An antibody–drug conjugate (GSK2857916) consisting of a humanized, afucosylated IgG1 monoclonal antibody targeting BCMA (TNFRSF17) conjugated to the cytotoxic payload monomethyl auristatin F (MMAF). It binds BCMA on plasma cells, is internalized, and releases MMAF to inhibit microtubules and induce apoptosis; the afucosylated antibody can also promote ADCC/ADCP.
Afucosylated anti-BCMA IgG1 ADC conjugated to MMAF. Binds BCMA on plasma cells, is internalized, and releases MMAF to inhibit tubulin polymerization causing G2/M arrest and apoptosis; afucosylation enhances ADCC/ADCP.
Belantamab mafodotin binds BCMA on target cells, is internalized, and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; its afucosylated Fc also mediates ADCC/ADCP against BCMA-expressing cells.
An autologous, genetically engineered T-cell therapy in which patient T cells are modified to express a chimeric antigen receptor targeting Claudin 18.2, with an iPD-1 design intended to counter PD-1/PD-L1–mediated inhibition. Administered as a single intravenous infusion to promote tumor cell killing via T-cell activation and cytotoxicity.
Autologous T cells genetically engineered to express a CAR targeting Claudin 18.2. Antigen engagement triggers T‑cell activation, proliferation, and cytotoxic killing of tumor cells. The iPD‑1 design counteracts PD‑1/PD‑L1–mediated inhibition in the tumor microenvironment to enhance T‑cell function and persistence.
CAR-T cells recognize Claudin 18.2 and, upon engagement, directly kill target cells via perforin/granzyme-mediated cytolysis and death-receptor pathways; the iPD-1 design sustains activity in PD-1/PD-L1–rich tumors.
Fully human anti-EGFR monoclonal antibody that binds EGFR on tumor epithelial cells, blocking downstream MAPK/PI3K signaling and inhibiting proliferation.
Fully human IgG1 monoclonal antibody targeting EGFR; binds and blocks EGFR activation to inhibit downstream MAPK/ERK and PI3K/AKT signaling, suppressing tumor cell proliferation and survival; may also induce ADCC and CDC against EGFR-expressing cells.
Binds EGFR on target cells and, via its IgG1 Fc, recruits immune effectors to mediate ADCC and complement-dependent cytotoxicity (CDC), causing lysis/apoptosis; also blocks EGFR survival signaling.
Intravenous CD20×CD3 bispecific antibody that redirects T-cell cytotoxicity against CD20-positive B cells; administered with step-up dosing to reduce cytokine release syndrome.
CD20xCD3 bispecific antibody that simultaneously binds CD3 on T cells and CD20 on B cells, crosslinking them to activate T-cell cytotoxicity (immune synapse formation, perforin/granzyme release) and kill CD20-positive B-cell malignancies.
Glofitamab links CD3 on T cells to CD20 on target cells, forming an immune synapse and inducing T‑cell cytotoxicity (perforin/granzyme-mediated apoptosis, +/- Fas/FasL).
Intravenous type II anti-CD20 monoclonal antibody used in a pre-phase to deplete B cells and mitigate cytokine release syndrome risk.
Glycoengineered humanized type II anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B cells and enhances FcγRIIIa engagement (via reduced fucosylation) to drive potent antibody‑dependent cellular cytotoxicity and phagocytosis, and induces caspase‑independent direct cell death, resulting in efficient B‑cell depletion.
Binds CD20 on B cells and triggers FcγRIIIa-mediated ADCC and antibody-dependent phagocytosis (ADCP), and also induces caspase-independent direct cell death (type II anti-CD20).