CMX 001/444805-28-1 99% C27H52N3O7P Senwayer

Brincidofovir is under investigation for the prevention of Outcomes, Survival Rates, and Cytomegalovirus Disease. Brincidofovir has been investigated for the prevention and treatment of CMV, Adenovirus, BK Virus (BKV), Adenoviruses (AdV), and Epstein-Barr (EBV), among others. Brincidofovir is an oral antiviral drug candidate for the treatment of smallpox infections and complications resulting from smallpox vaccine. It is a lipid mimic of cidofovir formed by linking a lipid 3-hexadecyloxy-1-propanol, to the phosphonate group of cidofovir. Brincidofovir is designed to cross cellular membranes by passive diffusion (vida supra, Phospholipid Mimics Designed to Facilitate Uptake in the Small Intestine). Uptake by this mechanism should be more efficient and lead to a more rapid accumulation of cidofovir in the cytoplasm of the target cell. Once it has reached the cytoplasm, CDV is phosphorylated by host cell nucleoside kinases to form the active antiviral agent cidofovir diphosphate.|Brincidofovir is an alkoxyalkyl ester prodrug containing the synthetic, acyclic nucleoside monophosphate analog cidofovir linked, through its phosphonate group, to a lipid, 3-hexadecyloxy-1-propanol, with antiviral activity against double-stranded DNA viruses. Upon oral administration, brincidofovir crosses the intestinal wall and penetrates target viral-infected cells before being cleaved to the free antiviral agent cidofovir. In turn, cidofovir is phosphorylated by pyruvate kinases to its active metabolite cidofovir diphosphate. Cidofovir diphosphate, bearing structural similarity to nucleotides, competes with deoxycytosine-5-triphosphate (dCTP) for viral DNA polymerase and gets incorporated into the growing viral DNA strands. As a result, it prevents further DNA polymerization and disrupts DNA replication of viruses. Compared to cidofovir, which is given intravenously, hexadecyloxypropyl-cidofovir shows better oral bioavailability, less toxicity and enhanced cellular penetration.