PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11160877-8	2001	Among the catechol drugs used in the L-DOPA treatment of Parkinson"s disease, the COMT inhibitors entacapone and tolcapone were not methylated, whereas the DOPA decarboxylase inhibitor benserazide was 15 times more specific substrate than L-DOPA, the target of COMT inhibition.	Benserazide	185-196	catechol-O-methyltransferase	Homo sapiens	261-265	
19922897-2	2009	Coadministration of a COMT inhibitor with levodopa and a dopa-decarboxylase inhibitor (carbidopa or benserazide) increases levodopa exposure and its therapeutic effect.	Benserazide	100-111	catechol-O-methyltransferase	Homo sapiens	22-26	
14517707-0	2003	Pharmacokinetic-pharmacodynamic interaction between BIA 3-202, a novel COMT inhibitor, and levodopa/benserazide.	Benserazide	100-111	catechol-O-methyltransferase	Homo sapiens	71-75	
14517707-12	2003	In conclusion, the novel COMT inhibitor BIA 3-202 was well tolerated and significantly increased the bioavailability of levodopa and reduced the formation of 3-OMD when administered with standard release levodopa/benserazide.	Benserazide	213-224	catechol-O-methyltransferase	Homo sapiens	25-29	
890572-0	1977	Competitive inhibition of catechol O-methyltransferase by RO-4-4602.	Benserazide	58-67	catechol-O-methyltransferase	Homo sapiens	26-54	
7447951-0	1980	Benserazide and carbidopa as substrates of catechol-O-methyltransferase: new mechanism of action in Parkinson"s disease.	Benserazide	0-11	catechol-O-methyltransferase	Homo sapiens	43-71	
10882160-1	2000	When peripheral decarboxylation is blocked by carbidopa or benserazide, the main metabolic pathway of levodopa is O-methylation by catechol-O-methyltransferase (COMT).	Benserazide	59-70	catechol-O-methyltransferase	Homo sapiens	131-159	
10882160-1	2000	When peripheral decarboxylation is blocked by carbidopa or benserazide, the main metabolic pathway of levodopa is O-methylation by catechol-O-methyltransferase (COMT).	Benserazide	59-70	catechol-O-methyltransferase	Homo sapiens	161-165	
11147507-3	2000	Even when levodopa is co-administered with an inhibitor of AAAD such as benserazide or carbidopa, the bulk (90%) of levodopa is converted by COMT to the therapeutically inactive 3-O-methyldopa.	Benserazide	72-83	catechol-O-methyltransferase	Homo sapiens	141-145	
11147508-1	2000	Catechol-O-methyl transferase (COMT) is one of the principal levodopa-metabolizing enzymes, particularly when aromatic amino acid decarboxylase (AAAD) is partially inhibited by carbidopa or benserazide.	Benserazide	190-201	catechol-O-methyltransferase	Homo sapiens	0-29	
11147508-1	2000	Catechol-O-methyl transferase (COMT) is one of the principal levodopa-metabolizing enzymes, particularly when aromatic amino acid decarboxylase (AAAD) is partially inhibited by carbidopa or benserazide.	Benserazide	190-201	catechol-O-methyltransferase	Homo sapiens	31-35	
9403227-1	1997	Tolcapone (Ro 40-7592) is a novel inhibitor of catechol-O-methyltransferase that is being developed for clinical use in the treatment of Parkinson"s disease as add-on therapy to a combination of levodopa and a peripheral amino acid decarboxylase inhibitor (benserazide or carbidopa).	Benserazide	257-268	catechol-O-methyltransferase	Homo sapiens	47-75	
8255368-5	1993	Acute and subchronic administration of CGP 28,014 alone or in combination with the peripherally acting decarboxylase inhibitor benserazide decreased plasma 30MD as an index of COMT inhibition by about 50%.	Benserazide	127-138	catechol-O-methyltransferase	Homo sapiens	176-180	
890572-1	1977	RO-4-4602, a peripheral L-DOPA decarboxylase (EC 4.1.1.28) inhibitor was shown to also inhibit the activity of catechol O-methyltransferase (COMT) (EC 2.1.1.6).	Benserazide	0-9	catechol-O-methyltransferase	Homo sapiens	111-139	
890572-1	1977	RO-4-4602, a peripheral L-DOPA decarboxylase (EC 4.1.1.28) inhibitor was shown to also inhibit the activity of catechol O-methyltransferase (COMT) (EC 2.1.1.6).	Benserazide	0-9	catechol-O-methyltransferase	Homo sapiens	141-145	
33220276-9	2021	Opicapone potentiated the improvements in Parkinson s-like symptoms produced by levodopa/benserazide combinations with concomitant increase in plasma levodopa exposure, reduction of plasma 3-O-methyldopa levels and erythrocyte catechol-O-methyltransferase activity, results that were later demonstrated in 2 large Phase 3 studies in Parkinson s disease patients.	Benserazide	89-100	catechol-O-methyltransferase	Homo sapiens	227-255