| Class | Serine protease inhibitor |
|---|---|
| Chemistry |
Monocarboxylic acid (a synthetic derivative of the amino acid lysine)
|
| Routes of administration |
IV, nebulised, topical, oral |
| Absorption |
50% absorbed from the GI tract; bioavailability is about 30-35%. Most of it is not metabolised.
|
| Solubility |
pKa of 10.22; highly water soluble, but minimally fat-soluble
|
| Distribution |
VOD = 0.18 L/kg; minimally protein bound (3%, all of which is binding to plasminogen). After some loading (eg. several doses over 24-36 hrs), enough of it distributes to the tissues to continue having a sustained antifibrinolytic effect for many hours
|
| Metabolism |
Minimally metabolised
|
| Elimination |
95% of the dose is excreted unchanged in the kidneys; half-life is 2 hours
|
| Time course of action |
Relatively short-acting, very rapid onset of effect
|
| Target receptor |
Plasminogen |
| Mechanism of action | |
| Clinical effects |
Prevents the breakdown of fibrin, thus maintaing clot integrity. Numerous other effects (as it also inhibits other proteases), as well as indirect effects via plasminogen inhibition (eg. on complement activation, where by reducing plasmin activity it reduces the consumption of C1 esterase inhibitor) |
| Literature reference | |
| CICM details of understanding | Level 3 |
| Mentioned around Deranged Physiology | |
| Related SAQs |
Question 6 from the first paper of 2024 Question 19 from the second paper of 2021 Question 4 from the first paper of 2013 Question 3 from the first paper of 2010 Question 19 from the second paper of 2015 |