An intramuscular mRNA nanoparticle vaccine encoding mutant KRAS neoantigens; taken up by antigen-presenting cells and presented on MHC I/II to prime KRAS-specific CD8+ and CD4+ T cells.
Intramuscular mRNA nanoparticle vaccine encoding mutant KRAS neoantigens; taken up by antigen-presenting cells, translated, and presented on MHC I and II to prime and expand KRAS-specific CD8+ cytotoxic and CD4+ helper T cells, promoting immune-mediated killing of KRAS-mutant tumor cells.
YES
INDIRECT
The mRNA vaccine primes and expands KRAS-mutant–specific CD8+ T cells, which recognize KRAS neoantigen peptides presented on MHC and kill tumor cells via perforin/granzyme-mediated cytotoxicity.
Allogeneic T cells from a new donor engineered to express an anti-CD7 chimeric antigen receptor; CAR engagement drives cytotoxic killing of CD7+ malignant T cells through TCR-like signaling, perforin/granzyme release, and cytokine secretion. Expected on-target depletion of normal CD7+ T cells and some NK cells, leading to T-cell aplasia.
Allogeneic donor-derived T cells are engineered to express an anti-CD7 chimeric antigen receptor. Upon binding CD7 on malignant T cells, the CAR triggers TCR-like signaling that activates cytotoxic effector functions, including perforin/granzyme-mediated killing and cytokine secretion. On-target effects also deplete normal CD7+ T cells and some NK cells, leading to T-cell aplasia.
YES
DIRECT
Anti-CD7 CAR T cells bind CD7 and are activated to kill CD7+ cells via perforin/granzyme-mediated cytolysis (and related T-cell effector pathways).
A CD20×CD3 bispecific monoclonal antibody T‑cell engager that binds bivalently to CD20 on B cells and monovalently to CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and drive T‑cell–mediated cytotoxicity against CD20+ lymphoma.
CD20×CD3 bispecific antibody that binds bivalently to CD20 on B cells and monovalently to CD3 on T cells, forming an immune synapse that activates TCR/CD3 signaling and drives T‑cell–mediated cytotoxicity against CD20‑positive lymphoma cells.
NO
INDIRECT
The bispecific antibody binds CD3 on T cells and CD20 on B cells, forming an immune synapse that activates T cells to kill CD20+ lymphoma cells (perforin/granzyme, FasL). CD3+ T cells are not killed by the drug.
A type II anti‑CD20 monoclonal antibody used as priming to deplete circulating B cells and reduce cytokine release syndrome risk prior to glofitamab administration.
Obinutuzumab is a glycoengineered, humanized type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them by enhanced FcγRIIIa-mediated antibody-dependent cellular cytotoxicity and phagocytosis, and by inducing direct, caspase-independent cell death; it has reduced reliance on complement-dependent cytotoxicity.
YES
DIRECT
Binds CD20 on B cells and triggers FcγRIIIa-mediated ADCC by NK cells and phagocytosis by macrophages; also induces direct, caspase‑independent cell death (with reduced reliance on complement).
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2 that blocks receptor signaling and mediates ADCC.
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2; binds HER2 on tumor cells to block receptor signaling and dimerization, inhibiting PI3K/AKT/MAPK pathways, and engages Fc gamma receptors to trigger antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and engages Fc gamma receptors on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (and phagocytosis); it can also activate complement (CDC).