BUY Azelnidipine

Both L-type (Ca_V1) and T-type (Ca_V3) voltage gated Ca²⁺ channels are large (~0.5 MDa), transmembrane proteins which control the cellular influx of Ca²⁺ in response to electrical stimulus; while CaV1s require a strong depolarization (~+40 mV) to perform, a much weaker pulse (~-40 mV) is sufficient to activate Ca_V3s. Ca²⁺ channel blockers (CCBs) are a diverse class of pharmaceutical agents, usually targeting L-type channels, of which dihydropyridines (DHPs) constitute a major subgroup. Inhibitors of Ca²⁺-mediated smooth muscle contractions, CCBs produce vasodilation, thus therapeutically managing hypertension and coronary heart disease. An antagonist of both Ca_V1 (all subtypes) and Ca_V3 ((A)_1G and (A)_1H subtypes), azelnidipine (AZL) is a DHP derivate known to target Ca_Vs with an IC₅₀ of 3 nM. Its long-lasting interaction at multiple binding sites of L-type Ca²⁺ channels renders it resistant to S(-)-Bay K 8644 (Ca_V1 channel agonist) activating effects, otherwise shown to counteract nifedipine-induced inhibition; AZL thus confers significantly prolonged cardioactive time. Its reduced side effects and improved cardiovagal baroreflex sensitivity (BRS) when clinically administered make ALZ's therapeutic benefits superior to that of the potent antihypertensive, amlodipine. Additionally, ALZ possesses hydragogue, heart-protective, kidney-protective, and anti-arteriosclerosis capabilities.