opicapone profile

opicapone: structure in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

ID Source	ID
PubMed CID	135565903
CHEMBL ID	1089318
CHEBI ID	134699
SCHEMBL ID	539065
SCHEMBL ID	17559532
SCHEMBL ID	19205880
MeSH ID	M0546492

Synonym
CHEBI:134699
opicapone
ongentys
bia-9-1067
bia-91067
bia 9-1067
bdbm50019329
chembl1089318 ,
923287-50-7
2,5-dichloro-3-(5-(3,4-dihydroxy-5-nitrophenyl)-1,2,4-oxadiazol-3-yl)-4,6-dimethylpyridine 1-oxide
HY-14896
SCHEMBL539065
opicapone [jan]
5-(3-(2,5-dichloro-4,6-dimethyl-1-oxy-pyridin-3-yl)-(1,2,4)oxadiazol-5-yl)-3-nitrobenzene-1,2-diol
opicapone [inn]
opicapone [orange book]
opicapone [usan]
opicapone [who-dd]
opicapone [mi]
(4z)-4-[3-(2,5-dichloro-4,6-dimethyl-1-oxidopyridin-1-ium-3-yl)-2h-1,2,4-oxadiazol-5-ylidene]-2-hydroxy-6-nitrocyclohexa-2,5-dien-1-one
ontilyv
gtpl8988
compound 37d [pmid: 20334432]
SCHEMBL17559532
ZB1234
SCHEMBL19205880
bia 9-1067; bia 91067; bia-91067; bia91067
BCP24268
DB11632
Q27088208
SB17488
NCGC00390666-01
AT23149
MS-27141
(4e)-4-[3-(2,5-dichloro-4,6-dimethyl-1-oxidopyridin-1-ium-3-yl)-2h-1,2,4-oxadiazol-5-ylidene]-2-hydroxy-6-nitrocyclohexa-2,5-dien-1-one
bia 9-1067bia 9-1067
5-[3-(2,5-dichloro-4,6-dimethyl-1-oxidopyridin-1-ium-3-yl)-1,2,4-oxadiazol-5-yl]-3-nitrobenzene-1,2-diol
EX-A5000
A922596
DTXSID601026417
2,5-dichloro-3-[5-(3,4-dihydroxy-5-nitrophenyl)-1,2,4-oxadiazol-3-yl]-4,6-dimethylpyridin-1-ium-1-olate
EN300-20385166
opicapona
opicaponum
compound 37d (pmid: 20334432)
n04bx04

Excerpt	Reference
"Opicapone is a catechol-O-methyl-transferase (iCOMT) inhibitor authorized in Europe in 2016 and indicated as adjunctive therapy to preparations of levodopa/ DOPA decarboxylase inhibitors in adult patients with Parkinson's disease and end-of-dose motor fluctuations who cannot be stabilised on those combinations. "	( [Opicapone for the treatment of Parkinson's disease: real-life data in Spain]. Abril-Jaramillo, J; Almeida, F; Bermejo, P; Borrue, C; Caballol, N; Campins-Romeu, M; Clavero, P; García-Caldentey, J; Gómez-Mayordomo, V; Labandeira, C; López-Ariztegui, N; Martí-Andrés, G; Martínez-Castrillo, JC; Martinez-Poles, J; Mata-Alvarez Santullano, M; Muñoz, T; Rico-Villademoros, F; Rojo, R; Salom, JM; Sarasa, P; Tegel, I; Valderrama-Martín, C; Vinagre-Aragón, A, 2021)
"Opicapone is a novel, peripherally acting catechol-O-methyl transferase (COMT) inhibitor used as adjunctive therapy to carbidopa/levodopa for treatment and prevention of "off" episodes."	( Opicapone for the Treatment of Parkinson's Disease "Off" Episodes: Pharmacology and Clinical Considerations. Berger, AA; Cornett, EM; Izygon, J; Jacob, BM; Kaye, AD; Kaye, AM; Kaye, JS; Noonan, MJ; Robinson, C; Shah, RJ; Urits, I; Viswanath, O; Winnick, A, 2022)
"Opicapone (OPC) is a third-generation, once-daily catechol-O-methyltransferase inhibitor shown to be generally well tolerated and efficacious in reducing OFF-time in two pivotal trials in patients with PD and end-of-dose motor fluctuations."	( Opicapone versus placebo in the treatment of Parkinson's disease patients with end-of-dose motor fluctuation-associated pain: rationale and design of the randomised, double-blind OCEAN (OpiCapone Effect on motor fluctuations and pAiN) trial. Antonini, A; Bannister, K; Chaudhuri, KR; Costa, R; Ferreira, JJ; Kurtis, MM; Magalhães, D; Odin, P; Rascol, O; Rocha, JF; Soares-da-Silva, P; Storch, A, 2022)
"Opicapone is a once-daily COMT inhibitor approved in the US adjunctive to carbidopa (CD)/LD in patients with Parkinson disease experiencing "OFF" episodes."	( Opicapone Pharmacokinetics and Effects on Catechol- O -Methyltransferase Activity and Levodopa Pharmacokinetics in Patients With Parkinson Disease Receiving Carbidopa/Levodopa. Jimenez, R; Kieburtz, KD; Klepitskaya, O; LeWitt, P; Liang, GS; Loewen, G; Olanow, CW; Olson, K, )
"Opicapone (OPC) is a third-generation peripheral catechol-O-methyl transferase inhibitor (COMT-i) approved as add-on therapy to levodopa/DOPA decarboxylase inhibitors (DDCI) combinations in Parkinson's disease (PD) patients with end-of-dose motor fluctuations. "	( The role of opicapone in the management of Parkinson's disease: an Italian consensus through a combined Nominal Group Technique and Delphi approach. Antonini, A; Barone, P; Calabresi, P; Lopiano, L; Morgante, F; Pontieri, FE; Sensi, M; Stocchi, F, 2023)
"Opicapone is a catechol O-methyltransferase (COMT) inhibitor indicated for use as adjunct to levodopa therapy in patients with Parkinson's disease (PD) and motor fluctuations."	( Safety Profile of Opicapone in the Management of Parkinson's Disease. Ferreira, JJ; Gama, H; Lees, A; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P, 2019)
"Opicapone (OPC) is a well-established catechol-O-methyltransferase (COMT) inhibitor that is approved for the treatment of Parkinson's disease (PD) associated with L-DOPA/L-amino acid decarboxylase inhibitor (DDI) therapy allowing for prolonged activity due to a more continuous supply of L-DOPA in the brain. "	( The preclinical discovery and development of opicapone for the treatment of Parkinson's disease. Auladell, C; Busquets, O; Camins, A; Cano, A; Ettcheto, M; Folch, J; Manzine, PR; Olloquequi, J; Sánchez-Lopez, E; Verdaguer, E, 2020)
"Opicapone is a recent and selective third-generation COMT inhibitor which achieves marked increase in the bioavailability of levodopa."	( Optimized clinical management of Parkinson's disease with opicapone. Recommendations from Spanish experts. García Ruiz-Espiga, P; Linazasoro-Cristóbal, G; López Del Val, LJ; López-Manzanares, L; Luquin-Piudo, MR; Martínez-Castrillo, JC; Mir, P; Pagonabarraga-Mora, J, 2020)
"Opicapone (OPC) is a third-generation catechol-O-methyltransferase inhibitor developed to treat Parkinson disease and motor fluctuations. "	( Pharmacokinetics of Opicapone and Its Metabolites in Healthy White and Chinese Subjects. Cong, D; Hui, A; Li, K; Liu, X; Liu, Y; Qi, W; Song, J; Tan, Y; Wang, J; Xu, C; Xue, W; Zhong, L, 2021)
"Opicapone is a novel potent, reversible and purely peripheral catechol-O-methyltransferase inhibitor that has been developed to be used as an adjunct to levodopa/aromatic L-amino acid decarboxylase inhibitor therapy for Parkinson's disease. "	( Pharmacokinetics of opicapone, a third-generation COMT inhibitor, after single and multiple oral administration: A comparative study in the rat. Alves, G; Falcão, A; Fortuna, A; Gonçalves, D; Soares-da-Silva, P, 2017)
"Opicapone is a third generation, highly potent and effective catechol O‑methyltransferase (COMT) inhibitor that optimizes the pharmacokinetics and bioavailability of L-DOPA therapy. "	( Opicapone for the management of end-of-dose motor fluctuations in patients with Parkinson's disease treated with L-DOPA. Ferreira, J; Lees, AJ; Poewe, W; Rascol, O; Reichmann, H; Stocchi, F; Tolosa, E, 2017)
"Opicapone is a novel catechol-O-methyltransferase (COMT) inhibitor that emerged to fulfil the need of a safer and more efficacious COMT inhibitor. "	( A single- and multiple-dose study to investigate the pharmacokinetics and pharmacodynamics of opicapone, a novel COMT inhibitor, in rat. Alves, G; Bonifácio, MJ; Falcão, A; Fortuna, A; Gonçalves, D; Soares-da-Silva, P, 2017)
"Opicapone (OPC) is a novel, potent, reversible, and purely peripheral third-generation COMT inhibitor, which provides an enhancement in levodopa (L-Dopa) availability. "	( Pharmacokinetic drug evaluation of opicapone for the treatment of Parkinson's disease. Kostić, V; Kresojević, N; Svetel, M; Tomić, A, 2018)
"Opicapone is a novel, third generation COMT inhibitor approved for the treatment of Parkinson's disease. "	( The launch of opicapone for Parkinson's disease: negatives versus positives. Castro Caldas, A; Ferreira, JJ; Teodoro, T, 2018)
"Opicapone (BIA 9-1067) is a novel catechol-O-methyltransferase inhibitor presently under clinical development as an adjuvant in the pharmacotherapy of Parkinson's disease. "	( An HPLC-DAD method for the simultaneous quantification of opicapone (BIA 9-1067) and its active metabolite in human plasma. Alves, G; Falcão, A; Fortuna, A; Gonçalves, D; Soares-da-Silva, P, 2013)
"Opicapone is a strong candidate to fill the unmet need for COMT inhibitors that lead to more sustained levodopa levels in Parkinson's disease patients."	( Brain and peripheral pharmacokinetics of levodopa in the cynomolgus monkey following administration of opicapone, a third generation nitrocatechol COMT inhibitor. Bonifácio, MJ; Soares-da-Silva, P; Sutcliffe, JS; Torrão, L; Wright, LC, 2014)
"Opicapone (OPC) is a novel catechol-O-methyltransferase (COMT) inhibitor to be used as adjunctive therapy in levodopa-treated patients with Parkinson's disease. "	( Effect of moderate liver impairment on the pharmacokinetics of opicapone. Falcão, A; Lopes, N; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Soares-da-Silva, P, 2014)
"Opicapone is a novel third generation catechol-O-methyltransferase (COMT) inhibitor. "	( Effect of opicapone and entacapone upon levodopa pharmacokinetics during three daily levodopa administrations. Falcão, A; Lopes, N; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Soares-da-Silva, P; Vaz-da-Silva, M; Wright, LC, 2014)
"Opicapone (OPC) is a novel third generation catechol-O-methyltransferase (COMT) inhibitor that enhances levodopa availability. "	( Effect of opicapone on levodopa pharmacokinetics, catechol-O-methyltransferase activity and motor fluctuations in patients with Parkinson's disease. Falcão, A; Ferreira, JJ; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Soares-da-Silva, P, 2015)
"Opicapone is a novel potent, reversible and purely peripheral third generation catechol-O-methyltransferase inhibitor, currently under clinical trials as an adjunct to levodopa therapy for Parkinson's disease. "	( Development of a liquid chromatography assay for the determination of opicapone and BIA 9-1079 in rat matrices. Alves, G; Falcão, A; Fortuna, A; Gonçalves, D; Soares-da-Silva, P, 2016)
"Opicapone is a novel, once-daily, potent third-generation catechol-O-methyltransferase inhibitor. "	( Opicapone as an adjunct to levodopa in patients with Parkinson's disease and end-of-dose motor fluctuations: a randomised, double-blind, controlled trial. Ferreira, JJ; Lees, A; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P, 2016)
"Opicapone (OPC) is a novel third-generation catechol-O-methyltransferase (COMT) inhibitor. "	( Opicapone pharmacokinetics and pharmacodynamics comparison between healthy Japanese and matched white subjects. Falcão, A; Nunes, T; Rocha, JF; Santos, A; Soares-da-Silva, P, 2016)
"Opicapone (OPC) is a novel, long-acting, peripherally selective, once daily, third-generation catechol-O-methyl transferase inhibitor."	( Clinical pharmacology review of opicapone for the treatment of Parkinson's disease. Fabbri, M; Ferreira, JJ; Rosa, MM, 2016)
"Opicapone is a novel catechol-O-methyltransferase (COMT) inhibitor. "	( Pharmacokinetics, pharmacodynamics and tolerability of opicapone, a novel catechol-O-methyltransferase inhibitor, in healthy subjects: prediction of slow enzyme-inhibitor complex dissociation of a short-living and very long-acting inhibitor. Almeida, L; Bonifácio, MJ; Falcão, A; Loureiro, AI; Nunes, T; Palma, PN; Pinto, R; Rocha, JF; Soares-da-Silva, P; Wright, LC, 2013)

Excerpt	Reference
"Opicapone has a prolonged inhibitory effect on peripheral COMT, which extends the bioavailability of levodopa, without inducing toxicity. "	( Pharmacological profile of opicapone, a third-generation nitrocatechol catechol-O-methyl transferase inhibitor, in the rat. Bonifácio, MJ; Loureiro, AI; Palma, PN; Soares-da-Silva, P; Torrão, L; Wright, LC, 2015)
"Opicapone has been recently licensed for the management of Parkinson's disease (PD); however, it is unknown whether it possesses a protective effect in brain vessels against HHcy."	( Opicapone Protects Against Hyperhomocysteinemia-Induced Increase in Blood-Brain Barrier Permeability. Wang, J; Yang, S; Zheng, B; Zheng, H, 2021)
"Opicapone has been developed for use in combination with levodopa to reduce the occurrence of motor fluctuations and was shown to be effective in two large clinical trials."	( Opicapone in UK clinical practice: effectiveness, safety and cost analysis in patients with Parkinson's disease. Carroll, C; Chaudhuri, KR; Evans, J; Foltynie, T; Lees, A; Pavese, N; Reichmann, H; Schofield, C; Sharma, JC; Soares-da-Silva, P; Zurowska, L, 2022)

Excerpt	Reference
"Opicapone-treated pwPD were algorithm-matched (1:4) to entacapone-treated pwPD."	( Opicapone versus entacapone: Head-to-head retrospective data-based comparison of healthcare resource utilization in people with Parkinson's disease new to catechol-O-methyltransferase (COMT) inhibitor treatment. Castilla-Fernández, G; Chaudhuri, KR; Di Foggia, V; Harrison-Jones, G; Marston, XL; Morgante, F, 2023)
"Opicapone treatment was associated with an average of 1,187 fewer OFF-time hours per patient and an increase of 0.07 QALYs compared with entacapone. "	( Cost-effectiveness of opicapone and entacapone in reducing OFF-time in Parkinson's disease patients treated with levodopa/carbidopa. Hansen, RN; Serbin, M; Suh, K; Sullivan, SD; Yonan, C, )
"Treatment with opicapone 50 mg was superior to placebo (mean difference in change from baseline -60·8 min, 95% CI -97·2 to -24·4; p=0·0015) and non-inferior to entacapone (-26·2 min, -63·8 to 11·4; p=0·0051)."	( Opicapone as an adjunct to levodopa in patients with Parkinson's disease and end-of-dose motor fluctuations: a randomised, double-blind, controlled trial. Ferreira, JJ; Lees, A; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P, 2016)

Excerpt	Reference
"3% of opicapone-treated patients reported treatment-emergent adverse events (TEAEs) versus 57."	( Safety Profile of Opicapone in the Management of Parkinson's Disease. Ferreira, JJ; Gama, H; Lees, A; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P, 2019)
"Long-term use of opicapone once-daily over 1-year at doses of 25 mg or 50 mg was generally safe and well tolerated, supporting its clinical usefulness in the management of PD motor fluctuations."	( Safety Profile of Opicapone in the Management of Parkinson's Disease. Ferreira, JJ; Gama, H; Lees, A; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P, 2019)
" Safety assessments included evaluation of treatment-emergent adverse events (TEAEs) and serious adverse events (SAEs)."	( Effectiveness and safety of opicapone in Parkinson's disease patients with motor fluctuations: the OPTIPARK open-label study. Lees, A; Magalhães, D; Reichmann, H; Rocha, JF; Soares-da-Silva, P, 2020)
" Safety was monitored via adverse events, laboratory testing, and physical, cardiovascular and neurological examinations."	( Long-term safety and efficacy of opicapone in Japanese Parkinson's patients with motor fluctuations. Hattori, N; Maeda, T; Nishimura, A; Nomoto, M; Takahashi, R; Takeda, A; Tsuboi, Y; Yoshida, K, 2021)

Excerpt	Reference
" Based on the observation that the half-life of COMT inhibition is independent of the dose and that it reflects an underlying kinetic process that is consistent with the k(off) value of the COMT-opicapone complex, we propose that the sustained COMT inhibition, far beyond the observable point of clearance of circulating drug, is due to the long residence time of the reversible complex formed between COMT and opicapone."	( Pharmacokinetics, pharmacodynamics and tolerability of opicapone, a novel catechol-O-methyltransferase inhibitor, in healthy subjects: prediction of slow enzyme-inhibitor complex dissociation of a short-living and very long-acting inhibitor. Almeida, L; Bonifácio, MJ; Falcão, A; Loureiro, AI; Nunes, T; Palma, PN; Pinto, R; Rocha, JF; Soares-da-Silva, P; Wright, LC, 2013)
"Opicapone increased levodopa systemic exposure by 2-fold not changing Cmax values and reduced both 3-O-methyldopa (3-OMD) exposure and Cmax values by 5-fold."	( Brain and peripheral pharmacokinetics of levodopa in the cynomolgus monkey following administration of opicapone, a third generation nitrocatechol COMT inhibitor. Bonifácio, MJ; Soares-da-Silva, P; Sutcliffe, JS; Torrão, L; Wright, LC, 2014)
" Although apparent total clearance (CL/F) of opicapone was decreased by ∼35 %, similar elimination half-life and unbound/bound fractions of opicapone were observed between the two groups."	( Effect of moderate liver impairment on the pharmacokinetics of opicapone. Falcão, A; Lopes, N; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Soares-da-Silva, P, 2014)
" The purpose of this study was to compare the levodopa pharmacokinetic profile throughout a day driven by the COMT inhibition either following repeated doses of opicapone or concomitant administration with entacapone."	( Effect of opicapone and entacapone upon levodopa pharmacokinetics during three daily levodopa administrations. Falcão, A; Lopes, N; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Soares-da-Silva, P; Vaz-da-Silva, M; Wright, LC, 2014)
"To compare the levodopa/carbidopa (LC) and levodopa/benserazide (LB) pharmacokinetic profiles following repeated doses of opicapone (OPC) administered apart from levodopa."	( Effect of opicapone multiple-dose regimens on levodopa pharmacokinetics. Almeida, L; Bonifácio, MJ; Falcão, A; Fauchoux, N; Loureiro, AI; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Sicard, É; Soares-da-Silva, P, 2017)
" After quantifying opicapone and BIA 9-1079 in plasma, a non-compartmental pharmacokinetic analysis was performed."	( Pharmacokinetics of opicapone, a third-generation COMT inhibitor, after single and multiple oral administration: A comparative study in the rat. Alves, G; Falcão, A; Fortuna, A; Gonçalves, D; Soares-da-Silva, P, 2017)
" Despite having a short elimination half-life (≤2."	( A single- and multiple-dose study to investigate the pharmacokinetics and pharmacodynamics of opicapone, a novel COMT inhibitor, in rat. Alves, G; Bonifácio, MJ; Falcão, A; Fortuna, A; Gonçalves, D; Soares-da-Silva, P, 2017)
" Areas covered: The purpose of this study was to evaluate pharmacokinetic of OPC for the treatment of PD."	( Pharmacokinetic drug evaluation of opicapone for the treatment of Parkinson's disease. Kostić, V; Kresojević, N; Svetel, M; Tomić, A, 2018)
"Inhibiting catechol-O-methyltransferase extends the plasma half-life of levodopa, potentially allowing physicians to optimize the levodopa regimen in patients with Parkinson's disease (PD) experiencing motor fluctuations."	( Effect of Opicapone on Levodopa Pharmacokinetics in Patients with Fluctuating Parkinson's Disease. Antonini, A; Ferreira, JJ; Guimarães, B; Moreira, J; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P; Stocchi, F, 2022)
" Despite a 100 mg lower total levodopa/carbidopa daily dose, adding opicapone 50 mg at least doubled the levodopa plasma half-life and minimal concentrations, with a significant ≈30% increase in total exposure."	( Effect of Opicapone on Levodopa Pharmacokinetics in Patients with Fluctuating Parkinson's Disease. Antonini, A; Ferreira, JJ; Guimarães, B; Moreira, J; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P; Stocchi, F, 2022)
" Despite the lower levodopa dose, modifying the levodopa pharmacokinetic profile with opicapone was associated with decreased off time and increased on time."	( Effect of Opicapone on Levodopa Pharmacokinetics in Patients with Fluctuating Parkinson's Disease. Antonini, A; Ferreira, JJ; Guimarães, B; Moreira, J; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P; Stocchi, F, 2022)
" At steady-state (day 14), opicapone Cmax (peak plasma concentration) and AUC 0-last (area under the curve-time curve) were 459 ± 252 ng/mL and 2022 ± 783 ng/mL·h, respectively."	( Opicapone Pharmacokinetics and Effects on Catechol- O -Methyltransferase Activity and Levodopa Pharmacokinetics in Patients With Parkinson Disease Receiving Carbidopa/Levodopa. Jimenez, R; Kieburtz, KD; Klepitskaya, O; LeWitt, P; Liang, GS; Loewen, G; Olanow, CW; Olson, K, )

Excerpt	Reference
"The present study aimed at evaluating the effect of opicapone, a third generation nitrocatechol catechol-O-methyltransferase (COMT) inhibitor, on the systemic and central bioavailability of 3,4-dihydroxy-l-phenylalanine (levodopa) and related metabolites in the cynomolgus monkey."	( Brain and peripheral pharmacokinetics of levodopa in the cynomolgus monkey following administration of opicapone, a third generation nitrocatechol COMT inhibitor. Bonifácio, MJ; Soares-da-Silva, P; Sutcliffe, JS; Torrão, L; Wright, LC, 2014)
"The bioavailability of an orally administered single dose of 50 mg OPC was significantly higher in patients with moderate chronic hepatic impairment, perhaps by a reduced first-pass effect."	( Effect of moderate liver impairment on the pharmacokinetics of opicapone. Falcão, A; Lopes, N; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Soares-da-Silva, P, 2014)
"Opicapone, a novel third generation COMT inhibitor, when compared to entacapone, provides a superior response upon the bioavailability of levodopa associated to more pronounced, long-lasting, and sustained COMT inhibition."	( Effect of opicapone and entacapone upon levodopa pharmacokinetics during three daily levodopa administrations. Falcão, A; Lopes, N; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Soares-da-Silva, P; Vaz-da-Silva, M; Wright, LC, 2014)
"Opicapone has a prolonged inhibitory effect on peripheral COMT, which extends the bioavailability of levodopa, without inducing toxicity."	( Pharmacological profile of opicapone, a third-generation nitrocatechol catechol-O-methyl transferase inhibitor, in the rat. Bonifácio, MJ; Loureiro, AI; Palma, PN; Soares-da-Silva, P; Torrão, L; Wright, LC, 2015)
"Opicapone, as once-daily oral evening regimen and/or 1 h apart from levodopa therapy, increases the bioavailability of levodopa associated with its pronounced, long-lasting and sustained catechol-O-methyltransferase inhibition."	( Effect of opicapone multiple-dose regimens on levodopa pharmacokinetics. Almeida, L; Bonifácio, MJ; Falcão, A; Fauchoux, N; Loureiro, AI; Nunes, T; Pinto, R; Rocha, JF; Santos, A; Sicard, É; Soares-da-Silva, P, 2017)
"Opicapone is a third generation, highly potent and effective catechol O‑methyltransferase (COMT) inhibitor that optimizes the pharmacokinetics and bioavailability of L-DOPA therapy."	( Opicapone for the management of end-of-dose motor fluctuations in patients with Parkinson's disease treated with L-DOPA. Ferreira, J; Lees, AJ; Poewe, W; Rascol, O; Reichmann, H; Stocchi, F; Tolosa, E, 2017)
" Opicapone fills the unmet need for a compound with sustained COMT inhibition which will improve levodopa bioavailability in patients with Parkinson's disease."	( Inhibition of catechol-O-methyltransferase in the cynomolgus monkey by opicapone after acute and repeated administration. Bonifácio, MJ; Kitajima, T; Mizote, S; Moser, P; Soares-da-Silva, P; Tanaka, M; Umemura, T; Yoneda, K, 2018)
" Opicapone is a recent and selective third-generation COMT inhibitor which achieves marked increase in the bioavailability of levodopa."	( Optimized clinical management of Parkinson's disease with opicapone. Recommendations from Spanish experts. García Ruiz-Espiga, P; Linazasoro-Cristóbal, G; López Del Val, LJ; López-Manzanares, L; Luquin-Piudo, MR; Martínez-Castrillo, JC; Mir, P; Pagonabarraga-Mora, J, 2020)
" Levodopa bioavailability and its maximum concentration were higher with opicapone."	( Effects of One-Day Application of Levodopa/Carbidopa/Entacapone versus Levodopa/Carbidopa/Opicapone in Parkinson's Disease Patients. Müller, T; Schlegel, E; Thiede, HM; Zingler, S, 2022)
"Combining opicapone 50 mg with a 100 mg lower daily dose of levodopa provides higher levodopa bioavailability with avoidance of trough levels."	( Effect of Opicapone on Levodopa Pharmacokinetics in Patients with Fluctuating Parkinson's Disease. Antonini, A; Ferreira, JJ; Guimarães, B; Moreira, J; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P; Stocchi, F, 2022)

Excerpt	Reference
"The addition of opicapone 50 mg to levodopa treatment in patients with Parkinson's disease and end-of-dose motor fluctuations could enable a simplified drug regimen that allows physicians to individually tailor the existing levodopa daily regimen, by potentially reducing the total daily levodopa dose, increasing the dosing interval, and ultimately reducing the number of intakes, thereby maximising its benefit."	( Opicapone as an adjunct to levodopa in patients with Parkinson's disease and end-of-dose motor fluctuations: a randomised, double-blind, controlled trial. Ferreira, JJ; Lees, A; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P, 2016)
"This phase 3 international, multicenter outpatient study evaluated a 25- and a 50-mg/d dosage of opicapone in a randomized, double-blind, 14- to 15-week, placebo-controlled clinical trial, followed by a 1-year open-label phase during which all patients received active treatment with opicapone."	( Opicapone as Adjunct to Levodopa Therapy in Patients With Parkinson Disease and Motor Fluctuations: A Randomized Clinical Trial. Ferreira, J; Lees, AJ; McCrory, M; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P, 2017)
"8] years) were randomized to a 25-mg/d (n = 129) or a 50-mg/d (n = 154) dosage of opicapone or to placebo (n = 144)."	( Opicapone as Adjunct to Levodopa Therapy in Patients With Parkinson Disease and Motor Fluctuations: A Randomized Clinical Trial. Ferreira, J; Lees, AJ; McCrory, M; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P, 2017)
" Opicapone was quickly absorbed (time to reach the maximum plasma concentration≤2h) in both dosage regimens and the extent of systemic exposure to opicapone increased approximately in a dose-proportional manner after single-dosing within the studied dose range (30-90mg/kg)."	( Pharmacokinetics of opicapone, a third-generation COMT inhibitor, after single and multiple oral administration: A comparative study in the rat. Alves, G; Falcão, A; Fortuna, A; Gonçalves, D; Soares-da-Silva, P, 2017)
" Several factors hamper the use of current available catechol-O-methyl transferase inhibitors, that is, the moderate efficacy and multiple dosing for entacapone and the risk of liver toxicity with tolcapone."	( Opicapone for the treatment of Parkinson's disease: A review of a new licensed medicine. Fabbri, M; Ferreira, JJ; Lees, A; Poewe, W; Rascol, O; Stocchi, F; Tolosa, E, 2018)
" Plasma concentrations of OPC and its metabolites were measured at 0 to 72 and 0 to 144 hours after dosing for single dose and multiple dose, respectively."	( Pharmacokinetics of Opicapone and Its Metabolites in Healthy White and Chinese Subjects. Cong, D; Hui, A; Li, K; Liu, X; Liu, Y; Qi, W; Song, J; Tan, Y; Wang, J; Xu, C; Xue, W; Zhong, L, 2021)
"To evaluate the effects of once-daily opicapone on levodopa plasma pharmacokinetics and motor response when added to two different levodopa dosing regimens."	( Effect of Opicapone on Levodopa Pharmacokinetics in Patients with Fluctuating Parkinson's Disease. Antonini, A; Ferreira, JJ; Guimarães, B; Moreira, J; Poewe, W; Rascol, O; Rocha, JF; Soares-da-Silva, P; Stocchi, F, 2022)

Class	Description
ring assembly	Two or more cyclic systems (single rings or fused systems) which are directly joined to each other by double or single bonds are named ring assemblies when the number of such direct ring junctions is one less than the number of cyclic systems involved.
oxadiazole
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus	Potency	31.6228	0.0096	10.5250	35.4813	AID1479145
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Catechol O-methyltransferase	Mus musculus (house mouse)	Ki	0.0087	0.0015	0.0087	0.0159	AID1153924
Catechol O-methyltransferase	Homo sapiens (human)	Ki	0.0055	0.0010	0.0055	0.0100	AID1153918
Catechol O-methyltransferase	Rattus norvegicus (Norway rat)	Ki	0.0087	0.0015	0.0066	0.0159	AID1153925
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
behavioral fear response	Catechol O-methyltransferase	Homo sapiens (human)
response to hypoxia	Catechol O-methyltransferase	Homo sapiens (human)
synaptic transmission, dopaminergic	Catechol O-methyltransferase	Homo sapiens (human)
startle response	Catechol O-methyltransferase	Homo sapiens (human)
response to amphetamine	Catechol O-methyltransferase	Homo sapiens (human)
renin secretion into blood stream	Catechol O-methyltransferase	Homo sapiens (human)
glycogen metabolic process	Catechol O-methyltransferase	Homo sapiens (human)
prostaglandin metabolic process	Catechol O-methyltransferase	Homo sapiens (human)
response to oxidative stress	Catechol O-methyltransferase	Homo sapiens (human)
memory	Catechol O-methyltransferase	Homo sapiens (human)
visual learning	Catechol O-methyltransferase	Homo sapiens (human)
response to xenobiotic stimulus	Catechol O-methyltransferase	Homo sapiens (human)
response to wounding	Catechol O-methyltransferase	Homo sapiens (human)
response to toxic substance	Catechol O-methyltransferase	Homo sapiens (human)
response to inorganic substance	Catechol O-methyltransferase	Homo sapiens (human)
gene expression	Catechol O-methyltransferase	Homo sapiens (human)
dopamine secretion	Catechol O-methyltransferase	Homo sapiens (human)
cellular response to phosphate starvation	Catechol O-methyltransferase	Homo sapiens (human)
cerebellar cortex morphogenesis	Catechol O-methyltransferase	Homo sapiens (human)
response to food	Catechol O-methyltransferase	Homo sapiens (human)
methylation	Catechol O-methyltransferase	Homo sapiens (human)
glomerulus development	Catechol O-methyltransferase	Homo sapiens (human)
cholesterol efflux	Catechol O-methyltransferase	Homo sapiens (human)
response to cytokine	Catechol O-methyltransferase	Homo sapiens (human)
multicellular organism growth	Catechol O-methyltransferase	Homo sapiens (human)
exploration behavior	Catechol O-methyltransferase	Homo sapiens (human)
renal sodium excretion	Catechol O-methyltransferase	Homo sapiens (human)
norepinephrine metabolic process	Catechol O-methyltransferase	Homo sapiens (human)
dopamine catabolic process	Catechol O-methyltransferase	Homo sapiens (human)
catecholamine catabolic process	Catechol O-methyltransferase	Homo sapiens (human)
habituation	Catechol O-methyltransferase	Homo sapiens (human)
norepinephrine secretion	Catechol O-methyltransferase	Homo sapiens (human)
detection of temperature stimulus involved in sensory perception of pain	Catechol O-methyltransferase	Homo sapiens (human)
response to corticosterone	Catechol O-methyltransferase	Homo sapiens (human)
artery development	Catechol O-methyltransferase	Homo sapiens (human)
cellular response to cocaine	Catechol O-methyltransferase	Homo sapiens (human)
mastication	Catechol O-methyltransferase	Homo sapiens (human)
renal albumin absorption	Catechol O-methyltransferase	Homo sapiens (human)
renal filtration	Catechol O-methyltransferase	Homo sapiens (human)
response to salt	Catechol O-methyltransferase	Homo sapiens (human)
response to dopamine	Catechol O-methyltransferase	Homo sapiens (human)
response to angiotensin	Catechol O-methyltransferase	Homo sapiens (human)
dopamine metabolic process	Catechol O-methyltransferase	Homo sapiens (human)
developmental process	Catechol O-methyltransferase	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
magnesium ion binding	Catechol O-methyltransferase	Homo sapiens (human)
protein binding	Catechol O-methyltransferase	Homo sapiens (human)
methyltransferase activity	Catechol O-methyltransferase	Homo sapiens (human)
O-methyltransferase activity	Catechol O-methyltransferase	Homo sapiens (human)
catechol O-methyltransferase activity	Catechol O-methyltransferase	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
cytosol	Catechol O-methyltransferase	Homo sapiens (human)
plasma membrane	Catechol O-methyltransferase	Homo sapiens (human)
membrane	Catechol O-methyltransferase	Homo sapiens (human)
intracellular membrane-bounded organelle	Catechol O-methyltransferase	Homo sapiens (human)
synapse	Catechol O-methyltransferase	Homo sapiens (human)
extracellular exosome	Catechol O-methyltransferase	Homo sapiens (human)
dendrite	Catechol O-methyltransferase	Homo sapiens (human)
membrane	Catechol O-methyltransferase	Homo sapiens (human)
axon	Catechol O-methyltransferase	Homo sapiens (human)
virion membrane	Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
AID473662	Inhibition of COMT in Wistar rat plasma assessed as decrease in 3-O-methyl-L-Dopa level at 3 mg/kg, po co-administered with L-dopa and benserazide measured after 2 hrs by HPLC analysis relative to control	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473656	Inhibition of COMT in Wistar rat plasma assessed as increase L-DOPA level at 3 mg/kg, po co-administered with L-dopa and benserazide measured after 2 hrs by HPLC analysis	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473645	Inhibition of COMT in Wistar rat brain homogenates assessed as metanephrine formation at 3 mg/kg, po measured after 1 hr	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID1153925	Inhibition of catalytic activity of rat COMT expressed in Escherichia coli using [3H]-S-adenosylmethionine as substrate after 20 mins by liquid scintillation counting	2014	Journal of medicinal chemistry, Jun-26, Volume: 57, Issue:12	A fragment-based approach to identifying S-adenosyl-l-methionine -competitive inhibitors of catechol O-methyl transferase (COMT).
AID1153918	Inhibition of catalytic activity of human cloned COMT expressed in Escherichia coli using [3H]-S-adenosylmethionine as substrate after 20 mins by liquid scintillation counting	2014	Journal of medicinal chemistry, Jun-26, Volume: 57, Issue:12	A fragment-based approach to identifying S-adenosyl-l-methionine -competitive inhibitors of catechol O-methyl transferase (COMT).
AID473642	Cytotoxicity against mouse Neuro2a cells assessed as cell viability at 30 uM after 24 hrs	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID1153924	Inhibition of catalytic activity of mouse COMT expressed in Escherichia coli using [3H]-S-adenosylmethionine as substrate after 20 mins by liquid scintillation counting	2014	Journal of medicinal chemistry, Jun-26, Volume: 57, Issue:12	A fragment-based approach to identifying S-adenosyl-l-methionine -competitive inhibitors of catechol O-methyl transferase (COMT).
AID473647	Inhibition of COMT in Wistar rat brain homogenates assessed as metanephrine formation at 3 mg/kg, po measured after 3 hrs	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473640	Inhibition of COMT in Wistar rat liver homogenates assessed as metanephrine formation at 3 mg/kg, po measured after 3 hrs relative to control	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473643	Inhibition of COMT in po dosed Wistar rat liver homogenates assessed as metanephrine formation measured up to 3 hrs relative to control	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473644	Inhibition of COMT in Wistar rat liver homogenates assessed as metanephrine formation at 3 mg/kg, po measured after 1 hr	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473654	Inhibition of peripheral COMT in Wistar rat liver homogenates assessed as metanephrine formation at 3 mg/kg, po measured after 24 hrs	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473652	Inhibition of central COMT in Wistar rat liver homogenates assessed as metanephrine formation at 3 mg/kg, po measured up to 24 hrs	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473653	Inhibition of central COMT in Wistar rat brain homogenates assessed as metanephrine formation at 3 mg/kg, po measured up to 24 hrs	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473646	Inhibition of COMT in Wistar rat liver homogenates assessed as metanephrine formation at 3 mg/kg, po measured after 3 hrs	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473661	Inhibition of COMT in Wistar rat plasma assessed as decrease in 3-O-methyl-L-Dopa level at 3 mg/kg, po co-administered with L-dopa and benserazide measured after 24 hrs by HPLC analysis	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID473655	Inhibition of peripheral COMT in Wistar rat brain homogenates assessed as metanephrine formation at 3 mg/kg, po measured after 24 hrs	2010	Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8	Discovery of a long-acting, peripherally selective inhibitor of catechol-O-methyltransferase.
AID1346011	Rat Catechol-O-methyltransferase (Catecholamine turnover)	2014	Journal of medicinal chemistry, Jun-26, Volume: 57, Issue:12	A fragment-based approach to identifying S-adenosyl-l-methionine -competitive inhibitors of catechol O-methyl transferase (COMT).
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	0 (0.00)	29.6817
2010's	40 (51.28)	24.3611
2020's	38 (48.72)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	20 (25.00%)	5.53%
Reviews	22 (27.50%)	6.00%
Case Studies	2 (2.50%)	4.05%
Observational	0 (0.00%)	0.25%
Other	36 (45.00%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (46)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
An Open-Label, Single-Dose, Single-Period Study Designed to Assess the Mass Balance Recovery, Metabolite Profile and Metabolite Identification of [14C]-BIA 9-1067 in Healthy Male Subjects[NCT03119194]	Phase 1	7 participants (Actual)	Interventional	2017-01-27	Completed
Effect of Food on Opicapone Bioavailability and Pharmacodynamics in Healthy Subjects[NCT03116308]	Phase 1	28 participants (Actual)	Interventional	2014-11-21	Completed
A Randomized, Parallel Group, Multicentre, Multinational, Prospective, Open-label Exploratory Study to Evaluate the add-on Effect of Opicapone 50 mg or Levodopa 100 mg as First Strategy for the Treatment of Wearing-off in Patients With Parkinson's Disease[NCT04990284]	Phase 4	106 participants (Actual)	Interventional	2021-11-29	Active, not recruiting
A Randomized, Parallel Group, Multicenter, Prospective, Open-label, Exploratory, Phase 4 Study to Evaluate the Add-on Effect of Opicapone 50 mg or Levodopa 100 mg as First Strategy for the Treatment of Wearing-off in Patients With Parkinson's Disease[NCT04821687]	Phase 4	169 participants (Actual)	Interventional	2021-06-17	Completed
Randomised, Double-blind, Placebo-controlled, Clinical Study to Evaluate the Effect of Opicapone 50 mg on Parkinson's Disease Patients With End-of-dose Motor Fluctuations and Associated Pain.[NCT04986982]	Phase 4	140 participants (Anticipated)	Interventional	2021-02-25	Recruiting
Effect of Opicapone at Steady State on Warfarin Pharmacokinetics in Healthy Volunteers[NCT02305030]	Phase 1	20 participants (Actual)	Interventional	2014-03-31	Completed
A Phase 1, Open-Label Study to Assess the Pharmacokinetics, Pharmacodynamics, Safety and Tolerability of Repeated Doses of Opicapone, and Effect on Levodopa Pharmacokinetics in Subjects With Parkinson's Disease[NCT03496870]	Phase 1	16 participants (Actual)	Interventional	2018-02-08	Completed
Opicapone Treatment Initiation Open-Label Study[NCT04787965]		239 participants (Actual)	Observational	2021-03-01	Completed
A Comparative, Randomized, Open-label, Fasted, Single-dose, 2-way Crossover Bioavailability and Bioequivalence Study of Two Different Sources of Opicapone in Healthy Subjects[NCT03116295]	Phase 1	56 participants (Actual)	Interventional	2017-06-20	Completed
An Open Label, Randomised, Two Period, Crossover Study to Assess Bioavailability, Bioequivalence and S COMT Activity Between Two Active Pharmaceutical Ingredient Sources of Opicapone at Two Different Dosage Strengths (50 mg and 25 mg) After Single and Mul[NCT04265027]	Phase 1	72 participants (Actual)	Interventional	2018-02-20	Completed
Efficacy and Safety of Opicapone in Clinical Practice in Parkinson's Disease Patients With Wearing-off Motor Fluctuations[NCT02847442]	Phase 4	518 participants (Actual)	Interventional	2016-11-23	Completed
Continue Providing Care for Patient Who Participated in the BIA 9-1067-302 Clinical Trial[NCT01851850]	Phase 3	1 participants (Actual)	Interventional	2013-05-31	Completed
Pharmacokinetic-pharmacodynamic Interaction Between Each of Three Different Single Doses of BIA 9-1067 and a Single-dose of Controlled-release 100/25 mg Levodopa/Carbidopa: a Double-blind, Randomized, Four-way Crossover, Placebo-controlled Study in Health[NCT02169453]	Phase 1	12 participants (Actual)	Interventional	2008-10-31	Completed
Pharmacokinetic-pharmacodynamic Interaction Between Each of Three Different Single Doses of BIA 9-1067 and a Single-dose of Immediate-release 100/25 mg Levodopa/Benserazide: a Doubleblind, Randomized, Four-way Crossover, Placebo-controlled Study in Health[NCT02169895]	Phase 1	16 participants (Actual)	Interventional	2008-09-30	Completed
Pharmacokinetic-pharmacodynamic Interaction Between Each of Three Diferente Single Doses of BIA 9-1067 and a Single-dose of Immediate-release 100/25 mg Levodopa/Carbidopa: a Doubleblind, Randomized, Four-way Crossover, Placebo-controlled Study in Healthy [NCT02169479]	Phase 1	16 participants (Actual)	Interventional	2008-09-30	Completed
A Double-blind, Randomised, Placebo- and Active-controlled Multiple-dose Study of BIA 9-1067 to Investigate Its Effect on Levodopa Pharmacokinetics Following a Levodopa/Carbidopa 100/25 mg Single-dose in Healthy Subjects[NCT01519284]	Phase 1	82 participants (Actual)	Interventional	2009-11-30	Completed
Effect of BIA 9-1067 on the Pharmacokinetics of Repaglinide in Healthy Volunteers[NCT01536366]	Phase 1	27 participants (Actual)	Interventional	2009-06-30	Completed
A Randomized, Double-blind, Placebo-controlled and Open-label Active-controlled, 4-period Crossover Trial to Evaluate the Effect of BIA 9-1067 on Cardiac Repolarization in Healthy Adult Men and Women[NCT01532115]	Phase 1	64 participants (Actual)	Interventional	2010-05-31	Completed
A Multinational, Multicentre, Prospective Non-interventional Study to Assess Safety and Effectiveness of Opicapone Plus Standard of Care in Elderly Patients With Parkinson's Disease[NCT03959540]		39 participants (Actual)	Observational	2020-04-28	Completed
Single Dose Crossover Comparative Bioavailability Study of BIA 9-1067 25 mg Capsules in Healthy Male Volunteers Following Administration of a 50 mg Dose / Fasted and Fed States[NCT02071823]	Phase 1	12 participants (Actual)	Interventional	2008-05-31	Completed
Effect of Paracetamol on Opicapone Pharmacokinetics in Healthy Volunteers[NCT02305017]	Phase 1	28 participants (Actual)	Interventional	2014-03-31	Completed
Dosage Form Proportionality of Opicapone To-Be-Marketed Formulation in Healthy Subjects[NCT02305329]	Phase 1	56 participants (Actual)	Interventional	2014-02-28	Completed
Open-label, Single-dose, Multi-center Study, Investigating the Pharmacokinetics of BIA 9-1067 in Subjects With Hepatic Impairment[NCT02101190]	Phase 1	16 participants (Actual)	Interventional	2010-03-31	Completed
Effect of BIA 9-1067 at Steady-state on the Pharmacokinetics of a Single-dose of Immediate-release 100/25 mg Levodopa/Carbidopa and 100/25 mg Levodopa/Benserazide in Healthy Subjects[NCT01533116]	Phase 1	52 participants (Actual)	Interventional	2009-03-31	Completed
Relative Bioavailability and Bioequivalence Of Different Formulations of Opicapone in Healthy Volunteers[NCT02305277]	Phase 1	85 participants (Actual)	Interventional	2014-03-31	Completed
Single-dose Pharmacokinetics and Relative Bioavailability of Two Different Formulations of Opicapone in Healthy Volunteers[NCT02305316]	Phase 1	28 participants (Actual)	Interventional	2014-02-28	Completed
A Double-blind, Randomised, Placebo-controlled, Cross-over Study to Investigate the Tolerability and Effect of Three Single-dose Regimens of BIA 9-1067 on the Levodopa Pharmacokinetics, Motor Response, and Erythrocyte Soluble Catechol-O-methyltransferase [NCT01568034]	Phase 2	10 participants (Actual)	Interventional	2009-04-30	Completed
Effect of Rasagiline on BIA 9-1067 Pharmacokinetics in Healthy Subjects[NCT01532141]	Phase 1	25 participants (Actual)	Interventional	2009-11-30	Completed
An Open-label Study in Healthy Male Subjects to Assess the Absorption, Distribution, Metabolism and Excretion of [14C]-Labelled BIA 9-1067 and Metabolites Following a Single Dose Oral Administration[NCT02169427]	Phase 1	6 participants (Actual)	Interventional	2011-03-31	Completed
"Efficacy and Safety of BIA 9-1067 in Idiopathic Parkinson's Disease Patients With Wearing-off Phenomenon Treated With Levodopa Plus a Dopa Decarboxylase Inhibitor (DDCI): a Double-blind, Randomised, Placebo-controlled, Parallel-group, Multicentre Clinica[NCT01227655]	Phase 3	427 participants (Actual)	Interventional	2011-03-31	Completed
Randomized, Double-Blinded, Placebo-Controlled, Multiple Ascending Dose Study to Compare the Pharmacokinetics of BIA 9-1067 in Healthy Japanese and Caucasian Subjects[NCT01520987]	Phase 1	105 participants (Actual)	Interventional	2011-05-31	Completed
A Phase I, Open-Label, Randomised, Three-Period, Three-Sequence, Partial Replicate Crossover Study to Investigate the Relative Bioavailability and Bioequivalence of Opicapone Obtained From Two Different Sources, Under Fasting Conditions After Single-dose [NCT03820037]	Phase 1	45 participants (Actual)	Interventional	2019-03-19	Completed
"Efficacy and Safety of BIA 9-1067 in Idiopathic Parkinson's Disease Patients With Wearing-off Phenomenon Treated With Levodopa Plus a Dopa Decarboxylase Inhibitor (DDCI): a Double-blind, Randomised, Placebo- and Active-controlled, Parallel-group, Multice[NCT01568073]	Phase 3	600 participants (Actual)	Interventional	2011-03-31	Completed
An Open-label Study in Healthy Male Subjects to Assess the Absorption, Distribution, Metabolism and Excretion of [14C]-Labeled BIA 9-1067 and Metabolites Following a Single-dose Oral Administration[NCT01515891]	Phase 1	4 participants (Actual)	Interventional	2009-05-31	Completed
A Single Oral Ascending Dose Study to Investigate the Safety, Pharmacokinetics and Catechol-O-methyltransferase (COMT) Inhibition Profiles of BIA 9-1067 in Healthy Male Subjects[NCT01520727]	Phase 1	64 participants (Actual)	Interventional	2007-10-31	Completed
A Phase III, Double-Blind, Randomized, Placebo-Controlled and Parallel-Group Study to Evaluate the Efficacy and Safety of Opicapone, as Add-on to Stable Levodopa (L-DOPA) Plus a Dopa Decarboxylase Inhibitor (DDCI) Therapy in Early Idiopathic Parkinson's D[NCT04978597]	Phase 3	410 participants (Actual)	Interventional	2021-05-31	Active, not recruiting
Effect of Three Multiple-dose Regimens of BIA 9 1067 at Steady-state on the Levodopa Pharmacokinetics of a Single-dose of Immediate Release 100/25 mg Levodopa/Carbidopa and 100/25 mg Levodopa/Benserazide in Healthy Subjects[NCT02169414]	Phase 1	74 participants (Actual)	Interventional	2010-02-28	Completed
Open-label, Single-arm, Pilot Study to Evaluate the Effect of Opicapone 50 mg on Parkinson's Disease Patients With End-of-dose Motor Fluctuations and Associated Sleep Disorders[NCT04986995]	Phase 4	22 participants (Actual)	Interventional	2021-06-09	Active, not recruiting
Pharmacokinetic Interaction Between BIA 9-1067 and Standard-release Levodopa/Carbidopa in Healthy Subjects[NCT01533077]	Phase 1	18 participants (Actual)	Interventional	2009-03-31	Completed
Effect of BIA 9-1067 on the Pharmacokinetics and Pharmacodynamics of Warfarin in Healthy Volunteers[NCT02169440]	Phase 1	20 participants (Actual)	Interventional	2009-06-30	Completed
The Effect of BIA 9-1067 at Steady-state on the Levodopa Pharmacokinetics When Administered With Immediate-release 100/25 mg Levodopa/Carbidopa in Healthy Subjects[NCT02170376]	Phase 1	80 participants (Actual)	Interventional	2011-09-30	Completed
Single-dose and Steady-state Pharmacokinetics of BIA 9-1067 and Its Metabolites in Healthy Male Elderly Subjects Compared With Those in Healthy Male Young Subjects[NCT02092168]	Phase 1	24 participants (Actual)	Interventional	2008-10-31	Completed
Pharmacokinetic-pharmacodynamic Interaction Between Three Different Single Doses of BIA 9-1067 and a Single-dose of Controlled-release 100/25 mg Levodopa/Benserazide: a Double-blind, Randomized, Four-way Crossover, Placebo-controlled Study in Healthy Male[NCT02169466]	Phase 1	22 participants (Actual)	Interventional	2009-01-31	Completed
Effect of BIA 9-1067 on Rasagiline Pharmacokinetics in Healthy Subjects[NCT01532128]	Phase 1	24 participants (Actual)	Interventional	2009-11-30	Completed
A Double-blind, Randomised, Placebo-controlled Study to Evaluate the Tolerability, Pharmacokinetics and Pharmacodynamics of Four Multiple Rising Dose Regimens of BIA 9-1067 in Healthy Male Volunteers[NCT02071810]	Phase 1	34 participants (Actual)	Interventional	2008-04-30	Completed
"Multicentre, Double-blind, Randomised, Placebo-controlled Study in Four Parallel Groups of PD Patients Treated With Standard-release Levodopa/Carbidopa 100/25 mg (Sinemet®) or Levodopa/Benserazide 100/25 mg (Madopar®/Restex®) and With Motor Fluctuations [NCT01568047]	Phase 2	40 participants (Actual)	Interventional	2010-02-28	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT01227655 (4) [back to overview]	Parkinson's Disease Sleep Scale (PDSS)
NCT01227655 (4) [back to overview]	UPDRS (Unified Parkinson's Disease Rating Scale) Sections I (ON), II (ON and OFF), and III (ON)
NCT01227655 (4) [back to overview]	Non-motor Symptoms Scale (NMSS)
NCT01227655 (4) [back to overview]	Efficacy of 2 BIA 9-1067 (25 mg, and 50 mg) Compared With Placebo, When Administered With the Existing Treatment of L-DOPA Plus a DDCI (DOPA Decarboxylase Inhibitor)
NCT01515891 (4) [back to overview]	Time to Reach Maximum Plasma Concentration (Tmax)
NCT01515891 (4) [back to overview]	Area Under the Plasma-concentration Time Curve Until the Last Quantifiable Sampling Point (AUC0-t)
NCT01515891 (4) [back to overview]	Area Under the Plasma-concentration Time Curve With Extrapolation to Infinity (AUC0-∞)
NCT01515891 (4) [back to overview]	Maximum Plasma Concentration (Cmax)
NCT01519284 (4) [back to overview]	Cmax - Maximum Plasma Concentration of Levodopa
NCT01519284 (4) [back to overview]	Tmax - Time to Reach Maximum Plasma Concentration of Levodopa
NCT01519284 (4) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve (AUC) of Levodopa From Time Zero to Infinity
NCT01519284 (4) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve (AUC) of Levodopa From Time Zero to the Last Sampling Time at Which the Drug Concentration Was at or Above the Lower Limit of Quantification.
NCT01520727 (3) [back to overview]	Adverse Events (AEs)
NCT01520727 (3) [back to overview]	Cmax - BIA 9-1067
NCT01520727 (3) [back to overview]	Time to Cmax (Tmax)
NCT01520987 (8) [back to overview]	AUC0-∞ - Area Under the Concentration of BIA 9-1067-time Curve (AUC) From Time Zero to Infinity (Day 1)
NCT01520987 (8) [back to overview]	AUC0-∞ - Area Under the Concentration of BIA 9-1067-time Curve (AUC) From Time Zero to Infinity (Day 10)
NCT01520987 (8) [back to overview]	AUC0-t - Area Under the Concentration-time Curve (AUC) From Time Zero to Last Time Point With Concentrations Above the Lower Limit of Quantitation of BIA 9-1067 (Day 1)
NCT01520987 (8) [back to overview]	AUC0-t - Area Under the Concentration-time Curve (AUC) From Time Zero to Last Time Point With Concentrations Above the Lower Limit of Quantitation of BIA 9-1067 (Day 10)
NCT01520987 (8) [back to overview]	Cmax of BIA 9-1067 - Maximum Observed Plasma Concentration of BIA 9-1067 (Day 10)
NCT01520987 (8) [back to overview]	Tmax of BIA 9-1067 - Time Taken to Reach Maximum Observed Plasma Concentration of BIA 9-1067 (Day 10)
NCT01520987 (8) [back to overview]	Tmax of BIA 9-1067 - Time Taken to Reach Maximum Observed Plasma Concentration of BIA 9-1067 (Day 1)
NCT01520987 (8) [back to overview]	Cmax of BIA 9-1067 - Maximum Observed Plasma Concentration of BIA 9-1067 (Day 1)
NCT01532128 (3) [back to overview]	Tmax - Time of Occurrence of Cmax
NCT01532128 (3) [back to overview]	Cmax - Maximum Observed Plasma Concentration
NCT01532128 (3) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration
NCT01532141 (3) [back to overview]	Time of Occurrence of Cmax (Tmax)
NCT01532141 (3) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration
NCT01532141 (3) [back to overview]	Cmax - Maximum Observed Plasma Drug Concentration
NCT01533077 (16) [back to overview]	Tmax - Time of Occurrence of Cmax Maximum Observed Plasma Concentration (L-DOPA)
NCT01533077 (16) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point (L-DOPA)
NCT01533077 (16) [back to overview]	Tmax - Time to Occurrence of Cmax (3-OMD)
NCT01533077 (16) [back to overview]	Tmax - Time to Occurrence of Cmax (BIA 9-1067)
NCT01533077 (16) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point (3-OMD)
NCT01533077 (16) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve Extrapolated to Infinity (Carbidopa)
NCT01533077 (16) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve Extrapolated to Infinity (BIA 9-1067)
NCT01533077 (16) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point (Carbidopa)
NCT01533077 (16) [back to overview]	Tmax - Time to Occurrence of Cmax (Carbidopa)
NCT01533077 (16) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point (BIA 9-1067)
NCT01533077 (16) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve Extrapolated to Infinity (3-OMD)
NCT01533077 (16) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve (AUC) From Time Zero to Infinity (L-DOPA)
NCT01533077 (16) [back to overview]	Cmax - Maximum Observed Plasma Concentration (3-OMD)
NCT01533077 (16) [back to overview]	Cmax - Maximum Observed Plasma Concentration (BIA 9-1067)
NCT01533077 (16) [back to overview]	Cmax - Maximum Observed Plasma Concentration (Carbidopa)
NCT01533077 (16) [back to overview]	Cmax - Maximum Observed Plasma Concentration (L-DOPA)
NCT01533116 (5) [back to overview]	AUEC0-24 - Area Under the Effect-time Curve (AUEC) to 24 h Post-dose
NCT01533116 (5) [back to overview]	tEmax - Time of Occurrence of Maximum Observed Effect on S-COMT Activity
NCT01533116 (5) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point
NCT01533116 (5) [back to overview]	Tmax - Time to Maximum Plasma Concentration
NCT01533116 (5) [back to overview]	Cmax - Maximum Plasma Concentration
NCT01536366 (4) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve From Time 0 to Infinity
NCT01536366 (4) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration
NCT01536366 (4) [back to overview]	Cmax - Maximum Observed Plasma Concentration
NCT01536366 (4) [back to overview]	Tmax - Time of Occurrence of Cmax
NCT01568034 (3) [back to overview]	Cmax - Maximum Plasma Concentration Day 3
NCT01568034 (3) [back to overview]	Tmax = Time to Cmax Day 3
NCT01568034 (3) [back to overview]	AUC0-6 - Area Under the Plasma Concentration-time Curve From Time 0 to 6 Hours Post-dose (Day 3)
NCT01568047 (3) [back to overview]	AUC0-6 - Area Under the Plasma Concentration-time Curve (AUC) From Time Zero to to 6 h Postdose (AUC [0-6])
NCT01568047 (3) [back to overview]	Cmax - Observed Maximum Concentration
NCT01568047 (3) [back to overview]	Tmax - Time to Observed Maximum Concentration
NCT01568073 (4) [back to overview]	Non-motor Symptoms Scale (NMSS)
NCT01568073 (4) [back to overview]	Total UPDRS SCORE (I, II (ON), and III)
NCT01568073 (4) [back to overview]	Efficacy of 3 BIA 9-1067 (5 mg, 25 mg, and 50 mg) Compared With 200 mg of Entacapone or Placebo,
NCT01568073 (4) [back to overview]	Parkinson's Disease Sleep Scale (PDSS)
NCT02071810 (1) [back to overview]	Number of Patients With at Least One Adverse Event
NCT02071823 (3) [back to overview]	Cmax - Maximum Observed Plasma Concentration
NCT02071823 (3) [back to overview]	AUCt - Cumulative Area Under the Plasma Concentration Time Curve
NCT02071823 (3) [back to overview]	Area Under the Concentration-time Curve Extrapolated to Infinity (AUC∞)
NCT02092168 (3) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration
NCT02092168 (3) [back to overview]	Tmax - Time to Reach Cmax
NCT02092168 (3) [back to overview]	Cmax - Maximum Plasma Concentration
NCT02101190 (3) [back to overview]	Area Under the Curve (AUC0-t)
NCT02101190 (3) [back to overview]	Cmax - Maximum Plasma Concentration of BIA 9-1067
NCT02101190 (3) [back to overview]	Tmax - Time to Reach Cmax
NCT02169414 (8) [back to overview]	Cmax - Maximum Plasma Concentration of Levodopa (Levodopa/Benserazide )
NCT02169414 (8) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve (AUC) of Levodopa From Time Zero to the Last Sampling Time at Which the Drug Concentration Was at or Above the Lower Limit of Quantification. (Levodopa/Benserazide)
NCT02169414 (8) [back to overview]	Cmax - Maximum Plasma Concentration of Levodopa (Levodopa/Carbidopa)
NCT02169414 (8) [back to overview]	Tmax - Time to Reach Maximum Plasma Concentration of Levodopa (Levodopa/Benserazide)
NCT02169414 (8) [back to overview]	Tmax - Time to Reach Maximum Plasma Concentration of Levodopa (Levodopa/Carbidopa)
NCT02169414 (8) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve (AUC) of Levodopa From Time Zero to Infinity (Levodopa/Benserazide)
NCT02169414 (8) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve (AUC) of Levodopa From Time Zero to Infinity (Levodopa/Carbidopa)
NCT02169414 (8) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve (AUC) of Levodopa From Time Zero to the Last Sampling Time at Which the Drug Concentration Was at or Above the Lower Limit of Quantification. (Levodopa/Carbidopa)
NCT02169427 (3) [back to overview]	Cmax - Maximum Concentration
NCT02169427 (3) [back to overview]	Cumulative Recovery of [14C]-Radioactivity
NCT02169427 (3) [back to overview]	Tmax - Time to Attain Maximum Concentration
NCT02169440 (9) [back to overview]	Tmax - Time to Maximum Observed Plasma Concentration (Warfarin Alone)
NCT02169440 (9) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration (Warfarin Alone)
NCT02169440 (9) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration (Warfarin + BIA 9-1067)
NCT02169440 (9) [back to overview]	Cmax - Maximum Observed Plasma Concentration (BIA 9-1067 + Warfarin)
NCT02169440 (9) [back to overview]	Cmax - Maximum Observed Plasma Concentration (Warfarin + BIA 9-1067)
NCT02169440 (9) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration (BIA 9-1067 + Warfarin)
NCT02169440 (9) [back to overview]	Cmax = Maximum Plasma Concentration (Warfarin Alone)
NCT02169440 (9) [back to overview]	Tmax - Time to Maximum Observed Plasma Concentration (BIA 9-1067 + Warfarin)
NCT02169440 (9) [back to overview]	Tmax - Time to Maximum Observed Plasma Concentration (Warfarin + BIA 9-1067)
NCT02169453 (6) [back to overview]	Cmax - Maximum Observed Plasma Concentration
NCT02169453 (6) [back to overview]	Emax - Maximum Inhibition of COMT Activity
NCT02169453 (6) [back to overview]	tEmax - Time of Occurrence of Emax
NCT02169453 (6) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve Extrapolated to Infinity
NCT02169453 (6) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point
NCT02169453 (6) [back to overview]	AUEC0-24 - Area Under the Effect-time Curve From t=0h to t=24h
NCT02169466 (4) [back to overview]	Tmax - Time to Cmax
NCT02169466 (4) [back to overview]	Cmax - Maximum Observed Plasma Concentration of Levodopa
NCT02169466 (4) [back to overview]	AUC0-∞ - AUC From Time Zero to Infinity
NCT02169466 (4) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve
NCT02169479 (3) [back to overview]	Tmax - Time of Occurrence of Cmax of Levodopa
NCT02169479 (3) [back to overview]	Cmax - Maximum Observed Plasma Concentration of Levodopa
NCT02169479 (3) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve
NCT02169895 (3) [back to overview]	Tmax - Time of Occurrence of Cmax
NCT02169895 (3) [back to overview]	Maximum Observed Plasma Drug Concentration (Cmax)
NCT02169895 (3) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve
NCT02170376 (6) [back to overview]	AUC0-∞ - Area Under the Concentration-time Curve From Time Zero up to Infinity With Extrapolation of the Terminal Phase
NCT02170376 (6) [back to overview]	AUC0-5 - AUC Over 5 Hours
NCT02170376 (6) [back to overview]	AUC0-t - Area Under the Plasma Concentration Versus Time Curve From Time Zero to the Time (t) Corresponding to the Last Quantifiable Concentration.
NCT02170376 (6) [back to overview]	t1/2 - Terminal Plasma Half-life
NCT02170376 (6) [back to overview]	Tmax - Time of Occurrence of Maximum Plasma Concentration
NCT02170376 (6) [back to overview]	Cmax - Maximum Plasma Concentration of Levodopa
NCT02305017 (4) [back to overview]	Cmax - Maximum Plasma Concentration
NCT02305017 (4) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve (AUC) From Time Zero to the Last Sampling Time at Which the Drug Concentration Was at or Above the Lower Limit of Quantification
NCT02305017 (4) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve (AUC) From Time Zero to Infinity.
NCT02305017 (4) [back to overview]	Tmax - Time of Occurrence of Cmax
NCT02305277 (3) [back to overview]	Cmax - Maximum Observed Plasma Concentration
NCT02305277 (3) [back to overview]	Tmax - Time of Occurrence of Cmax
NCT02305277 (3) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve for BIA 9-1067
NCT02305316 (4) [back to overview]	AUC0-inf - Area Under the Plasma Concentration-time Curve From Time 0 to the Infinity
NCT02305316 (4) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to the Time of Last Quantifiable Concentration
NCT02305316 (4) [back to overview]	Cmax - Maximum Observed Plasma Concentration
NCT02305316 (4) [back to overview]	Tmax - Time of Occurrence of Cmax of BIA 9-1067
NCT02305329 (4) [back to overview]	AUC0-∞ - Area Under the Plasma Concentration-time Curve Extrapolated to Infinity
NCT02305329 (4) [back to overview]	AUC0-t - Area Under the Plasma Concentration-time Curve Calculated Between Time of Administration and Time t
NCT02305329 (4) [back to overview]	Cmax - Maximum Observed Plasma Concentration of 9-1067
NCT02305329 (4) [back to overview]	Tmax - Time of Occurrence of Cmax of 9-1067

Parkinson's Disease Sleep Scale (PDSS)

"The Parkinson's disease Sleep Scale (PDSS) is a specific scale for the assessment of sleep disturbances in subjects with PD. The PDSS score is calculated as the sum of all single items. If one or two items are missing, they will be imputed with the mean of the non-missing items. If three or more items are missing, no imputation will be done and the score will be set to missing.~Subscale has 0-10 ratings, where 0 = severe and 10 = normal~The PDSS total score is a sum score of all 15 questions and ranges from 0 to 150, with lower scores meaning more disability." (NCT01227655)
Timeframe: 14-15 weeks

Intervention	units on a scale (Mean)
	Baseline	Visit 5	Visit 7
BIA 9-1067 25 mg	95.75	97.99	98.79
BIA 9-1067 50 mg	102.62	103.05	103.25
Placebo	101.76	107.11	105.39

Intervention	units on a scale (Mean)
	Baseline	Endpoint
BIA 9-1067 25 mg	30.8	26.6
BIA 9-1067 50 mg	31.7	28.7
Placebo	31.5	28.1

Intervention	Number of Adverse Events (Number)
BIA 9-1067 10 mg	0
BIA 9-1067 25 mg	0
BIA 9-1067 50 mg	2
BIA 9-1067 100 mg	0
BIA 9-1067 200 mg	1
BIA 9-1067 400 mg	1
BIA 9-1067 800 mg	0
BIA 9-1067 1200 mg	1
Placebo	4

Intervention	ng/mL (Mean)
BIA 9-1067 10 mg	130.7
BIA 9-1067 25 mg	308.5
BIA 9-1067 50 mg	522.2
BIA 9-1067 100 mg	927.2
BIA 9-1067 200 mg	1287.5
BIA 9-1067 400 mg	2013.3
BIA 9-1067 800 mg	2786.7
BIA 9-1067 1200 mg	4883.3

Intervention	ng.h/mL (Mean)
Caucasian 5 mg OPC	338
Caucasian 25 mg OPC	2039
Caucasian 50 mg OPC	3756
Japanese 5 mg OPC	357
Japanese 25 mg OPC	1976
Japanese 50 mg OPC	4470

Intervention	ng.h/mL (Mean)
Caucasian 5 mg OPC	409
Caucasian 25 mg OPC	2056
Caucasian 50 mg OPC	4028
Japanese 5 mg OPC	465
Japanese 25 mg OPC	2240
Japanese 50 mg OPC	4510

Intervention	ng.h/mL (Mean)
Caucasian 5 mg OPC	267
Caucasian 25 mg OPC	2013
Caucasian 50 mg OPC	3727
Japanese 5 mg OPC	319
Japanese 25 mg OPC	1886
Japanese 50 mg OPC	4438

Intervention	ng.h/mL (Mean)
Caucasian 5 mg OPC	349
Caucasian 25 mg OPC	2024
Caucasian 50 mg OPC	3999
Japanese 5 mg OPC	441
Japanese 25 mg OPC	2222
Japanese 50 mg OPC	4464

Intervention	hours (Median)
Caucasian 5 mg OPC	1.00
Caucasian 25 mg OPC	2.00
Caucasian 50 mg OPC	1.50
Japanese 5 mg OPC	2.00
Japanese 25 mg OPC	2.00
Japanese 50 mg OPC	2.00

Intervention	hours (Median)
	BIA 9-1067	Rasagiline
Rasagiline 1 h After BIA 9-1067	2.00	0.50
Rasagiline Alone	NA	0.50
Rasagiline Concomitant BIA 9-1067	2.50	0.50

Intervention	hours (Median)
	BIA 9-1067	Rasagiline
BIA 9-1067 1h Before Rasagiline	3.00	0.5
BIA 9-1067 Alone	3.00	NA
BIA 9-1067 Concomitant Rasagiline	2.50	0.5

Intervention	hours (Median)
Sinemet® 100/25 mg	1.0
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	1.0
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	0.5

Intervention	ng.h/mL (Mean)
Sinemet® 100/25 mg	2289
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	2611
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	2459

Intervention	hours (Median)
Sinemet® 100/25 mg	6.00
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	5.00
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	5.00

Intervention	ng.h/mL (Mean)
Sinemet® 100/25 mg	10296
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	6940
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	8149

Intervention	ng.h/mL (Mean)
BIA 9-1067 50 mg	2165
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	2360
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	2678

Intervention	ng.h/mL (Mean)
BIA 9-1067 50 mg	2094
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	2130
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	2245

Intervention	ng.h/mL (Mean)
Sinemet® 100/25 mg	11193
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	7730
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	89962

Intervention	ng.h/mL (Mean)
Sinemet® 100/25 mg	2397
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	2730
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	2603

Intervention	ng/mL (Mean)
Sinemet® 100/25 mg	1070
BIA 9-1067 50 mg + Sinemet® 100/25 mg Separated 1 h	1105
BIA 9-1067 50 mg + Sinemet® 100/25 mg Concomitantly	1198

Intervention	pmol/mg Hb/h.h (Mean)
Placebo	906
5 mg BIA 9-1067	454
15 mg BIA 9-1067	319
30 mg BIA 9-1067	226

opicapone

Description

Cross-References

Synonyms (46)

Research Excerpts

Overview

Effects

Treatment

Toxicity

Pharmacokinetics

Bioavailability

Dosage Studied

Drug Classes (2)

Protein Targets (4)

Potency Measurements

Inhibition Measurements

Biological Processes (44)

Molecular Functions (5)

Ceullar Components (9)

Bioassays (18)

Research

Studies (78)

Study Types

Clinical Trials (46)

Trial Overview

Trial Outcomes

Parkinson's Disease Sleep Scale (PDSS)

UPDRS (Unified Parkinson's Disease Rating Scale) Sections I (ON), II (ON and OFF), and III (ON)

Non-motor Symptoms Scale (NMSS)

Efficacy of 2 BIA 9-1067 (25 mg, and 50 mg) Compared With Placebo, When Administered With the Existing Treatment of L-DOPA Plus a DDCI (DOPA Decarboxylase Inhibitor)

Time to Reach Maximum Plasma Concentration (Tmax)

Area Under the Plasma-concentration Time Curve Until the Last Quantifiable Sampling Point (AUC0-t)

Area Under the Plasma-concentration Time Curve With Extrapolation to Infinity (AUC0-∞)

Maximum Plasma Concentration (Cmax)

Cmax - Maximum Plasma Concentration of Levodopa

Tmax - Time to Reach Maximum Plasma Concentration of Levodopa

AUC0-∞ - Area Under the Plasma Concentration-time Curve (AUC) of Levodopa From Time Zero to Infinity

AUC0-t - Area Under the Plasma Concentration-time Curve (AUC) of Levodopa From Time Zero to the Last Sampling Time at Which the Drug Concentration Was at or Above the Lower Limit of Quantification.

Adverse Events (AEs)

Cmax - BIA 9-1067

Time to Cmax (Tmax)

AUC0-∞ - Area Under the Concentration of BIA 9-1067-time Curve (AUC) From Time Zero to Infinity (Day 1)

AUC0-∞ - Area Under the Concentration of BIA 9-1067-time Curve (AUC) From Time Zero to Infinity (Day 10)

AUC0-t - Area Under the Concentration-time Curve (AUC) From Time Zero to Last Time Point With Concentrations Above the Lower Limit of Quantitation of BIA 9-1067 (Day 1)

AUC0-t - Area Under the Concentration-time Curve (AUC) From Time Zero to Last Time Point With Concentrations Above the Lower Limit of Quantitation of BIA 9-1067 (Day 10)

Cmax of BIA 9-1067 - Maximum Observed Plasma Concentration of BIA 9-1067 (Day 10)

Tmax of BIA 9-1067 - Time Taken to Reach Maximum Observed Plasma Concentration of BIA 9-1067 (Day 10)

Tmax of BIA 9-1067 - Time Taken to Reach Maximum Observed Plasma Concentration of BIA 9-1067 (Day 1)

Cmax of BIA 9-1067 - Maximum Observed Plasma Concentration of BIA 9-1067 (Day 1)

Tmax - Time of Occurrence of Cmax

Cmax - Maximum Observed Plasma Concentration

AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration

Time of Occurrence of Cmax (Tmax)

AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration

Cmax - Maximum Observed Plasma Drug Concentration

Tmax - Time of Occurrence of Cmax Maximum Observed Plasma Concentration (L-DOPA)

AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point (L-DOPA)

Tmax - Time to Occurrence of Cmax (3-OMD)

Tmax - Time to Occurrence of Cmax (BIA 9-1067)

AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point (3-OMD)

AUC0-∞ - Area Under the Plasma Concentration-time Curve Extrapolated to Infinity (Carbidopa)

AUC0-∞ - Area Under the Plasma Concentration-time Curve Extrapolated to Infinity (BIA 9-1067)

AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point (Carbidopa)

Tmax - Time to Occurrence of Cmax (Carbidopa)

AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point (BIA 9-1067)

AUC0-∞ - Area Under the Plasma Concentration-time Curve Extrapolated to Infinity (3-OMD)

AUC0-∞ - Area Under the Plasma Concentration-time Curve (AUC) From Time Zero to Infinity (L-DOPA)

Cmax - Maximum Observed Plasma Concentration (3-OMD)

Cmax - Maximum Observed Plasma Concentration (BIA 9-1067)

Cmax - Maximum Observed Plasma Concentration (Carbidopa)

Cmax - Maximum Observed Plasma Concentration (L-DOPA)

AUEC0-24 - Area Under the Effect-time Curve (AUEC) to 24 h Post-dose

tEmax - Time of Occurrence of Maximum Observed Effect on S-COMT Activity

AUC0-t - Area Under the Plasma Concentration-time Curve to Last Measurable Time Point

Tmax - Time to Maximum Plasma Concentration

Cmax - Maximum Plasma Concentration

AUC0-∞ - Area Under the Plasma Concentration-time Curve From Time 0 to Infinity

AUC0-t - Area Under the Plasma Concentration-time Curve From Time 0 to Last Observed Concentration

Cmax - Maximum Observed Plasma Concentration

Tmax - Time of Occurrence of Cmax

Intervention	hours (Mean)
Placebo	8.12
5 mg BIA 9-1067	2.71
15 mg BIA 9-1067	4.67
30 mg BIA 9-1067	3.50

Intervention	ng.h/mL (Mean)
	AUC0-t (Levodopa) Sinemet® 100/25	AUC0-t (Levodopa) Prolopa® 100-25	AUC0-t (3-OMD) Sinemet® 100/25	AUC0-t (3-OMD) Prolopa® 100/25	AUC0-t (BIA 9-1067) Sinemet® 100/25	AUC0-t (BIA 9-1067) Prolopa® 100/25
15 mg BIA 9-1067	2952	3442	2836	3473	872	836
30 mg BIA 9-1067	2753	4056	1751	2623	1101	1185
5 mg BIA 9-1067	3386	4115	5147	6205	223	232
Placebo	1837	2438	7631	11371	NA	NA

Intervention	hours (Median)
	Tmax (Levodopa) Sinemet® 100/25	Tmax (Levodopa) Prolopa® 100-25	Tmax (3-OMD) Sinemet® 100/25	Tmax (3-OMD) Prolopa® 100/25	Tmax (BIA 9-1067) Sinemet® 100/25	Tmax (BIA 9-1067) Prolopa® 100/25
15 mg BIA 9-1067	0.5	1.0	6.0	6.0	3.0	2.5
30 mg BIA 9-1067	1.0	1.0	8.0	4.0	4.0	3.0
5 mg BIA 9-1067	0.75	1.0	8.0	8.0	1.5	3.0
Placebo	0.5	1.0	4.0	4.0	NA	NA

Intervention	ng/mL (Mean)
	Cmax (Levodopa) Sinemet® 100/25	Cmax (Levodopa) Prolopa® 100-25	Cmax (3-OMD) Sinemet® 100/25	Cmax (3-OMD) Prolopa® 100/25	Cmax (BIA 9-1067) Sinemet® 100/25	Cmax (BIA 9-1067) Prolopa® 100/25
15 mg BIA 9-1067	1200	1727	167	206	263	281
30 mg BIA 9-1067	944	1795	115	160	310	370
5 mg BIA 9-1067	1245	2100	307	360	75.0	95.5
Placebo	985	1704	456	688	NA	NA

Intervention	ng.h/mL (Mean)
	BIA 9-1067	Repaglinide
BIA 9-1067 + Repaglinide	1015	15.0
Repaglinide	NA	14.1

Intervention	ng/ml (Mean)
	Cmax (levodopa)	Cmax (3-OMD)	Cmax (BIA 9-067)
BIA 9-1067 100 mg	2657	4085	816
BIA 9-1067 25 mg	2112	4193	320
BIA 9-1067 50 mg	2366	4284	590
Placebo	2103	3996	NA

Intervention	hours (Median)
	Tmax (levodopa)	Tmax (3-OMD)	Tmax (BIA 9-067)
BIA 9-1067 100 mg	0.5	1.75	2.00
BIA 9-1067 25 mg	1.0	1.75	2.00
BIA 9-1067 50 mg	0.5	2.50	2.00
Placebo	0.5	2.00	NA

Intervention	ng.h/mL (Mean)
	AUC0-6 (levodopa)	AUC0-6 (3-OMD)	AUC0-6 (BIA 9-1067)
BIA 9-1067 100 mg	5440	22200	2647
BIA 9-1067 25 mg	4545	22026	776
BIA 9-1067 50 mg	4580	23515	1694
Placebo	3958	22334	NA

Intervention	ng.h/mL (Mean)
	AUC0-6 (levodopa) Baseline	AUC0-6 (levodopa) Test	AUC0-6 (3-OMD) Baseline	AUC0-6 (3-OMD) Test	AUC0-6 (BIA 9-067) Test
BIA 9-1067 15 mg	2734	4044	18748	6685	698
BIA 9-1067 30 mg	3862	6297	34177	9059	1188
BIA 9-1067 5 mg	3451	4041	23934	14883	627
Placebo	2841	2510	23301	21228	NA

Intervention	ng/mL (Mean)
	Cmax (levodopa) Baseline	Cmax (levodopa) Test	Cmax (3-OMD) Baseline	Cmax (3-OMD) Test	Cmax (BIA 9-067) Test
BIA 9-1067 15 mg	1753	1806	3529	1197	233
BIA 9-1067 30 mg	1832	2584	6222	1603	480
BIA 9-1067 5 mg	1446	1868	4631	2633	240
Placebo	1484	1203	4701	3770	NA