An autologous, gene-modified chimeric antigen receptor T-cell (CAR-T) therapy engineered to target GPRC5D on malignant plasma cells in relapsed/refractory multiple myeloma; CAR engagement activates T-cell signaling to drive activation, proliferation, cytokine release, and cytotoxic killing.
Autologous T cells engineered to express a chimeric antigen receptor specific for GPRC5D on malignant plasma cells; CAR engagement initiates CD3ζ/costimulatory signaling that activates and expands T cells, drives cytokine release, and induces cytotoxic killing of GPRC5D-positive multiple myeloma cells.
CAR engagement of GPRC5D activates T cells (CD3ζ/co-stim), leading to perforin/granzyme release and Fas–FasL–mediated apoptosis of GPRC5D-positive cells.
Anti-HER2 antibody–drug conjugate (humanized IgG1 linked to MMAE) that binds HER2, is internalized, and releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis; may mediate ADCC and bystander effects.
Disitamab vedotin is an anti-HER2 antibody-drug conjugate (humanized IgG1 linked to MMAE). It binds HER2 on tumor cells, is internalized, and releases MMAE that binds tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis; it may also mediate ADCC and bystander killing.
The anti-HER2 ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which disrupts microtubules causing G2/M arrest and apoptosis; it may also trigger ADCC and bystander killing.
Rocatinlimab (AMG 451/KHK4083) is a subcutaneous monoclonal antibody targeting OX40 (CD134). It inhibits OX40–OX40L costimulatory signaling and depletes OX40-expressing activated effector/memory T cells, reducing type 2/Th2 inflammation in atopic dermatitis.
Rocatinlimab is a subcutaneous monoclonal antibody that binds OX40 (CD134) on activated effector/memory T cells, blocking OX40–OX40L costimulatory signaling and depleting OX40-expressing T cells, thereby reducing T-cell activation and type 2/Th2-driven inflammation in atopic dermatitis.
The anti-OX40 IgG1 antibody binds OX40 on activated T cells and engages Fcγ receptor–bearing effector cells to mediate ADCC (and potentially CDC), depleting OX40-expressing T cells.
Chimeric IgG1 monoclonal antibody against endoglin (CD105), a TGF-β coreceptor on proliferating tumor endothelium; inhibits TGF-β/SMAD–mediated angiogenesis, may induce ADCC, and interferes with VEGF cross-talk.
Chimeric IgG1 monoclonal antibody targeting endoglin (CD105) on proliferating tumor endothelium; blocks endoglin-mediated TGF-β/SMAD signaling and VEGF cross-talk to inhibit angiogenesis, and can engage Fc-mediated ADCC against CD105+ endothelial cells.
IgG1 antibody binds CD105 on endothelial cells and engages Fcγ receptors on effector cells (e.g., NK cells) to trigger ADCC, killing CD105+ cells; angiogenesis blockade is indirect.
Chimeric IgG1 monoclonal antibody TNF-α inhibitor administered subcutaneously (120 mg every 2 weeks). Binds soluble and transmembrane TNF-α, preventing TNFR1/2 engagement, suppressing NF-κB signaling and downstream pro-inflammatory mediators; can mediate ADCC/CDC against TNF-expressing cells.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, blocking TNFR1/2 engagement and downstream NF-κB signaling to suppress pro‑inflammatory mediators; can also mediate ADCC/CDC against TNF‑expressing cells.
Infliximab binds membrane TNF-alpha on cells and, via its IgG1 Fc, recruits Fc gamma receptor effector cells for ADCC and activates complement (CDC); reverse signaling through mTNF can also trigger apoptosis.