IMPACT ARA reagent is sensitive to aspirin and NSAID like diclofenac or ibuprofen. It contains arachidonic acid.

Disorders in arachidonic acid metabolism or thromboxane synthesis can lead to blood clotting disorders. Most of these disorders are acquired by taking different types of medications like aspirin and other painkillers or NSAID (e.g. diclofenac, ibuprofen), which inhibit cyclooxygenase and reduce TXA2 production and thus platelet aggregation.

Arachidonic acid plays a crucial role in platelet activation by being converted to thromboxane A2 (TXA2) by cyclooxygenase. TXA2 is a potent agent that promotes platelet aggregation and vasoconstriction, which contributes to blood clotting.

The in vitro addition of arachidonic acid mimics the in vivo process of endothelial injury.

Upon endothelial injury, platelets are activated and release arachidonic acid from their cell membrane. Arachidonic acid is converted to TXA2 by cyclooxygenase, an enzyme found in platelets. TXA2 plays an important role in primary haemostasis, the first phase of blood clotting, in which a platelet clot is formed to stop bleeding.

TXA2 acts via the thromboxane receptor (TXA2-R) and stimulates platelet aggregation, i.e., the clumping of platelets. TXA2 also triggers vasoconstriction, a narrowing of blood vessels, which also contributes to blood clotting.