Literature DB >> 23594227

Pharmacokinetic-pharmacodynamic studies of the 11β-hydroxysteroid dehydrogenase type 1 inhibitor MK-0916 in healthy subjects.

D Hamish Wright1, Julie A Stone, Tami M Crumley, Larissa Wenning, Wei Zheng, Kerri Yan, Amy Yifan Yang, Li Sun, Caroline Cilissen, Steven Ramael, Anne Hermanowski-Vosatka, Ronald B Langdon, Keith M Gottesdiener, John A Wagner, Eseng Lai.   

Abstract

AIMS: To characterize pharmacokinetic parameters of MK-0916 and its safety and tolerability in lean, healthy male subjects following single and multiple oral doses. To assess (by stable-isotope labelling) the in vivo inhibition of cortisone-to-cortisol conversion following oral MK-0916.
METHODS: Data are presented from two randomized, controlled, double-blind, rising-dose phase I studies. In the first study, subjects received single oral doses of 0.4-100 mg MK-0916 (n = 16). In the second study, subjects received 0.2-225 mg MK-0916 followed by daily doses of 0.2-100 mg for 13 days beginning on day 2 or day 15 (n = 80). Plasma and urine drug concentrations were measured for pharmacokinetic analysis. For pharmacodynamic analysis, concentrations of plasma [(13)C4]cortisol were measured by high-pressure liquid chromatography and tandem mass spectrometry following a single oral dose of 5 mg [(13)C4]cortisone.
RESULTS: Doses ≥3 mg were rapidly absorbed (time at which maximal concentration was achieved in plasma, 1.1-1.8 h). Exposure (measured as the area under the concentration-time curve from 0 to 168 h) increased approximately in proportion to dose. Values for the maximal plasma concentration and the plasma concentration at 24 h increased in excess of dose proportionality at doses <6 mg and roughly in proportion to dose at doses >6 mg. In subjects dosed with 6 mg MK-0916 once daily for 14 days, the mean trough plasma concentration was 240 nm and in vivo cortisone-to-cortisol conversion was inhibited by 84%. The relationship between plasma MK-0916 and hepatic 11β-hydroxysteroid dehydrogenase type 1 inhibition was well represented by a simple Emax model with an IC50 of 70.4 nm. Exposure to MK-0916 was generally well tolerated.
CONCLUSIONS: These findings indicate that 11β-hydroxysteroid dehydrogenase type 1 is effectively inhibited in human subjects by doses of MK-0916 that are well tolerated.
© 2013 Merck, Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc.,. Whitehouse Station, NJ, USA. British Journal of Clinical Pharmacology © 2013 The British Pharmacological Society.

Entities:  

Keywords:  11β-hydroxysteroid dehydrogenase type 1; cortisol; cortisone; metabolic syndrome

Mesh:

Substances:

Year:  2013        PMID: 23594227      PMCID: PMC3845315          DOI: 10.1111/bcp.12131

Source DB:  PubMed          Journal:  Br J Clin Pharmacol        ISSN: 0306-5251            Impact factor:   4.335


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