Overview
- Alomone Labs Pterinotoxin-1 inhibits rat NaV1.3 and NaV1.8 channels heterologously expressed in HEK and ND7-23 cells, respectively.A. Dose response of NaV channels inhibition by Pterinotoxin-1 (#STT-100). The inhibition was measured in 3-5 cells for each dose in rat NaV1.3 channels expressed in HEK cells and 3-5 cells for rat NaV1.8 expressed in ND7-23 cells (in the presence of 600 nM Tetrodotoxin citrate (#T-550)). B. Example of superimposed current traces of rat NaV1.3 channel activity before and during application of 2 µM of Pterinotoxin-1. Holding potential was -100 mV and currents were stimulated every 10 seconds by a voltage ramp of 40 msec from holding potential to + 60 mV. C. Example of superimposed current traces of rat NaV1.8 channel activity before and during application of 2 µM of Pterinotoxin-1 (both in the presence of 600 nM Tetrodotoxin (with citrate)). The same voltage protocol was used as in graph B.
Pterinotoxin-1 is isolated from the Pterinochilus murinus (Usambara) spider venom and is a synthetic version of the peptide1.
Pterinotoxin-1 inhibits voltage-gated rat NaV1.3, NaV1.7 and NaV1.8 Na+ channels.
Voltage-gated Na+ channels (VGSC, NaV) play a critical role in excitability of nociceptors (pain-sensing neurons). The peripheral-specific Na+ channels NaV1.7, NaV1.8 and NaV1.9 are particularly important in the pathophysiology of different pain syndromes and, hence, thought to be potential targets for pain therapeutics2-3.
The expression and functional properties of NaV channels in peripheral sensory neurons can be dynamically regulated following axonal injury or peripheral inflammation4.
Pterinotoxin-1 shows high homology to Phrixotoxin-3 (#STP-720) (58%), Huwentoxin-IV (#STH-100) (50%) and Ceratotoxin-2 (#STC-100) (66%).