Overview
- 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). - Alomone Labs Jingzhaotoxin-34 enhances the current of NaV1.1 channels heterologously expressed in Xenopus oocytes.A. Representative time course of Jingzhaotoxin-34 (#STJ-500) effect on the normalized area of NaV1.1 channels current. Membrane potential was held at -80 mV and current was elicited by a 100 ms voltage step to 0 mV, applied every 10 sec. 0.5 µM Jingzhaotoxin-34 (green) were perfused as indicated by the horizontal bar. B. Superimposed traces of NaV1.1 current after application of control (black) and of 0.5 µM Jingzhaotoxin-34 (green), taken from the recording in A.
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- Chen J. et al. (2009) Peptides, 30, 1042.
- Zeng, X. et al. (2018) Toxins, 10, 64.
- Lopes, L. et al. (2023) Biomed Pharmacother., 165, 115173.
- Laedermann, C.J. et al. (2015) Front. Pharmacol., 6, 263.
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 was reported first as a potent and selective blocker of the voltage-gated sodium (NaV) 1.7 channel and a weak blocker of the Nav1.3 channel3. Recently, it has been found that JzTx-34 has more potent activity as an activator of hNav1.14. In addition, at higher concentrations than hNav1.1, this toxin activated hNav1.3 and hNav1.6 channels and also blocked hNav1.2, hNav1.4, hNav1.5, hNav1.7, and hERG channels4. Moreover, JzTx-34 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. NaV1.1 channel has been utilized as a therapeutic target for various brain disorders, including epilepsy, Alzheimer's disease, and autism. The NaV1.1 channel also contributes to mechanical pain by regulating the excitability of a specific subset of sensory neurons within the peripheral nervous system. 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 electrogenesis5. JZTX-34 exhibited analgesic activity in three rodent pain models3.
Jingzhaotoxin-34 (#STJ-500) is a highly pure, synthetic, and biologically active peptide toxin.