Oral small-molecule BCL-2 inhibitor that blocks anti-apoptotic BCL-2 to trigger mitochondrial apoptosis in MDS blasts.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, blocks its anti-apoptotic function, and releases pro-apoptotic effectors (BAX/BAK) to trigger mitochondrial apoptosis in MDS/tumor cells; relatively spares BCL-XL compared with navitoclax.
Venetoclax is a BH3 mimetic that binds and inhibits BCL-2, releasing pro-apoptotic effectors (BAX/BAK) to trigger mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL-2–dependent cells.
CD30-directed antibody-drug conjugate (anti-CD30 IgG1 linked to the microtubule inhibitor MMAE); administered IV 0.6 mg/kg every 3 weeks for up to 48 weeks. Binds CD30 on activated lymphocytes, internalizes, and releases MMAE to disrupt microtubules and induce apoptosis, depleting CD30+ inflammatory cells to reduce immune-driven inflammation and fibrosis.
CD30-directed antibody-drug conjugate: the anti-CD30 IgG1 binds CD30 on target cells, is internalized, and the valine-citrulline linker is cleaved to release monomethyl auristatin E (MMAE), which inhibits tubulin polymerization causing G2/M arrest and apoptosis, depleting CD30-positive cells.
Anti-CD30 antibody-drug conjugate binds CD30, is internalized, linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of CD30+ cells.
An intravenous anti-CD38 IgG1 monoclonal antibody (Sarclisa) used as immunotherapy; mediates ADCC, CDC, and ADCP, induces direct apoptosis, and inhibits CD38 ectoenzyme (NADase) activity to reduce adenosine-mediated immunosuppression; targets CD38+ plasma and lymphoma cells and depletes CD38+ regulatory immune populations.
Isatuximab is an anti-CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells and some lymphoma cells, mediating antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP), and inducing direct apoptosis. It also inhibits CD38 ectoenzyme (NADase) activity, reducing adenosine-mediated immunosuppression and depleting CD38+ regulatory immune cells.
Anti-CD38 IgG1 binds CD38 on target cells and triggers NK cell–mediated ADCC, complement-dependent cytotoxicity (CDC), macrophage ADCP, and can induce direct apoptosis.
Anti-HER2 antibody-drug conjugate that binds HER2, internalizes, and releases the microtubule-disrupting payload MMAE; may exert a bystander effect.
Anti-HER2 monoclonal antibody linked to the microtubule inhibitor MMAE. After binding HER2 on tumor cells, the ADC is internalized and the linker is cleaved to release MMAE, which disrupts microtubules causing cell-cycle arrest and apoptosis; the membrane-permeable payload can produce a bystander effect.
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE after linker cleavage; MMAE disrupts microtubules causing G2/M arrest and apoptosis, with possible bystander killing due to membrane-permeable payload.
A subcutaneous bispecific T‑cell–engager antibody that binds BCMA on myeloma/plasma cells and CD3 on T cells to redirect and activate cytotoxic T cells against BCMA-expressing cells.
Bispecific antibody that simultaneously binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to form an immune synapse and activate cytotoxic T cells, leading to targeted lysis of BCMA-expressing cells.
Elranatamab binds BCMA on target cells and CD3 on T cells, forming an immune synapse that activates T cells to kill BCMA-expressing cells via perforin/granzyme-mediated lysis.