Fisetin-d₅

Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs^[1].
Fisetin inhibits lipid accumulation and suppresses the expression of PPARγ in 3T3-L1 cells. Fisetin suppresses early stages of preadipocyte differentiation, and induces expression of Sirt1. Fisetin facilitates Sirt1-mediated deacetylation of PPARγ and FoxO1, and enhances the association of Sirt1 with the PPARγ promoter, leading to suppression of PPARγ transcriptional activity, thereby repressing adipogenesis^[2]. Fisetin binds to tubulin and stabilizes microtubules with binding characteristics far superior than paclitaxel. Fisetin treatment of human prostate cancer cells results in robust up-regulation of microtubule associated proteins (MAP)-2 and -4. Fisetin significantly inhibits PCa cell proliferation, migration, and invasion. Nudc, a protein associated with microtubule motor dynein/dynactin complex that regulates microtubule dynamics, is inhibited with Fisetin treatment^[3].

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