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- Alomone Labs Nimodipine blocks L-type Ca2+ currents in Xenopus oocytes.A. Time course of L-type channel (CaV1.2+α2δ1+β1a) activity before and during applications of 10 μM Nimodipine (#N-150) (green) and upon wash. Holding potential was -80 mV and currents were elicited every 10 seconds by 100 ms ramp to +50 mV. B. Superimposed example current traces (plotted against the corresponding ramp voltage) before and during application of 10 μM Nimodipine in green (taken from the experiment described in A).
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- 4. Xu, W. and Lipscombe, D. (2001) J. Neurosci. 21, 5944.
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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 affinity1-3. Nimodipine is a strongly selective L-type Ca2+ channel blocker, with IC50 of 139 nM for CaV1.2 channel currents in Xenopus oocytes4. At 1 µm, Nimodipine inhibits 90% of the CaV1.2 channel current at voltages between -20 and +40 mV4.
Ca2+ antagonists block Ca2+ entry into cells, resulting in relaxation of smooth muscle and limitation of the cytotoxic effects of ischaemia in various organ systems. They are most frequently used for clinical conditions requiring vasodilatation, i.e. hypertension and Raynaud's phenomenon. Other uses include treatment of supraventricular arrhythmias and angina. Nimodipine has been approved for treating vasospasm after subarachnoid haemorrhage5.
Cytosolic free Ca2+ increases with ageing and since this increase may be mediated by the voltage operated L-type Ca2+ channel on the neuronal cell body, chronic treatment with an L-channel blocker, like Nimodipine, might palliate the progression of and possibly prevent the majority of cases of Alzheimer’s disease6.
A migraine attack is initiated by a cellular hypoxia that can cause an increase in the flow of calcium into the intracellular space, resulting in calcium overload and cellular dysfunction. Nimodipine exhibits selective effects on cerebral vessels and seems to offer protection against the cerebral ischemia and hypoxia presumed to be operative during migraine attacks and indeed, the frequency and duration of migraine attacks are decreased by at least half in 69% of patients treated with this agent7.
Nimodipine (#N-150) is a highly pure, synthetic, and biologically active compound.
- Anti-CaV1.1 (CACNA1S) (extracellular) Antibody (#ACC-314)
- Anti-CaV1.2 (CACNA1C) Antibody (#ACC-003)
- Anti-CaV1.2 (CACNA1C)-ATTO-488 Antibody (#ACC-003-AG)
- Guinea pig Anti-CaV1.2 (CACNA1C) Antibody (#AGP-001)
- 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-CaV1.3 (CACNA1D) (extracellular) Antibody (#ACC-311)
- Blockers/Antagonists: peptides/peptide toxinsBlockers/Antagonists: small molecules