1. Membrane Transporter/Ion Channel
  2. Sodium Channel
  3. Hm1a

Hm1a is a venom peptide and a selective hNaV1.1 activator with an EC50 of 7.5 nM. Hm1a enhances hNaV1.1 and hNaV1.3 channel currents via delayed inactivation. Hm1a restores action potential firing in Dravet syndrome GABAergic inhibitory interneurons, reduces interictal epileptiform discharges and whole-brain hyperexcitability, lowers seizure frequency, and rescues premature death in Dravet syndrome mice. Hm1a can be used for the research of neurological disease, such as Dravet syndrome.

For research use only. We do not sell to patients.

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Hm1a

Hm1a Chemical Structure

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Description

Hm1a is a venom peptide and a selective hNaV1.1 activator with an EC50 of 7.5 nM. Hm1a enhances hNaV1.1 and hNaV1.3 channel currents via delayed inactivation. Hm1a restores action potential firing in Dravet syndrome GABAergic inhibitory interneurons, reduces interictal epileptiform discharges and whole-brain hyperexcitability, lowers seizure frequency, and rescues premature death in Dravet syndrome mice. Hm1a can be used for the research of neurological disease, such as Dravet syndrome[1].

IC50 & Target[1]

hNav1.1

7.5 nM (EC50)

hNav1.3

39.5 nM (EC50)

In Vitro

Hm1a potently and selectively modulates hNaV1.1 and hNaV1.3 channels with efficacy EC50 values of 7.5 and 39.5 nM in HEK293T cells[1].
Hm1a (50 nM; 2 min) has no functional effect on hNaV1.2, hNaV1.4, hNaV1.5, hNaV1.6, hNaV1.7, or hNaV1.8 channels in HEK293T cells[1].
Hm1a (300 nM) has no functional effect on Kv1.7, Kv10.1, Kv11.1, KCa1.1, KCa2.2, or KCa3.1 channels[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Hm1a (0.5 μM; ICV infusion; 0.1-0.2 μL/min; 1 h) significantly reduces interictal spike frequency in Dravet syndrome mice[1].
Hm1a (0.5 μM; continuous ICV infusion; 0.2 μL/min; up to 5 days) reduces seizure frequency to near zero over 4 days and maintains 90% survival at day 3 in Dravet syndrome mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Scn1a (R1407X) Dravet syndrome mice (N2 backcross generation on C57BL/6J background; aged postnatal day 18-26)[1]
Dosage: 0.5 μM
Administration: ICV infusion; 0.1-0.2 μL/min; 1 h
Result: Reduced mean interictal spike frequency from 27.6 spikes/h to 11.7 spikes/h.
Achieved a significant reduction in peak 0.5-2 Hz activity via power spectrum analysis.
Induced a spike-free period of ~1 hour following infusion cessation.
Animal Model: Scn1a (R1407X) Dravet syndrome mice (N2 backcross generation on C57BL/6J background; aged postnatal day 18-26)[1]
Dosage: 0.5 μM
Administration: continuous ICV infusion; 0.2 μL/min; up to 5 days
Result: Reduced mean seizure count from 3.50 seizures/day at day 0 to near 0 seizures/day by day 4.
Led 67% of treated mice to have significantly reduced or completely abolished seizures after 3 days.
Maintained 90% survival of treated mice to day 3, compared to 0% survival of vehicle-treated controls.
Molecular Weight

3997.39

Formula

C170H239N47O54S6

Sequence

Glu-Cys-Arg-Tyr-Leu-Phe-Gly-Gly-Cys-Ser-Ser-Thr-Ser-Asp-Cys-Cys-Lys-His-Leu-Ser-Cys-Arg-Ser-Asp-Trp-Lys-Tyr-Cys-Ala-Trp-Asp-Gly-Thr-Phe-Ser (Disulfide bridge: Cys2-Cys16; Cys9-Cys21; Cys15-Cys28)

Sequence Shortening

ECRYLFGGCSSTSDCCKHLSCRSDWKYCAWDGTFS (Disulfide bridge: Cys2-Cys16; Cys9-Cys21; Cys15-Cys28)

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Hm1a
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