Bepridil (hydrochloride)

Bepridil is a dihydropyridine that has anti-anginal and anti-arrhythmic actions by blocking calcium channels in heart and smooth muscle.^1,2 It is recognized as a non-selective channel blocker, altering myocardial Ca²⁺, Na⁺, and K⁺ currents.³ For example, it blocks voltage-gated Ca²⁺ (Ca_v3.2) and K⁺ (hERG and KCNQ4) channels, sarcoplasmic ATP-sensitive K⁺ (K_ATP) channels, and Na⁺-activated (K_Na) channels (IC₅₀s = 7.1, 22, 9.4, 10, and 2.2 µM, respectively).^4,5,6,2 It also activates mitochondrial ATP-sensitive K_ATP channels (ED₅₀ = 27.5 µM).⁷

≥98%

Store at -20℃

1.Singh, B.N. The mechanism of action of calcium antagonists relative to their clinical applications. Br. J. Clin. Pharmacol. 21, 109S-121S (1986).

2.Perez-Reyes, E.,Van Deusen, A.L. and Vitko, I. Molecular pharmacology of human Ca_v3.2 T-type Ca²⁺ channels: Block by antihypertensives, antiarrhythmics, and their analogs. Journal of Pharmacology and Experimental Therapeutics 328(2), 621-627 (2009).

3.Iijima, K.,Chinushi, M.,Izumi, D., et al. Effect of bepridil in atrial fibrillation inducibility facilitated by vagal nerve stimulation. Prevention of vagal nerve activation-induced shortening of the atrial action potential duration. Circulation Journal 74(5), 895-902 (2010).

4.Sinha, N. and Sen, S. Predicting hERG activities of compounds from their 3D structures: Development and evaluation of a global descriptors based QSAR model. European Journal of Medicinal Chemistry 46(2), 618-630 (2011).

5.Sogaard, R.,Ljungstrom, T.,Pedersen, K.A., et al. KCNQ4 channels expressed in mammalian cells: Functional characteristics and pharmacology. American Journal of Physiology.Cell Physiology 280(4), C859-C866 (2001).

6.Li, Y.,Sato, T. and Arita, M. Bepridil blunts the shortening of action potential duration caused by metabolic inhibition via blockade of ATP-sensitive K⁺ channels and Na⁺-activated K⁺ channels. Journal of Pharmacology and Experimental Therapeutics 291(2), 562-568 (1999).

7.Sato, T.,Costa, A.D.T.,Saito, T., et al. Bepridil, an antiarrhythmic drug, opens mitochondrial KATP channels, blocks sarcolemmal KATP channels, and confers cardioprotection. Journal of Pharmacology and Experimental Therapeutics 316(1), 182-188 (2006).