Both ASA and Ibuprofen are COX-1 inhibitors. However, ASA inhibits the formation of the enzyme Thromboxan A2 through inhibition of COX-1 at SER 529, which is responsible for thrombocytes. That in turn results in the coagulation inhibition of ASA. Basically, it disturbs the following process:

COX-1 -> Thromboxan A2 -> Thrombocytes -> Coagulation

Ibuprofen does not have anticoagulant properties. Where does Ibuprofen inhibit COX-1, and what is Ibuprofen‘s Mode of Action?

  • Rethinking it: is this mode of action or mechanism of action? Have no good definition for either to differentiate but acronym and tags would need reconsideration? Sep 17, 2018 at 14:47
  • We say Mechanism of Action but Mode probably works too. This is a good pharm question.
    – DoctorWhom
    Sep 18, 2018 at 9:23
  • @DoctorWhom It is. But I've used only 'mechanism' (% we have only this tag) and thought of 'mode' as synonymous. However on the two WP pages they are differentiated. So this 'criticism' is as much about language of the Q as my own edit. Sep 18, 2018 at 11:06
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    What's an ASS in this context? Sep 18, 2018 at 18:47
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    @GrahamChiu Oops, my bad. ASS Is the German abbreviation (AcetylSalicylSäure). I‘ve corrected it
    – Narusan
    Sep 18, 2018 at 21:26

1 Answer 1


I'm not clear why you're asking this as this information is readily available unless I missed something in your question.

As for anticoagulant activity, my recollection is that if anything Ibuprofen is one of the worse NSAIDs in terms of cardiovascular side effects being prothrombotic, though not as bad as Diclofenac.

ibuprofen mode of action

The main mechanism of action of ibuprofen is the non-selective, reversible inhibition of the cyclooxygenase enzymes COX-1 and COX-2 (coded for by PTGS1 and PTGS2, respectively).


Ibuprofen exerts its anti-inflammatory and analgesic effects through inhibition of both COX isoforms. In addition, ibuprofen scavenges HO . radical, . NO and ONOO - and can potentiate or inhibit nitric oxide formation through its effects on nitric oxide synthase (NOS) isoforms. Ibuprofen may activate anti-nociceptive axis through binding to the cannabinoid receptors and through inhibition of fatty acid amide hydrolase (FAAH) that metabolizes endocannabinoid anandamide.

The supplementary question is, why is that NSAIDs also don't have anti-coagulant effect?. And the answer is that they do but it is short lived and reversible as the drug concentration falls, where aspirin's effect is irreversible.

All conventional, non-COX selective NSAIDs, also block platelets by inhibiting thromboxane synthesis but in contrast to aspirin, this effect is reversible. This is why an NSAID is not a satisfactory substitute for low-dose aspirin as a prophylactic therapy for cardiovascular events. As the blood concentration of the NSAID declines, the effect on the platelets also declines and is lost. This loss of platelet inhibitory effect is more pronounced for NSAIDs with shorter half-lives in the body such as ibuprofen, where for significant parts of the 24 hour day, platelets will not be inhibited. This problem is compounded if compliance with the NSAID is not perfect.

There is one other important complication. This effect of aspirin is blocked by concomitant therapy with all non-selective, conventional NSAIDs, except for diclofenac. (2) Also, we now know that the non-selective, conventional NSAIDs also increase the risk of cardiovascular events occurring. Diclofenac happens to be the most risky of the non-selective NSAIDs, and approximately equivalent to available COX-II selective NSAIDs such as celecoxib. (3)

https://www.pharmgkb.org/pathway/PA166121942 https://www.bmj.com/content/346/bmj.f3195/rr/656306

Coxib and traditional NSAID Trialists’ (CNT) Collaboration. Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials. Lancet 2013; doi:10.1016/S0140-6736(13)60900

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    +1 But according to this, I would expect Ibuprofen to be as much an anticoagulant as ASA, not? They both inhibit PTGS, PGH2 and TxA2. Why is the anticoagulating effect of ASA so much stronger?
    – Narusan
    Sep 19, 2018 at 8:13
  • That's a supp question which I've answered as well. Sep 19, 2018 at 20:15

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