Repositioning Candidate Details
| Candidate ID: | R0342 |
| Source ID: | DB00946 |
| Source Type: | approved; investigational |
| Compound Type: | small molecule |
| Compound Name: | Phenprocoumon |
| Synonyms: | 3-(1-Phenylpropyl)-4-hydroxycoumarin; 3-(1'-Phenyl-propyl)-4-oxycoumarin; 3-(alpha-Ethylbenzyl)-4-hydroxycoumarin; 3-(alpha-Phenylpropyl)-4-hydroxycoumarin; 4-Hydroxy-3-(1-phenylpropyl)-2H-1-benzopyran-2-one; 4-hydroxy-3-(1-phenylpropyl)-2H-chromen-2-one; Fenprocumone; Phenprocoumarol; Phenprocoumarole; Phenprocoumon; Phenprocumone |
| Molecular Formula: | C18H16O3 |
| SMILES: | CCC(C1=CC=CC=C1)C1=C(O)C2=C(OC1=O)C=CC=C2 |
| Structure: |
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| DrugBank Description: | Coumarin derivative that acts as a long-acting oral anticoagulant. |
| CAS Number: | 435-97-2 |
| Molecular Weight: | 280.3178 |
| DrugBank Indication: | Used for the prevention and treatment of thromboembolic disease including venous thrombosis, thromboembolism, and pulmonary embolism as well as for the prevention of ischemic stroke in patients with atrial fibrillation (AF). |
| DrugBank Pharmacology: | Phenprocoumon, a coumarin anticoagulant, thins the blood by antagonizing vitamin K which is required for the production of clotting factors in the liver. Anticoagulants such as phenprocoumon have no direct effect on an established thrombus, nor do they reverse ischemic tissue damage (damage caused by an inadequate blood supply to an organ or part of the body). However, once a thrombus has occurred, the goal of anticoagulant treatment is to prevent further extension of the formed clot and prevent secondary thromboembolic complications which may result in serious and possibly fatal sequelae. |
| DrugBank MoA: | Phenprocoumon inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decreased prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots. |
| Targets: | Vitamin K epoxide reductase complex subunit 1 inhibitor |
| Inclusion Criteria: | Indication associated |
| Strategy ID | Strategy | Synonyms | Related Targets | Related Drugs |
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| Target ID | Target Name | GENE | Action | Class | UniProtKB ID | Entry Name |
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| Diseases ID | DO ID | Disease Name | Definition | Class | |
|---|---|---|---|---|---|
| I08 | 114 | Cardiovascular system disease | A disease of anatomical entity which occurs in the blood, heart, blood vessels or the lymphatic system that passes nutrients (such as amino acids and electrolytes), gases, hormones, blood cells or lymph to and from cells in the body to help fight diseases and help stabilize body temperature and pH to maintain homeostasis. http://en.wikipedia.org/wiki/Circulatory_system | disease of anatomical entity | Details |
| 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 |
| I17 | 1596 | Mental depression | Mental depression | disease of mental health/ cognitive disorder/ mood disorder | Details |