L-type Ca++ CP α1C Inhibitors
L-type calcium channel (Ca++) CP α1C inhibitors belong to a specific class of chemical compounds that exert their effects on the α1C subunit of L-type calcium channels. These calcium channels are integral membrane proteins found in various tissues, including cardiac and smooth muscle cells, as well as neurons. They play a pivotal role in regulating calcium ion influx into cells, thereby influencing processes such as muscle contraction, neurotransmitter release, and gene expression. The α1C subunit, also known as Cav1.2, is a critical component of these channels, and its inhibition can have profound physiological consequences.
L-type Ca++ CP α1C inhibitors are designed to selectively target and modulate the activity of the α1C subunit, ultimately affecting the function of L-type calcium channels. By binding to specific sites on this subunit, these inhibitors can either block or regulate the flow of calcium ions through the channels. This modulation of calcium ion influx can have widespread implications in various physiological systems, including the cardiovascular and nervous systems. Inhibition of α1C subunit activity can lead to alterations in cardiac muscle contraction, vascular tone, and neuronal excitability, depending on the specific context and distribution of these channels in different tissues. Understanding the mechanisms by which L-type Ca++ CP α1C inhibitors interact with their target can provide valuable insights into the regulation of calcium signaling and its potential impact on cellular physiology and function. These inhibitors are thus vital tools for researchers seeking to unravel the intricacies of calcium channel function and its role in health and disease.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Nifedipine | 21829-25-4 | sc-3589 sc-3589A | 1 g 5 g | $59.00 $173.00 | 15 | |
Nifedipine blocks CaV1.2 channels by binding to the channel's α1C subunit, inhibiting calcium influx into cardiac and smooth muscle cells, leading to vasodilation and decreased contractility. | ||||||
Verapamil | 52-53-9 | sc-507373 | 1 g | $374.00 | ||
Verapamil inhibits CaV1.2 channels by binding to the channel's α1C subunit, blocking calcium entry, and reducing cardiac contractility and vascular tone. | ||||||
Diltiazem | 42399-41-7 | sc-204726 sc-204726A | 1 g 5 g | $209.00 $464.00 | 4 | |
Diltiazem acts as a CaV1.2 inhibitor by binding to the channel's α1C subunit, thereby reducing calcium influx and relaxing both cardiac and smooth muscle. | ||||||
Amlodipine | 88150-42-9 | sc-200195 sc-200195A | 100 mg 1 g | $74.00 $166.00 | 2 | |
Amlodipine selectively inhibits CaV1.2 channels in vascular smooth muscle, reducing calcium entry and causing vasodilation. | ||||||
Isradipine | 75695-93-1 | sc-201467 sc-201467A | 10 mg 50 mg | $88.00 $324.00 | 1 | |
Isradipine inhibits CaV1.2 channels, particularly in vascular smooth muscle cells, leading to vasodilation and reduced blood pressure. | ||||||
Felodipine | 72509-76-3 | sc-201483 sc-201483A | 10 mg 50 mg | $91.00 $222.00 | 1 | |
Felodipine blocks CaV1.2 channels in vascular smooth muscle, reducing calcium entry and causing relaxation of blood vessels. | ||||||
trans Lacidipine | 103890-78-4 | sc-213066 | 10 mg | $153.00 | ||
Lacidipine inhibits CaV1.2 channels in vascular smooth muscle, leading to vasodilation and reduced peripheral resistance. | ||||||
Bepridil | 64706-54-3 | sc-507400 | 100 mg | $1620.00 | ||
Bepridil blocks CaV1.2 channels by binding to the α1C subunit, inhibiting calcium influx, and exerting anti-arrhythmic and vasodilatory effects. | ||||||
Manidipine | 89226-50-6 | sc-211774 | 10 mg | $278.00 | ||
Manidipine inhibits CaV1.2 channels in vascular smooth muscle, resulting in vasodilation and reduced blood pressure. | ||||||
Nimodipine | 66085-59-4 | sc-201464 sc-201464A | 100 mg 1 g | $61.00 $307.00 | 2 | |
Nimodipine selectively inhibits CaV1.2 channels in cerebral blood vessels, preventing calcium influx and protecting against vasospasm after subarachnoid hemorrhage. | ||||||