Polypeptide With Localisation/Targeting Motif TRIZ Cases

A stable, positively charged TB peptide carries nanobodies and neurotensin across the blood-brain barrier while preserving brain activity.

Antibodies binding the MUC1-C extracellular domain selectively detect and treat MUC1-positive cancers by inhibiting growth and inducing cell death.

Multi-cistronic boosted CARs combine targeting, cytokine support, and tumor-penetrating elements to improve solid tumor persistence and safety.

Modified HA cleavage loops in plant-made influenza VLPs reduce protease processing and improve particle yield and immune response.

Single-stimulus synthetic bioswitches enable sharp on/off gene expression control, reducing off-target effects and toxicity in live cells.

Covalently linked small molecules extend ADC half-life, improving antitumor activity while reducing dosing frequency and side toxicity.

Fc tuning preserves FcRn half-life while reducing FcγR cross-linking and cytokine release in CLDN18.2-CD3 tumor-targeting antibodies.

Modified cyclotides bind BBB transcytosis receptors to carry therapeutic and diagnostic agents into the central nervous system.

RNA-encoded docking and activation compounds let one CAR-T cell type expand and precisely target different cancer cells.

Engineered NK-92 cells with PD-L1 CAR and CD16 kill PD-L1-positive tumor cells and suppressive myeloid cells with lower variability.

Engineered ATFs target specific immune gene loci to control cytokine expression, reduce off-target effects, and improve therapeutic response.

Rationally designed meganuclease fusions target specific DNA loci to regulate gene expression while reducing non-specific cleavage, mutagenicity, and toxicity.

Targeted Cas12a mutations expand PAM compatibility and raise DNA cleavage at AT-rich and TTTT sites for more effective genome editing in eukaryotic cells.

Gene-edited CD19 CAR T cells disrupt TRAC and B2M and add HLA-E shielding to reduce immune rejection while enabling scalable allogeneic therapy.

A donor strand-stabilized FimH RNA vaccine avoids chaperone production burden while driving strong antibodies against E. coli adhesion.

Targeted FraC mutations tune pore diameter and electroosmotic capture, enabling higher-resolution peptide and protein analysis.

Engineered host cells use DAP10-based chimeric adaptor polypeptides to stabilize receptor signaling, resist downregulation, and improve tumor killing.

A knob-into-hole IL-15 mutant and IL-15Rα-Fc heterodimer boosts NK and T cell activity while improving pharmacokinetics and limiting capillary leak risk.

Engineered meganucleases target HBV recognition sequences to improve on-target cleavage while reducing off-target cutting in host DNA.

Sequence-specific zinc finger proteins target the HTLV-1 LTR to suppress HBZ, reduce CCR4, and inhibit infected cell proliferation.

Genetically modified non-pathogenic bacteria secrete PTD-fusion proteins that cross the blood-brain barrier, enabling oral protein therapy.

A recombinant anti-PLA2R antibody standard replaces human serum to enable absolute quantification, safer production, and consistent kit batches.

Variant CD3ζ ITAM patterns in CAR T cells improve persistence, effector function, and antigen bond lifetime for cancer targeting.

By recruiting endogenous stimulatory signaling through its transmembrane domain, ESMA-CAR lowers cytokine release while preserving antitumor activity.

Novel BCMA CAR iNKT cells pair stronger target binding with IL-15 secretion to improve cancer cell killing and in vivo persistence.

Conformation-specific antibodies and scFv peptides detect force-induced fibronectin states to distinguish diseased tissue and regulate integrin signaling.

Humanized anti-CLDN18.2 antibodies retain high tumor-cell binding while reducing CLDN18.1 off-target toxicity and immunogenic response.

Blocking CCR4-driven regulatory T-cell migration with a humanized IgG4 antibody can restore effector T-cell activity and reduce tumor burden.

CD28-hinge BCMA CAR-NK cells improve targeting of BCMA-positive tumors while addressing immune suppression and disease escape.

A Rhizopus oryzae lipase leader peptide improves Brazzein folding and secretion, raising sweetness while lowering purification cost.

Phosphatidylserine-binding CERs drive engulfment signaling to clear apoptotic tumor cells while limiting unnecessary inflammation.

Selective TSHR epitope recognition enables a CAAR to deplete autoreactive B cells while preserving broader immune function in Graves’ disease.

Cell-specific enhancers paired with minimal promoters limit CAR expression to T, NK, or B cells, reducing hazards from off-target activity.

Specific CDR sequences enable anti-CLL-1 antibodies to bind AML-cell receptors, offering a targeted alternative to limited conventional therapies.

Defined CDR sequences and identity thresholds support high-affinity GPRC5D binding while streamlining antibody characterization for myeloma therapy.

Specific binding and strong internalization address CLDN18.2 targeting gaps through antibody sequence optimization for cancer therapy and diagnosis.

Removing TCR components and adding CAR signaling helps allogeneic T cells avoid immune rejection while supporting scalable, persistent cell therapy.

Targeted amino acid changes in CAR hinge, transmembrane, and intracellular domains improve T cell proliferation, cytokine production, and cancer-cell killing.

CasP6 nucleases and guide RNAs expand CRISPR options for sequence-specific genome modification and nucleic acid detection.

An adhesion-binding fusion protein helps deliver modified mitochondria into recipient cells, addressing limited options for mitochondrial disease.

Combining CD20 and BCMA binding regions in one CAR broadens targeting across B-cell populations, including BCMA-expressing plasma cells.

Reversible activating and blocking receptor expression forms localized micro-clusters that enable target-cell killing while limiting non-target activation.

Positively charged mucoadhesive peptides retain ACE2-binding proteins on mucosal surfaces to block coronavirus entry and activate complement.

Low-dose cyclophosphamide and fludarabine reduce endogenous lymphocytes and limit toxicity before T cell therapy.