Drug Disease Interaction Discussion

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Question 4. As we discussed in class, Aspirin inhibits cyclooxygenase-1 (COX-1) by irreversibly acetylating a serine residue at position 529. It is also well-known that residue 523, an isoleucine -is a part of active site of COX-1. In its isoform, COX-2, this residue is a valine. Explain how this information can be used to design a molecule that can selectively bind to COX-2. (300 words; 10points)

Question 1. As I mentioned during the class, HIV-1 protease is an important drug target. Refer to this review – Konvalinka et al., Virology 2015 (Fig. 5, pages 408-409). Explain the strategies used by HIV-1 to evade clinically used protease inhibitors. Explain how and why these strategies are effective when interactions between the synthetic drugs and protease are always much stronger than that of interactions between protease and its natural substrate. (500 words; 15 points)

Question 2. Not many small therapeutic molecules have been on the cover of TIME magazine. However, Gleevec (Imatinib; Novartis) has had this honor on May 2001. See this web-article to gain more information about Gleevec – https://www.nature.com/scitable/topicpage/gleevec-thebreakthrough-

in-cancer-treatment-565/. Using this and other literature, explain why Gleevec – a tyrosine kinase inhibitor – has been such a trendsetter as a kinase inhibitor. (500 words; 15 points)

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