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.
    1. Diochot, S. et al. (1998) J. Biol. Chem273, 6744.
    2. 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.
    Our bioassay
    • 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.
    Scientific background

    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: 24/01/2020

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

    For research purposes only, not for human use



    Scientific Background


    Product citations
    1. Strege, P.R. et al. (2017) Sci. Rep. 7, 15650.
    2. Meneses, D. et al. (2016) Neural Plast. 2016, 8782518.
    3. Ubels, J.L. et al. (2016) Exp. Eye Res. 145, 26.
    4. Liu, P. et al. (2012) J. Neurophysiol. 107, 3155.
    5. Alle, H. et al. (2011) J. Neurosci. 31, 8001.
    6. Kanyshkova, T. et al. (2011) Pflugers Arch. 461, 545.
    7. Martel, P. et al. (2011) PLoS ONE 6, e20402.
    8. Min, M.Y. et al. (2010) Neuroscience 168, 633.
    9. Wu, Z.Z. et al. (2009) J. Biol. Chem. 284, 36453.
    10. Dallas, M.L. et al. (2008) Brain Res. 1189, 51.
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