Frentizole exhibits a diverse range of bioactivities, demonstrating significant suppressive activity on delayed type hypersensitivity (DTH) without affecting humoral immunity in mice at an oral dose of 50 mg/kg. It shows an increase in ear thickness by 3.5 1/100mm and an inhibition rate of 42.6%. As an inhibitor of the beta amyloid-ABAD interaction, it has an IC50 value of 200000.0 nM. Additionally, this compound modulates various biological processes, including gene expression, splicing, and promoter activation, and shows activity in multiple assays involving lamin A splicing, NF-kB expression, miRNA activation, tau fibril alteration, and histone lysine methyltransferase inhibition, among others.
Despite its broad bioactivity, Frentizole is associated with moderate liver toxicity, with hepatotoxicity occurring in 70% of clinical trials, and low incidences of acute liver toxicity and cirrhosis (2% and 0%, respectively). No severe liver complications such as choleostasis, granulomatous hepatitis, or steatosis were observed.
In cytotoxicity assays against CHOK1 cells, Frentizole has an LC50 value of 31000.0 nM. It shows minimal inhibition of Dyrk1B and weak inhibition of Dyrk1A. In antiviral activity assays, it inhibits SARS-CoV-2 induced cytotoxicity in Caco-2 cells and VERO-6 cells at 10 µM with varying inhibition percentages. The compound also inhibits the SARS-CoV-2 3CL-Pro protease, with inhibition percentages of 30.22% and 20.99% at 20 µM.
Furthermore, Frentizole displays potent inhibition of human HDAC6 in enzymatic assays, with inhibition percentages ranging from 58.18% to 108.65% and an IC50 value of 592.3 nM, indicating effective enzyme inhibition at a low concentration..
Note: Summary generated by AI. Data source: ChEMBL 