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Famotidine does not induce long QT syndrome: experimental evidence from in vitro and in vivo test systems.

Abstract：

:The effects of famotidine on the cardiac repolarization process were assessed using four different levels of test systems described in the draft stage guideline ICH S7B. A supratherapeutic concentration of famotidine (10(-5) M), which is >8 times higher than C(max) obtained after its therapeutic dose, neither inhibited human ether-a-go-go-related gene (HERG) K(+) current expressed in human embryonic kidney 293 (HEK293) cells nor affected any of the action potential parameters of guinea pig papillary muscles. Therapeutic (0.3 mg/kg, i.v.) to supratherapeutic doses (3-10 mg/kg, i.v.) of famotidine did not affect the repolarization process of the halothane-anesthetized canine model, while only supratherapeutic doses exerted the positive chronotropic, inotropic and dromotropic effects without affecting the mean blood pressure. Moreover, supratherapeutic doses of famotidine (1-10 mg/kg, i.v.) neither induced torsades de pointes nor prolonged QT interval in the canine chronic atrioventricular conduction block model. These results suggest that famotidine possesses no cardiovascular effects at a therapeutic dose, while it may exert cardiostimulatory actions after drug overdoses that might potentiate the proarrhythmic potential of co-administered cardiotonic agents by increasing the intracellular Ca(2+) concentration.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Sugiyama A,Satoh Y,Takahara A,Nakamura Y,Shimizu-Sasamata M,Sato S,Miyata K,Hashimoto K

doi

10.1016/s0014-2999(03)01559-0

keywords:

subject

Has Abstract

pub_date

2003-04-11 00:00:00

pages

137-46

issue

1-2

eissn

0014-2999

issn

1879-0712

pii

S0014299903015590

journal_volume

466

pub_type

杂志文章

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