Polypeptide With Localisation/Targeting Motif TRIZ Cases

Segmented ligand structures enable selective CAR activation, resolving systemic toxicity from natural ligand cross-reactivity.

Engineering TFH-like cells resolves the lack of CD4+ T cell understanding to boost anti-tumor immunity.

Engineered KASII variants elongate C14 and C16 acyl-ACP substrates to C18 acyl-ACP in microalgal host cells.

Co-displaying RDTR and SCF on HIV vectors achieves specific transduction of CD34+ cells without adjuvants.

Segmented inert drug system blocks off-target binding sites, reducing toxicity while enhancing tumor treatment efficacy.

Fusing the GB1 domain from Streptococcus protein G to target proteins enhances recombinant expression levels in plant systems.

Sortilin-derived peptides combined with cell-penetrating sequences overcome EGFR T790M resistance in non-small cell lung cancers.

Segmented Wnt compositions overcome insolubility to enable high-yield muscle regeneration via stem cell expansion.

Ezh2S21A modification boosts Ezh2 activity in CAR T cells, resolving the trade-off between effector function and memory potential.

Peptides modulate immune system activity to enhance anti-tumor responses while reducing chemotherapy side effects.

Segmented Fc domains assemble into multimers to neutralize immune complexes without enhancing C1q binding, preventing albuminuria.

A fusion polypeptide uses a cell penetrating peptide to transport therapeutic proteins across the blood brain barrier.

Fluorescent fusion protein foci formation replaces complex biochemical assays, enabling rapid high-throughput screening of bromodomain inhibitors.

Fusion protein comprising a solubility-enhancing peptide tag and self-aggregating moiety enables polypeptide production.

Engineered fusion polypeptide downregulates MHC class I and TCR molecules to enable universal allogeneic cell manufacturing.

Fusion proteins utilize exosomes as intermediary carriers to conceal therapeutic payloads, reducing immune recognition and improving tissue penetration.

Segmented antibody design with protease-sensitive linkers prevents premature binding, reducing off-target toxicity while maintaining therapeutic efficacy.

Engineered chimeric antigen receptor T cells target Glypican 3 epitopes to eliminate hepatocellular carcinoma xenografts.

Fused nucleic acid molecules encode cognate pairs of bipartite immunoreceptors for direct expression in host cells.

Irradiated recombinant NK cells deliver immune modulators to tumors, limiting cellular persistence and side effects.

Targeted ENPP1 therapy elevates plasma pyrophosphate concentrations, addressing stroke prevention reliability without chronic transfusion complexity.

A Zika virus fusion protein immunogen combines envelope proteins with multimerization domains to stimulate neutralizing immune responses.

Distinct epitope-specific chimeric antigen receptors maintain therapeutic efficacy despite residual rituximab blockade in lymphoma treatment.

Multi-functional recombinant antigen-presenting cells express IL-21 and IL-15 to overcome low expansion efficiency of rare NK and gamma/delta T cells.

IL21 mutants form disulfide bonds to stabilize protein conformation, extending plasma half-life and reducing systemic toxicity in tumor immunotherapy.

A viral SET domain histone lysine methyltransferase modifies chromatin to suppress specific gene transcription.

Modulating PI4KIIIα enhances Aβ42 secretion, reducing intraneuronal accumulation and ameliorating neural deficits in Alzheimer's models.

Controlled glucose uptake during tryptophan promoter induction reduces acetic acid accumulation, boosting fibroin-like protein expression.

RAR and RXR active agents mediate tumor microenvironment modulation to boost CAR-T efficacy while lowering systemic toxicity.

Cell-penetrating compstatin analogs internalize into cells to bind complement component C3, resolving inadequate extracellular inhibition of tissue damage.

Hybrid chRDNA guides incorporating deoxyribonucleotide bases enhance Cas12a complex stability, reducing off-target editing while improving on-target precision.

Separating high molecular weight DNA fractions isolates integrated transgene sequences from residual nucleic acids for precise copy number determination.

Co-cultured CAR and TCR T cells expand in vivo to reduce tumors despite limited persistence.

Replacing CD3ζ with an FcεRIγ signaling domain in NK-92 cells overcomes low genetic modification efficiency and high effector-to-target ratio requirements.

Nucleic acid construct encodes activating and inhibitory chimeric antigen receptors to modulate T-cell surface expression.

Retinal modulating agents adjust the cis/trans ratio of retinal to suppress all-trans-retinal toxicity and prevent retinal atrophy.

A 16-amino acid Noxa-derived peptide induces rapid necrotic cell death in cancer cells.

Zinc finger peptides bind expanded GGGGCC repeats to modulate gene expression.

Co-expressing phospholipase with recombinant protein directs secretion into culture medium, bypassing inclusion body formation and host stress to boost yield.

Antibodies targeting the ROR1 C-terminal portion enable specific binding to full-length protein isoforms.

Patsnap Eureka TRIZ analysis shows how detecting myeloid cell markers enables early intervention and reduces severe neurotoxicity or cytokine release syndrome.

Polypeptide antagonists inhibit Na/K-ATPase receptor function to reduce angiogenesis in retinal vasculature.

Systematically varying antigen binding domain strength balances therapeutic efficacy against cytokine storm risks in BCMA-targeted therapies.

Humanized CD47-CAR-T cells use composite receptor structures to eliminate tumor growth while minimizing systemic toxicity.

Modified Fc-binding proteins resist acid degradation through targeted amino acid substitutions at specific sequence positions.

Segmenting activation signals via distinct receptors prevents off-target toxicity in solid tumours while maintaining high killing efficacy.

Segmenting plasmid expression from peptide synthesis resolves low yield and laborious folding bottlenecks in personalized immunotherapy.

Engineered meganucleases recognize and cleave the PCSK9 gene to reduce circulating LDL cholesterol levels.

Local pH variations trigger protease-mediated linker cleavage, reducing chemical waste and cross-reactions.