Overview
- Olivera, B.M. et al. (1987) Biochemistry 26, 2086.
- Newcomb, R. et al. (1994) Brain. Res. 638, 95.
Alomone Labs ω-Conotoxin MVIIA inhibits CaV2.2 heterologously expressed in Xenopus oocytes.A. Time course of ω-Conotoxin MVIIA (#C-670) blocking action on CaV2.2 channels maximum current (expressing α1B + α2δ1 + β1 subunits). Maximum current amplitudes were plotted as a function of time. Membrane potential was held at -100 mV and oocytes were stimulated by a 100 ms voltage ramp to 60 mV. 50 nM ω-Conotoxin MVIIA was perfused as indicated by the bar (green) for 180 sec. B. Superimposed examples of CaV2.2 channel peak current in the absence (control) and presence (green) of 50 nM ω-Conotoxin MVIIA (taken from the experiment in A).
ω-Conotoxin MVIIA is a synthetic peptidyl toxin originally isolated from Conus magus snail venom. ω-Conotoxin MVIIA specifically blocks CaV2.2 (α1B, N-type) channels1. The effect of the toxin is modulated by CaVβ auxiliary subunit2 and by voltage (i.e. it is more potent for inactivated channels)3.
ω-Conotoxin MVIIA inhibits K+-induced 3H-GABA release in hippocampus in vivo4. This effect was with high affinity (50% block, 200 nM). The toxin was used to inhibit synaptic transmission in several peripheral preparations5,6,7. The toxin binds with high affinity to rat neocortical membranes8. It blocked cloned CaV2.2 channels transiently expressed in tsa-2019 and in Xenopus oocytes3.
The FDA recently approved Prialt (synthetic ω-Conotoxin MVIIA) to treat severe chronic pain in patients who are intolerant of or refractory to other treatments such as systemic analgesics or other pain medication such as opiates. This is the first ion channel blocker to be marketed for pain.
