TargetMol
Eprenetapopt (PRIMA-1Met) restores wild-type conformation and function to mutant p53, and triggers apoptosis in tumor cells. PRIMA-1MET also targets the selenoprotein thioredoxin reductase 1 (TrxR1), a key regulator of cellular redox balance.
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TargetMol
Eprenetapopt (PRIMA-1Met) restores wild-type conformation and function to mutant p53, and triggers apoptosis in tumor cells. PRIMA-1MET also targets the selenoprotein thioredoxin reductase 1 (TrxR1), a key regulator of cellular redox balance.
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Elafibranor
100 mg
| Purity Not Available
TargetMol
Elafibranor is an agonist of the peroxisome proliferator-activated receptor-α (PPAR-α) and peroxisome proliferator-activated receptor-δ (PPAR-δ) with EC50 values of 45 and 175 nM, respectively.
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Elafibranor
25 mg
| Purity Not Available
TargetMol
Elafibranor is an agonist of the peroxisome proliferator-activated receptor-α (PPAR-α) and peroxisome proliferator-activated receptor-δ (PPAR-δ) with EC50 values of 45 and 175 nM, respectively.
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Elafibranor
10 mg
| Purity Not Available
TargetMol
Elafibranor is an agonist of the peroxisome proliferator-activated receptor-α (PPAR-α) and peroxisome proliferator-activated receptor-δ (PPAR-δ) with EC50 values of 45 and 175 nM, respectively.
More Information
Supplier Page
TargetMol
Eprenetapopt (PRIMA-1Met) restores wild-type conformation and function to mutant p53, and triggers apoptosis in tumor cells. PRIMA-1MET also targets the selenoprotein thioredoxin reductase 1 (TrxR1), a key regulator of cellular redox balance.
More Information
Supplier Page
TargetMol
Eprenetapopt (PRIMA-1Met) restores wild-type conformation and function to mutant p53, and triggers apoptosis in tumor cells. PRIMA-1MET also targets the selenoprotein thioredoxin reductase 1 (TrxR1), a key regulator of cellular redox balance.
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TargetMol
UAMC00039 dihydrochloride is a potent, reversible and competitive dipeptidyl peptidase II inhibitor with an IC50 of 0.48 nM.
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TargetMol
CEP-18770 is an orally active inhibitor of the chymotrypsin-like activity of proteasome (IC50: 3.8 nM). It only marginally inhibits the tryptic and peptidylglutamyl activities of the proteosome.
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TargetMol
Clozapine N-oxide is a major metabolite of clozapine that can be detected in the earliest excretion time interval after clozapine administration [1]. It is produced by the action of cytochrome P450 (CYP) isoforms CYP1A2 and CYP3A4, whose activities, in turn, can be affected by drugs and disease [2]. Clozapine N-oxide is normally biologically inactive. However, […]
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