Phage display selects high-affinity antibodies against hypo-glycosylated B7-H4 mutants to reduce immune suppression.
TIM-4 CASTL fusion proteins bind phosphatidylserine on heterogeneous tumor cells, activating T cells to kill antigens that escape standard CAR therapies.
A carrier peptide fragment enables efficient introduction of foreign substances into eukaryotic cells.
Engineered T-cells use differential binding affinity to destroy malignant cells while sparing healthy B cells.
Anti-HLA-G chimeric antigen receptors selectively target solid tumors while sparing normal tissues to reduce off-target toxicity.
Radionuclide-labeled ligands penetrate tissue to detect surface-expressed lipocalin reporters, bypassing light scattering limits.
Surface-displayed endoglycosidase on engineered eukaryotic cells deglycosylates secreted proteins, eliminating enzyme contamination and purification steps.
Anti-LINGO-1 antibodies block inhibitory myelin proteins to overcome axon regeneration barriers in demyelinating disorders.
Plant-derived transcription activation domains replace viral components to provide robust gene expression without regulatory barriers.
Segmented surface stretching and affinity labeling resolve measurement precision versus throughput contradictions for comprehensive epigenome sequencing.
Humanized DAGRS peptides inhibit oncogenes via specific membrane translocation, resolving toxicity challenges in cancer treatments.
CAAR cells eliminate pathogenic B cells to resolve TTP relapse risks.
DENV4-specific antibodies target stable multimeric NS1 complexes to resolve cross-reactivity and low sensitivity in secondary infection diagnosis.
Tat-9R fused reprogramming factors improve delivery efficiency by escaping macropinosomes, avoiding viral integration risks.
Inhibitory RNA reduces p18 levels to correct abnormal mTORC1 activation and improve synaptic plasticity in Angelman syndrome models.
Optimized peptide sequences enhance binding affinity to the Dvl PDZ domain, resolving low efficacy in Wnt pathway modulation.
Anti-PD-L1 immunocytokines fuse cytokines to antibodies, reducing toxicity from excessive IL-2R binding while enhancing anti-tumor immunity.
Recombinant bispecific immunotoxin binds wild-type EGFR and mutant EGFRvIII receptors to deliver cytotoxic payloads directly to tumor cells.
Anti-BCMA CAR T cell compositions utilize specific dose ranges and formulation parameters to treat relapsed or refractory multiple myeloma.
Antimicrobial peptides alter resident microorganism metabolism to decrease insect vector fitness, reducing disease transmission capabilities.
Transgenic animals produce homogeneous reporter fusion antibodies, eliminating chemical conjugation heterogeneity and separation steps in immunoassays.
Lentiviral vector particles deliver genetic cargo to T cells using an inducible gene expression system, preventing malignant cell transduction.
Sheddase-resistant TREM2 chimeric receptors on Tregs reduce inflammation by binding extracellular ligands without direct cell targeting.
Donor selection based on Vδ2 index scores expands gamma-delta T cells with high cytotoxicity, resolving interindividual heterogeneity in treatment efficacy.
Nanobody-based heterodimers reduce immunogenicity while maintaining dual antigen binding capability.
A polypeptide sequence binds selectively to heparan sulfate glycosaminoglycans on cell surfaces.
Segmented deaminase fragments reconstitute at target sites via dimerization, reducing off-target mutations and oncogenic risks.
Chimeric antigen receptors bind oncofetal fibronectin domains to enhance immune cell infiltration into solid tumors.
A Pyk2-derived peptide binds the cortactin SH3 domain to inhibit invadopodia maturation and block cancer metastasis.
Chimeric antigen receptor polypeptides bind Epstein-Barr virus glycoproteins to redirect T cell cytotoxic activity.
Nanoparticle compositions linked to chloroplast-targeting peptides overcome limited transformation efficiency in diverse plant species.
ND2 peptides disrupt the ND2-Src protein interaction to modulate NMDA receptor activity, reducing stroke and pain side effects without blocking calcium flux.
Engineered CDRs target the CD160 transmembrane domain to amplify NK cell activation without systemic toxicity.
Mutated CD28 chimeric antigen receptors eliminate tonic signaling to prevent exhaustion while maintaining cytokine production and tumor killing.
Antibodies targeting Eva1 proteins eliminate resistant glioma stem cells via ADCC and CDC while sparing normal tissue.