ATX-II 

ATX-II is a selective sodium channel modulator toxin. ATX-II enhances late sodium current, prevents full sodium channel inactivation, and generates persistent current fractions. ATX-II has pro-arrhythmic effect. ATX-II slows intrinsic heart rate, prolongs QT interval and sinus node recovery time, and causes sinus pauses and arrests. ATX-II can be used for the research of atrial fibrillation, long QT syndrome, and long QT3 syndrome^[1][2][4].

ATX-II (5 nM; 1.5 min post-application) enhances tetrodotoxin sensitive resurgent and persistent sodium currents in large diameter mouse DRG neurons at both 22°C and 30°C, and shifts the voltage dependence of activation and steady-state fast inactivation of TTX_S sodium channels to more hyperpolarized potentials^[3].
ATX-II (5 nM) enhances resurgent and persistent sodium currents in Nav1.7-expressing HEK293 cells when the β4-subunit C-terminus peptide is present in the pipette solution, shifts Nav1.7 activation to more depolarized potentials, and prolongs the slow time constant of Nav1.7 current decay^[3].
ATX-II (5 nM) enhances resurgent and persistent sodium currents in Nav1.6-expressing N1E115 cells when the β₄-subunit C-terminus peptide is present in the pipette solution, shifts Nav1.6 activation to more hyperpolarized potentials, reduces the fractional amplitude of the fast component of current decay, and prolongs the slow time constant of Nav1.6 current decay^[3].
ATX-II (8.8-50 nM; 30 min) concentration-dependently increases diastolic tension and arrhythmia score in isolated rat right atrial tissue with IC₅₀ values of 8.8 nM and 22.4 nM, respectively^[4].
ATX-II (50 nM) significantly increases diastolic intracellular Ca²⁺ concentrations in isolated rat atrial myocytes^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

4934.62

C₂₁₃H₃₂₃N₆₃O₆₁S₆

60748-45-0

Solid

White to off-white

Gly-Val-Pro-Cys-Leu-Cys-Asp-Ser-Asp-Gly-Pro-Ser-Val-Arg-Gly-Asn-Thr-Leu-Ser-Gly-Ile-Ile-Trp-Leu-Ala-Gly-Cys-Pro-Ser-Gly-Trp-His-Asn-Cys-Lys-Lys-His-Gly-Pro-Thr-Ile-Gly-Trp-Cys-Cys-Lys-Gln (Disulfide bonds: Cys4-Cys44, Cys6-Cys34, Cys27-Cys45)

GVPCLCDSDGPSVRGNTLSGIIWLAGCPSGWHNCKKHGPTIGWCCKQ (Disulfide bonds: Cys4-Cys44, Cys6-Cys34, Cys27-Cys45)

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Lu YY, et al. ATX-II-induced pulmonary vein arrhythmogenesis related to atrial fibrillation and long QT syndrome. Eur J Clin Invest. 2012;42(8):823-831.  [Content Brief]

  [2]. Wu J, et al. Sinus node dysfunction in ATX-II-induced in-vitro murine model of long QT3 syndrome and rescue effect of ranolazine. Prog Biophys Mol Biol. 2008;98(2-3):198-207.  [Content Brief]

  [3]. Klinger AB, et al. Sea-anemone toxin ATX-II elicits A-fiber-dependent pain and enhances resurgent and persistent sodium currents in large sensory neurons. Mol Pain. 2012;8:69. Published 2012 Sep 15.  [Content Brief]

  [4]. Liang F, et al. Inhibitions of late INa and CaMKII act synergistically to prevent ATX-II-induced atrial fibrillation in isolated rat right atria. J Mol Cell Cardiol. 2016 May;94:122-130.  [Content Brief]