2. Others Neuronal Signaling Membrane Transporter/Ion Channel Apoptosis
  3. Calcium Channel Necroptosis Apoptosis Insecticide
  4. ω-Hexatoxin-Hv1a TFA

ω-Hexatoxin-Hv1a TFA  (Synonyms: ω-ACTX-Hv1 TFA; ω-Atracotoxin-HV1 TFA)

Cat. No.: HY-P5142A Purity: 97.49%
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ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) TFA is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a TFA blocks L-type voltage-dependent Ca2+ channels and reduces intracellular calcium ion concentration, thereby decreasing apoptosis, necroptosis and oxidative stress, and promoting cell recovery and energy level elevation. ω-Hexatoxin-Hv1a TFA causes larval paralysis and death by impairing neurotransmission in the central nervous system of insects. It shows high injectable toxicity against insects of multiple orders, but exhibits weak oral toxicity. ω-Hexatoxin-Hv1a TFA is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons.

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

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ω-Hexatoxin-Hv1a TFA

ω-Hexatoxin-Hv1a TFA Chemical Structure

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Based on 1 publication(s) in Google Scholar

Other Forms of ω-Hexatoxin-Hv1a TFA:

ω-Hexatoxin-Hv1a TFA Related Antibodies

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Description

ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) TFA is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a TFA blocks L-type voltage-dependent Ca2+ channels and reduces intracellular calcium ion concentration, thereby decreasing apoptosis, necroptosis and oxidative stress, and promoting cell recovery and energy level elevation. ω-Hexatoxin-Hv1a TFA causes larval paralysis and death by impairing neurotransmission in the central nervous system of insects. It shows high injectable toxicity against insects of multiple orders, but exhibits weak oral toxicity. ω-Hexatoxin-Hv1a TFA is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons[1][2][3].

In Vitro

ω-Hexatoxin-Hv1a TFA (10-50 nM; 3 h of reperfusion) inhibits ischemia/reperfusion-induced apoptosis, suppresses ischemia/reperfusion-induced necrosis, alleviates intracellular calcium overload, and promotes the recovery of cell index in CHO-K1 epithelial cells[1].
Recombinant ω-Hexatoxin-Hv1a TFA (100-200 ng) retains immunoreactivity after fusion with GNA, which is confirmed by Western blotting analysis of 200 ng and 100 ng loaded samples of the intact Hv1a/GNA fusion protein[2].
ω-Hexatoxin-Hv1a TFA (10-50 nM; 18 h) blocks AC-1001 H3-induced apoptosis in CHO-K1 cells in a dose-dependent manner in vitro. At 50 nM (18 h incubation), it reduces the apoptosis level to that of the control group, while 10 nM used alone does not alter the baseline apoptosis level[3].

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

ω-Hexatoxin-Hv1a TFA Related Antibodies

Apoptosis Analysis[1]

Cell Line: CHO-K1 Chinese hamster ovary epithelial cells
Concentration: 10 nM, 50 nM
Incubation Time: 3 h (reperfusion)
Result: Maintained CHO-K1 cell apoptosis levels at the normal condition level at 50 nM.
Showed no effect on apoptosis at 10 nM.
Maintained necrosis levels at the normal condition level at both 10 nM and 50 nM.
Reduced intracellular calcium ion concentration during reperfusion to levels correlating with reduced apoptosis and necrosis at both 10 nM and 50 nM. Caused the cell index to return to pre-reperfusion values within 1 h of reperfusion start at both 10 nM and 50 nM, compared to the no-toxin group which returned to normal levels only after 5 h.
In Vivo

ω-Hexatoxin-Hv1a (46-184 μg/g insect; injection) TFA causes dose-dependent paralysis and mortality in fifth stadium Mamestra brassicae larvae, with 90% mortality achieved at 184 μg/g insect[2].
ω-Hexatoxin-Hv1a (9.6 μg per larva; p.o.; daily; 4 days) TFA alone via daily sucrose droplets has no insecticidal activity against fifth stadium Mamestra brassicae larvae[2].

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

Animal Model: Mamestra brassicae Cabbage moth (fifth stadium, 40-70 mg)[2]
Dosage: 46 μg/g insect; 92 μg/g insect; 184 μg/g insect
Administration: Injection
Result: Caused 20% mortality at 72 hours post-injection at 46 μg/g insect.
Caused 80% mortality at 72 hours post-injection at 92 μg/g insect.
Caused 90% mortality at 72 hours post-injection at 184 μg/g insect.
Induced paralysis in larvae injected with doses of 46 μg/g insect and above.
Significantly reduced survival compared to controls.
Molecular Weight

4049.38 (free base)

Formula

C162H247N49O61S6·xC2HF3O2
Appearance

Solid

Color

White to off-white

Sequence

Ser-Pro-Thr-Cys-Ile-Pro-Ser-Gly-Gln-Pro-Cys-Pro-Tyr-Asn-Glu-Asn-Cys-Cys-Ser-Gln-Ser-Cys-Thr-Phe-Lys-Glu-Asn-Glu-Asn-Gly-Asn-Thr-Val-Lys-Arg-Cys-Asp (Disulfide bridge:Cys4-Cys18, Cys11-Cys22, Cys17-Cys36)
Sequence Shortening

SPTCIPSGQPCPYNENCCSQSCTFKENENGNTVKRCD (Disulfide bridge:Cys4-Cys18, Cys11-Cys22, Cys17-Cys36)
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Sealed storage, away from moisture

Powder -80°C 2 years
-20°C 1 year

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Solvent & Solubility
In Vitro: 

H2O : ≥ 50 mg/mL

*"≥" means soluble, but saturation unknown.

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This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
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ω-Hexatoxin-Hv1a TFA Related Classifications

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  • 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.

Keywords:

ω-Hexatoxin-Hv1aω-ACTX-Hv1ω-Atracotoxin-HV1Calcium ChannelNecroptosisApoptosisInsecticideCa2+ channelsCa channelsVenomspiderCa2+ channeltoxinneurotoxinInhibitorinhibitorinhibit

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