Every lot is tried & tested in a relevant biological assay.
Our Bioassay
- 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.
- Findeisen, F. et al. (2010) Channels (Austin) 4, 459.
- Godfraind, T. (2005) Philos. Trans. R. Soc. Lond. B. Biol. Sci. 360, 2259.
- Clunn, G.F. et al. (2010) Int. J. Cardiol. 139, 2.
- Furukawa, T. et al. (2009) Eur. J. Pharmacol. 613, 100.
- Hayashi, K. et al. (2010) Keio. J. Med. 59, 74.
- Zhu, H.L. et al. (2006) Br. J. Pharmacol. 149, 786.
- Li, D. et al. (2012) Chem. Pharm. Bull. 60, 995.
- 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.
Azelnidipine (#A-135) is a highly pure, synthetic, and biologically active compound.
Applications
Specifications
Scientific Background
Citations
Related Products
Antibodies
- 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 Fluor-594 Antibody (#ACC-021-AR)
- Anti-CaV3.2 (CACNA1H) Antibody (#ACC-025)
Pharmacological tools
Resources
Need Help With This Product?
Our reagent specialists are here to help you find the best product for your application. Please call or email us and we will be happy to help you find the right product for the job.
Call us at
+972 2587 2202 or Email Us