Polypeptide With Localisation/Targeting Motif TRIZ Cases

An antigen-derived epitope molecule competes with target-antigen binding to modulate CAR-T activity and limit cytokine storms and toxicity.

Conventional CAR T cells struggle with solid-tumor penetration and durable responses; AbTCRs and CSRs target GPC2/GPC3 with stronger activity.

Modified PPR proteins bind DM1 CUG repeats to reduce RNA foci, correct splicing abnormalities, and improve muscle differentiation.

Peptides block AMPKα1S496 and AMPKα2S491 phosphorylation to restore mitochondrial fission and oxidative activity.

Removing or relocating the IscB PLMP domain can improve RNA-guided DNA cleavage, polynucleotide binding, and editing activity.

A bridging molecule links immune-cell receptors to dysfunctional P2X7 on tumors, improving solid-tumor targeting and limiting antigen escape.

Atomic-resolution VQIINK structures guide substituted peptide inhibitors that block full-length Tau aggregation and cellular seeding.

Targeted CDR amino acid substitutions increase anti-mesothelin binding despite fibrous tissue around solid tumors.

Orthogonal split-inteins join smaller CAR subunits after transduction, while magnetic sorting enriches correctly spliced cells.

An engineered PD-L1 CAR binding domain recognizes glycosylated PD-L1 to boost tumor-cell cytotoxicity while limiting normal-tissue toxicity.

Changing the light-chain N-terminal sequence or secretory leader prevents truncation impurities and batch-to-batch variability in recombinant antibodies.

Attaching a hydrophilic sugar chain improves aqueous solubility and CNS retention for intranasal glycosylated neuropeptide delivery.

Destabilizing domains and stimulus-response elements tune membrane-bound IL-12 levels over time for safer gene therapy expression.

Cell-penetration and endosomal-escape sequences help a peptide derivative reach the eyeball and optic nerve through nasal administration.

Targeting the DCLK1 tumor marker helps focus antibody and CAR activity on cancer cells while addressing toxicity in solid-tumor treatment.

Mitochondrial-potential flow sorting can be slow and costly; Pgp-selective enrichment offers a simpler route to robust adoptive cell therapy.

Optimized Cas14-derived CasMINI effectors address weak eukaryotic activity while preserving compact size for AAV genome engineering.

An intra-articular PNA inhibitor of miR-574-5p targets prostaglandin synthesis and osteoclast maturation to address OA progression.

CD19 downregulation and resistance are addressed by switching to CD22 with antibody, bispecific, CAR, and ADC formats for B-cell leukemias and lymphomas.

RSV F ectodomain chimeras with BPIV3 membrane tails improve envelope incorporation while supporting bivalent vaccine responses.

Combining IL-15, IL-7, and IL-21 in Fc-linked fusion complexes simplifies delivery while limiting non-specific immune activity.

Limited NK-cell lifespan can restrict cancer therapy; chimeric signaling polypeptides and timed safety switches support persistence with controlled cell termination.

Limited monoclonal antibodies constrain CAR T coverage of AML and NETs; STAR retrieves tumor-binding nanobodies for CARs and ADCs.

Trastuzumab-insensitive HER2-overexpressed cancer cells motivate antibody and CAR designs that bind a distinct epitope and improve killing.

Drug-resistant relapse after chemotherapy is addressed with engineered canine T cells that target CD20-positive lymphoma cells for antigen-specific killing.

Conformation-specific antibodies target the FnIII9-10 domain to distinguish force-induced fibronectin states and regulate integrin binding.

Single-domain antibody mimics let one CAR-T construct recognize multiple epitopes while supporting proper folding and stronger tumor-cell activity.

Affinity-tuned human I-domain CARs recognize ICAM-1-high tumors while limiting targeting of healthy tissues with basal expression.

An anti-CD30 scFv paired with a tumor-associated antigen binder helps CAR T-cells target CD30-negative tumors with improved persistence and lysis.

See how ITAM-mutated CARs paired with inducible IL-18 receptors can improve T cell persistence and killing of low-antigen cancer cells.

Antigen-binding chimeric fusion proteins let engineered myeloid cells target and phagocytose cancer cells while activating T cells.

Inhibiting B2M, CIITA, and endogenous TCRs helps create standardized T-cells with lower rejection and graft-versus-host risks.

Engineered immune cells use GXM-binding scFv CARs with CD28 and CD3ξ signaling to target Cryptococcus and address antifungal drug resistance.

An anti-CD30 CAR combines antigen recognition with co-stimulatory domains to kill cancer cells while sparing healthy CD30+ cells.

Targeted TCR downregulation in engineered immune cells limits graft-versus-host disease while preserving anti-tumor immune activity.

CD33-targeted t-haNK cells eliminate suppressive MDSCs, helping restore NK cytotoxic activity against tumor cells in cancer and MDS.

ICE cells engage inhibitory immune checkpoints to protect allogeneic therapeutic cells from adaptive and innate immune rejection.

Engineered T cells use fusion receptors to convert PD-1 or BTLA inhibitory signals into activation while limiting systemic autoimmunity.

Small molecules reversibly control fusion-protein dimerization, helping adapt antigen targeting while improving signaling precision and safety.

Paired recombinant bacterial effector peptides use protein transduction domains to target NFkB, JNK, and p38 pathways with lower toxicity.

PD-L1+ EV testing identifies likely CAR T responders and helps guide treatment choices before T cell exhaustion develops.

Genetic reduction of HLA class I/II and T cell receptor expression helps CAR-engineered cells limit GVHD and immune rejection in allogeneic therapy.

RNA-guided dCas13-RBM25 binds downstream introns to activate or repress endogenous exons without permanent genomic changes.

Multimerization regions in SPA peptides induce constitutive activity to support CAR-T expansion, persistence, cytokine production, and tumor-cell killing.

Engineered immune cells activate on MSLN while an HLA-A*03 blocker restrains attacks on normal tissues, exploiting tumor loss of heterozygosity.

V-ATPase C/FcpA constructs and heterologous signal peptides enhance therapeutic antibody secretion in P. tricornutum, addressing low microalgal yields.

Mutated VSV-G envelope proteins target lymphocytes, enabling resting-cell transduction while limiting off-target uptake.

Ribozyme-linked prokaryotic tRNA and dsRNA-binding control improve processing and limit eIF-2α phosphorylation for higher ncAA expression.

Conventional scFv CARs can miss low-density antigens; a Fab binding domain helps improve signaling and target-cell killing.

This case combines an IgG4 Fc domain with receptor-selective IL-2 variants to reduce dosing frequency and toxicity.