A single bicyclic complex combines Nectin-4 and CD137 ligands to address affinity, specificity, and stability limits in cancer therapy.
Biomaterial-derived decellularized sheets combine controlled tensile properties with pressure resistance for artificial blood vessels.
Linked binding domains support viral capture on chromatography resin for more efficient purification and target-cell transduction.
Controlling swelling from 1.0 to 10.0 and post-swelling size to 1.0 nm–5.0 μm helps gelatin particles enter cells naturally while limiting activity loss.
When meniscus repair options are limited, protein tuned to 60–85% β-turns and random coils supports regeneration in a suitable gel state.
Recombinant E. coli expression produces human collagen XVII polypeptides with biological activity while reducing production cost and cycle time.
Controlled alcalase treatment makes collagen-containing tissue matrices softer and more pliable while limiting collagen alteration and immune response.
EDC/NHS cross-linking covalently attaches OPG to a mineralized collagen-GAG scaffold, promoting osteogenesis while limiting bone resorption.
Limited stability and bioavailability of soluble FNDC4 are addressed by an Fc-linked fusion protein that improves glucose tolerance and insulin sensitivity.
FN3 domains shield siRNA from plasma nucleases and bind CD71 to drive receptor-mediated intracellular delivery.
Removing redundant nephrin promoter regions preserves podocyte-specific transgene expression while freeing vector cargo capacity.
Plants, fungi, and bacteria express animal collagen genes to provide comparable-quality collagen while avoiding slaughter and unwanted animal-derived materials.
Homologous recombination replaces native silkworm fibroin genes with spider silk sequences to limit lower-strength Bombyx silk contamination.
Fibronectin scaffold proteins and HSA fusion support stable, concentrated PCSK9 formulations that reduce dosing volume and aggregation.
Combining GDNF variants with Fc or albumin-binding domains addresses short serum half-life while retaining GFRα1 binding for disease treatment.