CAS 67-99-2: Gliotoxin

Gliotoxin from Gliocladium fimbriatum

Gliotoxin is a bioactive mycotoxin and antibiotic compound, which is primarily derived from various species of Aspergillus and Penicillium fungi. This epipolythiodioxopiperazine (ETP) toxin possesses a unique disulfide bridge that plays a pivotal role in its biological activity. Gliotoxin exerts its effects through the induction of oxidative stress by generating reactive oxygen species (ROS) and disrupting cellular redox balance. Additionally, it can inhibit the activation of crucial transcription factors like NF-κB, thereby modulating immune responses. In scientific research, gliotoxin is extensively used to study fungal pathogenicity, particularly in Aspergillus fumigatus, a significant opportunistic pathogen. Its immunosuppressive properties make it a valuable tool for exploring immune system dynamics, especially in the context of transplantation and autoimmune diseases. However, due to its potent cytotoxicity, caution is warranted in handling this compound, emphasizing controlled experimental settings to unravel its complex biological roles.

Applications Gliotoxin is a sulfur-containing mycotoxin produced by species of fungi and pathogens of humans. Gliotoxin exhibits inhibitory activities against histone H3K9 methyltransferase, a key enzyme in the regulation of transcriptional activity by writing epigenetic marks. Gliotoxin also exhibits immunosuppressive properties by causing apoptosis of cells of the immune system. In addition, various studies suggests Gliotoxin may also be a potential anti-inflammatory, antibiotic, antifungal and antiviral agent. Not a dangerous good if item is equal to or less than 1g/ml and there is less than 100g/ml in the package References Takahashi, M., et al.: J. Antibiotics., 65, 263 (2012); Li., Y.G., et al.: Biochem. Biophy. Rsch. Commun., 422, 85 (2012); Zhang, H.C., et al.: Applied, Mech. Mater., 178, 783 (2012); Scharf, D.H., et al.: Appl. Microbiol. Biotechnol., 93, 467 (2012);

Gliotoxin, a mycotoxin, inhibits Wnt pathway, causing apoptosis in mutated colorectal cancer cells and blocks NF-κB by preserving IκB.