Chemokines TRIZ Cases
- IL-7/CCL19 NK Cells for Lesion-Focused T Cell Chemotaxis
Engineered NK cells secreting IL-7 and CCL19 recruit endogenous T cells to lesions, improving coordinated cancer and infection therapy.
- CXCR3 Ligand N-Terminal Modifications for DPPIV Resistance
N-terminal sequence changes help CXCR3 ligands resist DPPIV cleavage while preserving cell migration activity for immune modulation.
- Modified CXCR1/CXCR2 Ligands With Reduced GAG-Driven Inflammation
Modified GCP2-derived ligands reduce GAG binding and leukocyte chemotaxis while preserving CXCR1/CXCR2 activation for cartilage homeostasis.
- CCL22 Vaccine Compositions Against Cancer Immune Evasion
Using CCL22 as a vaccine antigen triggers cytotoxic T cells to kill CCL22-expressing cells and counter tumor immune suppression.
- Chemokine Biologics With High GAG Affinity for Neutrophil Imbalance
Higher-GAG-affinity chemokine biologics rebalance neutrophil-driven inflammation by modulating native chemokine binding and reducing cytokines.
- Cytotoxin-CCL8 Peptide Constructs for Targeted CCL8 Inhibition
A linked cytotoxin and CCL8 peptide uses receptor binding to suppress CCL8 activity and kill target cells in cancer and immune disorders.
- Chemokine Receptor Antagonist Peptide for Drug-Resistant Cancer
A CXCR1/CXCR2 antagonist peptide combined with chemotherapy targets cancer stem cells to overcome resistance, limit tumor growth, and reduce side effects.
- IL-7/CCL19 NK Cell Composition for Endogenous T-Cell Homing
Engineered iPSC-derived NK cells express IL-7 and CCL19 to recruit endogenous T cells to lesion sites and boost synergistic cancer or infection therapy.
- Polypeptide Biomarkers for Post-PCI Adverse Cardiac Event Risk
Polypeptide expression profiles such as NAP-2 help identify post-PCI STEMI patients at risk of major adverse cardiac events.
- Mutant E1A Stabilization for Oncolytic Adenovirus Replication
Ubiquitination degrades E1A and limits adenoviral replication; lysine substitutions stabilize the protein and improve tumor-cell killing.