Recombinant fully human anti-CD38 monoclonal antibody immunotherapy that binds CD38 and eliminates CD38+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependent cellular phagocytosis; may also induce apoptosis and modulate CD38 enzymatic signaling.
Fully human IgG1 anti-CD38 monoclonal antibody that binds CD38 on malignant and immune cells and eliminates CD38+ cells via ADCC, CDC, and ADCP; can also induce apoptosis and modulate CD38 ectoenzyme signaling, leading to antitumor and immunomodulatory effects.
Anti-CD38 IgG1 binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), CDC (complement), and ADCP (phagocytes); it may also induce direct apoptosis.
Anti-CD38 monoclonal antibody (reference product, DARZALEX) that depletes CD38+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependent cellular phagocytosis; may also induce apoptosis and modulate CD38 enzymatic signaling.
Human IgG1κ monoclonal antibody targeting CD38 that depletes CD38+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependent cellular phagocytosis; can also induce apoptosis and modulate CD38 enzymatic signaling, reducing CD38+ tumor and immunosuppressive cells.
Anti-CD38 IgG1 mAb binds CD38 on target cells and uses its Fc to recruit immune effectors, causing ADCC (NK cells), CDC (complement), and ADCP (macrophages); can also induce apoptosis of CD38+ cells.
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.
The ADC binds nectin-4 on target cells, is internalized, then releases MMAE via a cleavable linker; MMAE binds tubulin, inhibits microtubule polymerization, causes G2/M arrest, and induces apoptosis.
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.
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.
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.
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.