Overview
- Meir, A. et al. (2011). Novel peptides isolated from spider venom, and uses thereof. U.S. Patent Application Publication # US 2011/0065647 A1.
- Alomone Labs Pterinotoxin-2 inhibits rNav1.3 and hNaV1.7 channels heterologously expressed in HEK293 cells.A. Dose-response of NaV channels inhibition by Pterinotoxin-2 (#STT-150). The inhibition was measured in 3-5 cells for each dose in rat Nav1.3 channels expressed in HEK cells (open circles) and 3-5 cells for human NaV1.7 expressed in HEK cells (filled circles). B. Example of superimposed current traces of rat NaV1.3 channel activity before (black) and during (green) application of the indicated concentration of 0.5 µM Pterinotoxin-2. 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.
Pterinotoxin-2 is isolated from the Pterinochilus murinus (Usambara) spider venom and is a synthetic version of the peptide1.
Pterinotoxin-2 inhibits voltage-gated rat NaV1.3 and NaV1.7 Na+ channels.
Voltage-gated sodium channels (VGSC, NaV) play a critical role in excitability of nociceptors (pain-sensing neurons). The peripheral-specific sodium 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-2 shows high homology to ProTx-II (#STP-100) (75%), Phrixotoxin-2 (#STP-710) (76%) and Phrixotoxin-1 (#STP-700) (70%).