Autologous T cells genetically modified to express a chimeric antigen receptor that binds mesothelin on tumor cells, triggering T-cell activation, cytokine release, and cytotoxic killing; evaluated via IV or local delivery, with lymphodepleting chemotherapy used to enhance expansion and optional combination with immune checkpoint inhibitors.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes mesothelin on tumor cells. CAR engagement triggers T-cell activation, cytokine release, proliferation, and targeted cytotoxic killing of mesothelin-expressing cancer cells; lymphodepleting chemotherapy may be used to enhance expansion.
CAR-T cells bind mesothelin on target cells and, upon CAR engagement, directly kill them via perforin/granzyme-mediated cytolysis and Fas–FasL–mediated apoptosis.
Autologous, gene-modified T cells expressing a cooperative/dual chimeric antigen receptor targeting ADGRE2 (EMR2) and CLEC12A (CLL-1) to mediate cytotoxic killing of AML blasts/LSCs while aiming to spare normal myeloid cells.
Autologous T cells engineered to express a cooperative dual chimeric antigen receptor targeting ADGRE2 (EMR2) and CLEC12A (CLL-1) on AML blasts and leukemic stem cells; antigen binding activates CAR signaling leading to T-cell activation and cytotoxic killing of malignant cells while aiming to spare normal myeloid cells.
CAR T cells recognize ADGRE2 (with CLEC12A co-recognition) and directly lyse target cells via perforin/granzyme-mediated cytotoxicity.
CD30-directed antibody–drug conjugate; internalized into Hodgkin/Reed-Sternberg cells to release MMAE (a microtubule inhibitor), inducing apoptosis and potentially mediating ADCC.
CD30-directed antibody–drug conjugate that binds CD30 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE via proteolytic cleavage of a valine–citrulline linker, causing tubulin depolymerization, G2/M arrest, and apoptosis; may also mediate ADCC.
Anti‑CD30 ADC binds CD30, is internalized, linker is cleaved to release MMAE, which inhibits tubulin, causing G2/M arrest and apoptosis; ADCC may also contribute.
An antibody–drug conjugate (ADC) consisting of a humanized anti–B7‑H3 (CD276) IgG1 linked via a protease‑cleavable linker to a duocarmycin DNA‑alkylating payload. After binding B7‑H3 on tumor cells and internalization, it releases the payload to cause DNA minor‑groove alkylation, DNA damage, and tumor cell death. Administered IV (2.7 mg/kg q28d).
Humanized anti-B7-H3 (CD276) IgG1 ADC with a protease-cleavable linker to a duocarmycin payload; after B7-H3 binding and internalization by tumor cells, linker cleavage releases duocarmycin, which binds the DNA minor groove and alkylates adenine (N3), causing DNA damage and tumor cell death.
The ADC binds B7-H3 on target cells, is internalized, and a protease-cleavable linker releases a duocarmycin payload that alkylates DNA (minor groove, N3 adenine), causing DNA damage and cell death.
Autologous, gene-modified T cells expressing a cooperative/dual chimeric antigen receptor targeting ADGRE2 (EMR2) and CLEC12A (CLL-1) to mediate cytotoxic killing of AML blasts/LSCs while aiming to spare normal myeloid cells.
Autologous T cells engineered to express a cooperative dual chimeric antigen receptor targeting ADGRE2 (EMR2) and CLEC12A (CLL-1) on AML blasts and leukemic stem cells; antigen binding activates CAR signaling leading to T-cell activation and cytotoxic killing of malignant cells while aiming to spare normal myeloid cells.
CAR T cells engage CLEC12A (in a cooperative dual-CAR with ADGRE2), triggering CAR signaling that activates T-cell cytotoxicity (perforin/granzyme release and death-receptor pathways) to lyse CLEC12A-positive cells.