ATX-II

• Description:

  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.

• Specifications:

  Nav1.5 channel activator

• Target:

  Na channels

• Sequence:

  GVPCLCDSDGPSVRGNTLSGIIWLAGCPSGWHNCKKHGPTIGWCCKQ

• Peptide Number:

  ATX002

• Disulfide Bonds:

  Cys4-Cys44; Cys6-Cys34; Cys27-Cys45

• N Terminal Sequence:

  H

• C Terminal Sequence:

  OH

• CAS Number:

  60748-45-0