Autologous CAR T-cell therapy engineered to express a STEAP2-specific chimeric antigen receptor; upon binding STEAP2 on prostate cancer cells, it activates T cells to proliferate, release cytokines, and lyse STEAP2-positive tumor cells. Administered intravenously after lymphodepleting chemotherapy.
Autologous T cells engineered to express a STEAP2-specific CAR and a dominant-negative TGF-β receptor II. Upon binding STEAP2 on prostate cancer cells, CAR signaling activates T cells to proliferate, secrete cytokines, and kill target cells via cytotoxic mechanisms, while the dnTGFBRII blocks immunosuppressive TGF-β signaling to enhance activity in the tumor microenvironment.
STEAP2-specific CAR T cells bind STEAP2 on target cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and death receptor apoptosis); dnTGFBRII enhances activity by blocking TGF-β suppression.
An intravenous antibody-drug conjugate targeting Nectin-4; the monoclonal antibody binds Nectin-4 on tumor cells, is internalized, and releases a cytotoxic payload intracellularly to kill the cancer cell. Intended for Nectin-4-expressing epithelial tumors (e.g., urothelial carcinoma, TNBC, NSCLC, esophageal, pancreatic, ovarian, cervical, HNSCC, prostate).
A monoclonal antibody targets Nectin-4 on tumor cells, is internalized, and via a cleavable linker releases the camptothecin analog/topoisomerase I inhibitor LSN3889710, inhibiting DNA replication and inducing cell cycle arrest and apoptosis in Nectin-4–expressing tumors.
ADC binds Nectin-4 on tumor cells, is internalized, and a cleavable linker releases the topoisomerase I inhibitor LSN3889710, causing DNA replication inhibition/DNA damage leading to cell cycle arrest and apoptosis.
Patient-derived T cells genetically engineered to express a CD19-targeted chimeric antigen receptor (with CD3ζ/costimulatory signaling) and infused IV to eliminate CD19+ B cells, leading to B-cell aplasia.
Autologous T cells are genetically engineered to express a CD19-targeted chimeric antigen receptor with CD3ζ and costimulatory domains. Upon binding CD19 on malignant and normal B cells, CAR signaling activates T-cell cytotoxicity (perforin/granzyme), cytokine release, and expansion, leading to elimination of CD19+ cells and B-cell aplasia.
CAR T cells recognize CD19 on target cells and induce cytolysis via perforin/granzyme release (and death-receptor pathways), eliminating CD19+ cells.
Autologous CD19-directed CAR T cells enriched for naïve/memory T cells, incorporating CD28 costimulation, CD3ζ signaling, and an EGFRt safety/tracking tag; administered intracerebroventricularly to target CD19+ malignant B cells in the CNS.
Autologous T cells engineered with a CD19-specific chimeric antigen receptor incorporating CD28 costimulation and a CD3ζ signaling domain. Binding to CD19 on malignant B cells triggers T‑cell activation, expansion, cytokine release, and cytotoxic killing, leading to depletion of CD19+ cells. An EGFRt tag allows cell tracking and potential ablation with cetuximab. Administered intracerebroventricularly to target CD19+ lymphoma cells in the CNS.
CAR T cells bind CD19 on target cells, become activated via CD28/CD3ζ signaling, and kill the CD19+ cells through perforin/granzyme-mediated cytolysis (and Fas/FasL), with supportive cytokine-driven effects.
An antibody–drug conjugate administered as monotherapy; a tumor‑antigen–binding monoclonal antibody delivers an intracellular topoisomerase I–inhibitor cytotoxic payload. After receptor‑mediated internalization and lysosomal release, the payload inhibits Top1, induces DNA damage, and triggers apoptosis, with potential bystander effects.
AMT-116 is a humanized IgG1 antibody–drug conjugate targeting CD44v9 on tumor cells. After antigen binding and receptor-mediated internalization, a hydrolysable linker is cleaved in lysosomes to release the belotecan-derived topoisomerase I inhibitor KL610023. The payload inhibits Top1, causing replication-associated DNA damage and apoptosis, with potential bystander killing of nearby tumor cells.
ADC binds CD44v9, is internalized, and lysosomal linker cleavage releases a topoisomerase I inhibitor (KL610023) that inhibits Top1, causing replication-associated DNA damage and apoptosis of CD44v9+ cells (with possible bystander effect).