Selective GRAIL-1 targeting of the DNAJA1-Hsp70 complex degrades mutant p53, while EGFR peptides track response in BE and EAC.
Oncolytic virus priming boosts CAR T targeting in solid tumors by selective tumor-cell replication and disruption of immunosuppressive barriers.
Dual-CRD and N-terminally deleted transposase fusion proteins improve PiggyBac site specificity, thermostability, and transposition efficiency.
By fusing AAV8 nuclear localization with AAV9 tropism regions, this engineered capsid boosts nuclear delivery and transgene expression.
Modular MESA receptors sense IL-23 and release a transcription factor to enable selective, precise gene expression without native pathway interference.
Targets pathogenic IgA1, gd-IgA1, and immune complexes with glycan-mediated internalization and degradation for faster, more specific therapy.
A short receptor-binding peptide on the nuclease enables cell uptake while reducing size for better diffusion and bioavailability in tumors.
A D-lysine change at position 12 boosts carrier peptide membrane permeability for efficient transfer of nucleic acids, drugs, and polypeptides.
Localizing orthogonal translation components to target mRNA enables selective ncAA insertion in mammalian cells while limiting background decoding.
Glycan-linked polypeptides bind ANCA autoantibodies and endocytic receptors to drive antibody internalization, degradation, and durable disease control.
Engineered Cas12b variants and single-vector delivery improve DNA base editing specificity while reducing off-target effects across cell types.
A compact MECP2 cassette preserves neural expression control within AAV capacity, improving delivery while limiting toxicity in Rett syndrome.
Modular synTFs use regulator proteins to tune immune cell gene expression, reducing toxicity while preserving therapeutic efficacy.
Hydrophilic changes at the 6th and 9th residues of the first PPR motif reduce aggregation while preserving strong target nucleic acid binding.
By splitting nuclease activity across Cas9 fusion proteins, this case reduces off-target DNA cleavage and enables more precise genomic modification.
A cell-penetrating SHP2/SHP1 SH2 fusion protein blocks checkpoint signaling inside cells to boost T cell killing and inhibit tumor growth.
Heavy-chain anti-CD19 binders with engineered CDRs improve CAR-T activation, T-cell expansion, and tumor control while simplifying antibody structure.
A soluble TRβC scaffold links two binding domains in one chain to improve antigen targeting and stimulate immune-cell killing.
Bispecific antibodies bridge CD3ε-positive T cells to TYRP1-expressing melanoma cells, enabling targeted lysis with fewer side effects.
Nanolipoprotein particles transfer functional CAR-like transmembrane proteins to immune cells with lower toxicity and no genetic modification.
A dual activator-inhibitor receptor strategy helps immune cells kill blood cancer cells while sparing normal blood cells.
A salicylic acid-triggered heterodimerization platform simplifies chemically induced proximity while enabling reversible, precise control of signaling and gene expression.
Mechanosensitive Piezo1 engineering helps CAR T-cells activate, infiltrate tumors, and persist despite microenvironment resistance.
Truncated T3SS effector polypeptides with protein transduction domains improve bioavailability and suppress host immune responses in chronic inflammation.
A peptide derivative with cell-penetration and endosomal-escape sequences reaches the eye or optic nerve without intravitreal injection.
CMV-specific CAR T cells target multiple HIV epitopes to kill infected cells, limit viral escape, and reduce dependence on lifelong ART.
Specific amino acid changes in SpCas9 improve target recognition, reducing off-target cleavage while preserving genome editing efficiency.
NK receptor-based CAR designs use inhibitory feedback to preserve tumor killing while reducing off-target attacks on normal tissues.
An IF1 peptide linked to an Fc region improves half-life, stability, and pharmacological efficacy while keeping the fusion protein well defined.
Novel low-homology Cas13 variants improve RNA nuclease activity and CRISPR editing performance while supporting sensitive nucleic acid detection.
Mutated IL13 CARs improve IL13Rα2 selectivity, reducing healthy-tissue receptor sink effects and off-target binding in cancer therapy.
Humanized BCMA scFv and CD28 or 4-1BB CAR domains improve BCMA-positive myeloma cell killing while reducing immunogenicity.
Using α-factor prepro and GLV secretion peptides boosts polypeptide secretion while reducing polynucleotide dose in mammalian and plant cells.
Single-domain VHH and VH binders overcome affinity and size limits to target B7-H3-positive solid tumors with CAR and conjugate options.
A CD27-equipped CAR-T structure improves tumor targeting and persistence while helping limit off-target toxicity and recurrence.
CRISPR disruption of PTPN2 helps engineered T cells resist exhaustion and improve cytokine secretion, persistence, and tumor killing.
Cell-penetrating MYB/CBP-interfering peptides block leukemogenic gene regulation, trigger apoptosis, and address chemoresistant AML.
Modular dCas9 or zinc finger repressors target PCSK9 transcription in vivo while limiting genome instability, off-target effects, and delivery risk.
Using dipeptide glutamine in the base medium and free glutamine in a frozen supplement limits degradation and precipitation during engineered cell culture.
Natural TSH α/β subunits replace scFv binding domains to target TSHR-positive thyroid cancer while reducing CAR-T immunogenicity and clearance.
Targets WT1 peptide fragments on MHC class II to broaden cancer cell recognition while reducing on- and off-target toxicity.
By combining antigen binding with co-stimulatory signaling, this case shows how engineered fusion polypeptides boost T-cell killing and persistence.
A BBB-penetrating TAT-P6 peptide blocks Syn2b-GluA2 binding to raise GluA2 membrane expression and restore AMPA signaling in cognitive impairment.
Chimeric signaling and IL-15 modules help modified NK cells persist longer in vivo while maintaining targeted cancer cell killing.
Dual CD19/CD22 CAR constructs improve T cell persistence and proliferation to better target B cell malignancies and reduce relapse.
An HLA-E single-chain trimer helps universal T cells evade NK killing, reduce rejection, and improve CAR/TCR cell persistence.
Engineered CD70-binding CARs and TCRs improve T-cell killing and cytokine production against CD70-expressing cancers such as multiple myeloma.
A linker-joined scFab enables one-step cell-free expression while preserving antibody affinity and stability for scalable production.
Humanized anti-EphA10 antibodies target resistant cancer cells, enabling selective killing and new options beyond checkpoint inhibitor non-response.
Cell-penetrating DAXXp and FADDp peptides block FAS-driven endothelial apoptosis to limit microvascular injury and preserve vascular density.