Rabbit polyclonal anti-thymocyte globulin (polyclonal IgG) given as a single IV dose (1 mg/kg) 48–72 hours after emergence from aplasia to reinforce GVHD prophylaxis after haploidentical allo-HSCT. Binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA‑DR) leading to T‑cell depletion via complement-dependent cytotoxicity and apoptosis, with Fc-mediated clearance and immunomodulatory effects; also impacts B cells, NK cells, and dendritic cells.
Rabbit polyclonal IgG that binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA‑DR), causing T‑cell depletion via complement‑dependent cytotoxicity and apoptosis, with Fc‑mediated clearance (ADCC/ADCP) and immunomodulatory effects; also impacts B cells, NK cells, and dendritic cells to reduce alloreactivity and GVHD risk.
Thymoglobulin contains antibodies that bind HLA‑DR (including DRB1) on leukocytes, leading to complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP, causing apoptosis/lysis of the bound cells.
An intravenous, half-life–extended bispecific T‑cell engager (BiTE) antibody construct that binds DLL3 on SCLC tumor cells and CD3 on T cells, redirecting and activating cytotoxic T lymphocytes to kill DLL3-positive tumor cells.
Tarlatamab is a half-life–extended BiTE that binds DLL3 on tumor cells and CD3 on T cells, bringing cytotoxic T lymphocytes into proximity with DLL3-positive cells to activate TCR/CD3 signaling, form an immune synapse, and induce target-cell killing via perforin/granzyme release and cytokine-mediated cytotoxicity.
A BiTE that bridges CD3 on T cells to DLL3 on target cells, forming an immune synapse and triggering T cell–mediated killing via perforin/granzyme release and cytokine-driven cytotoxicity.
A TROP-2–targeting antibody-drug conjugate (humanized anti–TROP-2 IgG1) linked to SN-38, the active metabolite of irinotecan. After binding TROP-2 on tumor cells, the ADC is internalized and releases SN-38 to inhibit topoisomerase I, causing DNA damage and apoptosis; the membrane-permeable payload may produce a bystander effect. Also known by the brand name Trodelvy.
Humanized anti-TROP-2 IgG1 antibody linked to SN-38; binds TROP-2 on tumor cells, is internalized and cleaved to release SN-38, which inhibits topoisomerase I by stabilizing topo I-DNA complexes, causing DNA damage and apoptosis; the membrane-permeable payload can produce a bystander effect.
Anti–TROP-2 ADC binds TROP-2, is internalized, then releases SN-38 that inhibits topoisomerase I, causing DNA damage and apoptosis in the target cell; the membrane-permeable payload can also produce bystander killing.
Gene-modified gamma-delta T cells engineered to express an anti-CD19 chimeric antigen receptor. Binding to CD19 on B-lineage cells triggers T-cell activation and perforin/granzyme-mediated cytotoxicity, leading to depletion of CD19+ B cells and plasmablasts, reduced autoantibody production, and modulation of antigen presentation and inflammatory cytokine signaling.
Gene-modified gamma-delta T cells expressing an anti-CD19 chimeric antigen receptor bind CD19 on B-lineage cells, triggering CAR-mediated activation and perforin/granzyme cytotoxicity. This depletes CD19+ B cells and plasmablasts, reducing autoantibody production and modulating antigen presentation and inflammatory cytokine signaling.
Anti-CD19 CAR gamma-delta T cells bind CD19 on B cells, activate via the CAR, and kill targets through perforin/granzyme-mediated cytolysis (apoptosis).
An antibody–drug conjugate consisting of a humanized monoclonal antibody targeting folate receptor alpha (FOLRα) that, upon internalization into FOLRα-positive tumor cells, releases a cleavable cytotoxic payload that inhibits microtubules/tubulin, leading to mitotic arrest and apoptosis.
Humanized anti-FOLRα monoclonal antibody binds FOLRα on tumor cells, is internalized, and releases a cleavable microtubule/tubulin-inhibiting cytotoxic payload, causing mitotic arrest and apoptosis in FOLRα-positive cancer cells.
ADC binds FOLR1 on tumor cells, is internalized, and releases a cleavable tubulin/microtubule‑inhibiting payload, causing mitotic arrest and apoptosis of FOLR1-positive cells.