| Class | Parenteral anticoagulant |
|---|---|
| Chemistry |
A mixture of heparan sulphate, dermatan sulphate, and chondroitin sulphate |
| Routes of administration |
IV ands subcut |
| Absorption |
Oral bioavailability is minimal, less than 1%. |
| Solubility |
pKa 3.0; good water solubility |
| Distribution |
VOD=0.1L/kg; minimal plasma protein binding |
| Metabolism |
Minimally metabolised |
| Elimination |
50% of danaparoid is eliminated via the kidneys. |
| Time course of action |
Half-life is about 25 hours |
| Target receptor |
Antithrombin III |
| Mechanism of action |
By binding to antithrombin III and causing the active site to undergo a conformational change, danaparoid increases its affinity for factor Xa (but not thrombin). The result is an increase in the activity of antithrombin on Factor Xa, which manifests in the form of the anticoagulant effect. Danaparoid has a low molecular weight, which means it does not have any effect on the activity of antithrombin III on thrombin. |
| Clinical effects |
Anticoagulation is the only clinically apparent effect; no significant side effects apart from bleeding; minimal risk of HITS |
| Literature reference |
Orgaran PI document |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |