Polypeptide With Localisation/Targeting Motif TRIZ Cases

Bispecific GPRC5D-CD3 antibodies use optimized CDR binding to activate T cells and lyse multiple myeloma target cells.

Modified CAR T cells overexpress JAK mutants or chimeric cytokine receptors to boost expansion, persistence, and cancer treatment efficacy.

Permeable peptide carriers ferry hydrophilic therapeutic and diagnostic agents across the blood-brain barrier for brain tissue delivery.

Dose-tuned cyclophosphamide and fludarabine conditioning improves CAR T cell engraftment by lowering lymphocytes and raising homeostatic cytokines.

Amyloid-reactive peptide antibody fusions bind fibrils more strongly, recruit macrophages, and improve clearance of amyloid deposits.

CAR-A*02 expressed in Treg cells selectively suppresses cytotoxic responses to HLA-A*02-positive transplants without broad immune suppression.

A three-domain fusion protein uses pHLIP, JAM, and CAR-T signaling to reduce metastasis while improving tumor cell targeting and eradication.

Engineered PSCA-targeted NKT cells co-expressing IL-15 improve persistence and tumor control in gemcitabine-resistant pancreatic cancer.

Small-molecule regulated SB transposase fusion proteins shorten activity windows to limit copy number, remobilization, and genotoxicity.

Transient anti-TCR CAR expression removes residual TCR-positive cells, enabling purer allogeneic CAR-T products with lower GVHD risk.

Specific anti-LILRB4 antibody CDRs expand AML treatment options by blocking immune-suppressive signaling and inhibiting leukemia cell proliferation.

A recombinant anti-PLA2R antibody standard replaces human serum to enable absolute quantification, reduce batch variation, and avoid pathogen risk.

Down-regulating death-receptor genes and adding immunosuppressive molecules helps allogeneic therapeutic cells resist rejection and persist longer.

Selective LTβR-NFκB inhibitors separate classical and non-classical signaling to control Treg migration and reduce inflammation and graft rejection.

Separate CAAR recognition and signaling modules let therapies target T cells and modified autoantigens with more selective autoimmune cell depletion.

PEBLs block CD3/TCRαβ surface expression in CAR-T cells, reducing GvHD risk while preserving proliferation and tumor killing.

Fast site-selective conjugation links α-hemolysin and DNA polymerase at low concentrations, improving nanopore sequencing accuracy and efficiency.

TLS-derived immortalized B cells yield PD1 binding antibodies that extend tumor immunotherapy beyond T-cell-only approaches.

Smaller Type V Cas proteins fit AAV delivery limits while enabling staggered DNA cuts, multiplexing, and more precise genome editing.

Local electroporation of plasmid cassettes expresses IL-12, CXCL9, anti-CTLA-4 scFv, and CD3 half-BiTE to boost tumor T cell infiltration with lower toxicity.

Anti-GPC3 constructs target cell surface-bound GPC3 to bypass chemotherapy export resistance and improve T-cell killing in HCC.

Membrane-bound IL-2 helps CAR or polyclonal Treg cells survive and stay suppressive in low-IL-2 settings without broadly activating other T cells.

Monomeric Cas12a adenine base editors expand targetable sites while improving editing specificity and activity in plants and other cells.

Hybrid scFv framework changes plus an alanine torsional linker curb CD20 CAR tonic signaling and preserve T-cell tumor killing.

Genetically engineered immune cells remove endogenous TCR activity to limit graft-versus-host disease, self-killing, and rejection.

Receptor-binding yolk protein precursors deliver CRISPR cargo into oocytes, avoiding difficult microinjection and enabling heritable editing.

Engineered D-domain binders replace antibody scaffolds in CAR adapters to target CS1-positive cancer cells with high affinity and fewer off-target effects.

Recombination proteins paired with CRISPR targeting enable kilobase-scale genome editing with higher fidelity and fewer off-target effects.

A humanized CD19 CAR preserves tumor-cell targeting while lowering immunogenicity and enabling shelf-type allogeneic CAR-T therapy.

Reporter T cells with luciferase signaling enable reproducible, high-throughput viral vector potency measurement with lower lot-to-lot variability.

CD19-directed B-cell depletion lowers anti-AAV neutralizing antibodies, enabling AAV re-administration and renewed transgene expression.

Selective fusion proteins bind sialylated cancer glycocalyx markers, enter lysosomes, and trigger caspase-3 apoptosis while sparing healthy cells.

Dual-target CAR T cells bind CD13 and TIM-3 to improve AML cell killing while sparing normal hematopoietic stem cells.

Engineered RSV F mutants use disulfide, cavity-filling, and electrostatic changes to hold the pre-fusion form and improve neutralizing responses.

Targeted IL12 Fc fusion proteins improve antitumor delivery while reducing systemic toxicity and off-target side effects.

Engineered NK-92 cells with PD-L1 CAR, CD16, and IL-2 target tumor cells plus MDSCs and TAMs while avoiding key CAR-T limitations.

Modified interferon chimeras reduce IFNAR binding and add cell targeting to extend half-life, limit side effects, and sustain antiviral activity.

Human-derived CD19 CAR sequences replace murine elements to target malignant B-cells while reducing cytokine toxicity and anti-mouse responses.

Engineered BCMA-targeting T cells use optimized CAR sequences and defined CD4/CD8 dosing to improve multiple myeloma response with low CRS and neurotoxicity.

IL-12, IL-15, and IL-18 pre-activation plus CD137 ligand aAPCs expands NK cells for off-the-shelf cancer therapy with stronger cytotoxicity.

Dual-hydrophobic cationic peptides improve cell entry and exon skipping at lower doses, reducing toxicity in Duchenne muscular dystrophy treatment.

Engineered CAR-T cells attack both tumor cells and suppressive Tregs or macrophages to overcome the solid tumor microenvironment.

Targeted TadA mutations reduce off-target RNA editing and indels while preserving efficient, specific DNA base editing.

Genetically modified CAR Treg cells target OxLDL in plaques to suppress inflammation, reverse plaque formation, and lower cardiovascular risk.

Humanized Il1rl2 and IL-36 ligand genes create a rodent model that reproduces DITRA-like IL-36R signaling for psoriasis and IBD drug testing.

Genetically reprogrammed Tregs express membrane-bound IL-10 to maintain a stable Tr1 phenotype and improve autoimmune therapy feasibility.

IL-12, IL-15, and IL-18 pre-activation plus CD137L aAPC expansion yields functional NK cells at scale without leukapheresis.

A bifunctional antigen-targeting approach helps CAR T cells hit multiple tumor antigens, improving solid and blood cancer response while limiting escape.

Engineered CAR-Tregs target HLA-A*02 or SLA-01*0401 to suppress cytotoxic transplant rejection with specific, stable immune control.