Overview
Veratridine (#V-110) is a highly pure, natural, and biologically active compound.
Structure
For research purposes only, not for human use
Applications
Citations (14)
Citations
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- Deuis, J.R. et al. (2016) Toxins 8, 78.
Specifications
Properties
Technical Specifications
Origin Veratrum officinale.
MW 673.8
Purity >98%
Molecular formula C36H51NO11.
CAS No. 71-62-5
Source Natural
Chemical name 4α,9-Epoxy-3β-veratroyloxy-5β-cevan-4β,12,14,16β,17,20-hexaol.
Biological Activity
Target Various NaV Na+ channels
Effective concentration 1-200 μM.
Activity Veratridine is an alkaloid which is a potent modulator of voltage-dependent Na+ channels and hence, of transmitter release1,2. Veratridine reduces the single channel conductance and increases the persistent opening probability3.
References
- Catterall, W.A. (1975) J. Biol. Chem. 250, 4053.
- Blaustein, M.P. (1975) J. Physiol. 247, 617.
- Wang, G.K. and Wang, S.Y. (2003) J. Physiol. 548, 667.
Solubility and Storage
Shipping and storage Shipped at room temperature. Product as supplied can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.
Solubility DMSO. Centrifuge all product preparations before use (10000 x g 5 min).
Storage of solutions Up to four weeks at 4°C or three months at -20°C.
Scientific Background
References
Scientific background Veratridine is an alkaloid extracted from the Veratrum officinale plant. It is a potent modulator of voltage-dependent Na+ channels and hence, of transmitter release1,2. Veratridine reduces the single channel conductance and increases the persistent opening probability of NaV1.4 channels expressed in a mammalian cell line3. Veratridine affects differentially the TTX-sensitive and TTX-resistant components of NaV currents in rat DRG neurons. Although veratridine inhibits both components at the peak current, it is much more effective in increasing the persistent component (channel opening) of the TTX-sensitive current4. Veratridine is widely used in different excitable preparations to induce NaV channel dependent transmitter release (see for example reference #5).
References
- Catterall, W.A. (1975) J. Biol. Chem. 250, 4053.
- Blaustein, M.P. (1975) J. Physiol. 247, 617.
- Wang, G.K. and Wang, S.Y. (2003) J. Physiol. 548, 667.
- Farrag, K.J. et al. (2007) Pflugers Arch. Eur. J. Physiol. 455, 929.
- Westphalen, R.I. et al. (2011) Neuropharmacology 61, 699.
Last Update: 08/01/2025
