| Catalog No. | HY257146 |
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| Description | Glofitamab is a T-cell-engaging bispecific antibody possessing a novel 2:1 structure with bivalency for CD20 on B cells and monovalency for CD3 on T cells. Glofitamab is an investigational, T-cell bispecific antibody with a distinctive design that features 2 Fab arms for binding CD20 on B cells, along with 1 Fab arm for binding CD3 on T cells. The CD3 binding arm is fused directly to one of the CD20-binding arms in a head-to-tail fashion via a short flexible linker. |
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| Species reactivity | Human |
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| Applications | ELISA, Bioactivity: FACS, Functional assay, Research in vivo |
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| Host species | Humanized |
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| Isotype | IgG1-kappa-lambda |
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| Expression system | Mammalian Cells |
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| Species | Human |
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| Clonality | Monoclonal |
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| Target | B-lymphocyte surface antigen B1, Membrane-spanning 4-domains subfamily A member 1, MS4A1, Leukocyte surface antigen Leu-16, B-lymphocyte antigen CD20, Bp35, CD20, T3E, T-cell surface antigen T3/Leu-4 epsilon chain, CD3e, CD3E, T-cell surface glycoprotein CD3 epsilon chain |
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| Endotoxin level | Please contact with the lab for this information. |
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| Purity | >95% as determined by SDS-PAGE. |
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| Purification | Protein A/G purified from cell culture supernatant. |
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| Accession | P11836 & P07766 |
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| Form | Liquid |
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| Storage buffer | 0.01M PBS, pH 7.4. |
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| Stability and Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles. Store at 4°C short term (1-2 weeks). Store at -20°C 12 months. Store at -80°C long term. |
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| Alternate Names | Bispecific, CD20-TCB (2:1), RG-6026, 2229047-91-8 |
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| Background | Epcoritamab (DuoBody-CD3xCD20, GEN3013) is a novel bispecific IgG1 antibody redirecting T-cells toward CD20+ tumor cells. Here, we assessed the preclinical efficacy of epcoritamab against primary tumor cells present in the lymph node biopsies from newly diagnosed (ND) and relapsed/refractory (RR) B-NHL patients. In the presence of T-cells from a healthy donor, epcoritamab demonstrated potent activity against primary tumor cells, irrespective of prior treatments, including CD20 mAbs. Median lysis of 65, 74, and 84% were achieved in diffuse large B-cell lymphoma (n = 16), follicular lymphoma (n = 15), and mantle cell lymphoma (n = 8), respectively. Furthermore, in this allogeneic setting, we discovered that the capacity of B-cell tumors to activate T-cells was heterogeneous and showed an inverse association with their surface expression levels of the immune checkpoint molecule Herpesvirus Entry Mediator (HVEM). In the autologous setting, when lymph node (LN)-residing T-cells were the only source of effector cells, the epcoritamab-dependent cytotoxicity strongly correlated with local effector cell-to-target cell ratios. Further analyses revealed that LN-residing-derived or peripheral blood-derived T-cells of B-NHL patients, as well as heathy donor T-cells equally mediated epcoritamab-dependent cytotoxicity. These results show the promise of epcoritamab for treatment of newly-diagnosed or relapsed/refractory B-NHL patients, including those who became refractory to previous CD20-directed therapies.
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| Note | For research use only. Not suitable for clinical or therapeutic use. |
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