protein

Ectatotoxin-Rm4a

STR-010

STR-010_1 mg

Ectatotoxin-Rm4a

Non Antibodies

Proteins

A0A8U0LTF0

https://www.uniprot.org/uniprotkb/A0A8U0LTF0/entry

Electrophysiology

Lyophilized Powder.

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.

Centrifuge the vial (10,000 × 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. Soluble in DMSO. Prepare a concentrated stock solution by dissolving the lyophilized peptide in DMSO first (e.g., at a concentration between 100-1000x of the final working concentration). Once the peptide is completely dissolved in DMSO, slowly dilute the solution into the working buffer (or water) to the desired final working concentration. Centrifuge all product preparations before use. Avoid multiple freeze-thaw cycles to maintain biological activity. It is recommended to keep the DMSO concentration as low as possible. For cell assays, a final concentration of 0.1%–0.5% DMSO (v/v) is considered safe. For other experiments, a 5% DMSO (v/v) concentration is recommended.

The product is shipped as a lyophilized powder at room temperature. Upon receipt, store the product at -20°C. Protect from moisture.

Rhytidoponera metallica (Australian green-headed ant) (Ponera metallica)

Synthetic peptide

SCN8A, SCN9A, SCN10A

Ectatotoxin-Rm4a (Rm4a), originally isolated from the venom of Rhytidoponera metallica (Australian green-headed ant), is a 26-amino acid cysteine-free peptide toxin that modulates voltage-gated sodium (NaV) channels, particularly NaV1.6 and NaV1.7 subtypes. Rm4a toxin induces sustained sodium currents by delaying inactivation and causing a hyperpolarizing shift in activation voltage. It exhibits higher potency for human Nav1.6 channels (EC50 = 196 ± 23 nM) compared to Nav1.7 (EC50 = 1.9 ± 0.4 µM) and Nav1.8 (EC50 = 8.4 ± 1.0 µM)1. Rm4a toxin, along with other closely related ant venom peptides such as Delta-myrmicitoxin-Ta3a, Myrmicitoxin1-Pm1a, Myrmicitoxin1-Pm2a and Poneratoxin, represents a new class of NaV channel modulators. These toxins are structurally and functionally distinct from previously characterized peptide-based NaV modulators, offering valuable insights into the evolutionary adaptations of ant venom. The effects of these toxins on NaV channel currents more closely resemble those of “site 2” alkaloid toxins, such as batrachotoxin1,2. The toxin's ability to prevent channel inactivation and shift the voltage-dependence of activation can lead to increased neuronal excitability and prolonged action potentials, ultimately resulting in enhanced pain signaling. In mice, Rm4a causes dose-dependent spontaneous nocifensive behaviors, further supporting its potential to induce pain1.

Alomone Labs

Nav1.6, Nav1.7 channels

2994.6 Da

Rm4a, ECTX-Rm4a

Asn25 – C-terminal amidation

C148H225N33O33

200 nM - 3 µM

Rm4a toxin induces sustained sodium currents by delaying inactivation and causing a hyperpolarizing shift in activation voltage. It exhibits higher potency for human NaV1.6 channels (EC50 = 196 ± 23 nM) compared to NaV1.7 (EC50 = 1.9 ± 0.4 µM) and NaV1.8 (EC50 = 8.4 ± 1.0 µM)1.

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.

1-2 Business Days

Israel/IL

≥98% (HPLC)

Lyophilized

Contact Alomone Labs for technical support and product customization

FPPLLLLAGLFSLPALQHYIETKWIN – NH2

Yes

12352202

yes

no