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Dendrotoxin-I

Venom basic protease inhibitor 1, Dendrotoxin-1, DTX-I, DTX-1

A Potent Blocker of KV1.1 and KV1.2 Channels

Cat #: D-390
Alternative Name Venom basic protease inhibitor 1, Dendrotoxin-1, DTX-I, DTX-1
Lyophilized Powder yes
  • Bioassay Tested
    • Origin Natural peptide isolated from Dendroaspis polylepis polylepis (Black mamba).
    MW: 7149 Da
    Purity: >98% (HPLC)
    Effective concentration 10-100 nM.
    Sequence QPLRKLCILHRNPGRCYQKIPAFYYNQKKKQCEGFTWSGCGGNSNRFKTIEECRRTCIRK.
    Modifications Disulfide bonds between Cys7-Cys57, Cys16-Cys40, and Cys32-Cys53.
    Structure
    Molecular formula C312H497N99O83S6.
    CAS No.: 107950-33-4
    Activity Dendrotoxin-I is a highly selective blocker of voltage-gated K+ channels (KV1.1 and KV1.2), as well as heteromultimeric channels containing these, with other KV1 isoforms1. The inhibition effect is higher in Xenopus oocytes compared to mammalian cells2.
    References-Activity
    1. Hopkins, W.F. (1998) J. Pharmacol. Exp. Therap. 285, 1051.
    2. Harvey, A.L. (2001) Toxicon 39, 15.
    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 one week at 4°C or three months at -20°C.
    Our bioassay
    • Alomone Labs Dendrotoxin-I inhibits KV1.1 and KV1.2 channel currents heterologously expressed in Xenopus oocytes.
      Alomone Labs Dendrotoxin-I inhibits KV1.1 and KV1.2 channel currents heterologously expressed in Xenopus oocytes.
      KV1.1 (left, in 2 mM K+) and KV1.2 (right, in 5 mM K+) channel currents, elicited by 200 ms depolarization from holding potential of -100 mV to +20 mV, before and during application of 100 nM Dendrotoxin-I (#D-390). 92% (n = 4) of the KV1.1 and 84% (n = 4) of the KV1.2 channels currents were inhibited by 100 nM Dendrotoxin-I, respectively.
    References - Scientific background
    1. Schweitz, H. et al. (1990) Toxicon 28, 847.
    2. Hopkins, W.F. (1998) J. Pharmacol. Exp. Therap. 285, 1051.
    3. Harvey, A.L. (2001) Toxicon 39, 15.
    Scientific background

    Dendrotoxin-I is isolated from Dendroaspis p.polylepis snake venom by modification of the procedure of Schweitz1 and purified to homogeneity.

    Dendrotoxin-I blocks KV1.2 and KV1.1 channels (IC50=0.13 and 3.1 nM in oocytes respectively, with higher values for mammalian cells)3 as well as heteromultimeric channels containing these, with other KV1 isoforms2 (for review see 3).

    Target KV1.1, KV1.2 K+ channels
    Peptide Content: 100%
    Lyophilized Powder
    Image & Title Dendrotoxin-I
    Alomone Labs Dendrotoxin-I shifts the resting potential of avian high characteristic frequency region of nucleus magnocellularis neurons.Voltage responses of a high characteristic frequency (CF) neuron in control (left panel) and in presence of Dendrotoxin-I (#D-390), (right panel). Application of Dendrotoxin-I shifts the resting potential from -75 to -64 mV and reduces the threshold current. Neurons show multiple action potentials in the presence of Dendrotoxin-I.Adapted from Fukui, I. and Ohmori, H. (2004) J. Neurosci. 24, 7514. with permission of the Society for Neuroscience.
    Last update: 06/12/2022

    Dendrotoxin-I (#D-390) is a highly pure, natural, and biologically active peptide toxin.

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    For research purposes only, not for human use

    Applications

    Citations

    Citations
    Product citations
    1. Wright, T. et al. (2016) Sci. Rep. 6, 28584.
    2. Sforna, L. et al. (2015) J. Neurophysiol. 113, 2653.
    3. Hardman, R.M. and Forsythe, I.D. (2009) J. Physiol. 587, 2487.
    4. Johnston, J. et al. (2008) Eur. J. Neurosci. 27, 1391.
    5. Johnston, J. et al. (2008) J. Physiol. 586, 3493.
    6. Sinha, K. et al. (2006) J. Neurophysiol. 95, 1683.
    7. Eftekharpour, E. et al. (2005) Exp. Neurol. 193, 334.
    8. Shibukawa, Y. et al. (2005) Biophys. J. 88, 3924.
    9. Svirskis, G. et al. (2004) J. Neurophysiol. 91, 2465.
    10. Svirskis, G. et al. (2002) J. Neurosci. 22, 11019.
    11. Monsivais, P and Rubel, E.W. (2001) J. Neurosci. 21, 7823.
    12. Petersson, J. et al. (1997) Br. J. Pharmacol. 120, 1344.

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