Modified aspirin-LAW JIA JUIN

Aspirin inhibits the production of thromboxane (reduces blood clot) and prostaglandin (reduces inflammation) by inactivating cyclooxygenase enzymePTGS or COX.

This is done when Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX or PTGS enzyme. 

Aspirin actually make changes to two types of cyclooxygenase (COX), first it inhibited COX1 ,in addition to that it modified COX2 ,this COX2 is previously in charge of the production of pro inflammatory agent eg prostanoid which will then changed to prostaglandin, but after been modified by aspirin, COX2 now works in a reverse way, it is now producing anti inflammatory agent eg lipoxin. these also make the effect of aspirin to become irreversible and "special" other NSAID drugs eg ibuprofen where their effect is reversible.

So indirectly,aspirin actually produces an inhibitory effect on platelet aggregation and inflammation. This antithrombotic property also makes aspirin an useful agent to reduce the incidence of heart attacks. (As we know heart attacks can be caused by blood clots, and low doses of aspirin can effective reduces the mortality of myocardial infarction.

As I had mentioned ,aspirin effect is irreversible and "special" as compared to other NSAID drugs, but does it means it is good to be irreversible? By selectively inhibiting COX2 //PTGS2, prostaglandin production (to be specific, PGI2; prostacyclin) is downregulated with respect to thromboxane levels. Thus, the natural protective anticoagulative effect of PGI2 is removed, so there is a chance for the increases of risk of thrombus and also heart attacks as well as other circulatory problems.

Furthermore, as we know,platelets have no DNA, they are unable to synthesize new COX2 once aspirin has irreversibly inhibited the effect of it.

BUT DONNT WORRY ,I HAVE A GOOD NEWS HERE ,there is currently an analogue of aspirin synthesized through a single-step reaction in which the carboxyl group was replaced by an ethyl ester, and/or the acetoxy group was replaced by an N-substituted sulfonamide . It had been found that this new drug not only inactivate cyclooxygenase but also act as a strong inhibitor for lipo-oxygenase, by inhibiting this lipo oxygenase ,inflamatory agent like leukotrine failed to be produced, in addition to that this new drug also acts as a donor of nitric oxide which in charge of the DILATION of capillaries and vessels, so overall the extra anti-inflammation effect ,blood thinning effect and vessel dilation effect can over-compensate the problem of down regulation of Prostaglandin I successfully, despite this new analogue also increases the inhibition of COX2, but the net effect is considered better and faster.