Autologous genetically modified T cells engineered to express a chimeric antigen receptor targeting mesothelin (MSLN), intended to recognize and kill MSLN-positive tumor cells after lymphodepletion.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting mesothelin (MSLN). Upon binding MSLN on tumor cells, the CAR provides activation and costimulatory signaling, driving T‑cell cytotoxicity (perforin/granzyme release) and cytokine production to kill MSLN‑positive cancer cells, typically after lymphodepleting conditioning to enhance expansion.
Anti-mesothelin CAR-T cells bind mesothelin on target cells and, upon activation, kill them via T-cell cytotoxicity (perforin/granzyme release and death-receptor–mediated apoptosis).
HER2-targeted antibody-drug conjugate (anti-HER2 monoclonal antibody linked to the topoisomerase I inhibitor deruxtecan); binds HER2, is internalized, and releases cytotoxic payload causing DNA replication inhibition with bystander killing.
HER2-targeted antibody-drug conjugate (trastuzumab linked via a cleavable linker to the topoisomerase I inhibitor deruxtecan). Binds HER2 on tumor cells, is internalized, and releases the DXd payload that inhibits Top1, blocking DNA replication and inducing cell-cycle arrest and apoptosis; also mediates ADCC and bystander killing.
The ADC binds HER2, is internalized, and releases the deruxtecan (DXd) payload, a topoisomerase I inhibitor, causing DNA damage/replication arrest and apoptosis; Fc engagement can also induce ADCC and bystander killing.
A HER2-targeted dual antibody–drug conjugate (ADC) administered intravenously every 3 weeks as neoadjuvant therapy. It binds HER2 (ErbB2) on tumor cells, is internalized, and releases an intracellular cytotoxic payload to kill HER2-expressing cells; it may also dampen HER2 signaling and engage Fc-mediated immune effector functions, impacting downstream PI3K/AKT and MAPK pathways.
HER2-targeted antibody–drug conjugate that binds HER2 (ErbB2) on tumor cells, is internalized, and releases an intracellular cytotoxic payload to kill HER2-expressing cells; it may also attenuate HER2 signaling and recruit Fc-mediated immune effector functions, impacting downstream PI3K/AKT and MAPK pathways.
HER2-targeted ADC binds HER2 on tumor cells, is internalized, and releases an intracellular cytotoxic payload that kills HER2-expressing cells; Fc-mediated ADCC/ADCP may also contribute.
Autologous anti-CD19 CAR T-cell therapy with 4-1BB costimulation that redirects a patient’s T cells to lyse CD19-positive B cells.
Autologous T cells are lentivirally engineered to express an anti-CD19 chimeric antigen receptor with a 4-1BB costimulatory domain and CD3-zeta signaling. After infusion, these CAR T cells recognize CD19 on B cells, become activated, expand, and lyse CD19-positive malignant B cells, leading to B-cell depletion and antitumor activity.
Anti-CD19 CAR T cells recognize CD19 on target cells and kill them via T-cell cytotoxicity (perforin/granzyme release and Fas/FasL-mediated apoptosis), leading to lysis of CD19+ cells.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
ULBP6 is an NKG2D ligand. Vγ9Vδ2 T cells express NKG2D; engagement of NKG2D by ULBP6 on target cells activates these T cells to kill via perforin/granzyme (and death receptor) pathways.