Page last updated: 2024-11-06

remacemide

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

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

Cross-References

ID SourceID
PubMed CID60511
CHEMBL ID25843
CHEBI ID91654
SCHEMBL ID151148
MeSH IDM0185124

Synonyms (68)

Synonym
128298-28-2
BRD-A36074203-003-03-5
fpl-12944aa
2-amino-n-(1-methyl-1,2-diphenylethyl)acetamide
acetamide, 2-amino-n-(1-methyl-1,2-diphenylethyl)-, (+-)-
acetamide, 2-amino-n-(1-methyl-1,2-diphenylethyl)-, (-)-
fpl 12924
(+-)-2-amino-n-(1-methyl-1,2-diphenylethyl)acetamide
fpl 14145
(+)-2-amino-n-(1-methyl-1,2-diphenylethyl)acetamide
remacemide
acetamide, 2-amino-n-(1-methyl-1,2-diphenylethyl)-, (+)-
pr 934-423
pr1032-646
pr 1032-644
(-)-2-amino-n-(1-methyl-1,2-diphenylethyl)acetamide
remacemide [inn]
remacemida [inn-spanish]
fpl 14144
pr-934-423
remacemidum [inn-latin]
ar-r-12924
fpl-12924
CHEMBL25843
pr-934423a
2-amino-n-(1,2-diphenylpropan-2-yl)acetamide
A805806
2-azanyl-n-(1,2-diphenylpropan-2-yl)ethanamide
ramacemide
remacemida
unii-eh6763c1ic
remacemidum
eh6763c1ic ,
sve7vvm49x ,
unii-sve7vvm49x
unii-y65k7hq8fu
118754-12-4
118754-14-6
remacemide, (+)-
y65k7hq8fu ,
remacemide, (-)-
n-(1,2-diphenylpropan-2-yl)glycinamide
STL371204
SCHEMBL151148
(+/-)-2-amino-n-(1-methyl-1,2-diphenylethyl)acetamide
remacemide [who-dd]
135252-01-6
2-amino-n-(1,2-di(phenyl)propan-2-yl)acetamide
acetamide, 2-amino-n-(1-methyl-1,2-diphenylethyl)-, (+/-)-
acetamide, 2-amino-n-(1-methyl-1,2-diphenylethyl)-
(+/-)-remacemide
n-(1-methyl-1,2-diphenylethyl)glycinamide
remacemide [mi]
AKOS025247578
DTXSID6048250
ar-r 12924
(.+/-.)-remacemide
2-amino-n-(1,2-diphenyl-1-methylethyl)acetamide
YSGASDXSLKIKOD-UHFFFAOYSA-N
CHEBI:91654
FT-0721535
DB06458
Q7311505
fpl-14144
pr-1032-646
pr-1032-644
fpl-14145
DTXSID601030460

Research Excerpts

Overview

Remacemide (RMC) is a non-competitive, low-affinity N-methyl-D-aspartate (NMDA) receptor antagonist that does not cause the behavioural and neuropathological side effects seen with other NMDA receptor antagonists. It is a safe and tolerable adjunct to dopaminergic therapy for patients with PD and motor fluctuations.

ExcerptReferenceRelevance
"Remacemide hydrochloride is a low-affinity NMDA receptor blocker as well as Na(+) fast-channel blocker."( Remacemide--a novel potential antiepileptic drug.
Borowicz, KK; Czuczwar, SJ; Kimber-Trojnar, Z; Małek, R; Piskorska, B; Sobieszek, G,
)
2.3
"Remacemide hydrochloride is an anticonvulsant, neuroprotective compound with antagonist activity at the N-methyl-D-aspartate receptor ion channel."( Antiparkinsonian effects of remacemide hydrochloride, a glutamate antagonist, in rodent and primate models of Parkinson's disease.
Eller, RV; Gash, DM; Greenamyre, JT; Kurlan, R; Ovadia, A; Zhang, Z, 1994
)
1.3
"Remacemide hydrochloride is a low affinity NMDA channel blocker that might improve parkinsonian symptoms by modulating glutamatergic overactivity in the basal ganglia or slow worsening by decreasing excitotoxicity."( A multicenter randomized controlled trial of remacemide hydrochloride as monotherapy for PD. Parkinson Study Group.
, 2000
)
1.29
"Remacemide (RMC) is a non-competitive, low-affinity N-methyl-D-aspartate (NMDA) receptor antagonist that does not cause the behavioural and neuropathological side effects seen with other NMDA receptor antagonists. "( Remacemide: current status and clinical applications.
Schachter, SC; Tarsy, D, 2000
)
3.19
"Remacemide is a safe and tolerable adjunct to dopaminergic therapy for patients with PD and motor fluctuations. "( A randomized, controlled trial of remacemide for motor fluctuations in Parkinson's disease.
Adler, C; Alderfer, V; Baker, D; Bardram, K; Bateman-Rodriguez, D; Belden, J; Blasucci, L; Brewer, M; Broshjeit, S; Brown, D; Carrion, A; Casaceli, C; Cha, JH; Chase, T; Colcher, A; Comella, C; Cooper, J; Cox, C; Craun, AM; Davies, R; Day, D; Deleo, A; Dilllon, S; Dingmann, C; Dobson, J; Elmer, L; Factor, S; Fahn, S; Feigin, A; Florack, M; Ford, B; Frey, J; Friedlander, J; Gauger, L; Gray, P; Greenamyre, JT; Grimes, D; Hall, J; Hammerstad, J; Harrison, M; Hauser, R; Hodgeman, K; Holdich, T; Janko, K; Jennings, D; Johnston, L; Kayson, E; Kennedy, L; Lafontaine, AL; Lang, A; Lannon, M; Laroia, N; Leventhal, C; Lew, MF; Lewitt, P; Lloyd, M; Locke, B; Marek, K; Martin, W; Matthews, M; Mazurkiewicz, J; McCree, L; McDermott, J; McDermott, M; McGuire, D; Mistura, K; Miyasaki, J; Newman, S; Nobel, R; Orme, C; Pahwa, R; Panniset, M; Pantella, C; Pearson, N; Penney, J; Read, B; Rexo, L; Rodnitzky, R; Rost, E; Rothenburgh, K; Ruzicka, D; Ryan, P; Schuman, S; Schwid, S; Seeberger, L; Shoulson, I; Shulman, L; Siderowf, A; Siemers, E; Stacy, M; Stone, C; Suchowersky, O; Sulimowicz, K; Tariot, P; Tarsy, D; Tennis, M; Tetrud, J; Watts, A; Wiener, W; Wratni, E, 2001
)
2.03
"Remacemide is a potential anticonvulsant drug with an active metabolite, desglycinyl-remacemide (DGR). "( Differential effects of remacemide and desglycinyl-remacemide on epileptiform burst firing in the rat hippocampal slice.
Brodie, MJ; Santangeli, S; Sills, GJ; Stone, TW, 2002
)
2.06
"Remacemide hydrochloride is a low-affinity, non-competitive NMDA receptor channel blocker under investigation for the treatment of epilepsy. "( Remacemide hydrochloride as an add-on therapy in epilepsy: a randomized, placebo-controlled trial of three dose levels (300, 600 and 800 mg/day) in a B.I.D. regimen.
Blume, WT; Guberman, A; Holdich, TA; Jones, MW; Lee, MA; Pillay, N; Veloso, F; Weaver, DF, 2002
)
3.2
"Remacemide hydrochloride is a low-affinity, non-competitive N-methyl-D-aspartic acid (NMDA) receptor channel blocker, under investigation in epilepsy. "( Remacemide hydrochloride as an add-on therapy in epilepsy: a randomized, placebo-controlled trial of three dose levels (300, 600 and 1200 mg/day) in a Q.I.D. regimen.
Betts, TA; Boddie, HG; Chadwick, DW; Crawford, PM; Holdich, TA; Lindstrom, P; Newman, PK; Soryal, I; Wroe, S, 2002
)
3.2

Effects

Remacemide hydrochloride has been shown to possess anticonvulsant activity in a wide range of animal models of epilepsy with ED50s in the 6-60 mg/kg range, depending on the species and route of administration.

ExcerptReferenceRelevance
"1. Remacemide hydrochloride has been shown to possess anticonvulsant activity in a wide range of animal models of epilepsy with ED50s in the 6-60 mg/kg range, depending on the species and route of administration. "( Remacemide hydrochloride: a novel antiepileptic agent.
Davies, JA, 1997
)
2.36
"Remacemide hydrochloride has demonstrated neuroprotection in animal models of hypoxia and ischemic stroke."( Remacemide hydrochloride: a double-blind, placebo-controlled, safety and tolerability study in patients with acute ischemic stroke.
Dyker, AG; Lees, KR, 1999
)
2.47

Treatment

Treatment with remacemide hydrochloride significantly ameliorated vasospasm (27.3 +/- 5.4%, p < 0.001) The area-under-the-curve for levodopa did not change.

ExcerptReferenceRelevance
"With remacemide treatment, the area-under-the-curve for levodopa did not change."( The impact of remacemide hydrochloride on levodopa concentrations in Parkinson's disease. Parkinson Study Group.
,
)
0.95
"Treatment with remacemide hydrochloride significantly ameliorated vasospasm (27.3 +/- 5.4%, p < 0.001)."( Effect of remacemide hydrochloride on subarachnoid hemorrhage-induced vasospasm in rabbits.
Anderson, DK; Farmer, JB; Lewis, AI; Upputuri, S; Zuccarello, M, 1994
)
1.03

Toxicity

ExcerptReferenceRelevance
" Patient safety was assessed by clinical observation, laboratory tests, and ECGs, while tolerability was assessed by recording adverse events."( Remacemide hydrochloride: a double-blind, placebo-controlled, safety and tolerability study in patients with acute ischemic stroke.
Dyker, AG; Lees, KR, 1999
)
1.75
"The most common adverse events considered by the investigator to be possibly treatment related were related to the central nervous system (CNS), and these events appeared to increase with dose."( Remacemide hydrochloride: a double-blind, placebo-controlled, safety and tolerability study in patients with acute ischemic stroke.
Dyker, AG; Lees, KR, 1999
)
1.75
" Assessments included routine physical examination and laboratory tests, recording of adverse events and seizure frequency, and neuropsychological tests."( Remacemide hydrochloride: a placebo-controlled, one month, double-blind assessment of its safety, tolerability and pharmacokinetics as adjunctive therapy in patients with epilepsy.
Chadwick, D; Crawford, P; Harrison, B; Smith, D, 2000
)
1.75
" The most common adverse events associated with remacemide were nausea, vomiting, dizziness, headache, abnormal vision, and hypokinesia."( A randomized, double-blind, placebo-controlled, ascending-dose tolerability and safety study of remacemide as adjuvant therapy in Parkinson's disease with response fluctuations.
Clarke, CE; Cooper, JA; Holdich, TA,
)
0.61
" Adverse events were similar to those reported in adults, with central nervous system and gastrointestinal events being the most common."( Safety, tolerability, and pharmacokinetics of remacemide in children.
Besag, FM; Blakey, GE; Dean, AD; Newton, RE, 2001
)
0.57

Pharmacokinetics

Remacemide and its desglycinyl metabolite in children is similar to that seen in adult patients. The mean area under the concentration-time curve, peak concentration and pre-dose concentration of VPA were unchanged by remacemides hydrochloride.

ExcerptReferenceRelevance
" Three of the new drugs, gabapentin, topiramate and vigabatrin, are more promising on the basis of their pharmacokinetic features."( Comparative pharmacokinetics of the newer antiepileptic drugs.
Bialer, M, 1993
)
0.29
" The mean area under the concentration-time curve, peak concentration and pre-dose concentration of VPA were unchanged by remacemide hydrochloride in three patients on the higher and in 10 patients on the lower dose of remacemide."( Lack of pharmacokinetic interaction between remacemide hydrochloride and sodium valproate in epileptic patients.
Brodie, MJ; Girvan, J; Jamieson, V; Jones, T; Leach, JP; Richens, A, 1997
)
0.77
"To determine whether there is a pharmacokinetic interaction between the antiepileptic drugs remacemide and phenobarbitone."( Evaluation of a pharmacokinetic interaction between remacemide hydrochloride and phenobarbitone in healthy males.
Blakey, GE; Eadie, MJ; Hooper, WD; Lockton, JA; Manun'Ebo, M, 2001
)
0.78
"Apparent remacemide clearance (CL/F) and elimination half-life values were unchanged after 7 days intake of the drug in the absence of phenobarbitone (1."( Evaluation of a pharmacokinetic interaction between remacemide hydrochloride and phenobarbitone in healthy males.
Blakey, GE; Eadie, MJ; Hooper, WD; Lockton, JA; Manun'Ebo, M, 2001
)
0.98
" The pharmacokinetic profile for remacemide and its desglycinyl metabolite in children is similar to that seen in adult patients."( Safety, tolerability, and pharmacokinetics of remacemide in children.
Besag, FM; Blakey, GE; Dean, AD; Newton, RE, 2001
)
0.85
" In the case of add-on studies, the inconclusive findings may be related to pharmacokinetic interactions between RMD and established antiepileptic drugs."( Influence of cytochrome P450 induction on the pharmacokinetics and pharmacodynamics of remacemide hydrochloride.
Brodie, MJ; Forrest, G; Santangeli, S; Sills, GJ, 2002
)
0.54

Dosage Studied

Remacemide hydrochloride was well tolerated up to a dosage of 300 mg/d on a twice daily schedule. The primary objective was to assess the short-term tolerability and safety of four dosage levels of remacemides.

ExcerptRelevanceReference
" Tolerance to MES was not apparent after 5 days of oral daily dosing of remacemide."( Preclinical profile of remacemide: a novel anticonvulsant effective against maximal electroshock seizures in mice.
Becker, CN; Frankenheim, JM; Garske, GE; Gentile, RJ; Griffith, RC; Napier, JJ; Ordy, JM; Palmer, GC; Stagnitto, ML; Woodhead, JH,
)
0.67
" To examine this further, the levels and activities of the major drug metabolizing cytochrome P450 (CYP) subfamilies (CPY1, CYP2, and CYP3) were monitored in microsomal samples from male Sprague-Dawley rats dosed by gavage with FPL 12924AA (250 mg base."( Induction of rodent hepatic drug-metabolizing enzyme activities by the novel anticonvulsant remacemide hydrochloride.
Clark, B; Cooper, AE; Hall, M; Jordan, MC; Lambert, C; Logan, CJ; Richmond, H; Riley, RJ, 1995
)
0.51
" Plasma concentration profiles of PHT, remacemide, and its active desglycinyl metabolite (ARL12495XX) were determined following single and multiple dosing with remacemide hydrochloride."( Mutual interaction between remacemide hydrochloride and phenytoin.
Brodie, MJ; Girvan, J; Jamieson, V; Jones, T; Leach, JP; Richens, A, 1997
)
0.86
" Plasma concentration profiles of VPA, remacemide, and its active desglycinyl metabolite (ARL12495XX) were determined following single (300 mg) and multiple dosing (150 or 300 mg twice daily) of remacemide hydrochloride for 14 days with a 300-mg final dose."( Lack of pharmacokinetic interaction between remacemide hydrochloride and sodium valproate in epileptic patients.
Brodie, MJ; Girvan, J; Jamieson, V; Jones, T; Leach, JP; Richens, A, 1997
)
0.83
"Patients taking CBZ entered a 4-week run-in period to stabilise their dosage regimen to Tegretol tablets and blinded capsules containing Tegretol tablets."( Adjustment of carbamazepine dose to offset the effects of the interaction with remacemide hydrochloride in a double-blind, multicentre, add-on drug trial (CR2237) in refractory epilepsy.
Jamieson, V; Lucas, SB; Mawer, GE; Wild, JM, 1999
)
0.53
"CBZ dosage reductions ranging from 14 to 50% were required by 63% of patients who received REM."( Adjustment of carbamazepine dose to offset the effects of the interaction with remacemide hydrochloride in a double-blind, multicentre, add-on drug trial (CR2237) in refractory epilepsy.
Jamieson, V; Lucas, SB; Mawer, GE; Wild, JM, 1999
)
0.53
" Blood sampling was included to determine plasma concentrations of remacemide and the desglycinyl metabolite at fixed points during the dosing period."( Remacemide hydrochloride: a double-blind, placebo-controlled, safety and tolerability study in patients with acute ischemic stroke.
Dyker, AG; Lees, KR, 1999
)
1.98
" The primary objective was to assess the short-term tolerability and safety of three dosage levels of remacemide."( A multicenter randomized controlled trial of remacemide hydrochloride as monotherapy for PD. Parkinson Study Group.
, 2000
)
0.78
" Most patients who experienced intolerable side effects on the BID schedule, however, could tolerate the same daily dosage on a QID schedule."( A multicenter randomized controlled trial of remacemide hydrochloride as monotherapy for PD. Parkinson Study Group.
, 2000
)
0.57
" The primary objective was to assess the short-term tolerability and safety of four dosage levels of remacemide during 7 weeks of treatment."( A randomized, controlled trial of remacemide for motor fluctuations in Parkinson's disease.
Adler, C; Alderfer, V; Baker, D; Bardram, K; Bateman-Rodriguez, D; Belden, J; Blasucci, L; Brewer, M; Broshjeit, S; Brown, D; Carrion, A; Casaceli, C; Cha, JH; Chase, T; Colcher, A; Comella, C; Cooper, J; Cox, C; Craun, AM; Davies, R; Day, D; Deleo, A; Dilllon, S; Dingmann, C; Dobson, J; Elmer, L; Factor, S; Fahn, S; Feigin, A; Florack, M; Ford, B; Frey, J; Friedlander, J; Gauger, L; Gray, P; Greenamyre, JT; Grimes, D; Hall, J; Hammerstad, J; Harrison, M; Hauser, R; Hodgeman, K; Holdich, T; Janko, K; Jennings, D; Johnston, L; Kayson, E; Kennedy, L; Lafontaine, AL; Lang, A; Lannon, M; Laroia, N; Leventhal, C; Lew, MF; Lewitt, P; Lloyd, M; Locke, B; Marek, K; Martin, W; Matthews, M; Mazurkiewicz, J; McCree, L; McDermott, J; McDermott, M; McGuire, D; Mistura, K; Miyasaki, J; Newman, S; Nobel, R; Orme, C; Pahwa, R; Panniset, M; Pantella, C; Pearson, N; Penney, J; Read, B; Rexo, L; Rodnitzky, R; Rost, E; Rothenburgh, K; Ruzicka, D; Ryan, P; Schuman, S; Schwid, S; Seeberger, L; Shoulson, I; Shulman, L; Siderowf, A; Siemers, E; Stacy, M; Stone, C; Suchowersky, O; Sulimowicz, K; Tariot, P; Tarsy, D; Tennis, M; Tetrud, J; Watts, A; Wiener, W; Wratni, E, 2001
)
0.81
"Remacemide was well tolerated up to a dosage of 300 mg/d on a twice daily schedule and 600 mg/d on a four times daily schedule."( A randomized, controlled trial of remacemide for motor fluctuations in Parkinson's disease.
Adler, C; Alderfer, V; Baker, D; Bardram, K; Bateman-Rodriguez, D; Belden, J; Blasucci, L; Brewer, M; Broshjeit, S; Brown, D; Carrion, A; Casaceli, C; Cha, JH; Chase, T; Colcher, A; Comella, C; Cooper, J; Cox, C; Craun, AM; Davies, R; Day, D; Deleo, A; Dilllon, S; Dingmann, C; Dobson, J; Elmer, L; Factor, S; Fahn, S; Feigin, A; Florack, M; Ford, B; Frey, J; Friedlander, J; Gauger, L; Gray, P; Greenamyre, JT; Grimes, D; Hall, J; Hammerstad, J; Harrison, M; Hauser, R; Hodgeman, K; Holdich, T; Janko, K; Jennings, D; Johnston, L; Kayson, E; Kennedy, L; Lafontaine, AL; Lang, A; Lannon, M; Laroia, N; Leventhal, C; Lew, MF; Lewitt, P; Lloyd, M; Locke, B; Marek, K; Martin, W; Matthews, M; Mazurkiewicz, J; McCree, L; McDermott, J; McDermott, M; McGuire, D; Mistura, K; Miyasaki, J; Newman, S; Nobel, R; Orme, C; Pahwa, R; Panniset, M; Pantella, C; Pearson, N; Penney, J; Read, B; Rexo, L; Rodnitzky, R; Rost, E; Rothenburgh, K; Ruzicka, D; Ryan, P; Schuman, S; Schwid, S; Seeberger, L; Shoulson, I; Shulman, L; Siderowf, A; Siemers, E; Stacy, M; Stone, C; Suchowersky, O; Sulimowicz, K; Tariot, P; Tarsy, D; Tennis, M; Tetrud, J; Watts, A; Wiener, W; Wratni, E, 2001
)
2.03
" Immediately prior to dosing, 5 days per week (M--F), throughout the 2-year dosing period, an incremental repeated acquisition (IRA) task was used to assess learning and a progressive ratio (PR) task was used to assess motivation."( Differential effects of two NMDA receptor antagonists on cognitive-behavioral development in nonhuman primates I.
Allen, RR; Hammond, TG; Paule, MG; Pearson, EC; Popke, EJ,
)
0.13
" Throughout the 2-year dosing period, a conditioned position responding (CPR) task was used to assess color and position discrimination and a delayed matching-to-sample (DMTS) task was used to assess memory."( Differential effects of two NMDA receptor antagonists on cognitive--behavioral performance in young nonhuman primates II.
Allen, RR; Hammond, TG; Paule, MG; Pearson, EC; Popke, EJ,
)
0.13
"To compare the effects of carbamazepine, remacemide, and placebo on actual driving performance during a 12-day incremental dosing regimen."( A comparative study of the effects of carbamazepine and the NMDA receptor antagonist remacemide on road tracking and car-following performance in actual traffic.
Lamers, J; Lewis, M; Lockton, A; Mobbs, E; Muntjewerff, D; Ramaekers, G; Sanders, N; Verhey, F, 2002
)
0.8
" In general, both drugs were well tolerated and produced no treatment-related effects during 2 years of dosing and assessment."( Assessing the potential toxicity of MK-801 and remacemide: chronic exposure in juvenile rhesus monkeys.
Allen, RR; Fogle, CM; Hammond, TG; Newport, GD; Patton, R; Paule, MG; Pearson, EC; Popke, EJ; Rushing, LG,
)
0.39
" Dosing began at weaning and continued for nine months."( Chronic exposure to NMDA receptor and sodium channel blockers during development in monkeys and rats: long-term effects on cognitive function.
Allen, RR; Fogle, CM; Hammond, TG; Paule, MG; Pearson, EC; Popke, EJ, 2003
)
0.32
" Subsequent dosage adjustments were allowed while maintaining the blind."( The cognitive and psychomotor effects of remacemide and carbamazepine in newly diagnosed epilepsy.
Dean, AD; Edgar, C; Wesnes, KA; Wroe, SJ, 2009
)
0.62
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (1)

ClassDescription
stilbenoidAny olefinic compound characterised by a 1,2-diphenylethylene backbone.
[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 Targets (1)

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Bile salt export pumpHomo sapiens (human)IC50 (µMol)288.10000.11007.190310.0000AID1449628
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (22)

Processvia Protein(s)Taxonomy
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (8)

Processvia Protein(s)Taxonomy
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (12)

Processvia Protein(s)Taxonomy
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (23)

Assay IDTitleYearJournalArticle
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID197754Minimum effective dose (MED) was determined in the rat middle cerebral artery occlusion (MCAO) model of focal stroke of rotarod assay2001Journal of medicinal chemistry, Jan-18, Volume: 44, Issue:2
Medicinal chemistry of neuronal voltage-gated sodium channel blockers.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1449628Inhibition of human BSEP expressed in baculovirus transfected fall armyworm Sf21 cell membranes vesicles assessed as reduction in ATP-dependent [3H]-taurocholate transport into vesicles incubated for 5 mins by Topcount based rapid filtration method2012Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 40, Issue:12
Mitigating the inhibition of human bile salt export pump by drugs: opportunities provided by physicochemical property modulation, in silico modeling, and structural modification.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID185053Neuroprotective activity was determined in the rat middle cerebral artery occlusion (MCAO) model of focal stroke2001Journal of medicinal chemistry, Jan-18, Volume: 44, Issue:2
Medicinal chemistry of neuronal voltage-gated sodium channel blockers.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (81)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's41 (50.62)18.2507
2000's35 (43.21)29.6817
2010's5 (6.17)24.3611
2020's0 (0.00)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 22.74

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be moderate demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index22.74 (24.57)
Research Supply Index4.77 (2.92)
Research Growth Index4.18 (4.65)
Search Engine Demand Index26.67 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (22.74)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials24 (25.81%)5.53%
Reviews14 (15.05%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other55 (59.14%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]