Also known as STRO-002 or Luvelta, this is an antibody-drug conjugate targeting folate receptor-α (FOLR1). It is an IgG1 (SP8166) linked via a cathepsin-cleavable linker to the 3-aminophenyl hemiasterlin cytotoxic payload SC209. After FRα binding and internalization, lysosomal cleavage releases SC209, a tubulin polymerization inhibitor, causing mitotic arrest and tumor cell death.
Anti-FOLR1 IgG1 antibody-drug conjugate. After binding folate receptor-alpha on tumor cells, the ADC is internalized and a cathepsin-cleavable linker is lysosomally cleaved to release SC209 (a 3-aminophenyl hemiasterlin tubulin polymerization inhibitor), causing microtubule disruption, mitotic arrest, and tumor cell death in FOLR1-positive cells.
ADC binds FOLR1 on target cells, is internalized, and lysosomal cleavage releases the SC209 tubulin polymerization inhibitor, disrupting microtubules and causing mitotic arrest and cell death in FOLR1+ cells.
Anti-CD47 monoclonal antibody immunotherapy that blocks the CD47–SIRPα "don’t‑eat‑me" signal to promote macrophage-mediated phagocytosis and innate antitumor immunity.
Anti-CD47 monoclonal antibody that blocks the CD47–SIRPα inhibitory ('don’t‑eat‑me') signal on tumor cells, enabling macrophage-mediated phagocytosis (ADCP) and enhancing innate antitumor immunity, with potential downstream priming of adaptive responses.
Blocks the CD47–SIRPα ‘don’t‑eat‑me’ signal and opsonizes CD47+ cells; macrophages engage the antibody Fc via Fcγ receptors and directly phagocytose/kill the target cells (ADCP).
Anti-HER2 antibody–drug conjugate that delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells, causing mitotic arrest and apoptosis.
Disitamab vedotin is an anti‑HER2 monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE. Upon binding HER2 on tumor cells, the ADC is internalized and the linker is proteolytically cleaved in lysosomes to release MMAE, which disrupts tubulin polymerization, causing G2/M mitotic arrest and apoptosis; the membrane‑permeable payload can mediate bystander killing, with potential additional Fc‑mediated effector activity.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE in lysosomes; MMAE disrupts microtubules, causing G2/M arrest and apoptosis. The membrane-permeable payload can also cause bystander killing; Fc functions may add ADCC.
Autologous gene-engineered T cells modified ex vivo to express a chimeric antigen receptor targeting CD147, enabling antigen-specific activation and cytotoxic killing of CD147-positive malignant T cells in relapsed/refractory T-cell non-Hodgkin’s lymphoma; administered in a dose-escalation range of 0.1–2.0×10^6 CAR T cells/kg.
Autologous T cells engineered ex vivo to express a chimeric antigen receptor targeting CD147; CAR binding to CD147 activates T cells via CD3ζ and costimulatory signaling, driving antigen-specific cytotoxic killing of CD147-positive malignant T cells.
CD147-targeted CAR T cells recognize CD147 on tumor cells and, upon CAR activation (CD3ζ/costimulatory signaling), kill CD147+ cells via perforin/granzyme-mediated cytolysis and death receptor pathways.
Anti-BCMA antibody–drug conjugate that delivers the microtubule inhibitor MMAF; binds BCMA, is internalized, disrupts microtubules to kill malignant plasma cells, and also mediates ADCC/ADCP.
Afucosylated anti-BCMA antibody–drug conjugate linked to MMAF (auristatin). Binds BCMA on malignant plasma cells, is internalized, and delivers MMAF to inhibit tubulin polymerization causing G2/M arrest and apoptosis; Fc afucosylation enhances ADCC/ADCP.
Belantamab mafodotin binds BCMA, is internalized, and delivers the MMAF auristatin payload to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; its afucosylated Fc also enhances ADCC/ADCP.