CYP2C9 Polymorphism is not a Major Determinant of Bosentan Exposure in Healthy Volunteers

Clinical Pharmacology and Therapeutics

Volumn 95, Issue 3, 2014, Pages 250-251

  Markert, C ^a   Burhenne, J ^a   Weiss, J ^a   Mikus, G ^a   Haefeli, W E ^a  

^a UNIVERSITY OF HEIDELBERG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ARYL HYDROCARBON HYDROXYLASES; DRUG-INDUCED LIVER INJURY; FEMALE; HUMANS; HYPERTENSION, PULMONARY; MALE; RECEPTORS, ENDOTHELIN; SULFONAMIDES;

EID: 84894486504     PISSN: 00099236     EISSN: 15326535     Source Type: Journal    
DOI: 10.1038/clpt.2013.188     Document Type: Letter

References (5)

1. Markova, S.M. et al. Association of CYP2C9*2 with bosentan-induced liver injury. Clin. Pharmacol. Ther. 94, 653-661 (2013).
2. Markert, C. et al. Clarithromycin substantially increases steady-state bosentan exposure in healthy volunteers. Br. J. Clin. Pharmacol. (2013); e-pub ahead of print 6 June 2013.
3. Dingemanse, J. & van Giersbergen, P.L. Clinical pharmacology of bosentan, a dual endothelin receptor antagonist. Clin. Pharmacokinet. 43, 1089-1115 (2004).
4. Chaudhry, A.S. et al. CYP2C9*1B promoter polymorphisms, in linkage with CYP2C19*2, affect phenytoin autoinduction of clearance and maintenance dose. J. Pharmacol. Exp. Ther. 332, 599-611 (2010).
5. Fattinger, K. et al. The endothelin antagonist bosentan inhibits the canalicular bile salt export pump: a potential mechanism for hepatic adverse reactions. Clin. Pharmacol. Ther. 69, 223-231 (2001).