Polypeptide With Localisation/Targeting Motif TRIZ Cases

HLA-G specific chimeric antigen receptor overcomes solid tumor immunosuppression by targeting conserved HLA-G antigens.

Fusion proteins couple tafazzin with permeability peptides to restore mitochondrial function in Barth syndrome patients.

Segmenting the receptor into stable and exchangeable parts resolves manufacturing cost trade-offs while enabling flexible antigen targeting.

TE-exon fusion-derived chimeric proteins isolate tumor-specific antigens to eliminate off-tumor side effects while maintaining therapeutic efficacy.

Single-domain antibodies bind transferrin to extend target protein serum half-life, reducing manufacturing complexity compared to albumin fusion.

Replacing Cas9 nickase with inactive LbCpf1 eliminates unwanted indels while expanding editing windows to positions 8 through 22.

LR004 antibody replaces galactose with N-acetylneuraminic acid to reduce hypersensitivity reactions while maintaining therapeutic efficacy.

Segmented heavy and light chains with transmembrane domains expand antibody library diversity while maintaining system complexity.

Multi subunit protein modules transmit activating signals through extracellular binding domains on immune cells.

Engineered chimeric antigen receptors target CD33 on leukemia cells to redirect T cell specificity and improve remission rates.

Membrane-tethered RBD constructs with engineered glycosylation sites mask non-neutralizing epitopes to elicit focused neutralizing antibody responses.

A V27G mutation in the CD19 scFv CDR1 region improves CAR-T cell specificity and IFN-gamma secretion while reducing off-target toxicity.

Tandem CAR structures merge two targeting domains to mitigate antigen escape caused by tumor heterogeneity in pancreatic cancer treatment.

Replacing conventional IgG domains with nanobodies resolves the failure of prior anti-STn therapies by enabling robust cytotoxic activity against solid tumors.

Engineered T-cell receptors bind specific IGF2BP3 peptide epitopes, resolving low targeting specificity in existing immunotherapies.

An artificial transmembrane protein enables label-free detection of intracellular interactions via an evanescent field.

Cell-free expression systems bypass transgenic immunogenicity to yield highly stable cholinesterases for efficient detoxification.

CAR T cells engineered with anti-CD99 receptors resolve the contradiction between treatment reliability and targeting precision in leukemia therapy.

Redirecting glucose metabolites out of the glycolysis pathway enables immune cells to survive and proliferate in nutrient-deprived tumor microenvironments.

A signaling and antigen-presenting bifunctional receptor combines MHC binding with signal transduction domains to enable bidirectional cellular communication.

A CD5-specific chimeric antigen receptor minimizes fratricide against normal T cells while eliminating CD5-positive malignancies.

Altering CD28 phosphorylation sites Y206 and Y218 modulates CAR activity to reduce T cell activation toxicity while maintaining anti-tumor efficacy.

An NK cell-specific chimeric antigen receptor integrates DAP10 and 2B4 cytoplasmic domains to enhance cytolytic activity.

A regulatable chimeric antigen receptor uses a dimerization switch to couple intracellular signaling domains with extracellular recognition elements.

A FasL-binding receptor neutralizes tumor microenvironment signals to prevent activation-induced cell death and improve CAR-T persistence.

Single-domain antibodies replace complex four-chain structures to maintain CD33 binding while reducing molecular weight and improving stability.

Fusion polypeptides link the receptor binding domain dimer to the N-terminal domain via non-immunogenic linkers.

Engineered human anti-CD19 antibodies target CD19-positive cells to resolve specificity gaps in B-cell malignancy treatments.

Mutating CDR regions boosts TCR affinity two-fold, improving targeting of AFP-related tumors.

A chimeric stimulating molecule fuses an extracellular checkpoint receptor domain with an intracellular co-stimulatory domain to activate modified immune cells.

Targeted amino acid substitutions in variant PD-L2 polypeptides increase binding affinity to PD-1 while preserving selectivity against RGMb.

Humanized antibodies target cleaved MUC1 peptides to reduce off-tumor effects from healthy tissue expression.

Composite chimeric antigen receptors using D7 scFv and CD28 overcome tumor microenvironment suppression to eliminate PSMA-positive tumors.

Self-assembling depsipeptide nanostructures protect peptides from rapid hydrolysis, extending in vivo retention and improving anticancer efficacy.

Mutated ARSA enzymes achieve extended half-life and improved CNS delivery via an apoE-II tag, reducing adverse effects from high doses.

Orthogonal synthetic promoter-transcription factor pairs regulate plant gene expression with high precision.

Chimeric peptides combine active sequences with cell-penetrating tags to cross the blood-brain barrier.

VHH fusion proteins bind biomaterials and growth factors to improve implant integration by controlling spatial release.

RPtag large protein resists gastrointestinal degradation, enabling systemic absorption without intravenous injection.

A retroviral integrase-Cas9 fusion protein enables targeted integration of large DNA sequences into the genome.

Recombinant exosomes present clustered SIRPα proteins to block the CD47-SIRPα interaction.

Engineered myeloid cells deliver immune inhibitory agents to prepare the patient microenvironment for cellular therapy.

Humanized anti-CD19 chimeric antigen receptors improve T cell survival and reduce toxicity by minimizing immune responses against the therapeutic agent.

Notch pathway modulation preserves stem-like properties in engineered T cells, reducing exhaustion susceptibility and improving antitumor persistence.

Recombinant fusion proteins form stable polymeric structures through spontaneous self-assembly of C-terminal spider silk moieties.

Engineered receptors enable antigen-presenting cells to internalize extracellular vesicles and present tumor antigens.

Segmented HingeW peptides antagonize c-Jun by blocking DNA binding while maintaining high affinity and stability.

An OGA-intein fusion protein self-splices upon 4-HT treatment to restore catalytic activity.