Ochratoxin A (OTA)-methyl ester was the main metabolite produced after ochratoxin A exposure. It is known, that OTA shows potent renal toxicity and carcinogenicity in rodents, with a tendency to develop a renal tumor. Recent experiments revealed that the hybrid Caco-2/HepG2 co-culture system might be a promising tool for assessing the cytotoxicity parameters and the biotransformation of OTA. Both cells Caco-2 and HepG2 metabolized OTA to OTA methyl ester at the concentrations where this mycotoxin shows not cytotoxic effect. In this sense, the use of the methylated metabolite of OTA reported as the major metabolite could be a novel biomarker of OTA in biological samples.

Piericidin A (also named piericidin A1 in some references) was reported as a new insecticidal metabolite, produced by cultures of the soil-derived actinomycete Streptomyces mobaraensis. Piericidin A resembles coenzyme Q in its overall structure containing a pyridine ring with two adjacent methoxy groups. The most widely recognized biological target of Piericidin A is the mitochondrial electron transport chain protein NADH-ubiquinone reductase (Complex I). Respiratory inhibition by piericidin A can be reversed by the addition of vitamin-K3 (menadione) to the inhibited respiratory chain in mammalian mitochondria. Piericidin A increases ROS production. Piericidin A showed significant cytotoxic activities against several tumor cells, such as mouse leukemia cell line, human colon carcinoma cells and was selectively cytotoxic toward human multiple myeloma cells. Moreover, it was identified as a highly selective antitumor agent with greater selectivity and potency than the comparison standard mitomycin C. Piericidin A aggravates the course of genetically determined tau pathology.

Lavendustin A is a selective inhibitor of epidermal growth factor (EGF) receptor-associated tyrosine kinase; it does not inhibit protein kinase A or C. It was shown, that lavendustin A inhibited histamine release from human mast cell line.