Biological ActivitySelective NaV1.7 channel blocker. Shifts activation gating positively and decreases current magnitude. Displays 100-fold selectivity over other sodium channel subtypes.
(Modifications: Disulfide bridge: 2-16, 9-21, 15-25)
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Structural basis of Nav1.7 inhibition by a gating-modifier spider toxin.
Xu et al.
Molecular interactions of the gating modifier toxin ProTx-II with NaV 1.5: implied existence of a novel toxin binding site coupled to activation.
Smith et al.
Evidence for multiple effects of ProTxII on activation gating in NaV 1.5.
Edgerton et al.
ProTx-II, a selective inhibitor of NaV 1.7 sodium channels, blocks action potential propagation in nociceptors.
Schmalhofer et al.
Citations for ProTx II
The citations listed below are publications that use Tocris products. Selected citations for ProTx II include:
2 Citations: Showing 1 - 2
Structures of human Nav1.7 channel in complex with auxiliary subunits and animal toxins.
Authors: Shen Et al.
Membrane protein Nav1.7 contributes to the persistent post-surgical pain regulated by p-p65 in dorsal root ganglion (DRG) of SMIR rats model.
Authors: Li Et al.
BMC Anesthesiol 2017;17:150
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