Pharmacology 4350A/B Lecture Notes - Lecture 8: Rifabutin, Bosentan, Muromonab-Cd3
Document Summary
Fda sped up process in 1990 + biopharmaceutical in 1980. High throughput screening assays best serves this strategy. Automated system in conducting chemical, genetic, pharmacological tests and allow identification of active compounds + ab + genes involved in a biomolecular pathway. Universities use this to make money and allow academia teaching. Sometimes the target is not actually related to pathogenesis. Target ab1 tyrosine kinase 3d structure allowed binding pocket structure. Discovery pre-clinical development took many years but clinical development took only 3 years to be registered on market. Drug approved without knowing what the mechanism/target was. Later found to target npc1l1 (cholesterol transporter) + metabolite ezetimibe glucuronide is more effective. Strategy more successful for infectious disease + cns diseases. When target is identified and related to pathogenesis. Ex: mono ab for pcsk9 (proprotein covertase substillin/kexin 9) increase ldl-receptors + lower blood cholesterol. Successful in phase 2 trials + ab cannot be oral administered (iv only)