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.
YES
DIRECT
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.
IBRX-042 (hAd5-HPV E6.ETSD-IRES-E7.ETSD) is an adenoviral serotype 5 viral vector therapeutic cancer vaccine encoding HPV E6 and E7 antigens engineered with an endosomal/lysosomal targeting domain (ETSD) to enhance MHC I/II presentation, inducing a Th1-biased CD8+ and CD4+ T-cell response against HPV-expressing tumor cells.
A non-replicating adenoviral serotype 5 vector delivers genes encoding HPV E6 and E7 fused to an endosomal/lysosomal targeting domain, enhancing MHC I/II antigen presentation in APCs and inducing a Th1-biased, HPV-specific CD8+ and CD4+ T-cell response to kill HPV-expressing tumor cells.
YES
INDIRECT
Viral-vector vaccine transduces APCs to present HPV E6 peptides on MHC I/II, inducing Th1-biased HPV-specific CD8+ T cells that recognize E6 peptide–MHC on tumor cells and kill them via perforin/granzyme-mediated cytolysis.
IBRX-042 (hAd5-HPV E6.ETSD-IRES-E7.ETSD) is an adenoviral serotype 5 viral vector therapeutic cancer vaccine encoding HPV E6 and E7 antigens engineered with an endosomal/lysosomal targeting domain (ETSD) to enhance MHC I/II presentation, inducing a Th1-biased CD8+ and CD4+ T-cell response against HPV-expressing tumor cells.
A non-replicating adenoviral serotype 5 vector delivers genes encoding HPV E6 and E7 fused to an endosomal/lysosomal targeting domain, enhancing MHC I/II antigen presentation in APCs and inducing a Th1-biased, HPV-specific CD8+ and CD4+ T-cell response to kill HPV-expressing tumor cells.
YES
INDIRECT
Adenoviral vaccine delivers HPV E7 (with ETSD) to APCs, enhancing MHC I/II presentation and priming Th1-biased HPV-specific T cells; resulting CD8+ CTLs recognize E7 peptides on tumor cells and kill them via perforin/granzyme-mediated cytotoxicity (with CD4+ T-cell help).
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.
YES
DIRECT
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.
YES
DIRECT
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.