Polypeptide With Localisation/Targeting Motif TRIZ Cases

A split intein system covalently links transmembrane domains to soluble proteins within phospholipid bilayers.

Constitutively active chimeric cytokine receptors boost CAR-T cell expansion and cytotoxicity while avoiding systemic toxicity from bystander immune activation.

A fusion polypeptide links ziconotide to a cell membrane penetrating peptide for systemic delivery.

Optimized CD19 antibody CDR sequences resolve insufficient binding affinity and specificity in B cell leukemia treatments.

Antibodies targeting HER2 domains I, II, or III overcome MUC4 glycoprotein masking that blocks trastuzumab binding to domain IV.

Engineered chimeric F proteins combine hMPV and RSV segments to stabilize the prefusion conformation for robust immune response induction.

Albumin and disaccharide additives in the cryopreservation medium maintain osmotic equilibrium to prevent intracellular water loss and solute toxicity.

Fusion proteins dephosphorylate TCR signaling components to prevent graft-vs-host disease while preserving CAR efficacy.

Segmented chimeric antigen receptors target Globo H antigens to activate T cell killing of cancer cells.

A dCas9-TET1 fusion protein enables precise epigenetic editing by targeting specific genomic sequences.

A heterodimeric VEGF fusion protein blocks endothelial cell proliferation and migration through receptor competition.

A combination therapy merges an ERK translocation-blocking peptide with a MEK inhibitor to overcome rapid resistance in BRAF and NRAS mutant melanomas.

A signal peptide directs lysostaphin secretion into the culture medium, resolving purification complexity and host protein contamination.

Lipid nanoparticle delivery of coding RNA overcomes reduced efficacy in developing countries by inducing strong immunity without reactive adjuvants.

Targeted mRNA localization guides translation at the mitochondrial surface, overcoming hydrophobicity barriers to enable stable therapeutic protein delivery.

An IgG4 hinge in GPC1-targeting CARs boosts cytolytic activity and cytokine secretion against solid tumors with low antigen expression.

Bispecific antibodies link NKG2D receptors to tumor antigens via IgG4 hinges, overcoming antigen heterogeneity in solid tumors.

Peptide inhibitors disrupt the POSH/JIP-1 scaffold network to modulate JNK1 activation, addressing specificity gaps in targeting immune responses.

A modified T-cell receptor targets tumor cells expressing the KASEKIFYV-HLA A0201 complex through engineered CDR mutations.

Engineered CAR polypeptides adjust ITAM counts on a DAP12 backbone to balance tumor killing efficiency against T cell toxicity and persistence.

Genetic modification of tumor cells to express distinct HLA haplotypes overcomes mismatch barriers and expands eligibility for TCR-engineered T cell therapy.

Deleting toxic genes from Clostridium genomes enables stable, non-toxigenic spores to deliver recombinant antigens without harmful effects.

Adding p38 MAPK inhibitors during culture prevents terminal differentiation, resolving the trade-off between cell quantity and antitumor persistence.

Fusion peptides inhibit GrB-EHITSN activity, reducing pulmonary vascular resistance in pulmonary arterial hypertension.

N264Q mutation on sulfamidase boosts secretion and uptake, resolving inadequate cross-correction in MPS IIIA therapy.

Engineered rAAV vectors restore NEU1 enzyme function to reduce toxic sialylated compound accumulation in sialidosis patients.

Sortase-mediated attachment of chimeric polypeptides to pili tips resolves folding reliability and exposure trade-offs.

Chimeric antigen receptors incorporate endogenous T cell receptor complexes to limit cytokine release syndrome and off-tumor toxicity.

Membrane-bound IL-15 fusion polypeptides anchor cytokine signaling to maintain T cell persistence and cytotoxic activity in the tumor microenvironment.

Phospholipid ether complexes link chimeric antigen receptors to tumor cells, reducing adverse side effects from non-specific binding.

Hypo-BioNVs deliver tailored CARs to tumor cells, bypassing liver sinking and immune neutralization.

A fusion protein integrates costimulatory receptor and CD3 signaling domains on T cells to enable direct ligand detection.

Replacing threonine-rich and basic regions in assembly activating proteins increases capsid stability and vector yield by up to 200 percent.

Engineered chimeric receptors use modular intracellular signaling domains to tune immune cell activation and proliferation.

Fusion polypeptides combine Leishmania antigens to stimulate protective immunity, addressing limited sub-unit vaccine effectiveness.

Engineered trigger nucleic acids and ILF3 proteins recruit transcription factors to upregulate gene expression.

Reporter gene translocation quantifies oncogenic activity through subcellular localization shifts, resolving mutation pool ambiguity.

Fusing endonucleases with DNA modifying enzymes generates 3' OH overhangs, resolving low mutagenesis efficiency caused by dominant error-free repair pathways.

Catalytic antibodies in CAR-T cells form covalent bonds with adapters, reducing cytokine release syndrome and off-target effects.

Photothermal electrospun nanofibers deliver macromolecules into T cells, maintaining homeostasis and viability lost with electroporation.

A T lymphocyte expresses a chimeric antigen receptor with dual single-chain antibodies targeting CD19 and CD22 antigens.

Antigen binding proteins targeting HLA-peptide complexes enable precise tumor cell cytotoxicity while minimizing off-target effects on normal tissues.

Recombinant SIRPα switch receptors invert native inhibitory signaling to enhance NK and T cell cytotoxicity against CD47-expressing tumor cells.

Self-assembling virus-like particles present exposed neutralizing epitopes on the surface to overcome structural shielding of HIV antigens.

Segmented Fcγ receptor design boosts tumor killing while reducing genetic complexity compared to CAR T therapies.

Mutant luciferases utilize aminoluciferins to produce bioluminescence, overcoming product inhibition that limits wild-type enzyme duration.