Selective BCL-2 inhibitor inducing apoptosis in malignant B cells.
Selective BCL-2 inhibitor (BH3-mimetic) that binds the hydrophobic groove of BCL-2, blocks its anti-apoptotic function, releases pro-apoptotic effectors (e.g., BAX/BAK), and induces mitochondrial apoptosis in malignant B cells; sparing BCL-XL reduces thrombocytopenia.
BH3-mimetic binds and inhibits BCL-2, releasing BAX/BAK to induce mitochondrial outer membrane permeabilization and caspase-dependent intrinsic apoptosis in target-expressing cells.
An in vivo gene therapy using a lentiviral vector that delivers a CD20-specific chimeric antigen receptor (CAR20) transgene. Following a single IV infusion, it transduces the patient’s immune cells to generate CAR-T and CAR-NK cells in vivo, which bind CD20 on malignant B cells and mediate cytotoxic killing.
INT2104 is an in vivo lentiviral gene therapy that delivers a CD20-specific CAR transgene (CAR20) to the patient’s immune cells after IV infusion. The transduced T and NK cells express CAR20, recognize CD20 on malignant B cells, form an immune synapse, and mediate cytotoxic killing via perforin/granzyme release and cytokine-driven mechanisms, depleting CD20-positive tumor cells.
CAR20-expressing T and NK cells recognize CD20, form an immune synapse, and kill target cells via perforin/granzyme-mediated cytolysis and cytokine-driven mechanisms.
An investigational anti-CD38 therapeutic monoclonal antibody administered intravenously (16 mg/kg weekly for 8 weeks) to deplete CD38-expressing long-lived plasma cells and plasmablasts, aiming to reduce pathogenic antiplatelet autoantibodies and improve platelet counts in refractory ITP.
Anti-CD38 monoclonal antibody that binds CD38 on long-lived plasma cells and plasmablasts, triggering ADCC, CDC, and ADCP to deplete these cells and reduce pathogenic antiplatelet autoantibodies; may also inhibit CD38 ectoenzyme activity.
The anti-CD38 antibody binds CD38 on target cells and, via its Fc, recruits immune effectors to kill through ADCC, CDC, and ADCP; it may also induce apoptosis and inhibit CD38 ectoenzyme activity.
HER2-directed antibody-drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to disrupt microtubules and induce apoptosis.
HER2-targeted antibody-drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor monomethyl auristatin E (MMAE); MMAE inhibits tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis in HER2-expressing cells.
The ADC binds HER2 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, leading to G2/M arrest and apoptosis of HER2-expressing cells.