Repositioning Candidate Details
| Candidate ID: | R1059 |
| Source ID: | DB06607 |
| Source Type: | approved; investigational; withdrawn |
| Compound Type: | biotech |
| Compound Name: | Catumaxomab |
| Synonyms: | Catumaxomab |
| Molecular Formula: | -- |
| SMILES: | -- |
| DrugBank Description: | Catumaxumab is a trifunctional monoclonal antibody developed for use in cancer treatment. It has affinity for T-cells, accessory immune cells, and cancer cells. Catumaxumab was initially authorized for market by the European Medicines Agency in April 2009 for the treatment of malignant ascites . Its market authorization was withdrawn in the EU in June 2017 at the manufacturer's request due to the company's insolvency. Catumaxumab was approved for market in Canada in May 2012 for the same condition . It is currently available under the brand name Removab. |
| CAS Number: | 509077-98-9 |
| Molecular Weight: | |
| DrugBank Indication: | For use in the management of malignant ascites tumours via intraperitoneal infusion where standard therapy is not available or feasible . |
| DrugBank Pharmacology: | Catumaxomab brings cancer cells, T cells, and accessory immune cells into close proximity and stimulates activation and of immune cells . This facilitates immune system-mediated destruction of the cancer cells. |
| DrugBank MoA: | Catumaxomab contains epitopes for human CD3 and human epithelial cell adehesion molecule. It also has an intact immunoglobulin gamma constant region allowing it to bind to Fcγ I, IIa, and III receptors . By binding to CD3 on killer T cells, EpCAM on cancer cells, and Fcγ receptors on accessory immune cells like macrophages and NK cells, Catumaxomab brings immune cells into close proximity to EpCAM positive cancer cells. As a functional antibody, Catumaxomab also stimulates bound NK cells to release cytotoxic mediators like granzyme or bound macrophages to phagocytose the cancer cell. Phagocytosed cancer cells can be processed and have their antigens presented on major histocompatibililty complex II to activate helper T cells and contribute to humoural immunity and activation of killer T cells against EpCAM postive cancer cells. These macrophages also release inflammatory cytokines to attract additional immune cells to EpCAM positive tissues. When antibodies reach higher concentrations, they can stimulate complement-mediated cytotoxicity against EpCAM positive cancer cells. Bound killer T cells are activated resulting in proliferation and release of cytotoxic mediators resulting in antibody-dependent cell-mediated cytotoxicity against the cancer cell. |
| Targets: | Epithelial cell adhesion molecule ligand; Low affinity immunoglobulin gamma Fc region receptor II-a agonist; Low affinity immunoglobulin gamma Fc region receptor III-A agonist; Low affinity immunoglobulin gamma Fc region receptor III-B agonist; T-cell surface glycoprotein CD3 epsilon chain agonist; High affinity immunoglobulin gamma Fc receptor I agonist |
| 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 |
|---|