Anti-CD79b antibody–drug conjugate delivering MMAE; internalization releases a microtubule inhibitor causing G2/M arrest and apoptosis.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE; binding to CD79b on B cells triggers internalization and intracellular release of MMAE, which inhibits tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
NO
INDIRECT
Polatuzumab vedotin targets CD79b on B cells, is internalized, and releases MMAE that binds the vinca site on beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; beta-tubulin expression alone does not make cells susceptible.
ImmTAC bispecific (IMC‑F106C): affinity‑enhanced PRAME‑specific TCR fused to anti‑CD3 scFv that binds PRAME peptide presented by HLA‑A*02:01 on tumor cells and recruits/activates T cells via CD3 to kill PRAME+ cells.
ImmTAC bispecific composed of an affinity‑enhanced PRAME‑specific TCR fused to an anti‑CD3 scFv; binds PRAME peptide presented by HLA‑A*02:01 on tumor cells and simultaneously engages CD3 on T cells, activating and redirecting polyclonal T cells to kill PRAME‑positive cells.
YES
DIRECT
Affinity‑enhanced TCR binds PRAME peptide–HLA‑A*02:01 on tumor cells while anti‑CD3 engages T cells, forming an immune synapse and triggering T‑cell–mediated killing (perforin/granzymes, apoptosis) of PRAME/HLA‑A*02:01–positive cells.
Autologous dendritic cell (DC) vaccine made from the patient’s monocytes and loaded ex vivo with autologous glioblastoma (GBM) tumor antigens to activate tumor-specific T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-derived glioblastoma antigens and administered to present these antigens via MHC I/II, priming tumor-specific CD8+ cytotoxic and CD4+ helper T-cell responses that drive CTL-mediated lysis of GBM cells; GM-CSF is used to enhance dendritic cell maturation and activity.
YES
INDIRECT
The DC vaccine primes/expands neoantigen-specific CD8+ T cells, which recognize the GBM neoantigen peptides on HLA class I and kill the tumor cells via CTL cytotoxicity (perforin/granzyme, Fas–FasL).
An antibody-drug conjugate (ADC) comprising a humanized anti-CLDN18.2 monoclonal antibody linked via a cleavable linker to a cytotoxic payload (DDDXD), with a drug–antibody ratio of 8; administered IV every 3 weeks (0.5–5.0 mg/kg). It binds CLDN18.2 on tumor cells, is internalized, and releases the cytotoxic agent intracellularly to kill cancer cells.
Humanized anti‑CLDN18.2 monoclonal antibody conjugated via a cleavable linker to a cytotoxic payload. Binds CLDN18.2 on tumor cells, is internalized, linker is cleaved in lysosomes, releasing the payload that induces DNA damage and kills CLDN18.2‑expressing cells, with potential bystander killing of adjacent tumor cells.
YES
DIRECT
ADC binds CLDN18.2, is internalized, linker cleaved in lysosomes, releasing a cytotoxic payload that induces DNA damage and kills the target-expressing cell (with possible bystander effect).
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.
YES
DIRECT
A bispecific T‑cell engager binds EpCAM on tumor cells and CD3 on T cells (activated in the acidic TME), forming immune synapses that activate cytotoxic T cells to kill EpCAM+ cells via perforin/granzyme-mediated cytolysis.