Polypeptide With Localisation/Targeting Motif TRIZ Cases

Chimeric antigen receptors with FKBP-rapamycin binding domains reduce T cell exhaustion while maintaining antitumor activity kinetics.

Engineering CAR-T cells with T-bet, STAT1, or STAT4 transcription factors to overcome costimulatory signal deficiency and improve persistence.

Early cytokine monitoring enables targeted tocilizumab intervention, reducing severe neurotoxicity and CRS complexity.

Macrophage CAR therapy targets TK1-expressing tumors via localized M1 responses, avoiding cytokine storms and long-term immune activation risks.

Lipid nanoparticles deliver modified nucleic acids encoding viral proteins, inducing neutralizing antibodies to reduce coronavirus replication.

Modifying framework regions reduces human immune response while maintaining CD19 binding specificity for sustained therapeutic efficacy.

Polymer-coated viral nanoparticles reduce unintended transduction and immunogenicity while maintaining high transduction efficiency.

Modifying coryneform bacteria to reduce RegX3 activity enhances heterologous protein secretion efficiency.

A chimeric ligand receptor fuses antigen recognition with suppressive signaling to inactivate specific immune cells.

Segmented biosensors with subtype-specific ligand binding domains achieve high selectivity for dopamine receptor D1 without compromising sensitivity.

Fusion polypeptides target nitrogenase components to plant mitochondria, resolving oxygen sensitivity and complex multigene assembly bottlenecks.

CAR-MAIT cells eliminate T-cell lymphoma without allogeneic feeder cells, avoiding graft-versus-host disease.

Multimodal chromatography purifies refolded Ranibizumab fragments from microbial inclusion bodies.

Peptide-modified T cell engagers reduce healthy tissue toxicity by blocking antigen binding until tumor proteases cleave the inhibitor.

Co-expressing vasoactive intestinal peptide receptor antagonists in CAR-T cells blocks immunosuppressive tumor microenvironments to improve cancer cell lysis.

Monoclonal antibodies target surface PRDX4 on intact cancer cells, resolving the inability of prior intracellular antibodies to bind and treat malignancies.

Attaching chorionic gonadotropin carboxy-terminal peptides extends serum half-life and reduces dosing frequency.

A peptide inhibitor of L-plastin targets osteoclasts to reduce bone resorption activity.

Co-localizing glycosidases with recombinant proteins in plant cells removes immunogenic sugar residues to produce safe therapeutic proteins.

Exogenous terminal cannabinoid synthases paired with specific chaperones improve enzyme solubility and expression in recombinant hosts.

A yeast vector system co-expresses a biotin acceptor site and Golgi-localized ligase to generate secreted, biotinylated recombinant polypeptides.

Engineered CAR-T cells eliminate drug-resistant Aspergillus infections through specific antigen binding, overcoming conventional therapy limitations.

CD28H-containing chimeric antigen receptors overcome inhibitory signals to boost anti-tumor cytotoxicity and safety.

Chimeric MyD88 receptors integrate alternative costimulatory signaling to overcome limited efficacy of conventional CAR-T therapies against solid tumors.

Linking CD3 chains to co-stimulatory domains in a modified TCR-CD3 complex overcomes immune suppression and improves anti-tumor efficacy.

A chimeric antigen receptor uses a humanized single-chain variable fragment to target p95HER2-expressing tumor cells.

Segmented fusion proteins merge growth hormone with carrier chains to maintain therapeutic levels without supraphysiological spikes.

Anti-idiotype antibodies target anti-BCMA domains to resolve low detection specificity in CAR-T cell assessment.

Model predicts tumor extinction and survival by analyzing lymphodepletion effects on T cell expansion.

A cell membrane-permeable peptide complex transfers genome editing enzymes directly into plant cells.

Replacing conserved motif residues within the 4-1BB co-stimulatory domain to improve tumor-killing efficiency while reducing cytokine storm toxicity.

A synthetic peptide combining S1PR1 binding and cell-penetrating sequences increases exosome yield while lowering native protein content.

Monoclonal antibodies bind human CD73 to inhibit enzymatic activity, overcoming immunosuppression in solid tumors.

Engineered cells express cleavable fluorescent reporters to measure botulinum neurotoxin activity, replacing time-consuming animal toxicity tests.

Engineered host cells express functional T cell receptors to isolate high-affinity binders against cancer-specific peptide-MHC complexes.

Peptides with specific sequences target HDM-2 overexpression to selectively kill malignant cells while sparing normal tissue.

Recombinant adeno-associated virus delivers modified beta-subunit gene to nervous system cells, resolving frequent protein administration requirements.

A CSF1-granzyme B fusion protein targets CSF1 receptor-expressing cells to deliver cytotoxicity.

A chimeric antigen receptor fusion protein with CD95 ligand and CD137 domains enhances immune cell specificity.

Fluorescent fusion proteins replace immunoassays to enable high-throughput single-cell secretion screening.

Humanized anti-5T4 antibodies resolve binding specificity limitations by enabling potent cross-reactivity with cynomolgus monkey targets.

A synthetic operon co-transcribes a gene of interest with an essential bacterial gene to ensure stable chromosomal integration.

Engineering humanized receptors with P329G mutations eliminates off-target toxicity while maintaining precise tumor cell recognition.

LIPG-binding peptides block viral entry into hepatocytes, reducing HBV DNA and cccDNA levels.

A dual-specific chimeric antigen receptor combines anti-CD19 and anti-CD22 binding domains to redirect T-cell specificity.

Optimized AAV vectors deliver GLA genes to hepatocytes, resolving antibody interference and reducing frequent intravenous administration needs.

Engineered CAR T and NK cells target PSCA-positive solid tumors using interleukin-15 domains to overcome intrinsic resistance to conventional chemotherapy.

An antibody fusion protein links variable regions to an NKG2D ligand domain.

Intermediary agents preserve blood-brain barrier integrity by sparing pericytes during CD19 cancer treatment.