Antibody–drug conjugate targeting Nectin-4 on urothelial tumor cells; after binding and internalization it releases the microtubule toxin monomethyl auristatin E (MMAE), disrupting tubulin polymerization and causing G2/M arrest and apoptosis.
Enfortumab vedotin is an antibody–drug conjugate targeting Nectin‑4 on tumor cells. Upon binding and internalization, a cleavable linker releases the cytotoxic payload MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis in Nectin‑4–expressing cells.
YES
DIRECT
ADC binds Nectin-4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
Antibody–drug conjugate targeting Nectin-4 on urothelial tumor cells; after binding and internalization it releases the microtubule toxin monomethyl auristatin E (MMAE), disrupting tubulin polymerization and causing G2/M arrest and apoptosis.
Enfortumab vedotin is an antibody–drug conjugate targeting Nectin‑4 on tumor cells. Upon binding and internalization, a cleavable linker releases the cytotoxic payload MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis in Nectin‑4–expressing cells.
NO
INDIRECT
The ADC targets Nectin-4 on the cell surface, is internalized, and releases MMAE, which binds the vinca site on beta-tubulin to inhibit microtubules, causing G2/M arrest and apoptosis. Beta-tubulin is not the recognition target of the drug.
A patient-specific therapeutic cancer peptide vaccine composed of synthetic peptides representing tumor-specific somatic mutations selected via whole-exome/RNA sequencing and HLA typing to generate high-affinity HLA-binding peptides. Designed to prime and expand neoantigen-specific CD8+ and CD4+ T cells via dendritic cell antigen presentation, enabling recognition and killing of tumor cells expressing the targeted neoantigens.
Patient-specific synthetic neoantigen peptides are selected by tumor sequencing and HLA typing and administered to be taken up and presented by antigen-presenting cells (HLA class I/II). This primes and expands neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, enabling immune recognition and killing of tumor cells expressing the targeted mutations.
YES
INDIRECT
Vaccine peptides are presented by APCs to prime/expand neoantigen-specific CD8+ T cells, which then recognize neoantigen–HLA on tumor cells and kill them via perforin/granzyme and apoptotic pathways.
A patient-specific therapeutic cancer peptide vaccine composed of synthetic peptides representing tumor-specific somatic mutations selected via whole-exome/RNA sequencing and HLA typing to generate high-affinity HLA-binding peptides. Designed to prime and expand neoantigen-specific CD8+ and CD4+ T cells via dendritic cell antigen presentation, enabling recognition and killing of tumor cells expressing the targeted neoantigens.
Patient-specific synthetic neoantigen peptides are selected by tumor sequencing and HLA typing and administered to be taken up and presented by antigen-presenting cells (HLA class I/II). This primes and expands neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, enabling immune recognition and killing of tumor cells expressing the targeted mutations.
NO
INDIRECT
The vaccine primes neoantigen-specific T cells, which kill tumor cells presenting the mutant peptide in HLA class I (e.g., HLA-A) via perforin/granzyme or Fas–FasL. HLA-A expression alone is not targeted.
A patient-specific therapeutic cancer peptide vaccine composed of synthetic peptides representing tumor-specific somatic mutations selected via whole-exome/RNA sequencing and HLA typing to generate high-affinity HLA-binding peptides. Designed to prime and expand neoantigen-specific CD8+ and CD4+ T cells via dendritic cell antigen presentation, enabling recognition and killing of tumor cells expressing the targeted neoantigens.
Patient-specific synthetic neoantigen peptides are selected by tumor sequencing and HLA typing and administered to be taken up and presented by antigen-presenting cells (HLA class I/II). This primes and expands neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, enabling immune recognition and killing of tumor cells expressing the targeted mutations.
NO
INDIRECT
The vaccine primes neoantigen-specific CD8+ T cells that kill tumor cells presenting the specific mutated peptide–HLA class I complex via TCR recognition and perforin/granzyme; HLA-B expression alone is not targeted.