A conditionally active biologic (CAB) bispecific T‑cell engager antibody that simultaneously binds EpCAM on tumor cells and CD3 on T cells to redirect and activate cytotoxic T cells against EpCAM-expressing cancer cells; designed for conditional activation within the tumor microenvironment.
Conditionally active bispecific antibody that binds EpCAM on tumor cells and CD3 on T cells; in the acidic tumor microenvironment it becomes activated to recruit and activate cytotoxic T cells, forming an immune synapse and inducing T cell–mediated killing of EpCAM‑expressing cancer cells while aiming to limit systemic toxicity.
NO
INDIRECT
BA3182 binds CD3ε on T cells and EpCAM on tumor cells; in the tumor microenvironment it activates and redirects T cells to kill EpCAM-positive cancer cells via immune-synapse formation and perforin/granzyme-mediated cytotoxicity. CD3ε-expressing T cells are not the cells killed.
An HPV-16–targeted therapeutic mRNA vaccine that delivers mRNA encoding HPV-16 antigens; after intramuscular injection, host cells translate the mRNA and present antigens on MHC I/II to activate antigen-presenting cells and prime HPV-16–specific CD8+ and CD4+ T-cell responses to eliminate HPV-16–positive lesions and tumors.
Delivers mRNA encoding HPV-16 antigens to host cells; translated antigens are presented on MHC I/II, activating antigen-presenting cells and priming HPV-16–specific CD8+ cytotoxic and CD4+ helper T-cell responses to eliminate HPV-16–positive lesions and tumors.
YES
INDIRECT
The mRNA vaccine primes HPV-16–specific CD8+ T cells that recognize HPV-16 peptides on MHC I of infected/tumor cells and kill them via perforin/granzyme-mediated cytolysis (with CD4+ T-cell help).
Monoclonal antibody inhibitor of CCR8 that targets CCR8-expressing intratumoral regulatory T cells (Tregs) to block CCR8 signaling and/or deplete CCR8+ Tregs, aiming to relieve immunosuppression in the tumor microenvironment.
Humanized IgG1 anti-CCR8 monoclonal antibody that binds CCR8 on intratumoral regulatory T cells, blocks CCR8 signaling and depletes CCR8+ Tregs via ADCC, reducing immunosuppression in the tumor microenvironment and restoring antitumor immunity.
YES
DIRECT
The IgG1 anti-CCR8 antibody binds CCR8 on target cells and recruits FcγR-expressing effector cells (e.g., NK cells) to mediate ADCC, depleting CCR8+ cells.
Anti-CD20 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant and normal B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via NK cell–mediated ADCC, complement-dependent cytotoxicity (CDC), and can trigger apoptosis of the bound cells.
HER2-targeted antibody-drug conjugate composed of an anti-HER2 monoclonal antibody linked to a topoisomerase I/camptothecin-class cytotoxic payload; binds HER2 on tumor cells, is internalized, and releases the payload to cause DNA damage and tumor cell death; Fc-mediated ADCC may also contribute.
Anti-HER2 monoclonal antibody linked to a topoisomerase I (camptothecin-class) cytotoxic payload. Binds HER2 on tumor cells, is internalized, and releases the payload to induce DNA damage and tumor cell death; Fc-mediated ADCC may also contribute.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases a topoisomerase I (camptothecin-class) cytotoxic payload that causes DNA damage and apoptosis; Fc effector function may add ADCC.