Integrated long-read transcriptomics (PacBio Iso-Seq / Oxford Nanopore), immunopeptidomics (LC-MS/MS), and computational filtering to systematically identify patient-specific alternative splicing– and fusion-derived MHC class I peptides beyond somatic mutations.
Precision targeting at the level of peptide-MHC-TCR interactions. 3D structural modeling of peptide-MHC complexes and TCR-pMHC docking to quantify binding energies and predict recognition potential.
Validation of immunogenicity and TCR recognition of prioritized neoepitopes in autologous patient-derived T cells. Elucidation of regulatory mechanisms controlling expression of immunogenic AS-derived peptides.
Rational engineering of neoepitopes combined with displacement of antagonistic self-peptides. Peptide enhancement via computational mutagenesis and ProteinMPNN to convert transient immune activation into durable, precision-guided anti-tumor immunity.
| Feature | Mutation-Only Platforms | PeptideXme |
|---|---|---|
| Neoantigen sources | Somatic SNVs, indels | Somatic mutations + AS-derived + fusion-derived + non-canonical |
| Transcriptomics | Short-read RNA-seq (expression only) | Long-read + short-read RNA-seq (full isoform resolution) |
| Immunopeptidomics | Prediction only | Direct MS validation of presented peptides |
| Structural modeling | Binding affinity prediction | 3D peptide-MHC-TCR structural modeling + binding energy |
| Peptide engineering | None | Rational peptide enhancement + self-peptide displacement |
| TME characterization | Limited (gene signatures) | Full immune profiling (scRNA-seq, TCR repertoire, TME deconvolution) |