First lecture 22/9/2008

Click the following link about the discovery of Captopril
http://en.wikipedia.org/wiki/Captopril

Here are some examples of true/false questions from previous exams:
1- Mechanism-based drug design is a rationale drug design.
2- 5-FU inhibits DNA biosynthesis in cancer cells because of its structure analogy to deoxyguanosine.
3- Mevalonic acid is the natural substrate of HMG-CoA reductase enzyme in cholesterol biosynthesis.
4- The mechanism of the antidiabetic effect of rosiglitasone is not a receptor mediated process.
5- The molecular lead of captopril is the nonapeptide ‘teprotide’.
6- Although, cimetidine is not structurally related to histamine, yet it is a potent H2-receptor antagonist.
The answers are : T, F, F, F, T, F.

After studying the lecture you should:
* Be able to differentiate between traditional and rationale drug design.
* Differentiate between pharmacological action of a drug and its therapeutic application.
*Notice the mimicry (resemblence) between natural metabolites or endogenous components and their antagonists.
*Be able to identify the biological targets (enzyme or receptor) for each drug.
*Know how to modify lead compounds to improve binding of the drug molecule to its target protein. (Example of Captopril,..).
*Relate between the physicochemical properties of a drug (E.g. polymixin) and its mechanism of action.