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Sekhar Surapaneni

Researcher at Bristol-Myers Squibb

Publications -  7
Citations -  70

Sekhar Surapaneni is an academic researcher from Bristol-Myers Squibb. The author has contributed to research in topics: Metabolite & Active metabolite. The author has an hindex of 2, co-authored 7 publications receiving 12 citations.

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Absorption, Metabolism, and Excretion, In Vitro Pharmacology, and Clinical Pharmacokinetics of Ozanimod, a Novel Sphingosine 1-Phosphate Receptor Modulator.

TL;DR: Ozanimod was extensively metabolized, with 14 metabolites identified, including two major active metabolites (CC112273 and CC1084037) and one major inactive metabolite (RP101124) in circulation as discussed by the authors.
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Evaluation of iberdomide and cytochrome p450 drug-drug interaction potential in vitro and in a phase 1 study in healthy subjects.

TL;DR: Caution should be taken when coadministering iberdomide with strong CYP3A inducers is not advised, and exploratory assessment of metabolite M12 concentrations demonstrated that CYP 3A is responsible for M12 formation.
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Physiologically based pharmacokinetic modeling to assess metabolic drug-drug interaction risks and inform the drug label for fedratinib

TL;DR: The physiologically based pharmacokinetic (PBPK) model of fedratinib facilitated drug development by identifying DDI potential, optimizing clinical study designs, supporting waivers for clinical studies, and informing drug label claims.
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Excretion balance and pharmacokinetics following a single oral dose of [14C]-fedratinib in healthy subjects

TL;DR: Fedratinib derived radioactivity was primarily excreted in feces following a single oral dose of radiolabeled fedrat inib to healthy subjects, indicating limited distribution of fedratInib and/or its metabolites into red blood cells.
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Impact of fedratinib on the pharmacokinetics of transporter probe substrates using a cocktail approach.

TL;DR: In this paper, the authors evaluated the influence of fedratinib on the pharmacokinetics of digoxin (P-gp substrate), rosuvastatin (OATP1B1/1B3 and BCRP substrate), and metformin (OCT2 and MATE1/2-K substrate).