Anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); binds the receptor’s extracellular domain to inhibit HER2 signaling and dimerization (especially HER2/HER3) and engages Fcγ receptors to elicit antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and engages Fc gamma receptors on immune effector cells (e.g., NK cells) to trigger antibody-dependent cellular cytotoxicity (ADCC), killing HER2-expressing cells.
An antibody-drug conjugate (ADC) composed of a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE); binds HER2, is internalized, and releases MMAE to disrupt microtubules and induce tumor cell death, with a bystander killing effect.
Humanized anti-HER2 (ERBB2) monoclonal antibody linked via a cleavable linker to the microtubule-disrupting payload MMAE. After binding HER2 on tumor cells and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis; the membrane-permeable payload enables bystander killing of adjacent cells.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE intracellularly via a cleavable linker; MMAE inhibits microtubule polymerization, causing G2/M arrest and apoptosis (with a membrane-permeable payload enabling bystander killing).
An antibody-drug conjugate (ADC) composed of a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE); binds HER2, is internalized, and releases MMAE to disrupt microtubules and induce tumor cell death, with a bystander killing effect.
Humanized anti-HER2 (ERBB2) monoclonal antibody linked via a cleavable linker to the microtubule-disrupting payload MMAE. After binding HER2 on tumor cells and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis; the membrane-permeable payload enables bystander killing of adjacent cells.
NO
INDIRECT
Disitamab vedotin binds HER2 on tumor cells, is internalized, and releases MMAE, which binds tubulin and disrupts microtubules causing mitotic arrest and apoptosis. Tubulin beta is the payload’s intracellular target, not the recognition antigen, so cells aren’t killed because they express tubulin per se; killing occurs in HER2-targeted (and bystander) cells after payload release.
Personalized therapeutic mRNA cancer vaccine encoding patient-specific tumor neoantigens; administered intradermally to be taken up by antigen-presenting cells, translated and presented via MHC I/II to prime neoantigen-specific CD8+ and CD4+ T cells for tumor cell killing.
Personalized mRNA encoding patient-specific tumor neoantigens is delivered intradermally, taken up by antigen-presenting cells (e.g., dendritic cells), translated into neoantigen proteins, and processed for presentation on MHC class I and II. This primes and expands neoantigen-specific CD8+ cytotoxic T cells and CD4+ helper T cells, leading to immune-mediated tumor cell killing.
YES
INDIRECT
The mRNA vaccine primes neoantigen-specific CD8+ T cells; these CTLs recognize the neoantigen peptide presented on MHC I by tumor cells and kill them via perforin/granzyme-mediated cytotoxicity.
Personalized therapeutic mRNA cancer vaccine encoding patient-specific tumor neoantigens; administered intradermally to be taken up by antigen-presenting cells, translated and presented via MHC I/II to prime neoantigen-specific CD8+ and CD4+ T cells for tumor cell killing.
Personalized mRNA encoding patient-specific tumor neoantigens is delivered intradermally, taken up by antigen-presenting cells (e.g., dendritic cells), translated into neoantigen proteins, and processed for presentation on MHC class I and II. This primes and expands neoantigen-specific CD8+ cytotoxic T cells and CD4+ helper T cells, leading to immune-mediated tumor cell killing.
YES
INDIRECT
The mRNA vaccine is taken up by APCs, which present neoantigens on MHC I/II to prime T cells; vaccine-induced T cells then kill neoantigen-expressing tumor cells—primarily via CD8+ CTL perforin/granzyme or Fas–FasL, with CD4+ T cells providing help and potentially killing MHC II–positive tumor cells.