toxin ii

AK-Toxin II is a host-specific toxin to Japanese white pear.

AM Toxin II is a Cyclic tetradepsipeptide isolated from Alternaria mali.

AM Toxin III is a phytotoxic peptide.

Asebotoxin III is a diterpenoid obtained from the leaves of Asebi, Pieris japonica.

Grayanotoxins are a group of closely related neurotoxins named after Leucothoe grayana. Extract from leaves of Ericaceae.

Grayanotoxins are a group of closely related neurotoxins named after Leucothoe grayana, a plant native to Japan originally. Extract from leaves Leucothoe grayana (Ericaceae).

Toxin IIc is a biochemical.

Altertoxin III is a mutagenic agent that induces mutations in Salmonella typhimurium strains TA98, TA100, and TA1537. It is isolated from extracts of A. alternata strains that demonstrate mutagenic responses in the Ames Salmonella typhimurium test.

NaV1.5 channels blocker

Jingzhaotoxin-V is a peptide that suppresses potassium currents in Xenopus laevis oocytes with an IC50 of 604.2 nM, while targeting both tetrodotoxin-resistant and tetrodotoxin-sensitive sodium currents in rat dorsal root ganglion neurons with IC50 values of 27.6 nM and 30.2 nM, respectively [1].

Jingzhaotoxin-II, a neurotoxin composed of 32 amino acid residues featuring two acidic and two basic residues, selectively inhibits voltage-gated sodium channels (VGSC), notably slowing the rapid inactivation of TTX-resistant (TTX-R) VGSC in cardiac myocytes, with an IC50 of 0.26 μM [1].

Chloroquinoxaline sulfonamide (Chloroquinoxaline) is a topoisomerase II alpha/beta toxin with antitumor activity and immunosuppressive properties that inhibits the proliferation of B16 melanoma cells in mice, and can be used to study metastatic colorectal cancer. It can be used to study metastatic colorectal cancer.

β-Amanitin, a cyclic peptide toxin found in the poisonous Amanita phalloides mushroom, inhibits eukaryotic RNA polymerase II and III, thereby disrupting protein synthesis.

Trypacidin is a fungal metabolite originally isolated fromA. fumigatus.1It is active againstB. subtilisandM. bovis(MICs = 12.5 and 1.25 μg/ml, respectively), as well asT. cruziandT. gondii(MICs = 5-10 and 10-20 μg/ml, respectively).1,2It reduces viability and induces lysis of A549 human lung cancer cells (IC50s = 7.4 μM for both).3Trypacidin increases survival in a mouse model ofT. gondiiinfection when administered in six doses of 12.5 mg/kg each.1 1.Balan, J., Ebringer, L., Nemec, P., et al.Antiprotozoal antibiotics. II. Isolation and characterization of trypacidin, a new antibiotic, active against Trypanosoma cruzi and Toxoplasma gondiiJ. Antibiot. (Tokyo)16157-160(1963) 2.Song, Z., Liu, Y., Gao, J., et al.Antitubercular metabolites from the marine-derived fungus strain Aspergillus fumigatus MF029Nat. Prod. Res.1-8(2019) 3.Gauthier, T., Wang, X., Dos Santos, J.S., et al.Trypacidin, a spore-borne toxin from Aspergillus fumigatus, is cytotoxic to lung cellsPLoS One7(2)e29906(2012)

ATX-II, an Na+ channel modulator toxin derived from the sea anemone (Anemonia sulcata), causes delayed inactivation of the Na+ channels and has been linked to pulmonary vein arrhythmogenesis and atrial fibrillation [1] [2]. It exhibits interaction with halothane, caffeine, and ryanodine.

Aah II, a sodium channel modulator, is a toxin derived from the venom of the scorpion Androctonus australis [1] [2].

GsAF-II is a peptide toxin that selectively blocks hERG1 subtype potassium channels through a voltage-dependent mechanism and impedes Nav1.x subtype sodium channels [1].

BDS-II, a peptide toxin comprising 43 amino acids, selectively inhibits the Kv3.4 channel [1].

ATX-II TFA, a specific Na+ channel modulator toxin, is derived from the venom of the sea anemone (Anemonia sulcata). This compound impedes the inactivation of Na+ channels and has been associated with arrhythmogenesis in the pulmonary vein and atrial fibrillation [1] [2]. It interacts with halothane, caffeine, and ryanodine in this modulation.

Retro-2 (2-{[(5-methyl-2-thienyl)methylene]amino}) is a plant toxin ricin inhibitor, itprotects HeLa cells against Ricin, Stx1 and Stx2, selectively blocks retrograde toxin trafficking at the early endosome-TGN (trans-Golgi network) interface.