Satratoxin H 

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].

Satratoxin H (50 nM; 0.5-24 hr) induces apoptosis in PC12 cells via p38 MAPK/JNK-mediated cleavage of caspase-3 and subsequent PARP cleavage^[1].
Satratoxin H (5-20 nM; 24 hr) induces chromosome damage in PC12 cells^[1].
Satratoxin H (5-50 nM; 12-24 hr) induces DNA double-stranded breaks in PC12 cells, as indicated by increased γH2AX staining at 50 nM (12 and 24 hours) and 5, 10, and 20 nM (24 hours)^[1].
Satratoxin H (5-20 nM; 24 hr) does not induce DNA single-stranded breaks in PC12 cells at concentrations of 5, 10, and 20 nM after 24-hour exposure^[1].
Satratoxin H (10-100 nM; 6-48 h) induces time- and concentration-dependent cytotoxicity in undifferentiated PC12 cells^[2].
Satratoxin H (50 nM; 24 h) induces apoptotic morphological changes (condensed chromatin, nuclear fragmentation, apoptotic bodies) in undifferentiated PC12 cells after 24 h, with some concurrent necrosis^[2].
Satratoxin H (50 nM; 18-24 h) increases the percentage of apoptotic undifferentiated PC12 cells to 4.85% after 18 h and 13.25% after 24 h, as measured by flow cytometric subdiploid DNA content analysis^[2].
Satratoxin H (5-100 nM; 0.5-6 h) induces time- and concentration-dependent phosphorylation of p38 MAPK, ERK1/2, and JNK in undifferentiated PC12 cells, and co-treatment with antioxidants reduces satratoxin H-induced p38 MAPK phosphorylation^[2].
Satratoxin H (1-100 nM; 6-48 h) reduces PC12 cell viability in a concentration- and time-dependent manner^[3].
Satratoxin H (1 nM-50 nM; 24 h) inhibits B16F10 mouse melanoma cell proliferation with an IC₅₀ of approximately 20 nM and completely suppresses colony formation at 50 nM^[4].
Satratoxin H (1 nM-50 nM; 24 h) induces caspase-dependent apoptosis in B16F10 mouse melanoma cells by upregulating pro-apoptotic Bax and cleaved caspase-3, and downregulating anti-apoptotic Bcl-2, in a concentration-dependent manner^[4].
Satratoxin H (1 nM-50 nM; 24 h) induces concentration-dependent activation of endoplasmic reticulum stress pathways (IRE1, PERK, ATF6) and upregulates pro-apoptotic Bim and CHOP mRNA levels in B16F10 mouse melanoma cells^[4].
Satratoxin H (1 nM-50 nM; 2 h) induces concentration-dependent intracellular ROS production in B16F10 mouse melanoma cells, and this ROS generation is essential for its cytotoxic effects^[4].
Satratoxin H (50 nM; 10 min) induces mitochondrial ROS production in B16F10 mouse melanoma cells, and this effect is dependent on endoplasmic reticulum stress^[4].

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

528.59

C₂₉H₃₆O₉

53126-64-0

Solid

White to off-white

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]

Room temperature in continental US; may vary elsewhere.

• [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]