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Results for "

paralysis/death

" in MedChemExpress (MCE) Product Catalog:

8

Inhibitors & Agonists

2

Peptides

1

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-P5142
    ω-Hexatoxin-Hv1a

    ω-ACTX-Hv1; ω-Atracotoxin-HV1

    		 Insecticide Calcium Channel Apoptosis Necroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a 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 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 is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons .
    ω-Hexatoxin-Hv1a
  • HY-W339331
    Flubendiamide

    NNI-0001

    		 Insecticide Calcium Channel Reactive Oxygen Species (ROS) Apoptosis Infection Metabolic Disease
    Flubendiamide (NNI-0001) is an orally active phthalic diamide insecticide that acts by targeting insect ryanodine receptors (RyRs), causing insect muscle dysfunction, paralysis and death. Flubendiamide disrupts molting, metamorphosis and reproductive processes, induces oxidative stress by increasing the levels of ROS/RNS, MDA and 8OHdG and decreasing the levels of SOD, CAT and GST, activates the CncC/Maf apoptosis pathway, impairs calcium homeostasis, promotes adipogenesis, increases triglyceride accumulation, and upregulates the expression of regulatory factors for adipocyte differentiation and adipogenesis .
    Flubendiamide
  • HY-114899
    Azamethiphos

    		Environmental Pollutants Cholinesterase (ChE) Insecticide Infection Neurological Disease
    Azamethiphos is an acetylcholinesterase inhibitor and insecticide. Azamethiphos covalently binds to acetylcholinesterase via phosphorylation, inhibits its activity, causes acetylcholine to accumulate in cholinergic synapses, triggers uncontrolled excitation of cholinergic sites, induces paralysis and leads to death. Azamethiphos can be used as a bath insecticide in salmonid aquaculture to control sea lice infestations, and it exerts acute toxicity to European lobster larvae, including mortality and movement disorders .
    Azamethiphos
  • HY-Z8942
    Avermectin B2a

    		Insecticide Parasite Chloride Channel Infection
    Avermectin B2a is an insecticide targeting glutamate-gated chloride channels (GluCls). Avermectin B2a causes hyperpolarization of nematode/insect neurons and subsequent paralysis/death. Avermectin B2a is promising for research of agricultural pests .
    Avermectin B2a
  • HY-15308B
    Δ2-Avermectin B1a

    		Parasite Chloride Channel Neurological Disease
    Δ²-Avermectin B₁ₐ (Compound 3) is an antiparasitic agent targeting glutamate-gated chloride channels (GluCls) in the neuromuscular system of invertebrates. Δ²-Avermectin B₁ₐ enhances chloride ion influx, leading to hyperpolarization of the neuromuscular cell membrane, inhibition of neural signal transmission, and ultimately paralysis and death of parasites. Δ²-Avermectin B₁ₐ is promising for research of agricultural pests .
    Δ2-Avermectin B1a
  • HY-175339
    Insecticidal agent 25

    		nAChR Infection
    Insecticidal agent 25 (Compound WZ18) is an insecticide targeting the nicotinic acetylcholine receptors (nAChRs) in insect nervous systems. Insecticidal agent 25 disrupts neurotransmission by competitively binding to nAChRs, leading to insect paralysis and death .
    Insecticidal agent 25
  • HY-120131
    Cyanofenphos

    		Insecticide Cholinesterase (ChE) Neurological Disease
    Cyanofenphos is an orally active organophosphate insecticide and brain AChE inhibitor with neurotoxicity. Cyanofenphos induces delayed neurotoxicity such as ataxia and paralysis. Cyanofenphos also causes symptoms including somnolence, reduced feed intake and weight loss in hens. Cyanofenphos has a unique self-antagonistic effect: repeated low-dose pre-treatment not only reduces subsequent acute toxicity, but also exacerbates delayed neurotoxicity and attenuates enzyme inhibition, with the protective effect peaking at 24 h after the last pre-treatment. Cyanofenphos is commonly used in studies related to delayed neurotoxicity .
    Cyanofenphos
  • HY-P5142A
    ω-Hexatoxin-Hv1a TFA

    ω-ACTX-Hv1 TFA; ω-Atracotoxin-HV1 TFA

    		 Insecticide Apoptosis Calcium Channel Necroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    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 .
    ω-Hexatoxin-Hv1a TFA

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