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A Blocker of Small Conductance Ca2+-Activated K+ Channels (SK Type)

Cat #: STA-200
Lyophilized Powder yes
  • Bioassay Tested
  • Origin Synthetic peptide
    MW: 2028 Da
    Purity: >98% (HPLC)
    Effective concentration 100 nM - 1 µM.
    Modifications Disulfide bonds between Cys1-Cys11, and Cys3-Cys15. His18 - C-terminal amidation.
    Molecular formula C79H131N31O24S4.
    CAS No.: 24345-16-2
    Activity Apamin is a blocker of voltage-independent Ca2+-activated K(SK) channels1.
    1. Shahidi, S. et al. (1993) Biochem. Biophys. Acta 1157, 74.
    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 two months at -20°C.
    Our bioassay
    • Alomone Labs Apamin inhibits KCa2.1 (SK1) channel heterologously expressed in Xenopus oocytes.
      Alomone Labs Apamin inhibits KCa2.1 (SK1) channel heterologously expressed in Xenopus oocytes.
      Voltage clamped whole oocytes current expressing KCa2.1 was recorded continuously in low Cl- concentration at 5 mV holding potential. At the indicated time, Ca2+ was injected and an outward current developed. One minute later 1 µM Apamin (#STA-200) was perfused to the bath, resulting in about 66% inhibition in the amplitude of this Ca2+-dependent current, which completely recovered upon toxin wash.
    • Alomone Labs Apamin inhibits SK2 channels in transfected HEK-293 cells.
      Alomone Labs Apamin inhibits SK2 channels in transfected HEK-293 cells.
      A. Time course of Apamin (#STA-200) action on SK2 channels. Current amplitudes were plotted as a function of time. Membrane potential was held at -80 mV and cells were stimulated by a 150 ms voltage ramp from -120 mV to +60 mV every 10 sec. 1 nM Apamin was perfused during 2.5 min as indicated by the bar at -10 mV. B. Superimposed examples of SK2 channel current in the absence (control, black) and presence of 1 nM Apamin (green) (taken from the experiment in A).
    References - Scientific background
    1. Gauldie, J. et al. (1976) Eur. J. Biochem61, 369.
    2. Logsdon, N.J. et al. (1997) J. Biol. Chem272, 32723.
    3. Shah M. and Haylett D.G. (2000) Br. J. Pharm. 129, 627.
    4. Strobaek D. et al. (2000) Br. J. Pharm. 129, 991.
    5. Barfod, E.T. et al. (2001) Am. J. Physiol. 280, C836.
    6. Desai, R. et al. (2000) J. Biol. Chem275, 39954.
    7. Hosseini, R. et al. (2001) J. Physiol. 535, 323.
    8. Kong, I.D. et al. (2000) Am. J. Physiol. 278, C352.
    9. Nagayama, T. et al. (2000) Am. J. Physiol279, R1731.
    Scientific background

    Apamin is a natural peptide isolated and purified from Apis mellifera bee venom. Apamin blocks small conductance Ca2+-activated K+ channels (SK). It is specific for the SK1-3 isoforms, but ineffective in blocking other calcium activated K+ channels2. In mammalian cell lines, Apamin blocks expressed hSK1 with an IC50 of ~10 nM3, rSK1 and rSK2 with IC50 of ~3 and <1 nM respectively4 and liver rSK3 with IC50 <1 nM.5 In Jurkat T-cells, 5 nM of Apamin blocks 70% of hSK2 currents.6

    Blocking these channels with Apamin slows down neuronal activity after hyperpolarization7, as well as smooth muscle contraction8 and catecholamine secretion in adrenal glands.9 Electrophysiology application of long (~400 ms) voltage ramps, covering the whole physiological range (-160 to +40 mV), in the whole cell patch-clamp or voltage clamp configurations, before and after bath perfusion of the drug, allows the detection of the blocked channel currents (by comparison).1

    Target KCa2 K+ channels
    Peptide Content: 100%
    Image & Title Apamin
    Alomone Labs Apamin abolishes STOCs in rat MNTB neurons.Whole-cell voltage-clamp recordings of rat medial nucleus of the trapezoid body (MNTB) neurons display spontaneous transient outward currents (STOCs) at –65 mV. 100 nM Apamin (#STA-200) completely suppresses the STOCs indicating the involvement of SK channels in mediating the STOCs.Adapted from Zhang, Y. and Huang, H. (2017) J. Neurosci. 37, 10738. with permission of the Society for Neuroscience.
    Last update: 06/11/2022

    Apamin (#STA-200) is a highly pure, synthetic, and biologically active peptide toxin.

    For research purposes only, not for human use



    Published figures using this product
    • Blocking BK channels mimics the mAChR activation effects.
      Blocking BK channels mimics the mAChR activation effects.
      A. and B. uEPSC (left), uEPSP (middle), and ΔGuEPSP/Gsat (right) measured in the presence of Apamin (#STA-200) (A) and Iberiotoxin (#STI-400) (B). The range of amplitudes ±SEM of the uEPSP and ΔGuEPSP/Gsat measured in control conditions are shown by the gray shaded bars. C. Summary of the uEPSC amplitude, uEPSP amplitude, uEPSP decay time constant, and ΔGuEPSP/Gsat in each pharmacological condition.
      Adapted from He, S. et al. (2014) with permission of the Society for Neuroscience.
    1. Mouse α-cells (single cell).
      Dickerson, M.T. et al. (2019) Am. J. Physiol. 316, E646.
    2. Human beta cells.
      Vierra, N.C. et al. (2017) Sci. Signal. 10, eaan2883.
    Product citations
    1. Zhang, Y. and Huang, H. (2017) J. Neurosci. 37, 10738.
    2. Babiec, W.E. et al. (2017) J. Neurosci. 37, 1950.
    3. Li, Y. et al. (2016) PLoS ONE 11, e0155006.
    4. Mader, F. et al. (2016) Acta Pharmacol. Sin. 37, 617.
    5. Margas, W. et al. (2016) Phil. Trans. R. Soc. B 371, 20150430.
    6. Almog, M. and Korngreen, A. (2014) J. Neurosci. 34, 182.
    7. He, S. et al. (2014) J. Neurosci. 34, 5261.
    8. Brereton, M.F. et al. (2013) PLoS ONE 8, e57451.
    9. Cosyns, S.M.R. et al. (2013) Neurogastroenterol. Motil. 25, e339.
    10. Gonzalez Corrochano, R. et al. (2013) Br. J. Pharmacol. 169, 449.
    11. Jones, S.L. and Stuart, G.J. (2013) J. Neurosci. 33, 19396.
    12. Priem, E.K. et al. (2013) Eur. J. Pharmacol. 705, 156.
    13. Tsai, K.L. et al. (2013) Cell. Physiol. Biochem. 31, 938.
    14. Weisbrod, Det al. (2013) Proc. Natl. Acad. Sci. U.S.A. 110, E1685.
    15. Zhang, C. et al. (2013) Am. J. Physiol. 304, E1237.
    16. Zhong, L.R. et al. (2013) PLoS ONE 8, e78727.
    17. Cosyns, S.M. and Lefebvre, R.A. (2012) Eur. J. Pharmacol. 686, 104.
    18. So, E.C. et al. (2012) Eur. J. Pharmacol. 683, 1.
    19. Vandael, D.Het al. (2012) J. Neurosci. 32, 16345.
    20. Catacuzzeno, Let al. (2011) J. Cell. Physiol. 226, 1926.
    21. Wu, S.N. et al. (2011) Cell. Physiol. Biochem. 28, 959.
    22. Artinian, Let al. (2010) J. Neurosci. 30, 1699.
    23. Kita, M. et al. (2010) Am. J. Physiol. 298, R1310.
    24. Malinina, Eet al. (2010) J. Neurophysiol. 104, 200.
    25. Faber, E.Set al. (2008) J. Neurosci. 28, 10803.
    26. Liu, Y.C. et al. (2008) Eur. J. Pharmacol. 590, 93.
    27. Pelucchi, B. et al. (2008) J. Neurosci. Res. 86, 194.


    Scientific Background

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