IV bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand-driven activation, inhibits PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, promotes receptor internalization/degradation, and induces ADCC/ADCP via Fc engagement; studied in EGFR-amplified glioblastoma.
Bispecific IgG1 monoclonal antibody that binds EGFR and MET extracellular domains to block ligand-driven activation, inhibit downstream PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, promote receptor internalization and degradation, and engage Fcγ receptors to induce ADCC/ADCP by NK cells and macrophages.
YES
DIRECT
Amivantamab binds MET on target cells and its IgG1 Fc engages Fcγ receptors on NK cells and macrophages to trigger ADCC and ADCP, resulting in lysis/phagocytosis of MET-expressing cells.
A Nectin-4–directed antibody–drug conjugate (human IgG1 mAb) linked to the microtubule-disrupting payload monomethyl auristatin E (MMAE); delivers MMAE to Nectin-4–expressing tumor cells, disrupting tubulin, causing cell-cycle arrest and apoptosis; exposure to MMAE is associated with peripheral neuropathy.
Nectin-4–directed human IgG1 antibody-drug conjugate; after binding Nectin-4 on tumor cells and internalization, a cleavable linker releases monomethyl auristatin E (MMAE), which inhibits tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis.
YES
DIRECT
The ADC binds Nectin-4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
YES
DIRECT
Infused TILs recognize TERT peptide–MHC complexes via native TCRs and kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis), with supportive cytokine effects.
A Nectin-4–directed antibody–drug conjugate (human IgG1 mAb) linked to the microtubule-disrupting payload monomethyl auristatin E (MMAE); delivers MMAE to Nectin-4–expressing tumor cells, disrupting tubulin, causing cell-cycle arrest and apoptosis; exposure to MMAE is associated with peripheral neuropathy.
Nectin-4–directed human IgG1 antibody-drug conjugate; after binding Nectin-4 on tumor cells and internalization, a cleavable linker releases monomethyl auristatin E (MMAE), which inhibits tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis.
NO
INDIRECT
Enfortumab vedotin targets Nectin-4 on the cell surface; after internalization, MMAE is released and binds β‑tubulin to disrupt microtubules, causing G2/M arrest and apoptosis. β‑tubulin expression alone does not make cells susceptible—killing requires Nectin‑4–mediated delivery of MMAE.
An HPV-16–targeted therapeutic mRNA vaccine delivered intramuscularly that encodes HPV-16 antigens to drive intracellular antigen expression, dendritic cell activation, MHC I/II presentation, and robust HPV-16–specific CD8+ and CD4+ T-cell immunity to eliminate HPV-16–infected dysplastic and cancer cells.
Intramuscular mRNA delivery encoding HPV-16 antigens leads to in situ antigen expression in host antigen-presenting cells, dendritic cell activation, and MHC I/II presentation, inducing robust HPV-16–specific CD8+ cytotoxic and CD4+ helper T-cell responses that eliminate HPV-16–infected dysplastic and cancer cells.
YES
INDIRECT
The mRNA vaccine primes HPV‑16 E6–specific CD8+ T cells that recognize E6-derived peptides on MHC I and kill infected tumor cells via perforin/granzyme-mediated apoptosis (with CD4+ T-cell help).