
3149290-1	1988	Two patients with congenital dopamine beta-hydroxylase (DBH) deficiency were treated with d,l-threo-3,4-dihydroxyphenylserine (DOPS), 500 mg twice daily.	Droxidopa	127-131	dopamine beta-hydroxylase	Homo sapiens	56-59
3149290-3	1988	In vitro l-DOPS may serve as a substrate for aromatic-l-amino-acid decarboxylase (ALAAD) to form physiological (-)-noradrenaline.	Droxidopa	9-15	dopa decarboxylase	Homo sapiens	45-80
2890807-1	1987	A patient with severe orthostatic hypotension due to dopamine-beta-hydroxylase deficiency was treated with the unnatural aminoacid D,L-threo-3,4-dihydroxyphenylserine (DOPS) in the hope that it would serve as a substrate of aromatic-L-aminoacid decarboxylase to produce (-)-noradrenaline.	Droxidopa	168-172	dopamine beta-hydroxylase	Homo sapiens	53-78
3138156-9	1988	), an MAO inhibitor, enhanced the excitatory effects of low-dose L-DOPS (10 mg/kg, i.v.)	Droxidopa	65-71	monoamine oxidase A	Rattus norvegicus	6-9
3138156-20	1988	These results suggest that the moderate enhancing effects of L-DOPS on MSR and PSR are due to conversion of L-DOPS to noradrenaline in the spinal cord.	Droxidopa	61-67	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Rattus norvegicus	71-74
3138156-20	1988	These results suggest that the moderate enhancing effects of L-DOPS on MSR and PSR are due to conversion of L-DOPS to noradrenaline in the spinal cord.	Droxidopa	108-114	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Rattus norvegicus	71-74
3106991-0	1987	Studies on the central action of L-threo-3,4-dihydroxyphenyl-serine (L-threo-DOPS) in FLA-63-treated mice.	Droxidopa	33-67	4-hydroxyphenylpyruvic acid dioxygenase	Mus musculus	86-89
3613861-0	1987	Stimulation of prolactin secretion by L-3,4-dihydroxyphenyl-serine (L-DOPS) via central norepinephrine in the rat.	Droxidopa	68-74	prolactin	Rattus norvegicus	15-24
3613861-1	1987	Intracerebroventricular (icv) injection of L-3,4-dihydroxyphenylserine (L-DOPS) (50 and 250 micrograms/rat) raised in a dose-related manner both plasma prolactin (PRL) and CSF norepinephrine (NE) in urethane-anesthetized male rats.	Droxidopa	72-78	prolactin	Rattus norvegicus	152-161
3613861-1	1987	Intracerebroventricular (icv) injection of L-3,4-dihydroxyphenylserine (L-DOPS) (50 and 250 micrograms/rat) raised in a dose-related manner both plasma prolactin (PRL) and CSF norepinephrine (NE) in urethane-anesthetized male rats.	Droxidopa	72-78	prolactin	Rattus norvegicus	163-166
3613861-2	1987	Intravenous (iv) injection of larger doses of L-DOPS (5 and 10 mg/100 g BW) slightly but significantly increased plasma PRL and CSF NE.	Droxidopa	46-52	prolactin	Rattus norvegicus	120-123
3613861-3	1987	L-DOPS injection (50 micrograms/rat, icv or 5 mg/100 g BW, iv) also raised plasma PRL in conscious rats.	Droxidopa	0-6	prolactin	Rattus norvegicus	82-85
3613861-5	1987	Propranolol (100 micrograms/100 g BW, iv) inhibited plasma PRL responses to L-DOPS (50 micrograms/rat, icv) and NE injection (1 microgram/rat, icv) raised plasma PRL in anesthetized animals.	Droxidopa	76-82	prolactin	Rattus norvegicus	59-62
3613861-6	1987	These findings indicate that L-DOPS stimulates PRL secretion via central noradrenergic mechanisms in the rat.	Droxidopa	29-35	prolactin	Rattus norvegicus	47-50
3585225-8	1987	Administration of DL-treo-dihydroxyphenylserine (DOPS) increased noradrenaline content in the ectopic pituitary and reduced plasma prolactin concentrations in pituitary grafted rats.	Droxidopa	49-53	prolactin	Rattus norvegicus	131-140
3585225-9	1987	In contrast, injection of DOPS to control rats increased both hypothalamic noradrenaline content and plasma prolactin concentrations.	Droxidopa	26-30	prolactin	Rattus norvegicus	108-117
3108598-11	1987	These results suggest that the L-threo-DOPS-induced increase in brain MHPG is not likely to originate in peripheral organs including the brain capillary, and that L-threo-DOPS can be converted to NE by aromatic L-amino acid decarboxylase(AADC) in the brain parenchyma.	Droxidopa	31-43	dopa decarboxylase	Mus musculus	238-242
3108598-11	1987	These results suggest that the L-threo-DOPS-induced increase in brain MHPG is not likely to originate in peripheral organs including the brain capillary, and that L-threo-DOPS can be converted to NE by aromatic L-amino acid decarboxylase(AADC) in the brain parenchyma.	Droxidopa	163-175	dopa decarboxylase	Mus musculus	238-242
3106991-0	1987	Studies on the central action of L-threo-3,4-dihydroxyphenyl-serine (L-threo-DOPS) in FLA-63-treated mice.	Droxidopa	69-81	4-hydroxyphenylpyruvic acid dioxygenase	Mus musculus	86-89
3106991-2	1987	L-threo-DOPS in combination with nialamide markedly increased both the locomotor activity and the concentrations of the brain, heart and kidney norepinephrine (NE) in the FLA-63-treated mice.	Droxidopa	0-12	4-hydroxyphenylpyruvic acid dioxygenase	Mus musculus	171-174
4091266-3	1985	Purified AADC showed a single band with an Mr of 50,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and decarboxylated L-3,4-dihydroxyphenylalanine, L-5-hydroxytryptophan, and L-threo-3,4-dihydroxyphenylserine (a synthetic precursor of natural norepinephrine).	Droxidopa	194-227	dopa decarboxylase	Homo sapiens	9-13
3090204-3	1986	The inhibitory effect of L-threo-DOPS on both MAO-A and -B activity was confirmed in human liver mitochondria, and MAO-A was found to be more sensitive to the inhibitor.	Droxidopa	25-37	monoamine oxidase A	Homo sapiens	46-58
3090204-3	1986	The inhibitory effect of L-threo-DOPS on both MAO-A and -B activity was confirmed in human liver mitochondria, and MAO-A was found to be more sensitive to the inhibitor.	Droxidopa	25-37	monoamine oxidase A	Homo sapiens	46-51
6735152-6	1984	Similarly plasma concentrations of GH were elevated by dihydroxyphenylserine (DOPS, a precursor of NE/E) in chicks pretreated with DDC or carbidopa.	Droxidopa	78-82	growth hormone 1	Homo sapiens	35-37
6431755-4	1984	After administration of DL-threo-DOPS, the CSF level of 3-methoxy-4-hydroxyphenylglycol (MHPG), a major metabolite of norepinephrine, was 127.5% of the pretreatment level.	Droxidopa	24-37	colony stimulating factor 2	Homo sapiens	43-46
3938472-1	1985	L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) was administered at a maintenance dose of 600-900 mg/day, in 10 patients with Parkinson"s disease who exhibited a notable freezing phenomenon under the medication of L-DOPA/DCI (DOPA-decarboxylase inhibitor).	Droxidopa	0-33	dopa decarboxylase	Homo sapiens	227-245
3938472-1	1985	L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) was administered at a maintenance dose of 600-900 mg/day, in 10 patients with Parkinson"s disease who exhibited a notable freezing phenomenon under the medication of L-DOPA/DCI (DOPA-decarboxylase inhibitor).	Droxidopa	35-47	dopa decarboxylase	Homo sapiens	227-245
6735152-14	1984	Plasma concentrations of GH were reduced by the peripheral administration of NE, which might be expected not to cross the blood-brain-barrier (BBB), alpha 1/alpha 2 agonists clonidine and p-amino clonidine (which does not cross BBB), NE/E precursors L-DOPA and DOPS, and the beta agonist, isoproterenol.	Droxidopa	261-265	growth hormone 1	Homo sapiens	25-27
6121849-6	1981	These findings suggest that in newborn rats, L-threo-DOPS is effectively converted by AADC to NA which in turn acts on beta-receptors in the pacemaker cell membrane.	Droxidopa	45-57	dopa decarboxylase	Rattus norvegicus	86-90
4359658-0	1973	Antagonism by DL-threo-DOPS of the suppression of a conditioned avoidance response induced by a dopamine-beta-hydroxylase inhibitor.	Droxidopa	14-27	dopamine beta-hydroxylase	Homo sapiens	96-121
33538595-5	2021	We investigated the interaction of alpha-synuclein with vesicles of 1,2-dioleoyl-sn-glycero-3-phospho-l-serine (DOPS) or 1,2-dilauroyl-sn-glycero-3-phospho-l-serine (DLPS).	Droxidopa	112-116	synuclein alpha	Homo sapiens	35-50
32507202-3	2020	In vivo assays showed that D. officinale polysaccharides (DOPs) exerted significant hypoglycemic effects accompanying increased serum insulin and glucagon-like peptide-1 (GLP-1) levels in streptozotocin-induced diabetic rats.	Droxidopa	58-62	glucagon	Rattus norvegicus	171-176
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Droxidopa	133-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	52-71
33170712-3	2020	In this work, a G12D-mutated farnesylated GTP-bound Kirsten RAt sarcoma (KRAS) protein has been simulated at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Droxidopa	133-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	73-77
33144914-2	2020	Dendrobium officinale polysaccharides (DOPs) are the main active ingredients extracted from Dendrobium officinale, which have been reported to have antioxidant and anti-inflammatory activity as well as inhibition of mucin gene expression.	Droxidopa	39-43	solute carrier family 13 member 2	Rattus norvegicus	216-221
33144914-8	2020	DOPs ameliorated the CS-induced mucus hypersecretion and viscosity as shown by the downregulation of MUC5AC mRNA, MUC5AC secretary protein, and mucus viscosity via inhibition of mucus secretory granules in both in vitro and in vivo models.	Droxidopa	0-4	citrate synthase	Rattus norvegicus	21-23
33144914-9	2020	DOPs produced its effective effects on the CS-induced mucus hypersecretion and viscosity via the inhibition of the mucus secretory granules.	Droxidopa	0-4	citrate synthase	Rattus norvegicus	43-45
32507202-5	2020	These results indicated that DOPs may decrease fasting blood sugar levels by stimulating GLP-1 secretion and that intracellular DOP-induced GLP-1 secretion involved the Ca2+/calmodulin/CaMKII and MAPK pathways.	Droxidopa	29-33	glucagon	Rattus norvegicus	89-94
31101254-10	2019	By using differential pulse voltammetry, the droxidopa detection limit and linear range was determined as 0.01 muM and 0.1-500.0 muM, respectively.	Droxidopa	45-54	latexin	Homo sapiens	111-114
32326703-6	2020	Varying annexin V concentration, lipid composition and DOPS presence at each leaflet, fluorescence imaging and correlation spectroscopy confirmed that when DOPS was present at the external, Annexin V, contacting leaflet, the protein assembled rapidly at the membrane interface to form a layer.	Droxidopa	156-160	annexin A5	Homo sapiens	8-17
32326703-6	2020	Varying annexin V concentration, lipid composition and DOPS presence at each leaflet, fluorescence imaging and correlation spectroscopy confirmed that when DOPS was present at the external, Annexin V, contacting leaflet, the protein assembled rapidly at the membrane interface to form a layer.	Droxidopa	156-160	annexin A5	Homo sapiens	190-199
32326703-10	2020	Intense laser light applied to the membrane, in which DOPS is initially isolated at the lower leaflet, was found to simulate membrane damage, stimulating the rapid assembly of annexin V at the membrane interface confirmed by fluorescence imaging, correlation spectroscopy and electrochemical impedance measurements.	Droxidopa	54-58	annexin A5	Homo sapiens	176-185
31991138-9	2020	DPDPE and U69593 had full efficacy for beta-arrestin2 recruitment to the DOP-r and KOP-r respectively.	Droxidopa	73-76	arrestin beta 2	Homo sapiens	39-53
31452021-8	2019	Droxidopa (Northera ), a synthetic norepinephrine precursor, has shown efficacy in controlled trials of neurogenic orthostatic hypotension in patients with hereditary TTR amyloidosis and is now approved in the US and Asia.	Droxidopa	0-9	transthyretin	Homo sapiens	167-170
31101254-10	2019	By using differential pulse voltammetry, the droxidopa detection limit and linear range was determined as 0.01 muM and 0.1-500.0 muM, respectively.	Droxidopa	45-54	latexin	Homo sapiens	129-132
28770608-0	2017	Highly Enantioselective Synthesis of syn-beta-Hydroxy alpha-Dibenzylamino Esters via DKR Asymmetric Transfer Hydrogenation and Gram-Scale Preparation of Droxidopa.	Droxidopa	153-162	synemin	Homo sapiens	37-40
30776373-2	2019	In this study, we compared the properties of the DOP-KOP heteromer agonist, 6"-guanidinonaltrindole (6"-GNTI), with agonists for DOP ([D-Pen2,5]-enkephalin [DPDPE]) and KOP (U50488) in peripheral sensory neurons in culture and in vivo.	Droxidopa	49-52	serine peptidase inhibitor, Kunitz type 2	Homo sapiens	53-56
30828233-2	2019	Droxidopa is a synthetic amino acid analog that is directly metabolized to norepinephrine by dopa-decarboxylase, subsequently providing alpha and beta-agonist effects to increase blood pressure.	Droxidopa	0-9	dopa decarboxylase	Homo sapiens	93-111
23265352-9	2013	This result supports our hypothesis, at least in patients with levodopa-resistant FOG, and shows that the co-administration of L-DOPS and entacapone could be a new strategy for FOG treatment.	Droxidopa	127-133	zinc finger protein, FOG family member 1	Homo sapiens	82-85
28494751-7	2017	Droxidopa was effective in patients using inhibitors of dopa decarboxylase (DDCI; the enzyme that converts droxidopa to norepinephrine), but its efficacy was numerically greater in non-DDCI users.	Droxidopa	0-9	dopa decarboxylase	Homo sapiens	56-74
28494751-7	2017	Droxidopa was effective in patients using inhibitors of dopa decarboxylase (DDCI; the enzyme that converts droxidopa to norepinephrine), but its efficacy was numerically greater in non-DDCI users.	Droxidopa	107-116	dopa decarboxylase	Homo sapiens	56-74
26429909-8	2015	Experiments in proteoliposomes reconstituted with alpha1beta1 show analogous effects of FXYD1 on K0.5Na, which are abolished by phosphomimetic mutants and also by increasing mole fractions of DOPS in the proteoliposomes.	Droxidopa	192-196	FXYD domain containing ion transport regulator 1	Homo sapiens	88-93
24517276-9	2015	When chronically administered to CCl4 -cirrhotic rats, propranolol + droxidopa caused a decrease in PP, a significant reduction in SMABF and an increase in SMAR.	Droxidopa	69-78	C-C motif chemokine ligand 4	Rattus norvegicus	33-37
24966384-4	2014	Acute pharmacological replacement of NA by L-threo-DOPS partially restored phosphorylation of beta-CaMKII and spatial memory performance in APP/PS1 Ear2(-/-) mice.	Droxidopa	43-55	amyloid beta (A4) precursor protein	Mus musculus	140-152
24105627-3	2013	At low concentrations of the negatively charged lipid DOPS (<10 %), FXYD1 increases K(1/2) of Na+ ions for activation of the ion pump.	Droxidopa	54-58	FXYD domain containing ion transport regulator 1	Homo sapiens	71-76
23643891-5	2013	The interaction of TAT peptide with anionic lipid bilayer, composed of an 80:20 mixture of DOPC and DOPS, takes place at two locations.	Droxidopa	100-104	tyrosine aminotransferase	Homo sapiens	19-22
23242741-2	2013	Droxidopa, a drug that increases norepinephrine, treats orthostatic hypotension, cholinomimetic drugs sometimes help with FOG and difficulty with balance, pimavanserin, a drug that blocks serotonin receptors, treats paranoia and hallucinations, and anti-glutaminergic drugs treat dyskinesias.	Droxidopa	0-9	zinc finger protein, FOG family member 1	Homo sapiens	122-125
27148966-4	2016	Phenotypes associated with DBH deficiency are typically treated with L-3,4-dihydroxyphenylserine (DOPS), which can be converted to NE by aromatic acid decarboxylase (AADC) in the absence of DBH.	Droxidopa	98-102	dopa decarboxylase	Homo sapiens	166-170
27148966-4	2016	Phenotypes associated with DBH deficiency are typically treated with L-3,4-dihydroxyphenylserine (DOPS), which can be converted to NE by aromatic acid decarboxylase (AADC) in the absence of DBH.	Droxidopa	98-102	dopamine beta-hydroxylase	Homo sapiens	27-30
26092297-3	2015	Droxidopa, an orally active synthetic amino acid that is converted to norepinephrine by the enzyme aromatic L-amino acid decarboxylase (dopa-decarboxylase), was recently approved by the FDA for the short-term treatment of nOH.	Droxidopa	0-9	dopa decarboxylase	Homo sapiens	99-134
26092297-3	2015	Droxidopa, an orally active synthetic amino acid that is converted to norepinephrine by the enzyme aromatic L-amino acid decarboxylase (dopa-decarboxylase), was recently approved by the FDA for the short-term treatment of nOH.	Droxidopa	0-9	dopa decarboxylase	Homo sapiens	136-154
25303896-10	2014	Droxidopa is a synthetic amino acid that is converted to norepinephrine by dopa-decarboxylase, the same enzyme that converts levodopa into dopamine in the treatment of Parkinson disease.	Droxidopa	0-9	dopa decarboxylase	Homo sapiens	75-93
23265352-3	2013	Although L-threo-3,4-dihydroxyphenylserine (L-DOPS), a precursor of noradrenaline, has been on the market in Japan because of its beneficial effect for FOG, clinical use of L-DOPS has been far from satisfying.	Droxidopa	9-42	zinc finger protein, FOG family member 1	Homo sapiens	152-155
23265352-3	2013	Although L-threo-3,4-dihydroxyphenylserine (L-DOPS), a precursor of noradrenaline, has been on the market in Japan because of its beneficial effect for FOG, clinical use of L-DOPS has been far from satisfying.	Droxidopa	44-50	zinc finger protein, FOG family member 1	Homo sapiens	152-155
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	53-59	catechol-O-methyltransferase	Homo sapiens	188-217
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	catechol-O-methyltransferase	Homo sapiens	188-217
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	catechol-O-methyltransferase	Homo sapiens	219-223
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	zinc finger protein, FOG family member 1	Homo sapiens	340-343
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	catechol-O-methyltransferase	Homo sapiens	188-217
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	catechol-O-methyltransferase	Homo sapiens	219-223
23265352-9	2013	This result supports our hypothesis, at least in patients with levodopa-resistant FOG, and shows that the co-administration of L-DOPS and entacapone could be a new strategy for FOG treatment.	Droxidopa	127-133	zinc finger protein, FOG family member 1	Homo sapiens	177-180
22196467-6	2011	Interestingly, the addition of DOPS scores to small-scale OSCE scores [small-scale OSCE+DOPS-composited scores] increased it"s correlation with 360-degree evaluation scores of PGY(1) residents (r = 0.72, p < 0.036).	Droxidopa	31-35	ATP binding cassette subfamily B member 1	Homo sapiens	176-182
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	zinc finger protein, FOG family member 1	Homo sapiens	340-343
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	catechol-O-methyltransferase	Homo sapiens	188-217
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	catechol-O-methyltransferase	Homo sapiens	219-223
23265352-4	2013	However, the fact that there were some responders to L-DOPS encouraged us to hypothesize that the enhancement of L-DOPS concentration in the brain by the co-administration of L-DOPS and a catechol-O-methyl transferase (COMT) inhibitor, which is expected to interrupt L-DOPS metabolism in the peripheral circulation, would be beneficial for FOG.	Droxidopa	113-119	zinc finger protein, FOG family member 1	Homo sapiens	340-343
21705113-6	2012	L-DOPS reduced astrocyte activation and Thioflavin-S staining; increased mRNA levels of neprilysin and insulin degrading enzyme, and of several neurotrophins; and increased brain-derived neurotrophic factor protein levels.	Droxidopa	0-6	membrane metallo endopeptidase	Mus musculus	88-98
21705113-6	2012	L-DOPS reduced astrocyte activation and Thioflavin-S staining; increased mRNA levels of neprilysin and insulin degrading enzyme, and of several neurotrophins; and increased brain-derived neurotrophic factor protein levels.	Droxidopa	0-6	insulin degrading enzyme	Mus musculus	103-127
21705113-6	2012	L-DOPS reduced astrocyte activation and Thioflavin-S staining; increased mRNA levels of neprilysin and insulin degrading enzyme, and of several neurotrophins; and increased brain-derived neurotrophic factor protein levels.	Droxidopa	0-6	brain derived neurotrophic factor	Mus musculus	173-206
22610782-4	2012	The droxidopa effect on the Rho kinase (RhoK) / protein kinase B (AKT) / endothelial nitric oxide synthase (eNOS) pathways was analyzed by western blot in superior mesenteric artery (SMA).	Droxidopa	4-13	G protein-coupled receptor kinase 1	Rattus norvegicus	28-38
22610782-4	2012	The droxidopa effect on the Rho kinase (RhoK) / protein kinase B (AKT) / endothelial nitric oxide synthase (eNOS) pathways was analyzed by western blot in superior mesenteric artery (SMA).	Droxidopa	4-13	G protein-coupled receptor kinase 1	Rattus norvegicus	40-44
22610782-4	2012	The droxidopa effect on the Rho kinase (RhoK) / protein kinase B (AKT) / endothelial nitric oxide synthase (eNOS) pathways was analyzed by western blot in superior mesenteric artery (SMA).	Droxidopa	4-13	AKT serine/threonine kinase 1	Rattus norvegicus	66-69
22610782-7	2012	Carbidopa (DOPA decarboxylase inhibitor) blunted all effects of droxidopa.	Droxidopa	64-73	dopa decarboxylase	Rattus norvegicus	11-29
22610782-9	2012	Droxidopa-treated rats also showed a decreased ratio of p-eNOS/eNOS and p-AKT/AKT and increased activity of RhoK in SMA.	Droxidopa	0-9	AKT serine/threonine kinase 1	Rattus norvegicus	74-77
22610782-9	2012	Droxidopa-treated rats also showed a decreased ratio of p-eNOS/eNOS and p-AKT/AKT and increased activity of RhoK in SMA.	Droxidopa	0-9	AKT serine/threonine kinase 1	Rattus norvegicus	78-81
22610782-9	2012	Droxidopa-treated rats also showed a decreased ratio of p-eNOS/eNOS and p-AKT/AKT and increased activity of RhoK in SMA.	Droxidopa	0-9	G protein-coupled receptor kinase 1	Rattus norvegicus	108-112
22200605-0	2012	Embryonic lethality in mice lacking mismatch-specific thymine DNA glycosylase is partially prevented by DOPS, a precursor of noradrenaline.	Droxidopa	104-108	thymine DNA glycosylase	Mus musculus	54-77
22200605-6	2012	Consequently, we tested the effect of D, L-threo-3, 4-dihydroxyphenylserine (DOPS), a synthetic precursor of noradrenaline, on the survival of the Tdg (-/-) embryos.	Droxidopa	77-81	thymine DNA glycosylase	Mus musculus	147-150
22200605-7	2012	DOPS was given to pregnant Tdg (+/-) mice from 6.5 dpc through drinking water.	Droxidopa	0-4	thymine DNA glycosylase	Mus musculus	27-30
22200605-8	2012	Most of the Tdg (-/-) embryos were alive at 11.5 dpc, and they were partially rescued up to 14.5 dpc by the administration of DOPS.	Droxidopa	126-130	thymine DNA glycosylase	Mus musculus	12-15
22196467-6	2011	Interestingly, the addition of DOPS scores to small-scale OSCE scores [small-scale OSCE+DOPS-composited scores] increased it"s correlation with 360-degree evaluation scores of PGY(1) residents (r = 0.72, p < 0.036).	Droxidopa	88-92	ATP binding cassette subfamily B member 1	Homo sapiens	176-182
21104228-10	2011	Stratified analyses revealed that in the high weight group in AROS individuals homozygous for the variant allele had a decreased BMD (p <= 0.02), whereas the same pattern was found in the low weight group in DOPS (p <= 0.03).	Droxidopa	211-215	ribosomal protein S19 binding protein 1	Homo sapiens	62-66
20839079-11	2010	Aerosolisation of the DOPS-rSLPI dry powder yielded 38% emitted dose, with 2.44 mum MMAD.	Droxidopa	22-26	secretory leukocyte peptidase inhibitor	Rattus norvegicus	27-32
21104233-11	2011	A haplotype comprising all the common alleles (frequency 9%) was associated with decreased bone loss at the hip (p < 0.05) and decreased incidence of osteoporotic fractures (p < 0.05) in DOPS and increased femoral neck BMD in AROS (p < 0.05).	Droxidopa	193-197	ribosomal protein S19 binding protein 1	Homo sapiens	232-236
23933657-8	2011	alpha-Synuclein was particularly strongly associated with GUVs containing the anionic lipids cardiolipin or DOPS, whereas it did not associate with GUVs containing only zwitterionic DOPC.	Droxidopa	108-112	synuclein alpha	Homo sapiens	0-15
20839079-12	2010	When challenged with Cat L post-aerosolisation, DOPS-rSLPI dry powder was significantly better at retaining a protective function against Cat L-induced rSLPI inactivation compared to the aqueous DOPS-rSLPI liposome dispersion and was also more stable under storage.	Droxidopa	48-52	cathepsin L	Homo sapiens	21-26
20839079-12	2010	When challenged with Cat L post-aerosolisation, DOPS-rSLPI dry powder was significantly better at retaining a protective function against Cat L-induced rSLPI inactivation compared to the aqueous DOPS-rSLPI liposome dispersion and was also more stable under storage.	Droxidopa	48-52	secretory leukocyte peptidase inhibitor	Rattus norvegicus	53-58
20839079-12	2010	When challenged with Cat L post-aerosolisation, DOPS-rSLPI dry powder was significantly better at retaining a protective function against Cat L-induced rSLPI inactivation compared to the aqueous DOPS-rSLPI liposome dispersion and was also more stable under storage.	Droxidopa	48-52	cathepsin L	Homo sapiens	138-143
20839079-12	2010	When challenged with Cat L post-aerosolisation, DOPS-rSLPI dry powder was significantly better at retaining a protective function against Cat L-induced rSLPI inactivation compared to the aqueous DOPS-rSLPI liposome dispersion and was also more stable under storage.	Droxidopa	48-52	secretory leukocyte peptidase inhibitor	Rattus norvegicus	152-157
20839079-12	2010	When challenged with Cat L post-aerosolisation, DOPS-rSLPI dry powder was significantly better at retaining a protective function against Cat L-induced rSLPI inactivation compared to the aqueous DOPS-rSLPI liposome dispersion and was also more stable under storage.	Droxidopa	48-52	secretory leukocyte peptidase inhibitor	Rattus norvegicus	152-157
16899413-4	2006	Drug seeking was induced when NA was restored to the central nervous system of Dbh -/- mice by administration of l-threo-3,4-dihydroxyphenylserine (DOPS) and carbidopa.	Droxidopa	113-146	dopamine beta hydroxylase	Mus musculus	79-82
20132473-4	2010	Treatment of mice with the NA precursor l-threo-3,4-dihydroxyphenylserine induced the production of MCP-1 in astrocytes.	Droxidopa	40-73	chemokine (C-C motif) ligand 2	Mus musculus	100-105
18665822-4	2008	A chromogenic substrate that is cleaved by thrombin at a slow rate, 7 pm tissue factor and 20 mum phospholipid (DOPC : DOPE : DOPS, 60 : 20 : 20) with and without 5 nm APC.	Droxidopa	126-130	coagulation factor II, thrombin	Homo sapiens	43-51
18368304-11	2008	It also addresses the issue of whether addition of dopa decarboxylase inhibitors, when combined with l-dopa in the treatment of the motor deficit in Parkinson"s disease, impairs the pressor efficacy of Droxidopa.	Droxidopa	202-211	dopa decarboxylase	Homo sapiens	51-69
17603032-2	2007	The lipid dynamics near the gel-fluid transition, the chain length of saturated lipids and the presence of DOPE or DOPS in DOPC-vesicles modulate the aggregation kinetics of insulin in an indifferent, an aggregation-accelerating or an aggregation-inhibiting manner, subtly depending on the pH-value and the presence of salt.	Droxidopa	115-119	insulin	Homo sapiens	174-181
17603032-6	2007	Apart from weak dipole-dipole, dipole-monopole and hydrogen bonding interactions, the release of curvature elastic stress in mixed DOPC/DOPE-membranes and preferred interactions of insulin with carboxylic groups in DOPC/DOPS-membranes favour an increased surface accumulation.	Droxidopa	220-224	insulin	Homo sapiens	181-188
17603032-7	2007	At neutral pH, a partial insertion of insulin into the lipid bilayer is favoured, which accounts for the aggregation-inhibiting effect of all lipid bilayer systems studied except those containing DOPS.	Droxidopa	196-200	insulin	Homo sapiens	38-45
17603032-9	2007	The accelerating effect of DOPS on the aggregation of insulin under net electrostatic repulsion at pH 7.4 remains to be elucidated, yet, it might result from increased surface accumulation and/or faster/more extensive unfolding of the protein without a subsequent membrane insertion.	Droxidopa	27-31	insulin	Homo sapiens	54-61
17214596-9	2006	L-DOPS is very effective in treatment of deficiency of dopamine-beta-hydroxylase (DBH), the enzyme required for conversion of dopamine to NE in sympathetic nerves.	Droxidopa	0-6	dopamine beta-hydroxylase	Homo sapiens	55-80
17214596-9	2006	L-DOPS is very effective in treatment of deficiency of dopamine-beta-hydroxylase (DBH), the enzyme required for conversion of dopamine to NE in sympathetic nerves.	Droxidopa	0-6	dopamine beta-hydroxylase	Homo sapiens	82-85
17214596-10	2006	L-DOPS holds promise for treating other much more common conditions involving decreased DBH activity or NE deficiency, such as a variety of syndromes associated with neurogenic orthostatic hypotension.	Droxidopa	0-6	dopamine beta-hydroxylase	Homo sapiens	88-91
16899413-4	2006	Drug seeking was induced when NA was restored to the central nervous system of Dbh -/- mice by administration of l-threo-3,4-dihydroxyphenylserine (DOPS) and carbidopa.	Droxidopa	148-152	dopamine beta hydroxylase	Mus musculus	79-82
17017570-1	2006	In the 1950s it was found that an artificial aminoacid, 3,4-threo-dihydroxyphenylserine (DOPS), was converted to norepinephrine (NE) in a single step by the enzyme L-aromatic amino acid decarboxylase (AADC), bypassing the need for the rate limiting enzyme dopamine beta hydroxylase.	Droxidopa	89-93	dopa decarboxylase	Homo sapiens	201-205
17017570-1	2006	In the 1950s it was found that an artificial aminoacid, 3,4-threo-dihydroxyphenylserine (DOPS), was converted to norepinephrine (NE) in a single step by the enzyme L-aromatic amino acid decarboxylase (AADC), bypassing the need for the rate limiting enzyme dopamine beta hydroxylase.	Droxidopa	89-93	dopamine beta-hydroxylase	Homo sapiens	256-281
17017570-3	2006	DOPS improved orthostatic hypotension in patients with familial amyloid polyneuropathy, congenital deficiency of dopamine beta hydroxylase, pure autonomic failure and multiple system atrophy.	Droxidopa	0-4	dopamine beta-hydroxylase	Homo sapiens	113-138
17017570-4	2006	DOPS pressor effect is due to its conversion to NE outside the central nervous system because concomitant administration of carbidopa, an inhibitor of AADC that does not cross the blood-brain barrier, blunted both the increase in plasma NE and the pressor response.	Droxidopa	0-4	dopa decarboxylase	Homo sapiens	151-155
12083775-0	2002	Behavior of fluorinated analogs of L-(3,4-dihydroxyphenyl)alanine and L-threo-(3,4-dihydroxyphenyl)serine as substrates for Dopa decarboxylase.	Droxidopa	70-105	dopa decarboxylase	Homo sapiens	124-142
16212933-3	2005	Purified COX-1 and -2 spontaneously incorporate into large unilamellar vesicles produced from a mixture of DOPC:DOPS (7:3) that has been doped with oleic acid.	Droxidopa	112-116	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	9-21
16463138-5	2005	Both tBid and Bax interact moderately half as strongly with negatively charged DOPS and non-lamellar DOPE monolayers.	Droxidopa	79-83	BCL2 associated X, apoptosis regulator	Homo sapiens	14-17
15620318-2	2005	We use the technique of quartz crystal microbalance with dissipation monitoring (QCM-D) to follow the adsorption of prothrombin on SLBs formed from sonicated unilamellar vesicles containing mixtures of dioleoylphosphatidylcholine (DOPC) and dioleoylphospatidylserine (DOPS).	Droxidopa	268-272	coagulation factor II, thrombin	Homo sapiens	116-127
15620318-3	2005	The specific interaction of prothrombin with negatively charged lipids is quantified and serves as a reporter of the content of accessible DOPS in SLBs.	Droxidopa	139-143	coagulation factor II, thrombin	Homo sapiens	28-39
11901210-3	2002	LAT1-mediated [(14)C]phenylalanine uptake was strongly inhibited in a competitive manner by aromatic-amino acid derivatives including L-dopa, alpha-methyldopa, melphalan, triiodothyronine, and thyroxine, whereas phenylalanine methyl ester, N-methyl phenylalanine, dopamine, tyramine, carbidopa, and droxidopa did not inhibit [(14)C]phenylalanine uptake.	Droxidopa	299-308	solute carrier family 7 member 5 L homeolog	Xenopus laevis	0-4
12102462-6	2002	DOPS is converted directly to NE through decarboxylation by L-aromatic amino acid decarboxylase (AADC), thereby bypassing DBH.	Droxidopa	0-4	dopa decarboxylase	Homo sapiens	97-101
12102462-6	2002	DOPS is converted directly to NE through decarboxylation by L-aromatic amino acid decarboxylase (AADC), thereby bypassing DBH.	Droxidopa	0-4	dopamine beta-hydroxylase	Homo sapiens	122-125
10323317-0	1999	L-threo-3,4-dihydroxyphenylserine enhances the orthostatic responses of plasma renin activity and angiotensin II in multiple system atrophy.	Droxidopa	0-33	renin	Homo sapiens	79-84
11054296-3	2000	The structural and dynamic properties of cyt c bound to vesicles containing an anionic phospholipid (DOPS) were investigated by amide H-(2)H exchange using two-dimensional NMR spectroscopy and electrospray ionisation mass spectrometry.	Droxidopa	101-105	cytochrome c, somatic	Homo sapiens	41-46
10594079-7	1999	Enhanced seizure susceptibility to flurothyl and increased seizure-induced c-fos mRNA expression were reversed by pretreatment with L-threo-3, 4-dihydroxyphenylserine, which partially restores the NE content in Dbh -/- mice.	Droxidopa	132-166	FBJ osteosarcoma oncogene	Mus musculus	75-80
10594079-7	1999	Enhanced seizure susceptibility to flurothyl and increased seizure-induced c-fos mRNA expression were reversed by pretreatment with L-threo-3, 4-dihydroxyphenylserine, which partially restores the NE content in Dbh -/- mice.	Droxidopa	132-166	dopamine beta hydroxylase	Mus musculus	211-214
10821639-4	1999	AADC neurons in the human ACC might transform L-DOPA to dopamine, droxidopa to noradrenaline, and/or 5-hydroxytryptophan to serotonin.	Droxidopa	66-75	dopa decarboxylase	Homo sapiens	0-4
11454927-7	2001	In addition, desipramine significantly reduced immobility in the Dbh(-/-) mice following pretreatment with the synthetic NE precursor L-threo-3,4-dihydroxyphenylserine, but not saline.	Droxidopa	134-167	dopamine beta hydroxylase	Mus musculus	65-68
11479395-5	2001	Tandospirone is reported to activate noradrenergic neurons via the 5-HT 1A receptor, which could account for such striking improvement in a patient previously responsive to the noradrenergic precursor L-threo-DOPS given alone.	Droxidopa	201-213	5-hydroxytryptamine receptor 1A	Homo sapiens	67-83
10323317-0	1999	L-threo-3,4-dihydroxyphenylserine enhances the orthostatic responses of plasma renin activity and angiotensin II in multiple system atrophy.	Droxidopa	0-33	angiotensinogen	Homo sapiens	98-112
10323317-3	1999	In concordance with this result, we detected significant increases in postural changes in plasma renin activity and angiotensin II following L-threo-DOPS treatment.	Droxidopa	141-153	renin	Homo sapiens	97-102
10323317-3	1999	In concordance with this result, we detected significant increases in postural changes in plasma renin activity and angiotensin II following L-threo-DOPS treatment.	Droxidopa	141-153	angiotensinogen	Homo sapiens	116-130
8902314-6	1996	After L-DOPS for 4 weeks, BP reduction in the initial phase was significantly attenuated (delta SBP/DBP = -37 +/- 9/-17 +/- 7 mmHg, p < 0.05) and recovery time was normalized in all, although supine BP and HR were unchanged.	Droxidopa	6-12	selenium binding protein 1	Homo sapiens	96-99
9804294-3	1998	Pre- (but not post-) ischemic administration of DOPS rescued 73% of hippocampal CA1 neurons (p < 0.001, compared with ischemia only) 1 week after transient global ischemia in gerbils.	Droxidopa	48-52	carbonic anhydrase 1	Homo sapiens	80-83
9603211-8	1998	Ptosis and reductions in male fertility, hind-limb extension, postdecapitation convulsions, and uncoupling protein expression in dopamine beta-hydroxylase-deficient mice are all reversed by DOPS injection.	Droxidopa	190-194	dopamine beta hydroxylase	Mus musculus	129-154
9335575-1	1997	The interaction of cytochrome c with anionic lipid vesicles of DOPS induces an extensive disruption of the native structure of the protein.	Droxidopa	63-67	cytochrome c, somatic	Homo sapiens	19-31
8945750-0	1996	Enhancement of mRNA expression of tissue-type plasminogen activator by L-threo-3,4-dihydroxyphenylserine in association with ocular dominance plasticity.	Droxidopa	71-104	plasminogen activator, tissue type	Homo sapiens	34-67
8945750-2	1996	We found that the expression of tPA mRNA in the visual cortex was increased significantly by the peripheral administration of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS; 100 mg/kg, i.p.	Droxidopa	126-159	plasminogen activator, tissue type	Homo sapiens	32-35
8945750-2	1996	We found that the expression of tPA mRNA in the visual cortex was increased significantly by the peripheral administration of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS; 100 mg/kg, i.p.	Droxidopa	161-173	plasminogen activator, tissue type	Homo sapiens	32-35
8023359-1	1994	BACKGROUND AND PURPOSE: L-Threo-3,4-dihydroxyphenylserine (DOPS) is reported to increase the nerve growth factor (NGF) synthesis in cultured mouse L-M fibroblast and astroglial cells, and this effect is not blocked by treatment with decarboxylase inhibitor.	Droxidopa	24-57	nerve growth factor	Mus musculus	114-117
8023359-1	1994	BACKGROUND AND PURPOSE: L-Threo-3,4-dihydroxyphenylserine (DOPS) is reported to increase the nerve growth factor (NGF) synthesis in cultured mouse L-M fibroblast and astroglial cells, and this effect is not blocked by treatment with decarboxylase inhibitor.	Droxidopa	24-57	nerve growth factor	Mus musculus	93-112
8836986-5	1996	Only a minor part of L-threo-DOPS was metabolized into noradrenaline by aromatic L-amino acid decarboxylase, and it was metabolized mainly by two other enzymes, catechol-O-methyltransferase and DOPS-aldolase in the brain.	Droxidopa	21-33	catechol-O-methyltransferase	Homo sapiens	161-189
7834959-2	1994	Droxidopa is decarboxylated into NA by aromatic L-amino acid decarboxylase in the brain, but its effects on other monoamine neurotransmitters, such as dopamine (DA) and serotonin (5-HT) have not been systematically examined.	Droxidopa	0-9	dopa decarboxylase	Homo sapiens	39-74
7834959-8	1994	On the other hand, the metabolites of NA and DA by catechol-O-methyltransferase (COMT), normetanephrine (NMN) and 3-methoxytyramine (3-MT), decreased in the patients treated with droxidopa and L-DOPA compared with the patients administered with L-DOPA alone and control patients.	Droxidopa	179-188	catechol-O-methyltransferase	Homo sapiens	51-79
7834959-8	1994	On the other hand, the metabolites of NA and DA by catechol-O-methyltransferase (COMT), normetanephrine (NMN) and 3-methoxytyramine (3-MT), decreased in the patients treated with droxidopa and L-DOPA compared with the patients administered with L-DOPA alone and control patients.	Droxidopa	179-188	catechol-O-methyltransferase	Homo sapiens	81-85
7834960-3	1994	Droxidopa, an artificial amino acid, is decarboxylated by aromatic L-amino acid decarboxylase (AADC) into NA.	Droxidopa	0-9	dopa decarboxylase	Homo sapiens	67-93
7834960-3	1994	Droxidopa, an artificial amino acid, is decarboxylated by aromatic L-amino acid decarboxylase (AADC) into NA.	Droxidopa	0-9	dopa decarboxylase	Homo sapiens	95-99
7834960-11	1994	In the intraventricular fluid, in addition to NA, a large amount of a metabolite of droxidopa by catechol-O-methyltransferase (COMT), 3-O-methoxy-droxidopa (3OMD), was detected, followed by the metabolites by DOPS-aldolase (DOPS-ALD), protocatechualdehyde and protocatechuic acid.	Droxidopa	84-93	catechol-O-methyltransferase	Homo sapiens	97-125
7834960-11	1994	In the intraventricular fluid, in addition to NA, a large amount of a metabolite of droxidopa by catechol-O-methyltransferase (COMT), 3-O-methoxy-droxidopa (3OMD), was detected, followed by the metabolites by DOPS-aldolase (DOPS-ALD), protocatechualdehyde and protocatechuic acid.	Droxidopa	84-93	catechol-O-methyltransferase	Homo sapiens	127-131
7834960-12	1994	It indicates that considerable parts of administered droxidopa are catabolized by COMT and DOPS-ALD, but not by AADC.	Droxidopa	53-62	catechol-O-methyltransferase	Homo sapiens	82-86
8023359-1	1994	BACKGROUND AND PURPOSE: L-Threo-3,4-dihydroxyphenylserine (DOPS) is reported to increase the nerve growth factor (NGF) synthesis in cultured mouse L-M fibroblast and astroglial cells, and this effect is not blocked by treatment with decarboxylase inhibitor.	Droxidopa	59-63	nerve growth factor	Mus musculus	93-112
8023359-1	1994	BACKGROUND AND PURPOSE: L-Threo-3,4-dihydroxyphenylserine (DOPS) is reported to increase the nerve growth factor (NGF) synthesis in cultured mouse L-M fibroblast and astroglial cells, and this effect is not blocked by treatment with decarboxylase inhibitor.	Droxidopa	59-63	nerve growth factor	Mus musculus	114-117
8023359-3	1994	We evaluated the possible protective effect of DOPS against hippocampal CA1 cell death after transient forebrain ischemia in gerbils.	Droxidopa	47-51	carbonic anhydrase 1	Mus musculus	72-75
8023359-8	1994	RESULTS: Preservation of the hippocampal CA1 cells was found in the brains treated with 300 mg/kg DOPS plus benserazide (neuronal density, 125 +/- 24 cells per millimeter) compared with the vehicle-treated ones (49 +/- 11 cells per millimeter) (P < .01).	Droxidopa	98-102	carbonic anhydrase 1	Mus musculus	41-44
8023359-9	1994	The immunoreactive NGF was greatly reduced from 3 hours after recirculation in the vehicle group, but it was much less reduced in the 300-mg/kg-DOPS-plus-benserazide group as compared with the vehicle group.	Droxidopa	144-148	nerve growth factor	Mus musculus	19-22
8023359-10	1994	The immunoreactivity for NGF receptor was gradually induced from 1 hour after recirculation with the peak at 1 day in the vehicle group, but it was only slightly induced at 8 hours in the 300-mg/kg-DOPS-plus-benserazide group.	Droxidopa	198-202	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	25-37
8023359-12	1994	However, in the 300-mg/kg-DOPS-plus-benserazide group, the induction of HSP70 was found from 8 hours and was much less intensive.	Droxidopa	26-30	heat shock protein 1B	Mus musculus	72-77
8023359-13	1994	CONCLUSIONS: Treatment with DOPS is protective to the ischemic hippocampal CA1 cells, and the NGF-receptor system may play a role in this protective effect of DOPS.	Droxidopa	28-32	carbonic anhydrase 1	Mus musculus	75-78
8023359-13	1994	CONCLUSIONS: Treatment with DOPS is protective to the ischemic hippocampal CA1 cells, and the NGF-receptor system may play a role in this protective effect of DOPS.	Droxidopa	159-163	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	94-106
7936090-0	1994	Reduction of nerve growth factor receptor immunoreactivity in ischaemic gerbil hippocampal CA1 neurons after treatment with L-threo-3,4-dihydroxyphenylserine (DOPS).	Droxidopa	124-157	carbonic anhydrase 1	Mus musculus	91-94
7936090-0	1994	Reduction of nerve growth factor receptor immunoreactivity in ischaemic gerbil hippocampal CA1 neurons after treatment with L-threo-3,4-dihydroxyphenylserine (DOPS).	Droxidopa	159-163	carbonic anhydrase 1	Mus musculus	91-94
7936090-4	1994	In this study, we studied a possible protective effect of DOPS against the hippocampal CA1 cell death after transient forebrain ischaemia in gerbils in relation to the change of NGFR immunoreactivity.	Droxidopa	58-62	carbonic anhydrase 1	Mus musculus	87-90
7936090-4	1994	In this study, we studied a possible protective effect of DOPS against the hippocampal CA1 cell death after transient forebrain ischaemia in gerbils in relation to the change of NGFR immunoreactivity.	Droxidopa	58-62	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	178-182
7936090-5	1994	We found that treatment with DOPS (300 mg kg-1) in combination with a decarboxylase inhibitor (benserazide, 10 mg kg-1) protected ischaemic hippocampal CA1 cell against delayed neuronal death (neuronal density = 125 +/- 24 mm-1) as compared to the treatment with vehicle (49 +/- 11 mm-1) (p < 0.01).	Droxidopa	29-33	carbonic anhydrase 1	Mus musculus	152-155
7936090-8	1994	These data suggest that the protective role of DOPS on the ischaemic hippocampal CA1 cells may act through the NGF and its receptor system.	Droxidopa	47-51	carbonic anhydrase 1	Mus musculus	81-84
8579767-3	1994	In the brain L-threo-DOPS was metabolized by 3 different enzymes; aromatic L-amino acid decarboxylase, catechol-O-methyltransferase, and DOPS-aldolase.	Droxidopa	13-25	catechol-O-methyltransferase	Rattus norvegicus	103-131
2110272-1	1990	A synthetic amino acid, L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), can be converted to (-)-norepinephrine (NE) by aromatic L-amino acid decarboxylase (AADC) in various mammalian tissues.	Droxidopa	24-57	dopa decarboxylase	Homo sapiens	130-156
8216760-6	1993	Pretreatment with Ro 40-7592, a catechol-O-methyltransferase inhibitor, potentiated and prolonged the anticataleptic effect of DOPS.	Droxidopa	127-131	catechol-O-methyltransferase	Rattus norvegicus	32-60
8216760-9	1993	Moreover, the therapeutic effect of DOPS may be potentiated by COMT inhibition.	Droxidopa	36-40	catechol-O-methyltransferase	Rattus norvegicus	63-67
1449487-2	1992	We now report bioactivation of DOPS to the potent pharmacological agent, noradrenalone (arterenone), via sequential stereoselective action by two target enzymes--dopamine beta-monooxygenase (DBM) and L-aromatic amino acid decarboxylase (AADC)--acting in tandem.	Droxidopa	31-35	dopa decarboxylase	Homo sapiens	237-241
8414219-5	1993	The antioxidants, ascorbic acid and sodium pyrosulfite, completely prevented the stimulatory effect of L-DOPS, and radical scavengers (superoxide dismutase plus catalase) caused a significant partial inhibition of the response to L-DOPS.	Droxidopa	103-109	catalase	Homo sapiens	161-169
8414219-5	1993	The antioxidants, ascorbic acid and sodium pyrosulfite, completely prevented the stimulatory effect of L-DOPS, and radical scavengers (superoxide dismutase plus catalase) caused a significant partial inhibition of the response to L-DOPS.	Droxidopa	230-236	catalase	Homo sapiens	161-169
8486891-5	1993	Treatment with the synthetic amino acid, DL-threo-dihydroxyphenylserine, which is converted to noradrenaline by dopa-decarboxylase, resulted in a significant increase in blood pressure.	Droxidopa	41-71	dopa decarboxylase	Homo sapiens	112-130
1817730-0	1991	Effects of L-threo-DOPS, a noradrenaline precursor, on the long-term potentiation in the rat hippocampal mossy fiber-CA3 region.	Droxidopa	11-23	carbonic anhydrase 3	Rattus norvegicus	117-120
1817730-1	1991	The effects of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), a synthetic precursor of norepinephrine (NE), on the long-term potentiation (LTP) in the hippocampal mossy fiber-CA3 system was examined in urethane-anesthetized rats, the objective being to determine whether or not this drug acts as NE on the LTP.	Droxidopa	15-48	carbonic anhydrase 3	Rattus norvegicus	178-181
1817730-3	1991	The LTP, induced in CA3 by tetanic stimulation (100 Hz for 1 s) applied to the mossy fiber persisted for more than 4 h. When L-threo-DOPS (50 and 150 micrograms) was injected into the lateral ventricle 30 min prior to the tetanic stimulation, there were no significant alterations in the LTP.	Droxidopa	125-137	carbonic anhydrase 3	Rattus norvegicus	20-23
1817730-7	1991	These results suggest that NE converted from L-threo-DOPS plays an important role in inducing LTP in the mossy fiber-CA3 system in the animals deficient in catecholamines.	Droxidopa	45-57	carbonic anhydrase 3	Rattus norvegicus	117-120
2119267-0	1990	[The effect of L-threo-DOPS on P-300 in parkinsonism].	Droxidopa	15-27	E1A binding protein p300	Homo sapiens	31-36
2119267-5	1990	In the present study we investigate the effect of L-threo-DOPS on cognitive function in Parkinsonism by measuring P-300 component succeedingly.	Droxidopa	50-62	E1A binding protein p300	Homo sapiens	114-119
2119267-7	1990	The latencies of P-300 are significantly shortened after treatment of DOPS compared with those of the previous treatment and placebo administration respectively (p less than 0.05, p less than 0.01).	Droxidopa	70-74	E1A binding protein p300	Homo sapiens	17-22
2110272-1	1990	A synthetic amino acid, L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), can be converted to (-)-norepinephrine (NE) by aromatic L-amino acid decarboxylase (AADC) in various mammalian tissues.	Droxidopa	24-57	dopa decarboxylase	Homo sapiens	158-162
2110272-1	1990	A synthetic amino acid, L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), can be converted to (-)-norepinephrine (NE) by aromatic L-amino acid decarboxylase (AADC) in various mammalian tissues.	Droxidopa	59-71	dopa decarboxylase	Homo sapiens	130-156
2110272-1	1990	A synthetic amino acid, L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), can be converted to (-)-norepinephrine (NE) by aromatic L-amino acid decarboxylase (AADC) in various mammalian tissues.	Droxidopa	59-71	dopa decarboxylase	Homo sapiens	158-162
2110272-7	1990	Pretreatment with AADC inhibitor, benserazide, completely blocked both the pressor and diuretic effects of L-threo-DOPS.	Droxidopa	107-119	dopa decarboxylase	Rattus norvegicus	18-22
33034372-1	2021	OBJECTIVE: Dopamine beta hydroxylase (DBH) deficiency is an extremely rare autosomal recessive disorder with severe orthostatic hypotension, that can be treated with L-threo-3,4-dihydroxyphenylserine (L-DOPS).	Droxidopa	166-199	dopamine beta-hydroxylase	Homo sapiens	11-36
33034372-1	2021	OBJECTIVE: Dopamine beta hydroxylase (DBH) deficiency is an extremely rare autosomal recessive disorder with severe orthostatic hypotension, that can be treated with L-threo-3,4-dihydroxyphenylserine (L-DOPS).	Droxidopa	166-199	dopamine beta-hydroxylase	Homo sapiens	38-41
33034372-1	2021	OBJECTIVE: Dopamine beta hydroxylase (DBH) deficiency is an extremely rare autosomal recessive disorder with severe orthostatic hypotension, that can be treated with L-threo-3,4-dihydroxyphenylserine (L-DOPS).	Droxidopa	201-207	dopamine beta-hydroxylase	Homo sapiens	11-36
33034372-1	2021	OBJECTIVE: Dopamine beta hydroxylase (DBH) deficiency is an extremely rare autosomal recessive disorder with severe orthostatic hypotension, that can be treated with L-threo-3,4-dihydroxyphenylserine (L-DOPS).	Droxidopa	201-207	dopamine beta-hydroxylase	Homo sapiens	38-41
34767786-11	2021	Our findings might help researchers to better understand how existing and new drugs chemically similar to Droxidopa, which is used to treat Parkinson"s disease, interact with beta2 AR.	Droxidopa	106-115	adenosine A2a receptor	Homo sapiens	175-183
34767786-0	2021	Analysis of L-DOPA and Droxidopa binding to Human beta2-Adrenergic Receptor.	Droxidopa	23-32	adrenoceptor beta 2	Homo sapiens	50-75
35605320-10	2022	On the other hand, DEHP and DOP were found in both small- and large-sized turtles with similar concentrations, i.e. ~ 21.0/32.0 ng mL-1 and ~ 7.1/9.9 ng mL-1, respectively.	Droxidopa	28-31	L1 cell adhesion molecule	Mus musculus	131-135
34767786-3	2021	We show that molecular docking of L-DOPA and Droxidopa into rigid and flexible beta2 AR models leads for both ligands to binding anchor sites comparable to those experimentally reported for adrenaline, namely D113/N312 and S203/S204/S207 side chains.	Droxidopa	45-54	adenosine A2a receptor	Homo sapiens	79-87
34474340-6	2021	DOPs reduced CS-induced oxidative stress as evidenced by reducing malondialdehyde (MDA) levels in the lung.	Droxidopa	0-4	citrate synthase	Rattus norvegicus	13-15
34474340-8	2021	Additionally, DOPs inhibited the CS-induced activation of ERK, p38 MAPK and NF-kappaB signaling pathways.	Droxidopa	14-18	citrate synthase	Rattus norvegicus	33-35
34474340-8	2021	Additionally, DOPs inhibited the CS-induced activation of ERK, p38 MAPK and NF-kappaB signaling pathways.	Droxidopa	14-18	Eph receptor B1	Rattus norvegicus	58-61
34363819-6	2021	Further investigation showed that DOPS significantly inhibited the protein expression of TLR4, and apparently up-regulated proteins expressions of nuclear-Nrf2, HO-1 and NQO-1 in lung tissues of colitis mice and in BEAS-2B cells.	Droxidopa	34-38	toll-like receptor 4	Mus musculus	89-93
34363819-6	2021	Further investigation showed that DOPS significantly inhibited the protein expression of TLR4, and apparently up-regulated proteins expressions of nuclear-Nrf2, HO-1 and NQO-1 in lung tissues of colitis mice and in BEAS-2B cells.	Droxidopa	34-38	nuclear factor, erythroid derived 2, like 2	Mus musculus	155-159
34363819-6	2021	Further investigation showed that DOPS significantly inhibited the protein expression of TLR4, and apparently up-regulated proteins expressions of nuclear-Nrf2, HO-1 and NQO-1 in lung tissues of colitis mice and in BEAS-2B cells.	Droxidopa	34-38	heme oxygenase 1	Mus musculus	161-165
34363819-6	2021	Further investigation showed that DOPS significantly inhibited the protein expression of TLR4, and apparently up-regulated proteins expressions of nuclear-Nrf2, HO-1 and NQO-1 in lung tissues of colitis mice and in BEAS-2B cells.	Droxidopa	34-38	NAD(P)H dehydrogenase, quinone 1	Mus musculus	170-175
34363819-7	2021	These results indicated that DOPS significantly inhibited inflammation and oxidative stress to alleviate colitis-induced secondary lung injury, and its mechanisms are closely related to the inhibition of TLR4 signaling pathway and the activation of Nrf2 signaling pathway.	Droxidopa	29-33	toll like receptor 4	Homo sapiens	204-208
34363819-7	2021	These results indicated that DOPS significantly inhibited inflammation and oxidative stress to alleviate colitis-induced secondary lung injury, and its mechanisms are closely related to the inhibition of TLR4 signaling pathway and the activation of Nrf2 signaling pathway.	Droxidopa	29-33	NFE2 like bZIP transcription factor 2	Homo sapiens	249-253
34812056-2	2021	Results showed that the administration of L-threo-3,4-dihydroxyphenylserine (L-DOPS) for 21 days significantly increased the expression of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the striatum and substantia nigra (SN) of 23-month-old rats.	Droxidopa	42-75	solute carrier family 6 member 3	Rattus norvegicus	169-189
34812056-2	2021	Results showed that the administration of L-threo-3,4-dihydroxyphenylserine (L-DOPS) for 21 days significantly increased the expression of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the striatum and substantia nigra (SN) of 23-month-old rats.	Droxidopa	42-75	solute carrier family 6 member 3	Rattus norvegicus	191-194
34812056-2	2021	Results showed that the administration of L-threo-3,4-dihydroxyphenylserine (L-DOPS) for 21 days significantly increased the expression of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the striatum and substantia nigra (SN) of 23-month-old rats.	Droxidopa	77-83	solute carrier family 6 member 3	Rattus norvegicus	169-189
34812056-2	2021	Results showed that the administration of L-threo-3,4-dihydroxyphenylserine (L-DOPS) for 21 days significantly increased the expression of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the striatum and substantia nigra (SN) of 23-month-old rats.	Droxidopa	77-83	solute carrier family 6 member 3	Rattus norvegicus	191-194
34812056-6	2021	Moreover, treatments with L-DOPS, 2-methoxy idazoxan, or salmeterol significantly increased the protein levels of phosphorylated Akt in rat striatum and SN.	Droxidopa	26-32	AKT serine/threonine kinase 1	Rattus norvegicus	129-132
34572525-3	2021	Only for Sn2+ we observed the formation of binuclear complexes (M2L2 and M2LOH (charge omitted for simplicity); M = Sn2+, L = Dop-).	Droxidopa	126-129	solute carrier family 38 member 5	Homo sapiens	9-12
35605320-10	2022	On the other hand, DEHP and DOP were found in both small- and large-sized turtles with similar concentrations, i.e. ~ 21.0/32.0 ng mL-1 and ~ 7.1/9.9 ng mL-1, respectively.	Droxidopa	28-31	L1 cell adhesion molecule	Mus musculus	153-157
35350699-7	2022	When the pH of the solution bathing a 1,2-dioleyol-sn-glycero-3-phosphoserine (DOPS) bilayer is decreased from 7 to 3 (causing decreased head group repulsion and a more negative c 0), tau is decreased.	Droxidopa	79-83	microtubule associated protein tau	Homo sapiens	184-187
35142321-6	2022	We tested the methodology using a G12D mutated GTP bound oncogenic KRas-4B protein located at the interface of a DOPC/DOPS/cholesterol model anionic cell membrane.	Droxidopa	118-122	KRAS proto-oncogene, GTPase	Homo sapiens	67-74