PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
7398195-1	1980	In 14 patients with Parkinson"s disease on long-term therapy the erythrocyte catechol-O-methyltransferase activity was found to correlate with the average plasma concentration ratio of 3-O-methyldopa to levodopa and with the fasting plasma concentration ratio of 3-O methyldopa to levodopa.	3-methoxytyrosine	185-199	catechol-O-methyltransferase	Homo sapiens	77-105
7398195-1	1980	In 14 patients with Parkinson"s disease on long-term therapy the erythrocyte catechol-O-methyltransferase activity was found to correlate with the average plasma concentration ratio of 3-O-methyldopa to levodopa and with the fasting plasma concentration ratio of 3-O methyldopa to levodopa.	3-methoxytyrosine	263-277	catechol-O-methyltransferase	Homo sapiens	77-105
32111562-5	2020	RESULTS: Approximately 20,000 cerebrospinal fluid samples were received with a request for neurotransmitter metabolite analysis in the eight-year study period; 22 samples tested positive for AADC deficiency based on decreased concentrations of 5-hydroxyindoleacetic acid and homovanillic acid, and increased 3-O-methyldopa, establishing an estimated prevalence of approximately 0.112%, or 1:900.	3-methoxytyrosine	308-322	dopa decarboxylase	Homo sapiens	191-195
33136226-0	2021	Impact of the catechol-O-methyltransferase Val158Met polymorphism on the pharmacokinetics of L-dopa and its metabolite 3-O-methyldopa in combination with entacapone.	3-methoxytyrosine	119-133	catechol-O-methyltransferase	Homo sapiens	14-42
33136226-4	2021	Therefore, the present study aimed to clarify the effect of the COMT Val158Met polymorphism on the concentrations of L-dopa and 3-OMD in the presence of entacapone.	3-methoxytyrosine	128-133	catechol-O-methyltransferase	Homo sapiens	64-68
28823629-5	2017	In five non-AADC patients treated with carbidopa-levodopa, levels of 3-methoxytyrosine were elevated (7.65); however, the samples from non-AADC patients treated with DOPA-elevating drugs had normal or elevated levels of metabolites downstream of aromatic l-amino acid decarboxylase, including dopamine 3-O-sulfate (2.92), vanillylmandelate (0.33), and 3-methoxytyramine sulfate (5.07).	3-methoxytyrosine	69-86	dopa decarboxylase	Homo sapiens	12-16
28823629-5	2017	In five non-AADC patients treated with carbidopa-levodopa, levels of 3-methoxytyrosine were elevated (7.65); however, the samples from non-AADC patients treated with DOPA-elevating drugs had normal or elevated levels of metabolites downstream of aromatic l-amino acid decarboxylase, including dopamine 3-O-sulfate (2.92), vanillylmandelate (0.33), and 3-methoxytyramine sulfate (5.07).	3-methoxytyrosine	69-86	dopa decarboxylase	Homo sapiens	246-281
28823629-7	2017	CONCLUSIONS: These data demonstrate the power of combining broad-scale genotyping and phenotyping technologies to diagnose inherited neurometabolic disorders and suggest that metabolic phenotyping of plasma can be used to identify AADC deficiency and to distinguish it from non-AADC patients with elevated 3-methoxytyrosine caused by DOPA-raising medications.	3-methoxytyrosine	306-323	dopa decarboxylase	Homo sapiens	231-235
27456338-1	2016	BACKGROUND: We evaluated the effects of 3-O-methyldopa (3-OMD), a metabolite of L-DOPA which is formed by catechol-O-methyltransferase (COMT), on the uptake, metabolism, and neuroprotective effects of L-DOPA in striatal astrocytes.	3-methoxytyrosine	40-54	catechol-O-methyltransferase	Homo sapiens	106-134
27216367-0	2016	3-O-methyldopa levels in newborns: Result of newborn screening for aromatic l-amino-acid decarboxylase deficiency.	3-methoxytyrosine	0-14	dopa decarboxylase	Homo sapiens	67-102
27456338-1	2016	BACKGROUND: We evaluated the effects of 3-O-methyldopa (3-OMD), a metabolite of L-DOPA which is formed by catechol-O-methyltransferase (COMT), on the uptake, metabolism, and neuroprotective effects of L-DOPA in striatal astrocytes.	3-methoxytyrosine	56-61	catechol-O-methyltransferase	Homo sapiens	106-134
27456338-1	2016	BACKGROUND: We evaluated the effects of 3-O-methyldopa (3-OMD), a metabolite of L-DOPA which is formed by catechol-O-methyltransferase (COMT), on the uptake, metabolism, and neuroprotective effects of L-DOPA in striatal astrocytes.	3-methoxytyrosine	56-61	catechol-O-methyltransferase	Homo sapiens	136-140
25869243-13	2015	In vivo, a single intravenous dose of SAB decreased the plasma concentration of 3-OMD, with no obvious effect on the pharmacokinetics of l-DOPA.	3-methoxytyrosine	80-85	SH3-domain binding protein 5	Rattus norvegicus	38-41
24788355-4	2015	The increase of both 3-O-methyldopa and 5-hydroxytryptophan on CSF was the most relevant biochemical alteration denoting AADC defect in these subjects.	3-methoxytyrosine	21-35	dopa decarboxylase	Homo sapiens	121-125
25869243-14	2015	Multiple doses of SAB given to rats also decreased the plasma concentration of 3-OMD, while SAB increased the plasma concentration of l-DOPA.	3-methoxytyrosine	79-84	SH3-domain binding protein 5	Rattus norvegicus	18-21
24770794-5	2014	Catechol-O-methyltransferase inhibition caused less fluctuations and higher baseline levels of levodopa after the first intake and less 3-O-methyldopa appearance.	3-methoxytyrosine	136-150	catechol-O-methyltransferase	Homo sapiens	0-28
22136163-9	2012	Concentrations of the metabolite 3-O-methyldopa decreased gradually during catechol-O-methyltransferase inhibition.	3-methoxytyrosine	33-47	catechol-O-methyltransferase	Homo sapiens	75-103
24770794-8	2014	More continuous levodopa brain delivery and lower 3-O-methyldopa bioavailability caused a better motor response during catechol-O-methyltransferase inhibition.	3-methoxytyrosine	50-64	catechol-O-methyltransferase	Homo sapiens	119-147
22863920-1	2012	It has been well known that 3-O-methyldopa (3-OMD) is a metabolite of L-3,4-dihydroxyphenylalanine (L-DOPA) formed by catechol O-methyltransferase (COMT), and 3-OMD blood level often reaches higher than physiological level in Parkinson"s disease (PD) patients receiving long term L-DOPA therapy.	3-methoxytyrosine	28-42	catechol-O-methyltransferase	Homo sapiens	118-146
22863920-1	2012	It has been well known that 3-O-methyldopa (3-OMD) is a metabolite of L-3,4-dihydroxyphenylalanine (L-DOPA) formed by catechol O-methyltransferase (COMT), and 3-OMD blood level often reaches higher than physiological level in Parkinson"s disease (PD) patients receiving long term L-DOPA therapy.	3-methoxytyrosine	28-42	catechol-O-methyltransferase	Homo sapiens	148-152
22863920-1	2012	It has been well known that 3-O-methyldopa (3-OMD) is a metabolite of L-3,4-dihydroxyphenylalanine (L-DOPA) formed by catechol O-methyltransferase (COMT), and 3-OMD blood level often reaches higher than physiological level in Parkinson"s disease (PD) patients receiving long term L-DOPA therapy.	3-methoxytyrosine	44-49	catechol-O-methyltransferase	Homo sapiens	118-146
22863920-1	2012	It has been well known that 3-O-methyldopa (3-OMD) is a metabolite of L-3,4-dihydroxyphenylalanine (L-DOPA) formed by catechol O-methyltransferase (COMT), and 3-OMD blood level often reaches higher than physiological level in Parkinson"s disease (PD) patients receiving long term L-DOPA therapy.	3-methoxytyrosine	44-49	catechol-O-methyltransferase	Homo sapiens	148-152
21533995-2	2011	Degradation of levodopa to 3-O-methyldopa via the enzyme catechol-O-methyltransferase (COMT) is a methyl group demanding reaction.	3-methoxytyrosine	27-41	catechol-O-methyltransferase	Homo sapiens	57-85
21752681-7	2011	In contrast to the previously published patients with a FOLR1 gene defect, our patient presented with an abnormal l-dopa metabolism in CSF and high 3-O-methyl-dopa.	3-methoxytyrosine	148-163	folate receptor alpha	Homo sapiens	56-61
21533995-2	2011	Degradation of levodopa to 3-O-methyldopa via the enzyme catechol-O-methyltransferase (COMT) is a methyl group demanding reaction.	3-methoxytyrosine	27-41	catechol-O-methyltransferase	Homo sapiens	87-91
19676096-0	2010	Reduced 3-O-methyl-dopa levels in OCD patients and their unaffected parents is associated with the low activity M158 COMT allele.	3-methoxytyrosine	8-23	catechol-O-methyltransferase	Homo sapiens	117-121
19676096-4	2010	Therefore, the purpose of our study was to assess COMT activity in OCD by measuring plasma levels of 3-O-methyl-dopa (3-OMD), which result from the methylation of levodopa by COMT, and to investigate the relationship between 3-OMD levels and the V158M polymorphism.	3-methoxytyrosine	101-116	catechol-O-methyltransferase	Homo sapiens	50-54
19676096-4	2010	Therefore, the purpose of our study was to assess COMT activity in OCD by measuring plasma levels of 3-O-methyl-dopa (3-OMD), which result from the methylation of levodopa by COMT, and to investigate the relationship between 3-OMD levels and the V158M polymorphism.	3-methoxytyrosine	101-116	catechol-O-methyltransferase	Homo sapiens	175-179
19676096-4	2010	Therefore, the purpose of our study was to assess COMT activity in OCD by measuring plasma levels of 3-O-methyl-dopa (3-OMD), which result from the methylation of levodopa by COMT, and to investigate the relationship between 3-OMD levels and the V158M polymorphism.	3-methoxytyrosine	118-123	catechol-O-methyltransferase	Homo sapiens	50-54
19676096-4	2010	Therefore, the purpose of our study was to assess COMT activity in OCD by measuring plasma levels of 3-O-methyl-dopa (3-OMD), which result from the methylation of levodopa by COMT, and to investigate the relationship between 3-OMD levels and the V158M polymorphism.	3-methoxytyrosine	118-123	catechol-O-methyltransferase	Homo sapiens	175-179
19930170-8	2009	The levels of 3-O-methyldopa were significantly decreased in the S-COMT-deficient mice.	3-methoxytyrosine	14-28	catechol-O-methyltransferase	Mus musculus	67-71
19676096-4	2010	Therefore, the purpose of our study was to assess COMT activity in OCD by measuring plasma levels of 3-O-methyl-dopa (3-OMD), which result from the methylation of levodopa by COMT, and to investigate the relationship between 3-OMD levels and the V158M polymorphism.	3-methoxytyrosine	225-230	catechol-O-methyltransferase	Homo sapiens	50-54
19657587-2	2009	Aim was to investigate the impact of the peripheral COMT inhibitor entacapone (EN) on plasma concentrations of homocysteine, LD and 3-O-methyl-dopa (3-OMD).	3-methoxytyrosine	132-147	catechol-O-methyltransferase	Homo sapiens	52-56
19657587-2	2009	Aim was to investigate the impact of the peripheral COMT inhibitor entacapone (EN) on plasma concentrations of homocysteine, LD and 3-O-methyl-dopa (3-OMD).	3-methoxytyrosine	149-154	catechol-O-methyltransferase	Homo sapiens	52-56
15965309-9	2005	Entacapone significantly reduced plasma 3-OMD concentration by about 50% (P = 0.0001), indicating marked COMT inhibiting activity.	3-methoxytyrosine	40-45	catechol-O-methyltransferase	Homo sapiens	105-109
18520980-6	2008	The 3-OMD levels were significantly lower during catechol-O-methyltransferase (COMT) inhibition with entacapone.	3-methoxytyrosine	4-9	catechol-O-methyltransferase	Homo sapiens	49-77
18520980-6	2008	The 3-OMD levels were significantly lower during catechol-O-methyltransferase (COMT) inhibition with entacapone.	3-methoxytyrosine	4-9	catechol-O-methyltransferase	Homo sapiens	79-83
11278508-2	2001	When expressed in Xenopus oocytes, the encoded protein designated as TAT1 (T-type amino acid transporter 1) exhibited Na+-independent and low-affinity transport of aromatic amino acids such as tryptophan, tyrosine, and phenylalanine (Km values: approximately 5 mm), consistent with the properties of classical amino acid transport system T. TAT1 accepted some variations of aromatic side chains because it interacted with amino acid-related compounds such as l-DOPA and 3-O-methyl-DOPA.	3-methoxytyrosine	470-485	solute carrier family 16 member 10	Rattus norvegicus	69-73
15354384-1	2004	Levodopa and dopamine are metabolized to 3-O-methyldopa and 3-methoxytyramine, respectively, by the enzyme catechol-O-methyltransferase (COMT) leading to the production of the demethylated cofactor S-adenosylhomo-cysteine (SAH) and subsequently homocysteine (HC).	3-methoxytyrosine	41-55	catechol-O-methyltransferase	Homo sapiens	107-135
15354384-1	2004	Levodopa and dopamine are metabolized to 3-O-methyldopa and 3-methoxytyramine, respectively, by the enzyme catechol-O-methyltransferase (COMT) leading to the production of the demethylated cofactor S-adenosylhomo-cysteine (SAH) and subsequently homocysteine (HC).	3-methoxytyrosine	41-55	catechol-O-methyltransferase	Homo sapiens	137-141
12075857-1	2002	One main metabolizing pathway of levodopa is O-methylation to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	62-76	catechol-O-methyltransferase	Homo sapiens	88-116
12075857-1	2002	One main metabolizing pathway of levodopa is O-methylation to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	62-76	catechol-O-methyltransferase	Homo sapiens	118-122
12075857-1	2002	One main metabolizing pathway of levodopa is O-methylation to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	78-83	catechol-O-methyltransferase	Homo sapiens	88-116
12075857-1	2002	One main metabolizing pathway of levodopa is O-methylation to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	78-83	catechol-O-methyltransferase	Homo sapiens	118-122
11978145-16	2002	The COMT inhibitors entacapone and tolcapone dose-dependently inhibit the formation of the major metabolite of levodopa, 3-O-methyldopa, and improve the bioavailability and reduce the clearance of levodopa without significantly affecting its absorption.	3-methoxytyrosine	121-135	catechol-O-methyltransferase	Homo sapiens	4-8
11445284-2	2001	This increases conversion of levodopa to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	41-55	catechol-O-methyltransferase	Homo sapiens	67-95
11445284-2	2001	This increases conversion of levodopa to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	41-55	catechol-O-methyltransferase	Homo sapiens	97-101
11445284-2	2001	This increases conversion of levodopa to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	57-62	catechol-O-methyltransferase	Homo sapiens	67-95
11445284-2	2001	This increases conversion of levodopa to 3-O-methyldopa (3-OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	57-62	catechol-O-methyltransferase	Homo sapiens	97-101
15992091-6	1999	Preclinical studies confirmed decreased formation of COMT-dependent metabolites, including 3-O methyldopa and homovanillic acid.	3-methoxytyrosine	91-105	catechol-O-methyltransferase	Homo sapiens	53-57
11391126-12	2001	The study showed that repeated dosing of entacapone inhibits the COMT activity in a dose-dependent manner and thereby reduces the loss of L-Dopa to 3-OMD.	3-methoxytyrosine	148-153	catechol-O-methyltransferase	Homo sapiens	65-69
11290879-5	2001	A possible defense mechanism is by means of metabolic shunting of levodopa excess to 3-O-methyldopa by COMT in peripheral and central nervous system tissues.	3-methoxytyrosine	85-99	catechol-O-methyltransferase	Homo sapiens	103-107
11290879-6	2001	In this study we examine whether the use of COMT inhibitor, which reduced the levels of 3-O-methyldopa, affect levodopa toxicity.	3-methoxytyrosine	88-102	catechol-O-methyltransferase	Homo sapiens	44-48
11290879-13	2001	Catechol-O-methyltransferase attenuates toxicity of levodopa in vitro by its metabolism to nontoxic 3-O-methyldopa.	3-methoxytyrosine	100-114	catechol-O-methyltransferase	Homo sapiens	0-28
11346021-5	2001	A more recent strategy has centered on increasing the availability of intracellular levodopa and synaptic dopamine by inhibiting the peripheral and central metabolism of levodopa to 3-O-methyldopa with the use of a catechol-O-methyltransferase inhibitor.	3-methoxytyrosine	182-196	catechol-O-methyltransferase	Homo sapiens	215-243
9392574-3	1997	Entacapone, a peripherally acting, reversible inhibitor of catechol-O-methyltransferase, slows the elimination of levodopa in humans by reducing the formation of 3-O-methyldopa.	3-methoxytyrosine	162-176	catechol-O-methyltransferase	Homo sapiens	59-87
10047930-1	1999	Tolcapone, a central and peripheral catechol O-methyltransferase (COMT) inhibitor, reduces the conversion of L-Dopa into 3-O-methyl-Dopa (3-OMD), thus leading to more stable and sustained L-Dopa plasma levels.	3-methoxytyrosine	121-136	catechol-O-methyltransferase	Homo sapiens	36-64
10047930-1	1999	Tolcapone, a central and peripheral catechol O-methyltransferase (COMT) inhibitor, reduces the conversion of L-Dopa into 3-O-methyl-Dopa (3-OMD), thus leading to more stable and sustained L-Dopa plasma levels.	3-methoxytyrosine	121-136	catechol-O-methyltransferase	Homo sapiens	66-70
10047930-1	1999	Tolcapone, a central and peripheral catechol O-methyltransferase (COMT) inhibitor, reduces the conversion of L-Dopa into 3-O-methyl-Dopa (3-OMD), thus leading to more stable and sustained L-Dopa plasma levels.	3-methoxytyrosine	138-143	catechol-O-methyltransferase	Homo sapiens	36-64
10047930-1	1999	Tolcapone, a central and peripheral catechol O-methyltransferase (COMT) inhibitor, reduces the conversion of L-Dopa into 3-O-methyl-Dopa (3-OMD), thus leading to more stable and sustained L-Dopa plasma levels.	3-methoxytyrosine	138-143	catechol-O-methyltransferase	Homo sapiens	66-70
9429234-10	1997	Furthermore, UGT1A6*2 metabolized 3-O-methyl-dopa and methyl salicylate at 41-74% of that of the wild-type, and a series of beta-blockers at 28-69% of the normal level.	3-methoxytyrosine	34-49	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	13-19
10343151-2	1999	The objective of the study reported here was the investigation of the effect of catechol-O-methyl transferase (COMT) inhibition by tolcapone on the pharmacokinetics of levodopa and 3-O-methyldopa (3-OMD) after administration of a new dual-release formulation (dual-RF) of levodopa/benserazide (200/50).	3-methoxytyrosine	181-195	catechol-O-methyltransferase	Homo sapiens	80-109
10343151-2	1999	The objective of the study reported here was the investigation of the effect of catechol-O-methyl transferase (COMT) inhibition by tolcapone on the pharmacokinetics of levodopa and 3-O-methyldopa (3-OMD) after administration of a new dual-release formulation (dual-RF) of levodopa/benserazide (200/50).	3-methoxytyrosine	181-195	catechol-O-methyltransferase	Homo sapiens	111-115
10343151-2	1999	The objective of the study reported here was the investigation of the effect of catechol-O-methyl transferase (COMT) inhibition by tolcapone on the pharmacokinetics of levodopa and 3-O-methyldopa (3-OMD) after administration of a new dual-release formulation (dual-RF) of levodopa/benserazide (200/50).	3-methoxytyrosine	197-202	catechol-O-methyltransferase	Homo sapiens	80-109
10343151-2	1999	The objective of the study reported here was the investigation of the effect of catechol-O-methyl transferase (COMT) inhibition by tolcapone on the pharmacokinetics of levodopa and 3-O-methyldopa (3-OMD) after administration of a new dual-release formulation (dual-RF) of levodopa/benserazide (200/50).	3-methoxytyrosine	197-202	catechol-O-methyltransferase	Homo sapiens	111-115
9808337-3	1998	They induce a dose-dependent inhibition of COMT activity in erythrocytes and a significant decrease in the plasma levels of 3-O-methyldopa, indicating their effectiveness as COMT inhibitors.	3-methoxytyrosine	124-138	catechol-O-methyltransferase	Homo sapiens	174-178
9333106-8	1997	RESULTS: By inhibiting COMT, tolcapone reduced levodopa metabolism to 3-O-methyldopa, resulting in a twofold increase in levodopa exposure (area under the curve) and elimination half-life, without changing levodopa peak plasma concentration.	3-methoxytyrosine	70-84	catechol-O-methyltransferase	Homo sapiens	23-27
8341294-1	1993	L-Dopa is metabolized to 3-O-methyldopa (3OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	25-39	catechol-O-methyltransferase	Homo sapiens	50-78
7957769-7	1994	In conclusion, the inhibitory effect of tolcapone on the O-methylation of levodopa to 3-OMD by COMT is largely due to improved levodopa and dopamine availability in the brain, and to the reduced formation of 3-OMD.	3-methoxytyrosine	86-91	catechol-O-methyltransferase	Mus musculus	95-99
7957769-7	1994	In conclusion, the inhibitory effect of tolcapone on the O-methylation of levodopa to 3-OMD by COMT is largely due to improved levodopa and dopamine availability in the brain, and to the reduced formation of 3-OMD.	3-methoxytyrosine	208-213	catechol-O-methyltransferase	Mus musculus	95-99
8341294-1	1993	L-Dopa is metabolized to 3-O-methyldopa (3OMD) by catechol-O-methyltransferase (COMT).	3-methoxytyrosine	25-39	catechol-O-methyltransferase	Homo sapiens	80-84
34715572-1	2021	5-hydroxytryptophan (5HTP) and 3-O-methyldopa (3OMD) are CSF diagnostic biomarkers of the defect of aromatic L-amino acid decarboxylase (AADC), a rare inherited disorder of neurotransmitter synthesis which, if untreated, results in severely disabling neurological impairment.	3-methoxytyrosine	31-45	dopa decarboxylase	Homo sapiens	109-135
1913700-0	1991	Reduction of circulating 3-O-methyldopa by inhibition of catechol-O-methyltransferase with OR-611 and OR-462 in cynomolgus monkeys: implications for the treatment of Parkinson"s disease.	3-methoxytyrosine	25-39	catechol O-methyltransferase	Macaca fascicularis	57-85
1770109-3	1991	The validity of the method was confirmed by markedly decreased urinary 3-O-methyldopa levels after administration of an inhibitor of catechol-O-methyltransferase to rats, radioactivity in chromatographic fractions corresponding to 3-O-methyldopa in urine of rats undergoing infusion of [3H]-L-DOPA, and correlations between excretion rates of 3-O-methyldopa and catechols in humans.	3-methoxytyrosine	71-85	catechol-O-methyltransferase	Rattus norvegicus	133-161
1770109-3	1991	The validity of the method was confirmed by markedly decreased urinary 3-O-methyldopa levels after administration of an inhibitor of catechol-O-methyltransferase to rats, radioactivity in chromatographic fractions corresponding to 3-O-methyldopa in urine of rats undergoing infusion of [3H]-L-DOPA, and correlations between excretion rates of 3-O-methyldopa and catechols in humans.	3-methoxytyrosine	231-245	catechol-O-methyltransferase	Rattus norvegicus	133-161
1770109-3	1991	The validity of the method was confirmed by markedly decreased urinary 3-O-methyldopa levels after administration of an inhibitor of catechol-O-methyltransferase to rats, radioactivity in chromatographic fractions corresponding to 3-O-methyldopa in urine of rats undergoing infusion of [3H]-L-DOPA, and correlations between excretion rates of 3-O-methyldopa and catechols in humans.	3-methoxytyrosine	231-245	catechol-O-methyltransferase	Rattus norvegicus	133-161
2276119-2	1990	We studied the effect of nitecapone (OR-462), a novel inhibitor of catechol-O-methyltransferase (COMT), on OMD formation in cynomolgus monkeys following intravenous levodopa administration.	3-methoxytyrosine	107-110	catechol O-methyltransferase	Macaca fascicularis	97-101
2128511-0	1990	Effect of the new selective COMT inhibitor CGP 28014 A on the formation of 3-O-methyldopa (3OMD) in plasma of healthy subjects.	3-methoxytyrosine	75-89	catechol-O-methyltransferase	Homo sapiens	28-32
34715572-1	2021	5-hydroxytryptophan (5HTP) and 3-O-methyldopa (3OMD) are CSF diagnostic biomarkers of the defect of aromatic L-amino acid decarboxylase (AADC), a rare inherited disorder of neurotransmitter synthesis which, if untreated, results in severely disabling neurological impairment.	3-methoxytyrosine	31-45	dopa decarboxylase	Homo sapiens	137-141