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- Hu, H. and Marban, E. (1998) Mol. Pharmacol. 53, 902.
- Wei, X. et al. (1995) J. Biol. Chem. 270, 27106.
- Alomone Labs Nisoldipine inhibits CaV1.2 currents expressed in Xenopus oocytes.A. Time course of CaV1.2/α2-δ1/β2a (L-type) current inhibition by 200 and 1000 µM of Nisoldipine (#N-160). 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 200 and 1000 µM Nisoldipine as indicated.
- Furukawa, T. et al. (1999) J. Pharmacol. Exp. Ther. 291, 464.
- Hering, S. et al. (1998) Trends Pharmacol. Sci. 19, 439.
- Hockerman, G.H. et al. (1997) Ann. Rev. Pharmacol. Toxicol. 37, 361.
- Haller, H. (2008) Int. J. Clin. Practice 62, 781.
Native voltage-gated Ca2+ channels (VGCC, CaV) are pharmacologically classified into at least five different subclasses (L-, N-, P-, Q-, and R-type), the characteristics of which are determined by the pore-forming α1 subunit. The subunits CaV1.1-1.4 (α1S, α1C, α1D and α1F) form L-type Ca2+ channels and bind dihydropyridines (DHPs) with high affinity1,2. Nisoldipine, a DHP, is a selective L-type Ca2+ channel blocker.
L-type (CaV1), voltage-gated Ca2+ channels are plasma membrane protein complexes which allow the passage of Ca2+ ions into cells following depolarization of the membrane potential.
L-type channels are widely expressed in cardiac and smooth muscle in which they control contraction and therefore were recognized as a therapeutic target for cardiovascular diseases3,4.
10 nM of nisoldipine completely inhibited L-type currents expressed in HEK-293 cells1. The IC50 value of nisoldipine was 2.2 and 0.084 μM in oocytes injected with α1/β2a and α1/β2a/α2δ, respectively2.
Nisoldipine (#N-160) is a highly pure, synthetic, and biologically active compound.
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