Activity has not been tested. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first.

Alpha-toxin Amm8  Protein, Androctonus mauritanicus, Recombinant (His & Myc) is expressed in Baculovirus insect cells with N-10xHis and C-Myc tag. The predicted molecular weight is 11.3 kDa and the accession number is Q7YXD3.

Androctonus mauritanicus

Baculovirus Insect Cells

Neurotoxin 8,AmmVIII,Amm VIII,Alpha-anatoxin Amm VIII

LKDGYIVNDINCTYFCGRNAYCNELCIKLKGESGYCQWASPYGNSCYCYKLPDHVRTKGPGRCND

20-84 aa

> 85% as determined by SDS-PAGE.

Reconstitute the lyophilized protein in sterile deionized water. The product concentration should not be less than 100 μg/mL. Before opening, centrifuge the tube to collect powder at the bottom. After adding the reconstitution buffer, avoid vortexing or pipetting for mixing.

Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

Alpha toxins bind voltage-independently at site-3 of sodium channels (Nav) and inhibit the inactivation of the activated channels, thereby blocking neuronal transmission. The toxin principally slows the inactivation process of TTX-sensitive sodium channels. It discriminates neuronal versus muscular sodium channel, as it is more potent on rat brain Nav1.2/SCN2A (EC(50)=29 nM) than on rat skeletal muscle Nav1.4/SCN4A (EC(50)=416 nM). It also shows a weak activity on Nav1.7/SCN9A (EC(50)=1.76 uM). In vivo, the toxin produces pain hypersensibility to mechanical and thermal stimuli.(PubMed:23685008). It also exhibits potent analgesic activity (when injected intraperitoneally), increasing hot plate and tail flick withdrawal latencies in a dose-dependent fashion. This paradoxical analgesic action, is significantly suppressed by opioid receptor antagonists, suggesting a pain-induced analgesia mechanism that involves an endogenous opioid system. This led to hypothesis that pain relief induced by peripheral administration of Amm VIII may result from sensitization of primary afferent neurons and subsequent activation of an opioid-dependent noxious inhibitory control.