Description
ω-Conotoxin MVIID is a potent neurotoxin derived from the venom of marine cone snails, specifically the Conus magus species. This peptide toxin is recognized for its ability to selectively and irreversibly inhibit N-type voltage-gated calcium channels (VGCCs), which play a crucial role in neurotransmitter release in the nervous system. ω-Conotoxin MVIID has a greater discrimination for N-channel subtypes than any other ω-conotoxin variant to date. In addition, ω-conotoxin MVIID has been shown to inhibit voltage-sensitive calcium uptake in synaptosomes. These characteristics make ω-conotoxin MVIID a valuable tool for studying neuronal calcium channel regulation and its potential therapeutic applications.
Specification
| Item | ω-Conotoxin MVIID |
|---|
| Catalog | MC153887082 |
| CAS | 153887-08-2 |
| Molecular Formula | C99H164N42O33S7 |
| Molecular Weight | 2695.08 |
| Purity | >98% |
| Sequence | Cys-Gln-Gly-Arg-Gly-Ala-Ser-Cys-Arg-Lys-Thr-Met-Tyr-Asn-Cys-Cys-Ser-Gly-Ser-Cys-Asn-Arg-Gly-Arg-Cys-NH2 (Disulfide bridge: Cys1-Cys16, Cys8-Cys20, Cys15-Cys25) |
| Sequence Shortening | CQGRGASCRKTMYNCCSGSCNRGRC-NH2 (Disulfide bridge: Cys1-Cys16, Cys8-Cys20, Cys15-Cys25) |
| Length (AA) | 25 |
| Peptide Content | 100% |
| Form | Lyophilized powder |
| Source | Synthetic peptide |
| Storage | Product as supplied can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20 °C. |
| Solubility | Water and saline buffer |
| Storage of Solutions | Store up to two weeks at 4 °C or up to three months at -20 °C. |
Mechanism of Action
ω-Conotoxin MVIID is a potent and selective blocker of N-type VGCCs. Upon binding to the N-type VGCCs, ω-conotoxin MVIID induces a conformational change that prevents the channels from opening in response to membrane depolarization. This inhibition leads to a significant reduction in the influx of calcium ions into presynaptic neurons, which is essential for the release of neurotransmitters. Consequently, the blockade of calcium entry diminishes the release of various neuroactive substances, ultimately resulting in decreased neuronal excitability and modulation of pain pathways. This mechanism underlies its potential therapeutic applications in pain management, particularly in conditions associated with neuropathic pain.
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For Research Use Only. Not for use in diagnostic or therapeutic procedures.
