Human IgG1κ anti-CD38 monoclonal antibody immunotherapy that depletes CD38+ cells via ADCC, CDC, ADCP, and direct apoptosis/immune modulation; administered subcutaneously.
Human IgG1κ monoclonal antibody against CD38 that binds CD38 on malignant and immunosuppressive CD38+ cells, inducing cell death via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptotic/immune-modulatory effects; administered subcutaneously.
YES
DIRECT
Anti-CD38 IgG1 binds CD38 on target cells and elicits Fc-mediated ADCC (NK cells), ADCP (phagocytes), complement-dependent cytotoxicity, and can trigger direct apoptotic signaling.
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
Trastuzumab deruxtecan binds HER2, is internalized, and releases deruxtecan that inhibits topoisomerase I to cause DNA damage and apoptosis (plus ADCC/bystander effects); killing is driven by HER2 targeting, not by expression of topoisomerase I itself.
Multi-epitope synthetic peptide cancer vaccine comprising HLA-A*0201–restricted peptides from EphA2, CMV pp65, and survivin, each fused to the tetanus toxoid P30 CD4 helper epitope; designed to elicit antigen-specific CD8+ T cells with CD4+ T-cell help in GBM.
Multi-epitope synthetic peptide vaccine comprising HLA-A*0201–restricted peptides from EphA2, CMV pp65, and survivin, each fused to the tetanus toxoid P30 CD4 helper epitope. The peptides are presented by APCs to prime and expand antigen-specific CD8+ cytotoxic T cells with CD4+ T-cell help, generating anti-tumor immune responses against cells expressing EphA2, survivin, and CMV pp65.
YES
INDIRECT
The vaccine primes HLA-A*0201–restricted EphA2-specific CD8+ T cells, which recognize EphA2-derived peptide–MHC I on tumor cells and kill them via perforin/granzyme (and Fas–FasL) cytotoxicity.