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ω-Conotoxin MVIIC


A Blocker of Presynaptic CaV (N- and P/Q-Type) Channels

Cat #: C-150
Alternative Name SNX-230
Lyophilized Powder yes
  • Bioassay Tested
  • Origin Synthetic peptide
    MW: 2750 Da
    Purity: >99% (HPLC)
    Effective concentration 50 nM - 1 μM.
    Modifications Disulfide bonds between Cys1-Cys16, Cys8-Cys20 and Cys15-Cys26. Cys26 - C-terminal amidation.
    Molecular formula C106H178N40O32S7.
    CAS No.: 147794-23-8
    Activity ω-Conotoxin MVIIC blocks P/Q- and N-type CaV channels1. ω-Conotoxin MVIIC is also reported to block nicotinic receptors heterologously expressed in Xenopus oocytes with an IC50 of 1.3 μM2.
    1. McDonough, S.I. et al. (1996) J. Neurosci. 16, 2612
    2. Herrero, C.J. et al. (1999) Br. J. Pharmacol. 127, 1375.
    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 three months at -20°C.
    Our bioassay
    • Alomone Labs ω-Conotoxin MVIIC inhibits CaV2.2 heterologously expressed in Xenopus oocytes.
      Alomone Labs ω-Conotoxin MVIIC inhibits CaV2.2 heterologously expressed in Xenopus oocytes.
      A. Time course of ω-Conotoxin MVIIC (#C-150) 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 MVIIC was perfused as indicated by the bar (green) for 160 sec. B. Superimposed examples of CaV2.2 channel peak current in the absence (control) and presence (green) of 50 nM ω-Conotoxin MVIIC (taken from experiment in A).
    References - Scientific background
    1. McDonough, S.I. et al. (1996) J. Neurosci. 16, 2612.
    2. Liu, H. et al. (1996) J. Biol. Chem. 23, 13804.
    3. Stocker, J.W. et al. (1997) J. Neurosci. 17, 3002.
    4. Herrero, C.J. et al. (1999) Br. J. Pharmacol. 127, 1375.
    5. Newcomb, R. and Palma, A. (1994) Brain. Res638, 95.
    6. Vega, T. et al. (1995) Eur. J. Pharmacol. 276, 231.
    7. Hirata, H. et al. (1997) Eur. J. Pharmacol. 321, 217.
    Scientific background

    ω-Conotoxin MVIIC blocks CaV2.11A, P/Q-type) and CaV2.21B, N-type) channels.1 The toxin binds with high affinity to CaV2.1 and with lower affinity to CaV2.2 in rabbit brain.2 However, the block by ω-Conotoxin-MVIIC of N-type channels in DRG neurons developed much faster than the block of P-type currents in Purkinje cells.1 The effect of the toxin is modulated by voltage (i.e. it is more potent for inactivated channels).3

    In addition this toxin was reported to block nicotinic receptors (transiently expressed in Xenopus oocytes) with IC50 of 1.3 µM.4 It was also shown to inhibit K+-induced 3H-GABA release in hippocampus in vivo.5 This effect was with high affinity (50% block, 200 nM). The toxin was used to inhibit synaptic transmission in several peripheral preparations.6,7

    Target N-type and P/Q-type Ca2+ channels
    Peptide Content: 100%
    Image & Title ω-Conotoxin MVIIC
    Alomone Labs ω-Conotoxin MVIIC partially affects [Ca2+]i in nicotine-treated PC12 cells.
    Cells were loaded with fura 2 and incubated without (control) or with 500 nM ω-Conotoxin MVIIC (#C-150). Intracellular Ca2+ was measured at 15 sec intervals before and after addition of nicotine. ω-Conotoxin MVIIC reduced [Ca2+]i in response to nicotine by 65%.Adapted from Gueorguiev, V.D. et al. (1999) Am. J. Physiol. 276, C54. with permission of the American Physiological Society.
    Last update: 21/11/2022

    ω-Conotoxin-MVIIC (#C-150) is a highly pure, synthetic, and biologically active peptide toxin.

    For research purposes only, not for human use



    Product citations
    1. Eltes, T. et al. (2017) J. Neurosci. 37, 1910.
    2. Pollak, J. et al. (2017) PLoS ONE 12, e0172884.
    3. Resch, J.M. et al. (2017) Neuron 96, 190.
    4. Forostyak, O. et al. (2016) Stem Cell Res. 16, 622.
    5. Evans, R.C. et al. (2015) J. Neurophysiol. 113, 2979.
    6. Gerencser, A.A. et al. (2015) Biochem. J. 471, 111.
    7. Perez-Burgos, A. et al. (2014) FASEB J. 28, 3064.
    8. Craviso, G.L. et al. (2010) Cell. Mol. Neurobiol. 30, 1259.
    9. Chu, J.Y. et al. (2009) Proc. Natl. Acad. Sci. U.S.A. 106, 15961.
    10. Chen, S. and Yaari, Y. (2008) J. Physiol. 586, 1351.
    11. Wu, W.W. et al. (2008) J. Neurophysiol. 100, 1897.
    12. Gueorguiev, V.D. et al. (1999) Am. J. Physiol. 276, C54.


    Scientific Background

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