Non-fucosylated Anti-Human Sclerostin (Romosozumab) Therapeutic Antibody (CAT#: BioBet-012ZP) Datasheet

SOST

sclerostin

Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Loss-of-function mutations in this gene are associated with an autosomal-recessive disorder, sclerosteosis, which causes progressive bone overgrowth. A deletion downstream of this gene, which causes reduced sclerostin expression, is associated with a milder form of the disorder called van Buchem disease.

SOST; sclerostin; CDD; VBCH; SOST1

Extracellular region or secreted

Diseases associated with SOST include Sclerosteosis 1 and Craniodiaphyseal Dysplasia, Autosomal Dominant.

Its related pathways are Signaling by GPCR and Signaling by Wnt.

Negative regulator of bone growth that acts through inhibition of Wnt signaling and bone formation.

Glycosylation at Asn53 and Asn175

Protein Based Therapies
Monoclonal antibody (mAb)

IgG1

Romosozumab

Human

Human

Romosozumab is a humanized monoclonal antibody that targets sclerostin. It is used in postmenopausal women with a high risk of fracture and in patients who have failed treatment or are intolerant to other osteoporosis treatments. Osteoporosis in the treatment of osteoporosis. Studies have shown that the drug can increase bone formation and reduce bone resorption in postmenopausal women with low bone density. Romolimumab is approved for medical use in the United States in 2019. Romosozumab is sold in the United States by Amgen under the trade name Evinity.

Osteoporosis

Not Available

Osteoblasts secrete sclerostin, which promotes bone resorption through two mechanisms: a. Inhibition of bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, thereby inhibiting the Wnt signaling pathway; b Increase the production of nuclear factor kappa-ligand (RANKL) 2 receptor activators to promote bone resorption.
Romosozumab targets and inhibits sclerostin, and on the one hand prevents the inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins. Activation of the Wnt pathway leads to promotion of osteoblast survival and proliferation; on the other hand, the inhibitory effect of Romosozumab on sclerostin also inhibits RANKL-dependent osteoclast activity and bone resorption.

Osteoporosis