Repositioning Candidate Details
| Candidate ID: | R1414 |
| Source ID: | DB11856 |
| Source Type: | investigational |
| Compound Type: | biotech |
| Compound Name: | Ligelizumab |
| Synonyms: | Ligelizumab |
| Molecular Formula: | -- |
| SMILES: | -- |
| DrugBank Description: | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to , another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation. Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients, and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU. |
| CAS Number: | 1322627-61-1 |
| Molecular Weight: | |
| DrugBank Indication: | -- |
| DrugBank Pharmacology: | -- |
| DrugBank MoA: | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FcεRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators. IgE also binds to CD23/FcεRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis. Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Cε3 domain. It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FcεRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Targets: | Immunoglobulin heavy constant epsilon antibody |
| 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 |
|---|