Humanized monoclonal antibody targeting CD2; blocks the CD2–LFA-3 costimulatory interaction and depletes/modulates CD2+ lymphocytes, inhibiting T/NK cell activation and cytokine release to reduce neuroinflammation.
Humanized anti-CD2 monoclonal antibody that blocks the CD2–LFA-3 costimulatory interaction and depletes/modulates CD2+ T and NK lymphocytes, thereby suppressing T-cell activation and proinflammatory cytokine release to reduce neuroinflammation.
YES
DIRECT
Anti-CD2 antibody binds CD2 on T/NK cells and depletes them via Fc-mediated ADCC and complement-dependent cytotoxicity (with possible apoptosis upon cross-linking).
MET-targeting antibody-drug conjugate designed to bind MET on tumor cells, inhibit HGF/MET signaling, and deliver cytotoxic activity to MET-positive cells.
Anti-MET (c-MET/HGFR) monoclonal antibody conjugated to the microtubule-disrupting payload MMAE. RC108 binds MET on tumor cells, inhibits HGF/MET signaling, is internalized, and releases MMAE intracellularly to disrupt tubulin polymerization, causing G2/M arrest and apoptosis in MET-positive cells.
YES
DIRECT
Anti-MET ADC binds MET on target cells, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization causing G2/M arrest and apoptosis of MET-positive cells.
MET-targeting antibody-drug conjugate designed to bind MET on tumor cells, inhibit HGF/MET signaling, and deliver cytotoxic activity to MET-positive cells.
Anti-MET (c-MET/HGFR) monoclonal antibody conjugated to the microtubule-disrupting payload MMAE. RC108 binds MET on tumor cells, inhibits HGF/MET signaling, is internalized, and releases MMAE intracellularly to disrupt tubulin polymerization, causing G2/M arrest and apoptosis in MET-positive cells.
NO
INDIRECT
RC108 targets MET, is internalized, and releases MMAE that binds tubulin to disrupt microtubules, causing G2/M arrest and apoptosis; tubulin expression alone does not make cells targets—only MET-positive cells are killed.
Third-generation, irreversible covalent EGFR tyrosine kinase inhibitor selective for mutant EGFR (including T790M), blocking EGFR signaling to inhibit proliferation and induce death of EGFR-mutant tumor cells and overcome T790M-mediated resistance.
YES
DIRECT
Irreversible covalent inhibition of mutant EGFR (including T790M) blocks survival signaling (e.g., MAPK/PI3K-AKT), causing apoptosis of EGFR-mutant tumor cells.
Third-generation, irreversible covalent EGFR tyrosine kinase inhibitor selective for mutant EGFR (including T790M), blocking EGFR signaling to inhibit proliferation and induce death of EGFR-mutant tumor cells and overcome T790M-mediated resistance.