53126-64-0
Chemical Structure
Satratoxin H
- CAS No.: 53126-64-0
- Formula:C29H36O9
- Molecular Weight:528.59
InChIKey: MUACSCLQRGEGOE-AURGYWNQSA-N
SMILES: CC([C@]1([H])OC(/C=C\C=C\[C@@]2([C@@H](O)C)[C@H](O)/C(CCO2)=C\C3=O)=O)([C@@]4(OC4)[C@@]([H])(C1)O5)C6(CO3)CCC(C)=C[C@]65[H]
Biological Activity: Satratoxin H is a toxic metabolite of Stachybotrys atra. Satratoxin H induces caspase-3 and PARP cleavage via p38 MAPK and JNK pathways, stimulates JNK, ERK, and p38 MAPK phosphorylation, and activates JNK and p38 MAPK in a glutathione-sensitive manner. Satratoxin H induces DNA double-stranded breaks, apoptotic body formation, intracellular reactive oxygen species generation, and endoplasmic reticulum stress via ATF6, PERK, and IRE1 pathways. Satratoxin H can be used for the research of central nervous system disorders and melanoma[1][2][3][4].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Satratoxin H | 99.7% | Satratoxin H is a toxic metabolite of Stachybotrys atra. Satratoxin H induces caspase-3 and PARP cleavage via p38 MAPK and JNK pathways, stimulates JNK, ERK, and p38 MAPK phosphorylation, and activates JNK and p38 MAPK in a glutathione-sensitive manner. Satratoxin H induces DNA double-stranded breaks, apoptotic body formation, intracellular reactive oxygen species generation, and endoplasmic reticulum stress via ATF6, PERK, and IRE1 pathways. Satratoxin H can be used for the research of central nervous system disorders and melanoma. | ||||||||||||||||||||
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- [1]. Nusuetrong P, et al. Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells. J Toxicol Sci. 2012;37(4):803-812. [Content Brief]
- [2]. Nusuetrong P, et al. Involvement of reactive oxygen species and stress-activated MAPKs in satratoxin H-induced apoptosis. Eur J Pharmacol. 2005;507(1-3):239-246. [Content Brief]
- [3]. Nusuetrong P, et al. Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells. Biol Pharm Bull. 2008;31(6):1115-1120. [Content Brief]
- [4]. Lee J, et al. Roridin E and satratoxin H, macrocyclic trichothecene mycotoxins, induce endoplasmic reticulum stress-dependent apoptosis through ribosome interaction in B16 mouse melanoma cells. Bioorg Chem. 2025;164:108842. [Content Brief]
Keywords