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Clinical data | |
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Pronunciation | /vɒˈrɪnoʊstæt/ vorr-IN-oh-stat |
Trade names | Zolinza |
AHFS/Drugs.com | Monograph |
MedlinePlus | a607050 |
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Routes of administration | Oral (capsules) |
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Pharmacokinetic data | |
Bioavailability | 1.8–11%[1] |
Protein binding | ~71% |
Metabolism | Hepatic glucuronidation and β-oxidation CYP system not involved |
Metabolites | vorinostat O-glucuronide, 4-anilino-4-oxobutanoic acid (both inactive)[2] |
Elimination half-life | ~2 hours (vorinostat and O-glucuronide), 11 hours (4-anilino-4-oxobutanoic acid) |
Excretion | Renal (negligible) |
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ECHA InfoCard | 100.207.822 |
Chemical and physical data | |
Formula | C14H20N2O3 |
Molar mass | 264.325 g·mol−1 |
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Vorinostat (rINN),[3] also known as suberoylanilide hydroxamic acid (suberoyl+anilide+hydroxamic acid abbreviated as SAHA), is a member of a larger class of compounds that inhibit histone deacetylases (HDAC). Histone deacetylase inhibitors (HDI) have a broad spectrum of epigenetic activities.
Vorinostat is marketed under the name Zolinza (/zoʊˈlɪnzə/ zoh-LIN-zə) by Merck for the treatment of cutaneous manifestations in patients with cutaneous T cell lymphoma (CTCL) when the disease persists, gets worse, or comes back during or after two systemic therapies.[2][4] The compound was developed by Columbia University chemist Ronald Breslow and Memorial Sloan-Kettering researcher Paul Marks.[5][6]
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