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β-theraphotoxin-Gr1b, β-TRTX-Gr1b, GsAF1, GsAF-I, GsAFI

A Blocker of TTX-Sensitive NaV and KV11.1 Channels

Cat #: STG-300
Alternative Name β-theraphotoxin-Gr1b, β-TRTX-Gr1b, GsAF1, GsAF-I, GsAFI
Lyophilized Powder yes
  • Bioassay Tested
  • Origin Synthetic peptide
    MW: 3707.9 Da
    Purity: >98% (HPLC)
    Effective concentration 40 nM – 1.3 µM.
    Modifications Disulfide bonds between Cys2-Cys16, Cys9-Cys21 and Cys15-Cys25. C-terminal Leu29 amidation.
    Molecular formula C160H245N47O41S7.
    Activity GsAF-I is a blocker of TTX-sensitive NaV and hERG1 channels1.
    1. Redaelli, E. et al. (2010) J. Biol. Chem. 285, 4130.
    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 other 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 GsAF-I inhibits NaV1.7 currents in stably transfected HEK293T cells.
      Alomone Labs GsAF-I inhibits NaV1.7 currents in stably transfected HEK293T cells.
      A. Time course of GsAF-I (#STG-300) action on NaV1.7 peak currents. Peak current amplitudes were plotted as a function of time. Holding potential was -100 mV and currents were stimulated every 10 seconds by a voltage ramp of 50 msec from holding potential to 60 mV. 50 nM GsAF-I was perfused as indicated by the horizontal bar (green). B. Superimposed traces of NaV1.7 channel current in the absence (control) and presence of 50 nM (green) GsAF-I perfused during 2.5 min (taken from the experiment in A).
    References - Scientific background
    1. Catterall W.A. et al. (2005) Pharmacol. Rev57, 397.
    2. Garcia M.L. and Possani L. D. (2007) Toxicon 49, 123.
    3. Escoubas P. et al. (2004) Toxicon 43, 555.
    4. Redaelli, E. et al. (2010) J. Biol. Chem.   285, 4130.
    Scientific background

    The tetrodotoxin (TTX)-sensitive Na+ channels are differentially distributed in the central and peripheral nervous systems, in skeletal muscle, and in cardiac muscle1.

    Several venom-derived peptides are known to modify the gating properties of ion channels, and the study of their mechanisms of action is expected to contribute to the elucidation of the molecular motions associated with channel gating2. Tarantula venoms contain a library of interesting compounds, some of which are exquisite modulators of many types of ion channels. A large number of spider toxins have been demonstrated to modulate NaV channels3.

    GsAF-I (also termed β-theraphotoxin-Gr1b) is a peptidyl toxin originally isolated from the venom of Grammostola rosea spider. This toxin is reported to block the following voltage-gated Na+ channels: NaV1.1, NaV1.2, NaV1.3, NaV1.4, NaV1.6 and NaV1.7 with respective IC50 values of 0.4, 0.6, 1.3, 0.3, 1.2 and 0.04 µM. In addition, the toxin blocks the hERG1 isoform with an IC50 value of 4.8 µM4.

    Target TTX-sensitive NaV, KV11.1 channels
    Peptide Content: 100%
    Last update: 08/01/2023

    GsAF-I (#STG-300) is a highly pure, synthetic, and biologically active peptide toxin.

    For research purposes only, not for human use
    Shipping and Ordering information