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 Ca 2+ 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 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].
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].
References:
[1]. Iurova EV, et al. Effect of the Peptide Calcium Channel Blocker ω-hexatoxin-Hv1a on Cell Death during Ischemia/Reperfusion in vitro. Sovrem Tekhnologii Med. 2023;15(1):21-27.
[2]. Fitches EC, et al. Fusion to snowdrop lectin magnifies the oral activity of insecticidal ω-Hexatoxin-Hv1a peptide by enabling its delivery to the central nervous system. PLoS One. 2012;7(6):e39389.
[3]. Iurova E, et al. Arthropod toxins inhibiting Ca 2+ and Na + channels prevent AC-1001 H3 peptide-induced apoptosis. J Pept Sci. 2021;27(1):e3288.
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].
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].
References:
[1]. Iurova EV, et al. Effect of the Peptide Calcium Channel Blocker ω-hexatoxin-Hv1a on Cell Death during Ischemia/Reperfusion in vitro. Sovrem Tekhnologii Med. 2023;15(1):21-27.
[2]. Fitches EC, et al. Fusion to snowdrop lectin magnifies the oral activity of insecticidal ω-Hexatoxin-Hv1a peptide by enabling its delivery to the central nervous system. PLoS One. 2012;7(6):e39389.
[3]. Iurova E, et al. Arthropod toxins inhibiting Ca 2+ and Na + channels prevent AC-1001 H3 peptide-induced apoptosis. J Pept Sci. 2021;27(1):e3288.