Anti–nectin-4 antibody-drug conjugate that delivers MMAE (vedotin), a microtubule-disrupting cytotoxin, to nectin-4–expressing urothelial cancer cells, inducing apoptosis.
Anti–nectin-4 monoclonal antibody linked via a cleavable linker to the microtubule toxin MMAE. After binding nectin-4 on tumor cells and internalization, MMAE is released to bind tubulin, inhibit polymerization, cause G2/M arrest, and induce apoptosis in nectin‑4–expressing cells.
NO
INDIRECT
Enfortumab vedotin targets nectin-4 on the cell surface; after internalization, MMAE is released and binds beta-tubulin (vinca site) to inhibit microtubule polymerization, causing G2/M arrest and apoptosis. Cells expressing beta-tubulin alone are not selectively killed without nectin-4–mediated uptake.
Investigational anti–Claudin-6 (CLDN6) targeted immunotherapy administered by short IV infusion for CLDN6-expressing solid tumors (Phase 1, first-in-human); trial terminated due to sponsor decision.
Half-life extended bispecific antibody (BiTE) that binds CD3 on T cells and CLDN6 on tumor cells, redirecting cytotoxic T lymphocytes to CLDN6-expressing tumor cells to induce T-cell activation, cytokine release, and targeted tumor cell lysis.
YES
DIRECT
AMG 794 is a BiTE that links CD3 on T cells to CLDN6 on tumor cells, activating CTLs to kill CLDN6-expressing cells via perforin/granzyme-mediated cytolysis.
Investigational anti–Claudin-6 (CLDN6) targeted immunotherapy administered by short IV infusion for CLDN6-expressing solid tumors (Phase 1, first-in-human); trial terminated due to sponsor decision.
Half-life extended bispecific antibody (BiTE) that binds CD3 on T cells and CLDN6 on tumor cells, redirecting cytotoxic T lymphocytes to CLDN6-expressing tumor cells to induce T-cell activation, cytokine release, and targeted tumor cell lysis.
NO
INDIRECT
AMG 794 engages CD3 on T cells to redirect them to CLDN6+ tumor cells, triggering T-cell cytotoxicity (perforin/granzyme) against the tumor. CD3E+ T cells serve as effectors and are not the cells killed.
Donor-derived γδ T cells engineered to express a chimeric antigen receptor (CAR) targeting tumor-expressed HLA-G and to secrete a bispecific T-cell engager (BiTE) that binds CD3 on endogenous T cells, thereby recruiting bystander T cells for additional tumor killing. Intended for relapsed/refractory PD-L1+ solid tumors including NSCLC, TNBC, CRC, and GBM.
Allogeneic donor-derived gamma-delta T cells engineered to express a CAR targeting tumor HLA-G and to secrete a CD3-binding bispecific T-cell engager (BiTE). The CAR enables direct, MHC-independent recognition and killing of HLA-G–positive tumor cells, while the secreted BiTE recruits and activates endogenous alpha-beta T cells via CD3 to enhance bystander tumor killing through perforin/granzyme cytotoxicity and cytokine release, with inherently low GVHD risk.
YES
DIRECT
Engineered gamma-delta T cells express an HLA-G–specific CAR that binds HLA-G on target cells and induces perforin/granzyme-mediated cytotoxicity; the secreted CD3 BiTE additionally recruits endogenous T cells for bystander killing.
Donor-derived γδ T cells engineered to express a chimeric antigen receptor (CAR) targeting tumor-expressed HLA-G and to secrete a bispecific T-cell engager (BiTE) that binds CD3 on endogenous T cells, thereby recruiting bystander T cells for additional tumor killing. Intended for relapsed/refractory PD-L1+ solid tumors including NSCLC, TNBC, CRC, and GBM.
Allogeneic donor-derived gamma-delta T cells engineered to express a CAR targeting tumor HLA-G and to secrete a CD3-binding bispecific T-cell engager (BiTE). The CAR enables direct, MHC-independent recognition and killing of HLA-G–positive tumor cells, while the secreted BiTE recruits and activates endogenous alpha-beta T cells via CD3 to enhance bystander tumor killing through perforin/granzyme cytotoxicity and cytokine release, with inherently low GVHD risk.
NO
INDIRECT
CD3ε on T cells is bound by the secreted BiTE to activate and recruit T cells as effectors; these T cells (and the CAR γδ T cells) kill HLA‑G–positive tumor cells via perforin/granzyme, not the CD3+ cells themselves.