Blood depressing substance I, Blood depressing substance 1, DeltaKappa-actitoxin-Avd4a
A Blocker of KV3 Channels and a Modulator of NaV Channels
    Cat #: STB-400
    Alternative Name Blood depressing substance I, Blood depressing substance 1, DeltaKappa-actitoxin-Avd4a
  • Lyophilized Powder
  • Bioassay Tested
  • Origin Synthetic peptide
    MW: 4708 Da.
    Purity: >95% (HPLC)
    Effective concentration 100 nM - 5 µM.
    Modifications Disulfide bonds between Cys4-Cys39, Cys6-Cys32, and Cys22-Cys40.
      • BDS-I
    Molecular formula C210H303N57O56S6.
    Activity BDS-I inhibits 60% of KV3.4 current. The blocking effect is rapid, direct and reversible1. BDS-I also modulates voltage-gated Nachannels. It enhances TTX-sensitive Na+ channels (highly effective on NaV1.7 channels), and weakly inhibits TTX-resistant NaV channels2.
      • Diochot, S. et al. (1998) J. Biol. Chem273, 6744.
      • Liu, P. et al. (2012) J. Neurophysiol. 107, 3155.
    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 four weeks at 4°C or three months at -20°C.
      • BDS-I
        Alomone Labs BDS-I enhances the current of NaV1.7 channels expressed in Xenopus oocytes.
        A. Time course of BDS-I (#STB-400) effect on the normalized area of NaV1.7 channel current. Membrane potential was held at -100 mV, current was elicited by a 100 ms voltage step to 0 mV every 1 sec, and was significantly enhanced by 3.5 min application of 100 nM BDS-I, indicated by the horizontal bar. B. Superimposed traces of NaV1.7 current upon application of control and of 100 nM BDS-I (as indicated), taken from the recording shown in A.
    References - Scientific background
    • 1. Diochot, S. et al. (1998) J. Biol. Chem273, 6744.
    • 2. Yeung, S.Y. et al. (2005) J. Neurosci25, 8735.
    • 3. Kaab, S. et al. (2005) J. Physiol566, 395.
    • 4. Baranauskas, G. et al. (2004) Nature Neurosci6, 258.
    • 5. Shevchenko, T. et al. (2004) J. Neurophysiol92, 3043.
    • 6. Wang, L. et al. (2004) Invest. Ophthamol. Vis. Sci45, 1796.
    • 7. Sanchez, D. et al. (2002) J. Physiol542, 369.
    • 8. Riazanski, V. et al. (2001) J. Physiol537, 391.
    • 9. Liu, P. et al. (2012) J. Neurophysiol. 107, 3155.
      • BDS-I is a 43 amino acid peptidyl toxin isolated from the sea anemone Anemonia sulcata venom. It is reported to be a selective blocker of KV3.4 K+ channel. BDS-I blocks 60% of the KV3.4 current in COS-transfected cells at a concentration of 2.5 µM. The blocking effect is rapid, direct and reversible1. Recently it was shown that it blocks other KV3 channels with similar potencies2.

        BDS-I inhibits KV currents in carotid body cells3, an effect which disappears after chronic hypoxia, establishing the unique role played by KV3 channels in the response to hypoxia4. BDS-I (2.5 µM) also reduces the native transient K+ current and increases the action potential duration in hippocampal granule neurons5. In corneal epithelial cells BDS-I (400 nM) inhibits most of the detected KV current6. In magnocellular neurosecretory neurons of the hypothalamus, 100 nM BDS-I inhibits about half of the KV current and increases the action potential duration7. In fast spiking neurons from different brain areas, 2 µM BDS-I inhibits part of the KV current and broadened the action potential and reduces spike frequency8.

        BDS-I also produces broadening of the spike and accelerates the upstroke of the action potential by modulating voltage-gated Na+ channels. It enhances TTX-sensitive Na+ channels (highly effective on NaV1.7 channels), and weakly inhibits TTX-resistant NaV channels9.

    Target KV3 K+ channels, NaV Na+ channels
    Net Peptide Content: 100%
    Last update: 13/11/2019

    BDS-I (#STB-400) is a highly pure, synthetic, and biologically active peptide toxin.

    For research purposes only, not for human use
      • Strege, P.R. et al. (2017) Sci. Rep. 7, 15650.
      • Meneses, D. et al. (2016) Neural Plast. 2016, 8782518.
      • Ubels, J.L. et al. (2016) Exp. Eye Res. 145, 26.
      • Liu, P. et al. (2012) J. Neurophysiol. 107, 3155.
      • Alle, H. et al. (2011) J. Neurosci. 31, 8001.
      • Kanyshkova, T. et al. (2011) Pflugers Arch. 461, 545.
      • Martel, P. et al. (2011) PLoS ONE 6, e20402.
      • Min, M.Y. et al. (2010) Neuroscience 168, 633.
      • Wu, Z.Z. et al. (2009) J. Biol. Chem. 284, 36453.
      • Dallas, M.L. et al. (2008) Brain Res. 1189, 51.
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