Casprin Mechanism of Action

Aspirin is the most widely used drug in the world for pain relief. It has been used as an antiplatelet agent to prevent thrombosis and embolism and has been formulated as enteric-coated low-dose preparation for the prophylaxis and treatment of transient ischaemic attack (TIA) and other thromboembolic disorders.
Pharmacology: Aspirin is an analgesic, anti-inflammatory, antipyretic and an inhibitor of platelet aggregation. It acetylates the enzyme cyclooxygenase, thereby inhibiting the synthesis of prostaglandins, thromboxane in the circulation, platelets and prostacyclin in the systemic vascular endothelium. Thromboxane is a vasoconstrictor and inhibitor of platelet aggregation.
The antiplatelet aggregating effect of Casprin is postulated to retard or reduce the development of thromboembolic disorders. The low dose, enteric-coated and relatively slow rate of release of aspirin is observed to selectively and irreversibly inhibit thromboembolic synthesis. Aspirin inhibits thromboxane synthesis in the portal circulation and is presystemically metabolised to salicylate with negligible amount reaching the systemic circulation to inhibit prostacyclin synthesis. Salicylate is effectively inactive at the blood concentrations achieved clinically and prostacyclin is less sensitive than thromboxane to aspirin.
Pharmacokinetics: In order to eliminate the gastrointestinal adverse effects of aspirin, an enteric-coated, low-dose aspirin (as pellets) was developed. The advantages of enteric-microencapsulated capsules include ready distribution over a large area, thus minimizing the risk of local damage caused by the dumping effect of enteric-coated tablets. Furthermore, enteric-microencapsulated capsules are also less dependent on gastric transient time. They may attain more constant plasma level, achieve slow-release effect, give higher accuracy in reproducibility between doses and provide less decreases in bioavailability.
Following oral administration, absorption of aspirin occurs in the intestine. Some aspirin is hydrolysed to salicylate in the gut wall. Aspirin is bound to plasma protein and is widely distributed. Plasma aspirin concentrations decline rapidly (half-life: 15-20 min) as plasma salicylate concentrations increases.
Aspirin is rapidly converted by esterases present in plasma and many tissues, especially the liver, to salicylic acid which itself has some antipyretic, analgesic and anti-inflammatory actions but which has little effects on platelets. Salicylic acid is metabolised in the liver to the glycine conjugate salicyluric acid. Other metabolites include salicyl phenolic glucuronide; salicyl acyl glucuronide and gentisic acid. Excretion of salicylic acid in urine is pH-dependent; approximately 80% appears unchanged in urine at pH 8, but only around 10% at pH 4.
Since enteric-coated pellets of aspirin can reduce gastrointestinal side effects that may occur with conventional or other enteric-coated tablet preparations, it is an effective antiplatelet treatment of choice for long-term treatment and prevention of certain forms of ischaemic attacks.