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The **Voltage-gated L-type calcium channel alpha-1C subunit (CaV1.2)** is the main subunit forming the L-type calcium channel, a voltage-gated ion channel widely expressed in cardiac, smooth, and some neuronal tissue[5][7]. L-type calcium channels are responsible for the slow, long-lasting inward calcium current during the action potential, mediating calcium influx critical for the contraction of cardiac and smooth muscle, regulation of heart rate, and triggering other calcium-dependent signaling pathways[1][3][6]. These channels play important roles in the cardiovascular system and are implicated in multiple cardiovascular pathologies including hypertension, arrhythmias, and angina pectoris[6]. **Diltiazem** is a benzothiazepine class drug that acts as a selective inhibitor of L-type calcium channels by binding to the central cavity of the channel's pore, physically blocking calcium ion conduction[2][3]. This blockade leads to decreased intracellular calcium in cardiac and smooth muscle cells, resulting in reduced contractility (negative inotropy), lower heart rate (negative chronotropy), arterial vasodilation, and clinical benefit in arrhythmia, hypertension, and angina[2][3][1]. Diltiazem can interact allosterically with other channel blockers (such as dihydropyridines and phenylalkylamines), and its site overlaps with those of other calcium channel antagonists[2]. Notably, the target entry is incorrectly specified as "Diltiazem on L-type calcium channel"—the correct target is the L-type calcium channel itself, not the drug-channel combination[2][5][7]. Key clinical concerns for drugs targeting this channel include bradycardia, hypotension, heart block, worsening of heart failure, and substantial drug-drug interaction potential—especially via CYP3A4 inhibition by diltiazem[3]. No established biomarkers for patient selection or efficacy are clearly described in current results. The **canonical form** for this target is "Voltage-gated L-type calcium channel alpha-1C subunit (Cav1.2)", often referred to by its gene symbol CACNA1C[5].
Inhibition of calcium influx, Blockade of voltage-gated calcium channels, Negative inotropy, Negative chronotropy, Vasodilation
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