This case uses dual binding domains to connect MHC-MAGE tumor targets with T cells or NK cells for selective killing.
Covalent and non-covalent APP transmembrane binding inhibits γ-secretase cleavage, reducing Aβ42 with minimal impact on Notch substrates.
This case uses alphavirus replicon RNA to express focused SARS-CoV-2 spike RBD antigens, supporting immunity while limiting ADE risk.
This case sequences CAR T cells with a targeted small molecule ligand to limit off-target toxicity and cytokine release syndrome.
A modular immune complex platform combines dengue serotype antigens to improve multivalent immunogenicity and complement receptor binding.
Targeted cysteine substitutions form disulfide bonds that stabilize prefusion EBV gB as a vaccine antigen.
Point mutations, CHO-cell glycosylation, and FcRn recycling extend ENPP1 half-life while sustaining PPi levels for calcification treatment.
Targeting moieties guide reduced-affinity consensus interferon to specific cells, supporting longer serum half-life and fewer side effects.
A universal carrier peptide fragment improves delivery of proteins, nucleic acids, and drugs across eukaryotic cell membranes.
Anionic polymers stabilize CRISPR-Cas editing for precise transgene insertion.
This case uses plant expression to produce immunogenic rabies glycoprotein, addressing animal-cell cost, scale, and contamination risks.
Tailored CARs on iPSC-derived nanovesicles target tumor biomarkers while reducing immune neutralization and improving gene-editing delivery.
This case uses a humanized CD7 scFv and modular CAR domains to improve binding, persistence, and control in CAR-T therapy.
This case uses HLA-G-linked myelin peptides to suppress autoimmunity while limiting severe side effects in MS and MOGAD.
This case shows how localized proline substitutions preserve pre-fusion epitopes and improve recombinant RSV-A F protein stability.
This case shows how targeted Cas12i3 mutations improve eukaryotic editing activity and reduce off-target effects.
A segmented CAR design separates signaling until membrane assembly, reducing misfolding, aggregation, and cell exhaustion.
This case shows how humanized anti-CD3 CDR sequences preserve CD3 binding while limiting cytokine release and immunogenicity.
This case uses nanobodies fused to UBX to recruit p97, enabling degradation of large complexes and toxic aggregates.
This case uses bispecific NK engagers to bind Siglec-7 and ovarian tumor antigens, boosting NK cytotoxicity in cold, chemoresistant tumors.
This case combines retroviral packaging proteins with lipid components to improve targeted cargo delivery while limiting off-target effects.
Optimized CDR sequences improve GPRC5D antibody affinity and specificity for diagnostic and therapeutic constructs.
Defined HER2-binding CDRs and signaling domains focus CAR activity on cancer cells while reducing normal-tissue reactivity.
This case uses CD40 CAR signaling in engineered myeloid cells to address solid-tumor barriers and sustain anti-tumor activity.
This case uses HLA-restricted Claudin-18.2 epitopes and engineered receptors to target cancer cells while sparing normal cells.
This case combines CD37 binding with CD3ζ and optional 4-1BB signaling to target cancers affected by CD19 or CD20 antigen loss.
The case combines C5 binding with CFH or DAF regulation to inhibit C3b deposition and address intravascular and extravascular hemolysis.
Engineered bacterial signal sequences move silk and collagen proteins outward, avoiding cell lysis and easing scalable purification.
Engineered heVLPs use human-derived GAG and ENV proteins to deliver DNA, RNA, proteins, and chemicals with reduced immunogenicity.
A target enhancing sequence helps CPP-bearing fusion proteins reach non-nuclear organelles while reducing unwanted nuclear accumulation.
Cationic lipid or polymer complexes help supernegatively charged proteins cross cell membranes for low-toxicity effector delivery.
Targeted IRF5-binding peptides cross cells to inhibit nuclear translocation, offering focused control of cytokine expression in SLE.
This case combines antibodies, NLS, and sterol variants to bypass endosomal trapping and improve nuclear delivery and cytotoxicity.
This case uses localized SpCas9 amino acid changes to improve target recognition while reducing unintended gene modification.
Human-derived VLP membranes and GAG proteins deliver DNA, RNA, proteins, and chemicals while avoiding unwanted DNA integration.
High-affinity PICK1 peptides use a CPP and NPEG linker to improve delivery while limiting maladaptive AMPA receptor trafficking.
Specific MSLN-binding CDRs are integrated into CARs to support immune-cell proliferation, cytokine release, and tumor inhibition.
This case uses inducible promoters and signal peptides to activate and secrete defense proteins after plant injury.
Conventional CAR-T designs underperform in NK cells; NKG2D transmembrane structures tailor signaling for stronger, longer killing.
RGD/NGR-targeted saporin fusion proteins bind αv-integrins or CD13 to improve tumor-cell delivery and limit systemic toxicity.
With photoreceptors lost, AAV sorting motifs localize ChR2 and HaloR in retinal ganglion cells to recreate center-surround fields.
An inactive Cas13 fused to adenosine deaminase edits guided RNA transcripts for specific, scalable targeting.
Receptor-targeting peptides modify AAV particles to improve systemic delivery across the BBB and transduction in adult brain cells.
Specific four-vector ratios and a 24-hour harvest window improve lentiviral titer while reducing excess material in CAR-T manufacturing.
Fusion peptides use polyserine repeats to recruit degradation pathways toward tau aggregates without generating seeding-competent species.
A recombinant AAV vector uses a transferrin receptor-binding tag to deliver therapeutic enzymes into the CNS for sustained treatment.
Engineered Lactobacillus reuteri delivers ShK-235 and IbTX orally, targeting potassium channels while limiting systemic side effects.
IL-2/Fc chimeric proteins sustain CAR T-cell activation without exogenous cytokines.
This case combines TIR, CD3ζ, and other CAR signaling domains to strengthen engineered NK-cell activity against cancer.
A cell-permeable PI3Kγ peptide disrupts PI3Kγ/PKA binding, selectively inhibiting PDE4D to reduce intimal hyperplasia.