Overview
Cys22 - Cysteine amide
- McMahon, K.L. et al. (2020) Biomedicines, 8, 321.
- Alomone Labs μ-Conotoxin SxIIIC inhibits NaV1.4 channel currents heterologously expressed in Xenopus oocytes.A. Representative time course of μ-Conotoxin SxIIIC (#STC-130) inhibition of NaV1.4 channels current. Membrane potential was held at -100 mV, current was elicited by a 100 ms voltage step to 0 mV every 10 sec, and significantly inhibited by application of 50 nM μ-Conotoxin SxIIIC (green).
B. Superimposed traces of NaV1.4 channel currents in the absence (control) and presence (green) of 50 nM μ-Conotoxin SxIIIC (taken from the recording in A). - Alomone Labs μ-Conotoxin SxIIIC inhibits NaV1.7 channel currents heterologously expressed in Xenopus oocytes.A. Representative time course of μ-Conotoxin SxIIIC (#STC-130) inhibition of NaV1.7 channels current. Membrane potential was held at -100 mV, current was elicited by a 100 ms voltage step to 0 mV every 10 sec, and significantly inhibited by application of 1 µM μ-Conotoxin SxIIIC (green).
B. Superimposed traces of NaV1.7 channel currents in the absence (control) and presence (green) of 1 µM μ-Conotoxin SxIIIC (taken from the recording in A).
- McMahon, K.L. et al. (2020) Biomedicines, 8, 321.
- Huang, W. et al. (2017) Protein Cell, 8, 401.
- Mackieh, R. et al. (2021) Mar. Drugs, 19, 562.
µ-conotoxin SxIIIC (SxIIIC) is a 22 amino acid peptidyl toxin originally isolated from the venom of the cone snail, Conus striolatus1. SxIIIC is a potent and irreversible blocker of voltage-gated sodium (Nav) channels, which displays a unique µ-conotoxin selectivity profile of human (h)NaV1.4 > hNaV1.3 > hNaV1.1 ≈ hNaV1.6 ≈ hNaV1.7 > hNaV1.2 >> hNaV1.5 ≈ hNaV1.81.
Voltage-gated sodium channels (VGSCs) are transmembrane proteins that control the voltage-dependent increase in sodium permeability. VGSCs play a fundamental role in normal neurological function, especially in the initiation and propagation of action potentials. Nav channels have been the topic of significant research and discussion for a considerable amount of time given their unique functions in electrical cell signaling. These channels are very important for homeostasis, thus specific genetic abnormalities in VGSC genes can result in a range of muscle, cardiac, and neurological disorders known as “channelopathies”2. Marine toxins appear to be an emerging source of therapeutic tools that can relieve pain or treat VGSC-related human channelopathies3.
Mu-conotoxin SxIIIC (#STC-130) is a highly pure, synthetic, and biologically active peptide toxin.