Repositioning Candidate Details
| Candidate ID: | R1344 |
| Source ID: | DB11157 |
| Source Type: | approved |
| Compound Type: | small molecule |
| Compound Name: | Anthralin |
| Synonyms: | Anthralin; Dithranol |
| Molecular Formula: | C14H10O3 |
| SMILES: | OC1=CC=CC2=C1C(=O)C1=C(O)C=CC=C1C2 |
| Structure: |
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| DrugBank Description: | Anthralin (1,8‐dihydroxy‐9anthrone, dithranol) is an older anti-psoriatic agent that was first synthesized as a derivative of chrysarobin, obtained from the araroba tree in Brazil over 100 years ago. Adverse effects of anthralin include irritation and discoloration of the skin . This specific property of the molecule inspired workers to study details of its pharmacology. It is important to consider that the drug is relatively innocuous, yet effective, and systemic side effects have not been observed with this anthralin, in contrast to a wide variety of systemic and topical therapies for psoriasis . Anthralin is also known as dithranol. It is a main active ingredient in topical skin formulations for the treatment of psoriasis. Various formulations of the drug are available, including solutions, foams, and shampoos . The chemical structure of anthralin allows for dual solubility, permitting the compound to be absorbed well through the epidermis . Anthralin has also been studied in the treatment of warts, showing promising results . Salicylic acid is frequently added to anthralin to augment the stability of anthralin and to increase its penetration and efficacy . |
| CAS Number: | 1143-38-0 |
| Molecular Weight: | 226.231 |
| DrugBank Indication: | Stable plaque psoriasis of the skin and scalp . It is also used topically in the management of psoriasis, dermatoses, and alopecia areata. Anthralin is also used in biomedical research due to its effect on EGFR autophosphorylation . |
| DrugBank Pharmacology: | Anthralin is a natural anthraquinone derivative, anti-psoriatic and anti-inflammatory agent. It controls skin growth by reducing the synthesis of DNA and the mitotic activity in the hyperplastic epidermis, normalizing the rate of cell proliferation and keratinization . |
| DrugBank MoA: | Anthralin inhibits the proliferation of keratinocytes (epidermal skin cells), prevents the action of T-cells, and promotes cell differentiation, likely through mitochondrial dysfunction. In addition, the production of free radicals may contribute to its anti-psoriatic effect . In vitro studies demonstrate that anthralin prolongs the prophase component of mitosis for keratinocytes and leukocytes . Prophase is the first step of mitosis, the process separating the duplicated genetic material carried in the nucleus of a parent cell into two identical daughter cells . In vivo studies demonstrate that anthralin blocks DNA synthesis and can increase the release of reactive oxygen species . Anthralin is believed to normalize the rate of epidermal cell proliferation and keratinization by reducing the mitotic activity of the epidermal hyperplasia in psoriasis . Anti-proliferative and anti-inflammatory effects of anthralin have been demonstrated on both psoriatic and healthy skin. The anti-proliferative effects of anthralin are thought to be due to a combination of inhibition of DNA synthesis and its strong reducing properties. The effectiveness of anthralin as an anti-psoriatic agent is partly owed to its ability to promote lipid peroxidation and reduce the concentration of endothelial adhesion molecules, which are found to be elevated in psoriatic patients , . Recent studies suggest that its ability to prevent T-lymphocyte activation and normalize keratinocyte differentiation may occur by a direct effect on mitochondria . |
| Targets: | Keratin, type II cytoskeletal 2 epidermal antagonist; C-Jun-amino-terminal kinase-interacting protein 1 agonist; Keratin, type I cytoskeletal 12 antagonist |
| Inclusion Criteria: | Therapeutic strategy associated |
| Strategy ID | Strategy | Synonyms | Related Targets | Related Drugs | |
|---|---|---|---|---|---|
| S05 | Anti-inflammatory | inflammatory | Bile acid; TNF-a inhibitor; Dual PPAR-α and -δ agonists; Toll-Like Receptor; (TLR)-4 antagonist; Caspase inhibitor; ASK-1 inhibitor | Ursodeoxycholic Acid; Pentoxifylline; Elafibranor; JKB-121; Emricasan; Selonsertib; | Details |
| Diseases ID | DO ID | Disease Name | Definition | Class |
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