ATX-II

ATX-II is a Nav1.5 activator

ATX-II was originally discovered in 1976 by extraction from the tentacles of Anemonia sulcata (Bergman et al., 1976). At that time, it was already discovered that it has activity on voltage-dependent Na+ channels from the frog Rana esculenta by slowing the rate of inactivation. Later, it was found that the purified toxin has a positive inotropic effect on isolated guinea pig atria linked to delayed inactivation of the Na+ channel (Alsen et al., 1982). ATX-II acts as a late inward Na+ current inducer in the heart that produces atrial arrhythmias, partly because it also promotes Ca2+/calmodulin-dependent protein kinase activation and concomitant Nav1.5 channel phosphorylation and further activation (Liang et al., 2016). Because late inward Na+ current is difficult to witness, but is a risk factor for the induction of cardiac arrhythmias, it is now mandatory for the FDA that all drugs to be approved should lack effect on the ATX-II-induced late inward Nav1.5 Na+ current. ATX-II is a site 3 toxin and affects domain IV voltage-sensor movement. ATX-II is a carboxylated 47 amino acid peptides with 3 disulfide bridges and of 4934.7 Da molecular weight, recently produced by Smartox Biotechnology in its synthetic form.

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Product code: ATX002. Category: . Tag: .

AA sequence: GVPCLCDSDGPSVRGNTLSGIIWLAGCPSGWHNCKKHGPTIGWCCKQ
Disulfide bonds: Cys4-Cys44, Cys6-Cys34, Cys27-Cys45
Length (aa): 47
Formula: C213H323N63O61S6
Molecular Weight: 4934.63 g/mol
CAS number: 60748-45-0
Source: Synthetic
Purity rate: > 95 %

Inhibition of the sodium inactivation of the nodal membrane by anemonia sulcate toxin
Studies on the mechanism of the positive inotropic effect of ATX II...
Inhibitions of late Ina and CaMKII act synergistically to prevent ATX-II-induced...