Centrifuge the vial (10,000 x g for 5 minutes) before adding solvent to spin down all the powder to the bottom of the vial. The lyophilized product may be difficult to visualize. Add solvent directly to the centrifuged vial. Gently tap, tilt, and roll the vial to aid dissolution. Avoid vigorous vortexing, light vortexing for up to 3 seconds is acceptable if needed. The product is soluble in pure water at high micromolar concentrations (5 μM - 1 mM). For long-term storage in solution, we recommend preparing a stock solution by dissolving the product in double distilled water (ddH2O) at a concentration between 100-1000x of the final working concentration. Divide the stock solution into small aliquots and store at -20 °C. Before use, thaw the relevant vial(s) and dilute to the desired working concentration in your working buffer. Centrifuge all product preparations before use. It is recommended to prepare fresh solutions in working buffers just before use. Avoid multiple freeze-thaw cycles to maintain biological activity.
Buffer
Lyophilized from double distilled water (ddH2O). May contain TFA as a residual counter ion.
Lagerung
-20 °C
Informationen zur Lagerung
Store the reconstituted solution for the shortest time possible at -20°C. We do not recommend storing the product in working solution for longer than one day. Avoid multiple freeze-thaw cycles.,Store the reconstituted solution for the shortest time possible at -20°C. We do not recommend storing the product in working solution for longer than one day. Avoid multiple freeze-thaw cycles.
Target
Conotoxin MVIIC omega
Hintergrund
SNX-230, Omega-CgTx-MVIIC, Omega-conotoxin MVIIC,ω-Conotoxin MVIIC blocks CaV2.1 (α1A, P/Q-type) and CaV2.2 (α1B, N-type) channels.1 The toxin binds with high affinity to CaV2.1 and with lower affinity to CaV2.2 in rabbit brain.2 However, the block by ω-Conotoxin-MVIIC of N-type channels in DRG neurons developed much faster than the block of P-type currents in Purkinje cells.1 The effect of the toxin is modulated by voltage (i.e. it is more potent for inactivated channels).3 In addition, this toxin was reported to block nicotinic receptors (transiently expressed in Xenopus oocytes) with IC50 of 1.3 μM.4 It was also shown to inhibit K+-induced 3H-GABA release in hippocampus in vivo.5 This effect was with high affinity (50 % block, 200 nM). The toxin was used to inhibit synaptic transmission in several peripheral preparations.6,7