This product is freeze dried. All water molecules have been removed.
Every lot is tried & tested in a relevant biological assay.
- Zhu, H.L. et al. (2006) Br. J. Pharmacol. 149, 786.
- Alomone Labs Azelnidipine inhibits L-type voltage-gated Ca2+ currents heterologously expressed in Xenopus oocytes.A. Time course of CaV1.2/α2-δ1/β2a (L-type) current inhibition by 10 and 100 µM Azelnidipine (#A-135). Currents were elicited by application of voltage steps from a holding potential of -100 mV to 0 mV (100 msec). B. Superimposed example traces of current responses before and during perfusion of 10 and 100 µM Azelnidipine as indicated.
- 1. Findeisen, F. et al. (2010) Channels (Austin) 4, 459.
- 2. Godfraind, T. (2005) Philos. Trans. R. Soc. Lond. B. Biol. Sci. 360, 2259.
- 3. Clunn, G.F. et al. (2010) Int. J. Cardiol. 139, 2.
- 4. Furukawa, T. et al. (2009) Eur. J. Pharmacol. 613, 100.
- 5. Hayashi, K. et al. (2010) Keio. J. Med. 59, 74.
- 6. Zhu, H.L. et al. (2006) Br. J. Pharmacol. 149, 786.
- 7. Li, D. et al. (2012) Chem. Pharm. Bull. 60, 995.
- 8. Eguchi, K. et al. (2007) J. Cardiovasc. Pharmacol. 49, 394.
Both L-type (CaV1) and T-type (CaV3) voltage-gated Ca2+ channels are large (~0.5 MDa), transmembrane proteins which control the cellular influx of Ca2+ in response to electrical stimuli. While CaV1s require a strong depolarization (~+40 mV) to perform, a much weaker pulse (~-40 mV) is sufficient to activate CaV3s1.
Ca2+ channel blockers (CCBs) are a diverse class of pharmaceutical agents, usually targeting L-type channels, of which dihydropyridines (DHPs) constitute a major subgroup2,3. Inhibitors of Ca2+-mediated smooth muscle contractions, CCBs produce vasodilation, thus therapeutically managing hypertension and coronary heart disease2.
An antagonist of both CaV1 (all subtypes) and CaV3 (α1G and α1H subtypes)4, azelnidipine (AZL) is a DHP derivate5 known to target CaVs with an IC50 of 3 nM6. Its long-lasting interaction at multiple binding sites of L-type Ca2+ channels renders it resistant to S(-)-Bay K8644 (CaV1 channel agonist) activating effects, otherwise shown to counteract nifedipine-induced inhibition6; AZL thus confers significantly prolonged cardioactive time7. 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, amlodipine8. Additionally, ALZ possesses hydragogue, heart-protective, kidney-protective, and anti-arteriosclerosis capabilities7.
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Azelnidipine (#A-135) is a highly pure, synthetic, and biologically active compound.
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- Anti-CaV1.1 (CACNA1S) (extracellular) Antibody (#ACC-314)
- Anti-CaV1.2 (CACNA1C) Antibody (#ACC-003)
- Anti-Human CaV1.2 (CACNA1C) Antibody (#ACC-022)
- Anti-CaV1.2a (CACNA1C) Antibody (#ACC-013)
- Anti-CaV1.3 (CACNA1D) Antibody (#ACC-005)
- Guinea pig Anti-CaV1.3 (CACNA1D) Antibody (#AGP-061)
- Anti-CACNA1G (CaV3.1) Antibody (#ACC-021)
- Anti-CACNA1G (CaV3.1)-ATTO-594 Antibody (#ACC-021-AR)
- Anti-CaV3.2 (CACNA1H) Antibody (#ACC-025)
Blockers/Antagonists: small molecules
- Amlodipine besylate (#A-120)
- (R)(+)-Bay K8644 (#B-352)
- Benidipine hydrochloride (#B-120)
- Felodipine (#F-105)
- Isradipine (#I-100)
- L-Ascorbic acid (#L-140)
- Lercanidipine hydrochloride (#L-115)
- ML 218 hydrochloride (#M-166)
- (±)-Naringenin (#N-110)
- Nifedipine (#N-120)
- TTA-A2 (#T-140)
- Verapamil HCl (#V-100)
- CaV1.2 (CACNA1C) Channel Overexpressing Membrane Fraction (#LX-104)
- CaV1.2 (CACNA1C) Channel Antibody and Membrane Fractions Kit (#LK-104A)
- L-Type CaV Channel Blocker Explorer Kit (#EK-103)
- L-Type CaV Channel Antibody Explorer Kit (#AK-215)
- T-Type CaV Channel Blocker Explorer Kit (#EK-111)
- Cardiac Channel Blocker Explorer Kit (#EK-345)
- Cardiac CaV Channel Antibody Explorer Kit (#AK-310)