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ω-Conotoxin MVIIA

SNX-111, Omega-conotoxin MVIIA, Ziconotide

A Specific Blocker of CaV2.2 Channel

Cat #: C-670
Alternative Name SNX-111, Omega-conotoxin MVIIA, Ziconotide
Lyophilized Powder yes
  • Bioassay Tested
  • Origin Synthetic peptide
    MW: 2639.2 Da
    Purity: >99% (HPLC)
    Effective concentration 100 nM - 2 µM.
    Modifications Disulfide bonds between Cys1-Cys16, Cys8-Cys20 and Cys15-Cys25. Cys25 - C-terminal amidation.
    Molecular formula C102H172N36O32S7.
    CAS No.: 107452-89-1
    Activity ω-Conotoxin MVIIA specifically blocks N-type CaV channels1 and also inhibits K+-induced 3H-GABA release in the hippocampus in vivo2.
    1. Olivera, B.M. et al. (1987) Biochemistry 26, 2086.
    2. Newcomb, R. et al. (1994) Brain. Res638, 95.
    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 Any aqueous buffer. Centrifuge all product preparations before use (10000 x g 5 min).
    Storage of solutions Up to two weeks at 4°C or six months at -20°C.
    Our bioassay
    • Alomone Labs ω-Conotoxin MVIIA inhibits CaV2.2 heterologously expressed in Xenopus oocytes.
      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).
    References - Scientific background
    1. Olivera, B.M. et al. (1987) Biochemistry 26, 2086.
    2. Luchian, T. (2001) Biochim. Biophys. Acta. 1512, 329.
    3. Stocker, J.W. et al. (1997) J. Neurosci 17, 3002.
    4. Newcomb, R. et al. (1994) Brain. Res638, 95.
    5. Vega, T. et al. (1995) Eur. J. Pharmacol. 276, 231.
    6. Hirata, H. et al. (1997) Eur. J. Pharmacol. 321, 217.
    7. Sanger, G.J. et al. (2000) Eur. J. Pharmacol. 388, 89.
    8. Stoehr, S.J. et al. (1993) Neurosci. Lett. 161, 113.
    9. Feng, Z.P. et al. (2001) J. Biol. Chem276, 15278.
    Scientific background

    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 morphine. This is the first ion channel blocker to be marketed for pain.

    Target CaV2.2 Ca2+ channel
    Peptide Content: 100%
    Last update: 09/11/2022

    ω-Conotoxin MVIIA (#C-670) is a highly pure, synthetic, and biologically active peptide toxin.

    For research purposes only, not for human use



    Product citations
    1. Gao, S. et al. (2021) Nature 596, 143.
    2. Lv, P. et al. (2012) J. Neurosci. 32, 16314.
    3. Boesmans, W. et al. (2008) Gut 57, 314.
    4. Grimm, C. et al. (2008) Neurosci. Lett. 442, 44.
    5. Kim, S. et al. (2008) Biochem. Biophys. Res. Commun. 365, 399.
    6. Nimmrich, V. et al. (2008) J. Neurosci. 28, 788.


    Scientific Background

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