ATX-II

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.