Whole Human Antibody
ADCC-enhanced Burosumab is a non-fucosylated anti-FGF23 therapeutic biobetter antibody. Creative Biolabs' Afuco™ technology platform allows for the control of glycosylation level, thereby achieving ADCC-Enhanced Anti-FGF23 Burosumab, a biobetter by reducing fucosylation of the Fc region of Burosumab, leading to an increased binding affinity for the FcyR receptor on immune effector cells.
More specifically, the afucosylated therapeutic biobetter antibody was generated by recombinant DNA technology. It has been produced in CHO cells that are deficient for fucosylation and purified by affinity chromatography with protein G. The absence of the fucose residue from the N-glycans of IgG-Fc results in dramatic enhancement of antibody-dependent cellular cytotoxicity (ADCC).
Therapeutic antibody; biobetter
Creative Biolabs is interested in collaborating with potential partners (include but not limit to major pharma or biotech firms) to further co-develop ADCC-enhanced Burosumab. For commercial partners interested in our ADCC-enhanced therapeutic antibodies, Creative Biolabs welcomes collaboration. Here are two ways for your choice, and please contact us for more details.
1) Collaborate with us and co-develop the programs from discovery phase to IND enabling. Costs will be shared.
2) Become a licensed candidate of our programs.
Looking forward to cooperating with you in the near future.
Fibroblast growth factor 23
This gene encodes a member of the fibroblast growth factor family of proteins, which possess broad mitogenic and cell survival activities and are involved in a variety of biological processes. The product of this gene regulates phosphate homeostasis and transport in the kidney. The full-length, functional protein may be deactivated via cleavage into N-terminal and C-terminal chains. Mutation of this cleavage site causes autosomal dominant hypophosphatemic rickets (ADHR). Mutations in this gene are also associated with hyperphosphatemic familial tumoral calcinosis (HFTC).
ADHR; FGFN; HYPF; HFTC2; HPDR2; PHPTC
Extracellular region or secreted
Involvement in Disease
Diseases associated with FGF23 include Hypophosphatemic Rickets, Autosomal Dominant and Tumoral Calcinosis, Hyperphosphatemic, Familial, 2.
Its related pathways are RET signaling and Signaling by FGFR2 in disease.
Regulator of phosphate homeostasis. Inhibit renal tubular phosphate transport by reducing the level of SLC34A1. Up-regulate the expression of EGR1 in the presence of KL (via similarity). Acts directly on the parathyroid glands, reducing parathyroid secretion (similar). Vitamin d metabolism regulator. Negatively regulate osteoblast differentiation and matrix mineralization.
Field of research
Cancer antibody; Controls and Markers antibody; Developmental Biology antibody; Signaling Transduction antibody
1.Following secretion this protein is inactivated by cleavage into a N-terminal fragment and a C-terminal fragment. The processing is effected by proprotein convertases. 2.O-glycosylated by GALT3. Glycosylation is necessary for secretion; it blocks processing by proprotein convertases when the O-glycan is alpha 2,6-sialylated. Competition between proprotein convertase cleavage and block of cleavage by O-glycosylation determines the level of secreted active FGF23.
Protein Based Therapies
Monoclonal antibody (mAb)
Whole Human Antibody
Burosumab (KRN23) is a fully human monoclonal IgG1 antibody that specifically binds fibroblast growth factor 23 (FGF23). The U.S. Food and Drug Administration approved Burosumab for the treatment of X-linked hypophosphatemia (XLH) in 2018. It is a rare inherited disease that affects approximately 3,000 children and 12,000 adults in the United States. Burosumab is a breakthrough therapy classified as an orphan drug.
Burosumab (genetical recombination)