Desirudin
A recombinant copy of the leech anticoagulant that blocks thrombin directly, once approved in the US and EU to prevent clots after hip replacement
Desirudin is hirudin, the anticoagulant protein from the saliva of the medicinal leech, made by recombinant DNA technology without the sulfate group the natural protein carries. It binds thrombin, the enzyme that makes blood clot, directly and very tightly, including thrombin already inside a clot. Given as two injections a day, it prevented more deep vein thrombosis after hip replacement than heparin or enoxaparin. Europe authorised it as Revasc in 1997 and the US as Iprivask in 2003; both products have since been withdrawn or discontinued for commercial reasons.
Last FDA label of a product discontinued in the US (not a current US recommendation): 15 mg, Every 12 hours; first dose 5 to 15 minutes before surgery, after any regional block, Subcutaneous Details ↓
Recommended Dosing
Last FDA label of a product discontinued in the US (not a current US recommendation)
From the last US prescribing information of a product discontinued in the US (see the regulatory status on this page). It records what that label said while the product was sold there; it is not a current US recommendation. Other doses studied, if any, are in the full dosing data below.
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
Work out syringe units → · New to syringes? · All dosing data ↓
What is it?
Hirudin is the protein a medicinal leech injects to keep blood flowing while it feeds. Desirudin is a recombinant version of that protein, lacking the sulfate group the natural form carries, which is why early papers call it recombinant desulfatohirudin. Under the code CGP 39393 it was first studied in healthy volunteers in the early 1990s, given into a vein or under the skin.
It works on thrombin itself. Heparins act through antithrombin and cannot reach thrombin that is already bound inside a clot; desirudin binds thrombin's active site and its fibrinogen-binding site directly, whether the enzyme is circulating or clot-bound. Its effect shows up as a longer activated partial thromboplastin time (aPTT), which rose in proportion to the dose in volunteer studies, while thrombin time was too sensitive and prothrombin time too insensitive to be useful. The kidneys clear it, so blood levels and aPTT climb when kidney function falls.
Its main use was preventing deep vein thrombosis after hip replacement. In a European trial of 1,119 patients, 10, 15 and 20 mg twice daily all lowered clots against heparin, and 15 mg twice daily cut proximal clots from about 20% to 3%. A second double-blind trial against heparin found clots in 7% of patients on desirudin against 23% on heparin, and a 2,078-patient trial against enoxaparin later showed its advantage held, or grew, in patients with reduced kidney function. A 40 mg dose caused major bleeding and was abandoned. These trials led to European authorisation as Revasc in 1997 and US approval as Iprivask in 2003, at 15 mg every 12 hours with the first dose just before surgery.
It was also tried more widely. In heart attack and unstable angina trials, given intravenously with clot-dissolving drugs, results were mixed, and it did not become a heart drug. Later US studies looked for other roles: an open-label study of 516 surgical and medical patients found no major bleeding, a small trial in suspected heparin-induced thrombocytopenia found it cheaper than argatroban with no major bleeding, and in heart and chest surgery patients it did not trigger the antibodies that cause that heparin reaction. About one patient in ten developed antibodies to hirudin itself, without any change in its effect.
Neither product is available now. The EU authorisation was withdrawn at the holder's request in July 2014, and Drugs@FDA lists Iprivask as discontinued; its last US label, revised in 2014, is the source of the dosing below. Bivalirudin, a shorter synthetic peptide modelled on hirudin, and the related recombinant hirudin lepirudin have their own entries.
Mechanism of Action
Desirudin binds thrombin directly and almost irreversibly, so thrombin cannot turn fibrinogen into fibrin or amplify its own production, whether it is free in blood or held inside a clot.
Direct thrombin block
It occupies thrombin's active site and its fibrinogen-binding exosite, needing no antithrombin, and reaches clot-bound thrombin (2000 review).
Delayed thrombin burst
In plasma it slows the thrombin-driven activation of the clotting cofactors that amplify it, and so lengthens the lag before thrombin generation, though it cannot stop the burst entirely (1990 laboratory study).
Measured by aPTT
aPTT rises with its blood level over a wide range, which is why aPTT is the test used to monitor it (1993 volunteer studies).
Kidney clearance
About half to 60% leaves unchanged in urine; clearance follows creatinine clearance, so doses are cut in kidney impairment (1997 study).
Published Research
Studies of desirudin itself, under that name or its code CGP 39393, read from their PubMed abstracts: the hip-replacement trials behind its approval, volunteer pharmacology, kidney-impairment studies, later US studies in surgery and heparin-induced thrombocytopenia, and reviews. Trials that titled it only as 'hirudin' are not carded.
Dose-ranging against heparin, 1,119 patients
In a double-blind European trial in elective hip replacement, 10, 15 or 20 mg of CGP 39393 twice daily under the skin, started just before surgery for 8 to 11 days, cut venographic deep vein thrombosis from 34.2% on heparin 5,000 IU three times daily to 23.9%, 18.4% and 17.7%. Proximal clots fell from 19.6% to 8.5%, 3.1% and 2.4%.
15 mg twice daily against heparin
In 445 hip-replacement patients randomised double-blind, confirmed deep vein thrombosis occurred in 7% on desirudin 15 mg twice daily against 23% on heparin, and proximal thrombosis in 3% against 16%. All four pulmonary emboli in follow-up were in the heparin group; bleeding did not differ.
Finding the maximum dose
In an open safety study in 48 hip-replacement patients, doses of 10 to 20 mg twice daily were tolerated, with deep vein thrombosis in 42% at 10 mg and about 10% at 15 and 20 mg. The first three patients on 40 mg twice daily each had a major bleed, so that dose was stopped.
Kidney disease: fewer clots than enoxaparin
In a post hoc analysis of a 2,078-patient double-blind hip-replacement trial of desirudin 15 mg twice daily against enoxaparin 40 mg daily, the 577 patients with stage 3B kidney disease or worse had major venous thromboembolism in 3.4% on desirudin against 11.1% on enoxaparin, with no difference in major bleeding.
Antibodies to hirudin
Of 112 hip-surgery patients in a dose-finding study (10, 15 or 20 mg twice daily), 11 (9.8%) developed IgG antibodies to hirudin whatever the dose. The antibodies did not change desirudin levels and were not linked to clots, allergy or bleeding.
DESIR-ABLE: 516 surgical and medical patients
In an open-label, single-arm study at 19 US centres, 516 patients after major surgery or with prolonged immobility received 15 mg every 12 hours; many had low platelets, severe obesity or reduced kidney function. There were no major bleeds and no deaths from venous thromboembolism.
Knee replacement, first dose after surgery
In a case series of knee-replacement patients given 15 mg every 12 hours for about five days, starting the evening after surgery, there was no major bleeding, wound ooze or infection and no symptomatic deep vein thrombosis; two patients had pulmonary emboli found on CT.
PREVENT-HIT pilot against argatroban
Sixteen patients with suspected heparin-induced thrombocytopenia were randomised to fixed subcutaneous desirudin (15 or 30 mg every 12 hours) or intravenous argatroban. No one died or lost a limb; major bleeding occurred in two argatroban patients and none on desirudin, and drug cost per course was about $1,700 against $8,250.
No heparin-type antibodies after heart surgery
Of 120 cardiac and thoracic surgery patients randomised to desirudin 15 mg twice daily or heparin three times daily, new antibodies to the PF4-heparin complex appeared in none of the 36 desirudin patients without heparin exposure; deep vein thrombosis and bleeding were similar in the two groups.
Kidney impairment raises exposure
After intravenous doses scaled down for kidney function, exposure rose 1.15, 2.83 and 7 times in mild, moderate and severe impairment, and clearance followed creatinine clearance. About 55% to 60% left in urine; the authors advised a six-fold dose cut in severe kidney failure.
Moderate impairment may not need a cut
Pooled data from six studies and simulations found peak levels after 15 mg every 12 hours of 35 nmol/l with normal kidneys and 47 nmol/l with moderate impairment, supporting the full dose without aPTT monitoring in moderate impairment.
Intravenous pharmacology in 47 volunteers
Bolus doses of 0.1 to 1.0 mg/kg gave peaks of 154 to 1,691 nmol/l, and infusions of 0.1 to 0.3 mg/kg per hour gave steady levels of 78 to 312 nmol/l. Clearance averaged 2.2 ml/min/kg; aPTT doubled at 100 nmol/l and was judged the best monitoring test, and there was no clinically relevant bleeding.
Under the skin in 231 volunteers
Single subcutaneous doses of 0.1 to 0.75 mg/kg lengthened aPTT in proportion to the dose within 30 minutes, with a near-maximal effect for 3 to 4 hours; repeated doses for 3 or 6 days kept aPTT raised without lengthening bleeding time.
A weak allergen
In 263 healthy volunteers given CGP 39393 into a vein or under the skin, a first exposure caused no allergic signs, and after a second course a type I allergic reaction attributable to it was rare, under 1%; one volunteer developed low-level hirudin-specific IgE.
No important interaction with piroxicam
In 12 healthy men, 12 days of the anti-inflammatory piroxicam before a 6-hour infusion of 0.1 mg/kg per hour barely changed the aPTT response (peak 83 vs 84 seconds), and the drug did not lengthen bleeding time further.
Heart attack trials in context
This trial report on the HERO-2 rationale summarises that, in the GUSTO 2b trial, hirudin (desirudin) given with streptokinase cut death or reinfarction at 30 days from 14.4% to 8.6% against heparin, while drugs that block thrombin directly gave modest gains overall after clot-dissolving drugs.
More effective than heparin in hip surgery
This review found desirudin clearly better than unfractionated or low-molecular-weight heparin at preventing deep vein thrombosis after hip replacement, with similar bleeding, while its results in acute coronary syndromes were inconsistent between two large heart-attack trials and showed no lasting benefit at 30 days.
The first thrombin inhibitor for clot prevention
Described as the first direct thrombin inhibitor approved for deep vein thrombosis prophylaxis in Europe and a newcomer in the US, desirudin offered fixed dosing and less immunogenicity than heparin but needed dose changes in kidney impairment.
Compared with bivalirudin for stenting
This review compares desirudin, which binds thrombin more tightly, with bivalirudin, the direct thrombin inhibitor approved for coronary intervention, and their roles around stenting in acute coronary syndromes.
Better patency in microsurgery
In a blinded rat model of microvenous anastomosis, desirudin given 30 minutes before surgery kept 96.9% of vessels open against 53.1% with saline and cut non-occluding clots from 41% to 3%, while lengthening bleeding time modestly.
How it delays thrombin in plasma
In activated human plasma, CGP 39393 lengthened the lag before thrombin generation by slowing the thrombin-driven activation of the clotting cofactors (factor V and the antihaemophilic factor), but could not prevent the eventual burst of thrombin.
Dosing Data
The first rows are the last US label for Iprivask, revised in November 2014. The product is discontinued, so these are printed to explain the trials, not as a dose anyone can obtain. The trial rows below are doses given in the studies carded above.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Desirudin is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: we hold no copy of the preparation section of the label behind Desirudin's dose. Its label, named in Recommended Dosing above, is the source; the reconstitution calculator does the arithmetic for any vial.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Desirudin, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Desirudin stays intact once mixed.
How it is taken
As the approved label gives it: Subcutaneous (Every 12 hours; first dose 5 to 15 minutes before surgery, after any regional block; Last US label (Iprivask, discontinued): hip replacement).
Source: Last FDA label of a product discontinued in the US (not a current US recommendation): the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: a half-life of about 2 hours after a subcutaneous dose; 2 to 3 hours terminal after intravenous dosing; up to 12 hours in severe kidney impairment. After about five half-lives almost none is left.
How long the doses were given: Last US label (Iprivask, discontinued): hip replacement: Up to 12 days (average 9 to 12 days in trials); Last US label (Iprivask, discontinued): moderate kidney impairment (CrCl 31–60): Interrupt if aPTT exceeds twice control; Last US label (Iprivask, discontinued): severe kidney impairment (CrCl under 31): Interrupt if aPTT exceeds twice control.
When effects appear: unknown; no source on this page gives a time to effect for Desirudin. Results reported in the studies are under Published Research.
Source: half-life: Iprivask (desirudin for injection) US prescribing information, revised November 2014, Clinical Pharmacology (Drugs@FDA, BLA 021271); Last FDA label of a product discontinued in the US (not a current US recommendation), the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: Bleeding: any haemorrhage in 30% of desirudin patients in the hip-replacement trials against 22% on heparin and 33% on enoxaparin; serious bleeding in about 3% (label); Major bleeding at 40 mg twice daily, the reason that dose was dropped (PMID 7831657); Antibodies to hirudin in about 10% of patients, without loss of effect (PMID 12393696); Allergic reactions in under 2% of trial patients; rare type I allergy in volunteers (label; PMID 7719527). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Desirudin. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the trials above and the last US label”).
Interactions
Unknown: a PubMed search for human interaction studies of Desirudin (reviewed 2026-10-28) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Desirudin products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against Desirudin's expected mass, 6,963.0 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Discontinued (FDA-approved April 4, 2003 as Iprivask (BLA 021271) for deep vein thrombosis prophylaxis after elective hip replacement). Sport: Unsettled (S0 may apply).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
From the trials above and the last US label.
Contraindications & Cautions
Boxed warning, contraindications and warnings from the last US label (Iprivask, revised November 2014):
Legal Status
Desirudin was approved in the US and the EU; neither product is on the market now.
Frequently Asked Questions
?What is desirudin?
A recombinant form of hirudin, the anticoagulant protein in leech saliva. It blocks thrombin directly and was approved to prevent deep vein thrombosis after hip replacement.
?Is desirudin still available?
No. Drugs@FDA lists Iprivask as discontinued, and the EU authorisation for Revasc was withdrawn in 2014 for commercial reasons.
?What was the dose?
The last US label gave 15 mg under the skin every 12 hours, starting just before surgery, cut to 5 mg or 1.7 mg every 12 hours in moderate or severe kidney impairment.
?How did it compare with heparin?
In hip-replacement trials it prevented more deep vein thrombosis than unfractionated heparin and enoxaparin, with similar rates of serious bleeding.
?How is it different from bivalirudin and lepirudin?
Lepirudin is another recombinant hirudin with a slightly different sequence; bivalirudin is a short synthetic peptide modelled on hirudin. All three block thrombin directly, and each has its own entry.
References
- [fda] Drugs@FDA (openFDA): BLA021271, IPRIVASK (desirudin recombinant), Bausch; original approval April 4, 2003; marketing status Discontinued. Read October 28, 2026.
- [other] PubChem CID 16129703, Desirudin: formula C287H440N80O110S6, molecular weight 6963. Read October 28, 2026. https://pubchem.ncbi.nlm.nih.gov/compound/16129703
- [fda] Iprivask (desirudin for injection) US prescribing information, revised November 2014 (Drugs@FDA, BLA 021271, supplement 6; Marathon Pharmaceuticals): dosage, renal adjustment, boxed warning, contraindications and pharmacokinetics. Read October 29, 2026.
- [other] European Medicines Agency, Revasc (desirudin): authorised July 9, 1997; authorisation withdrawn July 18, 2014 at the holder's request for commercial reasons. Read October 29, 2026.
- [clinical-trial] Eriksson BI, et al. "Prevention of deep-vein thrombosis after total hip replacement: direct thrombin inhibition with recombinant hirudin, CGP 39393." Lancet, 1996;347(9002):635-9. PMID: 8596376.
- [clinical-trial] Eriksson BI, et al. "Prevention of thromboembolism with use of recombinant hirudin. Results of a double-blind, multicenter trial comparing the efficacy of desirudin (Revasc) with that of unfractionated heparin in patients having a total hip replacement." J Bone Joint Surg Am, 1997;79(3):326-33. PMID: 9070519.
- [clinical-trial] Eriksson BI, et al. "Direct thrombin inhibition with Rec-hirudin CGP 39393 as prophylaxis of thromboembolic complications after total hip replacement." Thromb Haemost, 1994;72(2):227-31. PMID: 7831657.
- [clinical-trial] Shorr AF, et al. "Impact of stage 3B chronic kidney disease on thrombosis and bleeding outcomes after orthopedic surgery in patients treated with desirudin or enoxaparin: insights from a randomized trial." J Thromb Haemost, 2012;10(8):1515-20. PMID: 22672318.
- [clinical-trial] Greinacher A, et al. "Antihirudin antibodies following low-dose subcutaneous treatment with desirudin for thrombosis prophylaxis after hip-replacement surgery: incidence and clinical relevance." Blood, 2003;101(7):2617-9. PMID: 12393696.
- [clinical-trial] Bergese SD, et al. "Multicenter trial of desirudin for the prophylaxis of thrombosis: an alternative to heparin-based anticoagulation (DESIR-ABLE)." Clin Appl Thromb Hemost, 2013;19(4):418-23. PMID: 22802554.
- [clinical-trial] Jove M, et al. "Safety of desirudin in thrombosis prevention after total knee arthroplasty: the DESIR-ABLE study." Am J Ther, 2014;21(6):496-9. PMID: 23344102.
- [clinical-trial] Boyce SW, et al. "A randomized, open-label pilot study comparing desirudin and argatroban in patients with suspected heparin-induced thrombocytopenia with or without thrombosis: PREVENT-HIT Study." Am J Ther, 2011;18(1):14-22. PMID: 21079512.
- [clinical-trial] Avidan MS, et al. "The occurrence of antibodies to heparin-platelet factor 4 in cardiac and thoracic surgical patients receiving desirudin or heparin for postoperative venous thrombosis prophylaxis." Thromb Res, 2011;128(6):524-9. PMID: 21794899.
- [clinical-trial] Lefèvre G, et al. "Effect of renal impairment on the pharmacokinetics and pharmacodynamics of desirudin." Clin Pharmacol Ther, 1997;62(1):50-9. PMID: 9246019.
- [pubmed] Nafziger AN, et al. "Desirudin dosing and monitoring in moderate renal impairment." J Clin Pharmacol, 2010;50(6):614-22. PMID: 19915180.
- [clinical-trial] Marbet GA, et al. "Clinical pharmacology of intravenously administered recombinant desulfatohirudin (CGP 39393) in healthy volunteers." J Cardiovasc Pharmacol, 1993;22(3):364-72. PMID: 7504125.
- [pubmed] Verstraete M, et al. "Biologic effects of recombinant hirudin (CGP 39393) in human volunteers. European Hirudin in Thrombosis Group." J Am Coll Cardiol, 1993;22(4):1080-8. PMID: 8409044.
- [clinical-trial] Close P, et al. "Weak allergenicity of recombinant hirudin CGP 39393 (REVASC) in immunocompetent volunteers. The European Hirudin in Thrombosis Group (HIT Group)." Coron Artery Dis, 1994;5(11):943-9. PMID: 7719527.
- [clinical-trial] Thürmann P, et al. "Influence of piroxicam coadministration on pharmacodynamic parameters and the plasma concentration/effect relationship of recombinant hirudin (CGP 39393)." Eur J Clin Pharmacol, 1995;48(3-4):241-6. PMID: 7589048.
- [clinical-trial] White HD, et al. "Hirudin (desirudin) and Hirulog (bivalirudin) in acute ischaemic syndromes and the rationale for the Hirulog/Early Reperfusion Occlusion (HERO-2) Study." Aust N Z J Med, 1998;28(4):551-4. PMID: 9777138.
- [review] Matheson AJ, et al. "Desirudin: a review of its use in the management of thrombotic disorders." Drugs, 2000;60(3):679-700. PMID: 11030473.
- [review] Graetz TJ, et al. "Desirudin: a review of the pharmacology and clinical application for the prevention of deep vein thrombosis." Expert Rev Cardiovasc Ther, 2011;9(9):1101-9. PMID: 21932952.
- [review] Vranckx P, et al. "Looking back into the future: desirudin in acute coronary syndromes and coronary stenting." EuroIntervention, 2011;7(2):263-9. PMID: 21646070.
- [pubmed] Lewis CM, et al. "Desirudin reduces the rate of microvenous thrombosis in a rat model." Laryngoscope, 2008;118(7):1149-52. PMID: 18401270.
- [pubmed] Lindhout T, et al. "The anticoagulant mechanism of action of recombinant hirudin (CGP 39393) in plasma." Thromb Haemost, 1990;64(3):464-8. PMID: 2096492.
Sources & Citations
Studies were read from their PubMed abstracts on October 29, 2026. The label is the last Iprivask prescribing information on Drugs@FDA (revised November 2014); approval and marketing status come from Drugs@FDA (openFDA) and the EMA Revasc page, read October 28-29, 2026. The formula is PubChem's. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.