Accession Number
Approved, Investigational

Ancrod (current brand name: Viprinex) is a defibrinogenating agent derived from the venom of the Malayan pit viper. The defribrinogenation of blood results in an anticoagulant effect. Currently, Viprinex®/ancrod is not approved or marketed in any country, but is being investigated as a stroke treatment in worldwide clinical trials. In January 2005, the U.S. FDA granted a 'fast-track status' for investigation of ancrod use in patients suffering from acute ischemic stroke, a life threatening condition caused by the blockage of blood vessels supplying blood and oxygen to portions of the brain, for which phase III trials are currently being conducted.

Not Available
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
ViprinexLiquid70 unitIntravenous; SubcutaneousAbbott1986-12-312007-07-31Canada
CAS number



For the treatment of established deep vein thrombosis; central retinal and branch vein thrombosis; priapism; pulmonary hypertension of embolic origin; embolism after insertion of prosthetic cardiac valves; rethrombosis after thrombolytic therapy and rethrombosis after vascular surgery. It is also indicated for the prevention of deep venous thrombosis after repair of the fractured neck of a femur.


The decreased viscosity is directly attributable to lowered fibrinogen levels and leads to important improvements in blood flow and perfusion of the microcirculation.Ancrod decreases the blood viscosity in affected arteries, leads to less intense pain, improves physical limb mobility, and facilitates physical and ergo therapy. Finally, ancrod decreases the likelihood of local thrombotic events.

Mechanism of action

Ancrod's anticoagulant effects are through the rapid removal of fibrinogen from the blood within hours following ancrod administration. Ancrod specifically cleaves only the alpha chain of fibrinogen, producing the characteristic fibrinopeptides A, AP and AY, not the B-fibrinopeptide. The resulting fibrin polymers are imperfectly formed and much smaller in size (1 to 2 µm long) than the fibrin polymers produced by the action of thrombin. These ancrod-induced microthrombi are friable, unstable, urea-soluble and have significantly degraded a-chains. They do not cross-link to form thrombi. They are markedly susceptible to digestion by plasmin and are rapidly removed from circulation by either reticuloendothelial phagocytosis or normal fibrinolysis, or both. The blood viscosity in patients receiving ancrod is progressively reduced by 30 to 40%. Ancrod does not activate plagminogen and does not degrade preformed, fully cross-linked thrombin fibrin. Consequently, unlike fibrinolytic agents, ancrod can be used postoperatively. Unlike thrombin, ancrod does not directly activate Factor XIII, nor does it produce platelet aggregation nor cause the release of ADP, ATP, potassium, nor serotonin from platelets.

UFibrinogen alpha chainNot AvailableHumans

100% after i.v. dosing

Volume of distribution
Not Available
Protein binding

95% bound to erythrocytes

Not Available
Route of elimination
Not Available
Half life

3 to 5 hours

Not Available

Currently, a new dosing strategy is being investigated in two international phase III trials as part of the 'Ancrod Stroke Program (ASP).' Each of these studies will enroll 650 patients and assess whether a brief, relatively rapid ancrod infusion with no maintenance dosing will be both effective and safe. Contraindications and precautions Known bleeding disorders of any origin or any unexplained excessive bleedings in the past. Platelet counts of less than 100,000 (even if asymptomatic), exemption : HIT (Heparin- induced thrombocytopenia). Planned surgery or short before delivery. Active ulcerations of the GIT. Any kind of malignant disease. Renal stones (increased likelihood of significant urological bleeding). Severe and uncontrolled arterial hypertension. Active pulmonary tuberculosis. Impaired fibrinolysis. Severe liver disease. Manifest or impending shock. I.M.-Injection : Ancrod should not be injected i.m., because of rapid induction of neutralizing antibodies and therefore drug resistance. Pregnancy Category X : Ancrod was not found to be teratogenic in animal studies, but some fetal deaths occurred as a result of placental hemorrhages in animals given high doses; therefore, it should not be used during pregnancy as the defibrinogenation mechanism of ancrod might be expected to interfere with the normal implantation of the fertilized egg. Side effects Hypersensitivity reactions : Local or generalized skin reactions (rash and urticaria); appearance of neutralizing antibodies to ancrod with partial or total loss of ancrod activity (drug resistance). Sometimes pain at injection site (normally mild)

Affected organisms
Not Available
Not Available
Pharmacogenomic Effects/ADRs
Not Available


Drug Interactions
(1,2,6,7-3H)TestosteroneThe therapeutic efficacy of Ancrod can be increased when used in combination with (1,2,6,7-3H)Testosterone.
(R)-warfarinThe risk or severity of bleeding can be increased when Ancrod is combined with (R)-warfarin.
(S)-WarfarinThe risk or severity of bleeding can be increased when Ancrod is combined with (S)-Warfarin.
1-TestosteroneThe therapeutic efficacy of Ancrod can be increased when used in combination with 1-Testosterone.
18-methyl-19-nortestosteroneThe therapeutic efficacy of Ancrod can be increased when used in combination with 18-methyl-19-nortestosterone.
3,5-diiodothyropropionic acid3,5-diiodothyropropionic acid may increase the anticoagulant activities of Ancrod.
4-hydroxycoumarinThe risk or severity of bleeding can be increased when Ancrod is combined with 4-hydroxycoumarin.
4-HydroxytestosteroneThe therapeutic efficacy of Ancrod can be increased when used in combination with 4-Hydroxytestosterone.
5beta-dihydrotestosteroneThe therapeutic efficacy of Ancrod can be increased when used in combination with 5beta-dihydrotestosterone.
AbaloparatideAbaloparatide may increase the anticoagulant activities of Ancrod.
Food Interactions
Not Available


General References
  1. Hennerici MG, Kay R, Bogousslavsky J, Lenzi GL, Verstraete M, Orgogozo JM: Intravenous ancrod for acute ischaemic stroke in the European Stroke Treatment with Ancrod Trial: a randomised controlled trial. Lancet. 2006 Nov 25;368(9550):1871-8. [PubMed:17126719]
  2. Kelton JG, Smith JW, Moffatt D, Santos A, Horsewood P: The interaction of ancrod with human platelets. Platelets. 1999;10(1):24-9. [PubMed:16801067]
External Links
PubChem Substance
ATC Codes
B01AD09 — Ancrod

Clinical Trials

Clinical Trials
1, 2CompletedTreatmentDeafness / Ear Diseases / Hearing Disorders / Hearing loss or impairment / Hearing Loss, Sensorineural1
3CompletedNot AvailableBrain Infarction / Ischemia, Cerebral / Stroke, Acute1
3TerminatedTreatmentBrain Infarction / Ischemia, Cerebral / Strokes2


Not Available
Not Available
Dosage forms
LiquidIntravenous; Subcutaneous70 unit
Not Available
Not Available


Experimental Properties
Not Available


Not classified


Pharmacological action
General Function
Structural molecule activity
Specific Function
Cleaved by the protease thrombin to yield monomers which, together with fibrinogen beta (FGB) and fibrinogen gamma (FGG), polymerize to form an insoluble fibrin matrix. Fibrin has a major function ...
Gene Name
Uniprot ID
Uniprot Name
Fibrinogen alpha chain
Molecular Weight
94972.455 Da

Drug created on October 21, 2007 16:23 / Updated on November 02, 2018 06:08