An antibody–drug conjugate consisting of patritumab (anti-HER3 monoclonal antibody) linked to the deruxtecan topoisomerase I inhibitor payload (DXd). It binds HER3 on tumor cells, is internalized, and releases DXd to inhibit Topo I, causing DNA damage and cell death, with a potential bystander effect.
Human anti-HER3 monoclonal antibody (patritumab) linked via a cleavable linker to a deruxtecan (DXd) topoisomerase I inhibitor payload. Binds HER3 (ERBB3) on tumor cells, is internalized, and releases DXd intracellularly; DXd inhibits Topo I by stabilizing the Topo I–DNA cleavage complex and blocking religation, causing DNA damage, replication arrest, and apoptosis. The membrane-permeable payload can produce a bystander effect.
ADC binds HER3 on target cells, is internalized, linker is cleaved to release the DXd topoisomerase I inhibitor; DXd stabilizes the Topo I–DNA cleavage complex causing DNA damage, replication arrest, and apoptosis, with a membrane-permeable payload enabling a bystander effect.
An mRNA therapeutic (injection) that encodes a bispecific T‑cell engager targeting CD19 and CD3. After in vivo translation, the expressed CD19×CD3 engager redirects and activates T cells to kill CD19+ B cells, depleting autoreactive B-cell compartments and reducing autoantibody-producing cells (BiTE-like mechanism).
Injected mRNA is translated in vivo into a bispecific CD19xCD3 T‑cell engager that links CD3 on T cells to CD19 on B cells, redirecting and activating T cells to kill CD19+ B cells and deplete autoreactive, autoantibody‑producing compartments.
An in vivo–expressed CD19xCD3 bispecific engages CD3 on T cells and CD19 on B cells, creating an immune synapse that redirects T cells to kill CD19+ cells via perforin/granzyme-mediated apoptosis.
A bispecific antibody–drug conjugate (izalontamab brengitecan; iza-bren; BMS-986507) targeting EGFR and HER3 that, upon internalization, releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after binding and internalization, it releases the camptothecin-class topoisomerase I inhibitor brengitecan, inducing DNA damage (via topo I inhibition) and tumor cell death, with potential bystander effect.
The ADC binds EGFR on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and cell death (with possible bystander effect).
A bispecific antibody–drug conjugate (izalontamab brengitecan; iza-bren; BMS-986507) targeting EGFR and HER3 that, upon internalization, releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after binding and internalization, it releases the camptothecin-class topoisomerase I inhibitor brengitecan, inducing DNA damage (via topo I inhibition) and tumor cell death, with potential bystander effect.
ADC binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and cell death (with potential bystander effect).
Off-the-shelf, partially HLA-matched allogeneic anti-CD19 chimeric antigen receptor (CAR) T-cell therapy administered intravenously after lymphodepletion; donor-derived T cells engineered to express a CD19-specific CAR that binds CD19 on malignant B cells, triggering T-cell activation, cytokine release, and cytotoxic killing.
Allogeneic donor-derived T cells engineered with a CD19-specific chimeric antigen receptor (with 1XX CD3zeta signaling) bind CD19 on malignant B cells, inducing T-cell activation, cytokine release, proliferation, and cytotoxic lysis of CD19+ cells; the EBV-sensitized allogeneic platform is intended to reduce GVHD risk.
Anti-CD19 CAR T cells bind CD19 on target B cells, become activated, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and apoptosis; Fas/FasL).