Every lot is tried & tested in a relevant biological assay.
- Zeng, X. et al. (2018) Toxins, 10, 64.
- Alomone Labs Jingzhaotoxin-34 inhibits NaV1.7 channel currents heterologously expressed in Xenopus oocytes.A. Representative time course of Jingzhaotoxin-34 (#STJ-500) inhibition of NaV1.7 channels current. Membrane potential was held at -80 mV, current was elicited by a 100 ms voltage step to 0 mV every 10 sec, and significantly inhibited by application of 0.5 µM Jingzhaotoxin-34 (green).
B. Superimposed traces of NaV1.7 channel currents in the absence (control) and presence (green) of 0.5 µM Jingzhaotoxin-34 (taken from the recording in A).
Jingzhaotoxin-34 (JZTX-34) is a 35 amino acid peptidyl toxin originally isolated from the venom of the Chinese earth tiger tarantula, Chilobrachys guangxiensis1,2. JZTX-34 is a potent and selective blocker of the voltage-gated sodium (NaV) 1.7 channel and a weak blocker of the Nav1.3 channel. In addition, this toxin inhibited voltage-gated potassium (Kv) channels in rat DRG neurons3.
Nav channels are transmembrane proteins that control the voltage-dependent increase in sodium permeability. They play a fundamental role in normal neurological function, especially in the initiation and propagation of action potentials. Nav channels are composed of nine different isoforms with distinct biophysical properties. Several studies, including the analysis of mutations associated with an increase or absence of pain sensitivity in humans, have revealed that Nav1.7, Nav1.8, and Nav1.9 are the most important contributors that control nociceptive neuronal electrogenesis4. JZTX-34 exhibited analgesic activity in three rodent pain models3.
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Jingzhaotoxin-34 (#STJ-500) is a highly pure, synthetic, and biologically active peptide toxin.