Overview
The product is soluble in pure water at high micromolar concentrations (100 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.
Alomone Labs Hm1a enhances the current of NaV1.1 channels expressed in Xenopus oocytes.A. Representative time course of Hm1a Toxin (#STH-600) effect on the normalized area of NaV1.1 channels current. Membrane potential was held at -90 mV, current was elicited by a 100 ms voltage step to -10 mV every 10 sec, and was significantly enhanced by the application of 250 nM Hm1a (green).
B. Superimposed traces of NaV1.1 current after application of control (black) and of 250 nM Hm1a Toxin (green), taken from the recording in A.
Delta-theraphotoxin-Hm1a (Hm1a) is a peptide toxin originally isolated from Heteroscodra maculate tarantula venom. Initially described as a moderate-affinity KV4.1 blocker¹, later studies confirmed it primarily targets NaV1.1 voltage-gated sodium channels²,3. It interacts with extracellular loops connecting transmembrane segments 1-2 and 3-4 in domain IV voltage sensor of the channel to inhibit NaV1.1 fast inactivation2,3. Hm1a inhibits human NaV1.1 channel inactivation expressed in Xenopus oocytes with EC50 value of 38 ± 6 nM.
Recent studies show Hm1a restores interneuron firing in Scn1a+/- mice, improving inhibition in Dravet Syndrome models⁴. Electrophysiology confirms it prolongs NaV1.1 activation with minimal effects on NaV1.2 and Na1.6⁵,⁶.
NaV1.1 channel is a therapeutic target for brain disorders, such as epilepsy, Alzheimer's disease, and autism. It also contributes to mechanical pain by regulating excitability in a specific subset of sensory neurons within the peripheral nervous system. Hm1a is a valuable tool for neuroscience and pharmacology research⁴-⁷.
