Investigational CLDN18.2-targeted antibody-drug conjugate that binds claudin 18.2 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death; may also engage immune effector functions.
CLDN18.2-targeted monoclonal antibody linked via a cleavable linker to MMAE; after binding CLDN18.2 on tumor cells and internalization, releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc region may engage immune effector functions.
NO
INDIRECT
LM-302 targets CLDN18.2 on the cell surface; after internalization it releases MMAE, which binds beta-tubulin to disrupt microtubules and induce G2/M arrest and apoptosis. Beta-tubulin expression alone does not lead to targeting or direct killing by the drug.
A human afucosylated IgG1 monoclonal antibody (HZN-7734) that binds ILT7 (LILRA4) on plasmacytoid dendritic cells, depleting them via enhanced ADCC to reduce type I interferon signaling; administered subcutaneously.
Afucosylated IgG1 monoclonal antibody that binds ILT7 (LILRA4) on plasmacytoid dendritic cells, enhancing FcγRIIIa-mediated ADCC to deplete pDCs and thereby reduce type I interferon production and downstream inflammatory signaling.
YES
DIRECT
Antibody-bound ILT7+ plasmacytoid dendritic cells are killed via enhanced FcγRIIIa-mediated ADCC, primarily by NK cells (perforin/granzyme-mediated lysis).
A human afucosylated IgG1 monoclonal antibody (HZN-7734) that binds ILT7 (LILRA4) on plasmacytoid dendritic cells, depleting them via enhanced ADCC to reduce type I interferon signaling; administered subcutaneously.
Afucosylated IgG1 monoclonal antibody that binds ILT7 (LILRA4) on plasmacytoid dendritic cells, enhancing FcγRIIIa-mediated ADCC to deplete pDCs and thereby reduce type I interferon production and downstream inflammatory signaling.
NO
INDIRECT
Daxdilimab binds ILT7 on pDCs; its afucosylated Fc engages FcγRIIIa (CD16A) on NK cells to trigger ADCC that kills ILT7+ pDCs. CD16A-expressing cells act as effectors and are not killed by the drug.
Autologous 4th-generation chimeric antigen receptor T-cell therapy engineered to target glypican-3 (GPC3) on hepatocellular carcinoma cells; administered intravenously. Antigen engagement triggers CAR signaling leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity.
Autologous T cells engineered to express a chimeric antigen receptor that binds glypican-3 (GPC3) on hepatocellular carcinoma cells; antigen engagement triggers CAR signaling (CD3ζ with costimulatory domains) leading to T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of GPC3-positive tumor cells.
YES
DIRECT
GPC3-specific CAR-T cells bind GPC3 on target cells, triggering CAR signaling and T-cell cytotoxicity with perforin/granzyme release (apoptotic lysis).
Autologous, lentiviral-transduced, gene-modified T-cell therapy expressing a CAR targeting the BT-001 tumor surface antigen; given via multiple IV infusions without lymphodepleting chemotherapy to redirect T cells to kill BT-001–positive solid tumor cells.
Autologous T cells are lentivirally transduced to express a chimeric antigen receptor that binds the BT-001 tumor surface antigen. Antigen engagement triggers CAR signaling (CD3ζ with costimulation), activating and expanding the T cells to mediate perforin/granzyme-dependent cytotoxicity and cytokine release, selectively killing BT-001–positive solid tumor cells; given as repeat IV infusions without lymphodepleting chemotherapy.
YES
DIRECT
CAR-T cells recognize BT-001 on tumor cells; CAR signaling activates T cells to kill targets via perforin/granzyme cytolysis (and death‑receptor pathways), lysing BT-001–positive cells.