Autologous genetically engineered CD22-directed chimeric antigen receptor (CAR) T-cell therapy administered after lymphodepleting chemotherapy to treat relapsed/refractory B-cell lymphomas by targeting and eliminating CD22-expressing B cells.
Autologous T cells are genetically engineered ex vivo to express a chimeric antigen receptor that recognizes CD22 on B cells. Upon CD22 binding, the CAR transmits activation and co-stimulatory signals, driving T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated cytolysis, resulting in targeted depletion of CD22‑expressing malignant (and normal) B cells.
CD22-specific CAR T cells bind CD22 on target B cells, triggering T-cell activation and immunologic synapse formation, leading to perforin/granzyme-mediated cytolysis and apoptosis of CD22+ cells.
Humanized, Fc-engineered anti-CTLA-4 monoclonal antibody that enhances T-cell priming by blocking CTLA-4 and may deplete CTLA-4high regulatory T cells via Fc-mediated effector functions.
Humanized, Fc‑engineered anti‑CTLA‑4 monoclonal antibody that blocks CTLA‑4 to enhance T‑cell priming/activation and leverages Fc‑mediated effector functions (e.g., ADCC/ADCP) to deplete CTLA‑4high regulatory T cells, thereby augmenting antitumor immunity.
The anti-CTLA-4 antibody binds CTLA-4 on target cells (especially CTLA-4–high Tregs) and engages Fcγ receptor–bearing effector cells to mediate ADCC/ADCP, depleting those CTLA-4–expressing cells.
An intravenous anti-FGFR2b antibody–drug conjugate that binds FGFR2b on tumor cells, is internalized, and releases an intracellular cytotoxic payload to induce tumor cell death; targeting may also attenuate FGFR2 signaling. Evaluated as monotherapy and in combination with other anticancer agents in advanced solid tumors with FGFR2b expression and/or FGFR2 amplification.
BG-C137 is an anti-FGFR2b monoclonal antibody linked to a topoisomerase-1 inhibitor. After binding FGFR2b on tumor cells and internalization, it releases the cytotoxic payload that inhibits DNA topoisomerase I, disrupting DNA replication and causing cell cycle arrest and apoptosis; target binding may also attenuate FGFR2 signaling.
Anti-FGFR2b antibody–drug conjugate binds FGFR2b on target cells, is internalized, and releases a topoisomerase I inhibitor payload that disrupts DNA replication, causing cell cycle arrest and apoptosis.
Oral selective BCL-2 inhibitor that promotes mitochondrial apoptosis in malignant cells.
Selective BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, neutralizing its anti-apoptotic function and restoring mitochondrial apoptosis (MOMP, cytochrome c release, caspase activation) in BCL-2–dependent malignant cells; spares BCL-XL relative to navitoclax.
Venetoclax binds and inhibits BCL-2 (BH3 mimetic), disabling its anti-apoptotic function and freeing pro-apoptotic effectors to trigger MOMP, cytochrome c release, caspase activation, and apoptosis in BCL-2–dependent cells.
Anti-CD22 antibody-drug conjugate delivering calicheamicin to CD22+ B cells, causing DNA breaks and cytotoxicity.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; after binding CD22 on B cells and internalization, releases calicheamicin that binds the DNA minor groove, causing double-strand breaks and apoptosis in CD22-positive cells.
The ADC binds CD22, is internalized, and releases calicheamicin inside the cell, causing DNA double-strand breaks and apoptosis in CD22-positive cells.