A patient-specific therapeutic cancer vaccine composed of mutated peptide epitopes derived from the patient’s tumor (selected by exome/RNA sequencing and HLA typing). Administered subcutaneously, the peptides are taken up by antigen-presenting cells and presented on HLA class I/II to prime and boost neoantigen-specific CD8+ cytotoxic and CD4+ helper T-cell responses for tumor-specific killing and immune memory.
Patient-specific mutated peptide epitopes from the tumor are administered subcutaneously and taken up by antigen‑presenting cells. The peptides are presented on HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific recognition and killing and establishing immunologic memory.
NO
INDIRECT
The vaccine primes neoantigen-specific T cells; activated CD8+ T cells kill tumor cells presenting the neoantigen peptides on HLA class I via perforin/granzyme. HLA-DPA1 (MHC II DP) on APCs is used for antigen presentation and is not itself a cytotoxic target.
A patient-specific therapeutic cancer vaccine composed of mutated peptide epitopes derived from the patient’s tumor (selected by exome/RNA sequencing and HLA typing). Administered subcutaneously, the peptides are taken up by antigen-presenting cells and presented on HLA class I/II to prime and boost neoantigen-specific CD8+ cytotoxic and CD4+ helper T-cell responses for tumor-specific killing and immune memory.
Patient-specific mutated peptide epitopes from the tumor are administered subcutaneously and taken up by antigen‑presenting cells. The peptides are presented on HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific recognition and killing and establishing immunologic memory.
NO
INDIRECT
The vaccine primes neoantigen-specific T cells; CD8+ T cells kill tumor cells presenting neoantigen peptides on MHC class I (perforin/granzyme). HLA-DPB1 is only an HLA class II presenter for helper T-cell priming and is not itself a killing target.
A patient-specific therapeutic cancer vaccine composed of mutated peptide epitopes derived from the patient’s tumor (selected by exome/RNA sequencing and HLA typing). Administered subcutaneously, the peptides are taken up by antigen-presenting cells and presented on HLA class I/II to prime and boost neoantigen-specific CD8+ cytotoxic and CD4+ helper T-cell responses for tumor-specific killing and immune memory.
Patient-specific mutated peptide epitopes from the tumor are administered subcutaneously and taken up by antigen‑presenting cells. The peptides are presented on HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific recognition and killing and establishing immunologic memory.
NO
INDIRECT
The vaccine primes neoantigen-specific T cells; activated CD8+ T cells kill tumor cells presenting neoantigen peptides on MHC I via perforin/granzyme or Fas–FasL. HLA-DQA1 (MHC II) on APCs is used for presentation, not targeted for killing.
Third-generation, irreversible EGFR tyrosine kinase inhibitor (also known as alflutinib) designed to target activating and T790M EGFR mutations.
Furmonertinib (alflutinib) is a third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds the ATP site (e.g., Cys797) of EGFR, potently inhibiting activating and T790M resistance mutations. This blocks EGFR phosphorylation and downstream MAPK and PI3K–AKT signaling, suppressing proliferation and inducing death of EGFR-mutant tumor cells, including those with T790M-mediated resistance.
YES
DIRECT
Small-molecule TKI covalently inhibits EGFR kinase (Cys797), blocking EGFR phosphorylation and downstream MAPK/PI3K–AKT signaling, causing growth arrest and apoptosis of EGFR-mutant (incl. T790M) tumor cells.
A patient-specific therapeutic cancer vaccine composed of mutated peptide epitopes derived from the patient’s tumor (selected by exome/RNA sequencing and HLA typing). Administered subcutaneously, the peptides are taken up by antigen-presenting cells and presented on HLA class I/II to prime and boost neoantigen-specific CD8+ cytotoxic and CD4+ helper T-cell responses for tumor-specific killing and immune memory.
Patient-specific mutated peptide epitopes from the tumor are administered subcutaneously and taken up by antigen‑presenting cells. The peptides are presented on HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific recognition and killing and establishing immunologic memory.
NO
INDIRECT
The vaccine primes neoantigen-specific T cells; CD8+ CTLs kill tumor cells presenting neoantigen peptides on HLA class I. HLA-DQB1 (class II) on APCs is used for CD4+ T-cell priming and is not a direct cytotoxic target.