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In cases where the possibility of developing CVD is significant, it may be imperative to implement pharmacological measures to modify risk factors

(2017) described the D-retro-inverso modification strategy that confers protease resistance while maintaining the binding surface topology needed for p53 interaction, establishing the pharmaceutical chemistry basis for FOXO4-DRI [1]

CP-25 reverses prostaglandin E4 receptor desensitization-induced fibroblast-like synoviocyte dysfunction via the G protein-coupled receptor kinase 2 in autoimmune arthritis

CYP2E1 catalyzes the oxidation of APAP to NAPQI, a highly reactive metabolite inducing severe massive hepatocellular necrosis (Ramachandran and Jaeschke, 2020)