Repositioning Candidate Details
| Candidate ID: | R0701 |
| Source ID: | DB05099 |
| Source Type: | approved; investigational |
| Compound Type: | biotech |
| Compound Name: | Ancrod |
| Synonyms: | Ancrod |
| Molecular Formula: | -- |
| SMILES: | -- |
| DrugBank Description: | Ancrod, marketed as Viprinex, is a defibrinogenating agent derived from Malayan pit viper venom. 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. |
| CAS Number: | 9046-56-4 |
| Molecular Weight: | |
| DrugBank Indication: | Ancrod is indicated for the treatment of deep vein thrombosis (DVT), central retinal branch vein thrombosis, pripaism, pulmonary hypertension of embolic origin, embolism after insertion of prosthetic cardiac valves, rethrombosis after thrombolytic therapy, rethrombosis after vascular surgery, and prevention of DVT after repair of a fractured neck of a femur. |
| DrugBank Pharmacology: | 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, facilitates physical and ergo therapy, and decreases the likelihood of local thrombotic events. |
| DrugBank MoA: | 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. Blood viscosity is reduced by 30-40%. Ancrod does not activate plagminogen and does not degrade preformed, fully cross-linked thrombin fibrin. Consequently, unlike fibrinolytic agents, ancrod can be used postoperatively. Ancrod does not activate Factor XIII, produce platelet aggregation, or release ADP, ATP, potassium, or serotonin from platelets. |
| Targets: | Fibrinogen alpha chain |
| Inclusion Criteria: | Therapeutic strategy associated |
| Strategy ID | Strategy | Synonyms | Related Targets | Related Drugs |
|---|
| Diseases ID | DO ID | Disease Name | Definition | Class | |
|---|---|---|---|---|---|
| I16 | 6713 | Cerebrovascular disease | An vascular disease that is characterized by dysfunction of the blood vessels supplying the brain. http://en.wikipedia.org/wiki/Cerebrovascular_disease, http://www.ncbi.nlm.nih.gov/books/NBK378/ | disease of anatomical entity/ cardiovascular system disease/ vascular disease/cerebrovascular disease | Details |
| I12 | 10763 | Hypertension | An artery disease characterized by chronic elevated blood pressure in the arteries. https://en.wikipedia.org/wiki/Hypertension, https://www.ncbi.nlm.nih.gov/pubmed/24352797 | disease of anatomical entity/ cardiovascular system disease/vascular disease/ artery disease | Details |