| Catalog No. | HV185036 |
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| Species reactivity | Human |
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| Applications | ELISA, Bioactivity: FACS, Functional assay, Research in vivo |
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| Host species | Human |
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| Isotype | IgG2-lambda |
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| Expression system | Mammalian Cells |
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| Clonality | Monoclonal |
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| Target | SOST, Sclerostin |
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| Endotoxin level | Please contact the lab for this information. |
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| Purity | >95% purity as determined by SDS-PAGE. |
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| Purification | Protein A/G purified from cell culture supernatant. |
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| Accession | Q9BQB4 |
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| Form | Liquid |
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| Storage buffer | 0.01M PBS, pH 7.4. |
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| Stability and Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles. Store at 4°C for short-term storage (1-2 weeks). Store at -20°C for up to 12 months. For long-term storage, store at -80°C. |
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| Alternate Names | BPS-804, MOR-05813, 1847394-95-9 |
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| Background | Blosozumab is an IgG4-kappa type mouse monoclonal antibody optimized by humanization engineering with a molecular weight of 144.63 kDa. The monoclonal antibody was developed by Eli Lilly for the treatment of osteoporosis. Blosozumab can target and bind sclerostin (SOST) to play a biological role. In 2014, blosozumab was conducted a different doses of clinical trial about blosozumab was conducted to evaluate including drug safety, tolerance, pharmacokinetics and pharmacodynamics in postmenopausal women. The results showed that blosozumab had well tolerance and anabolic effect on bone, which could be used as a potential treatment for osteoporosis. In 2015, a randomized double-blind phase Ⅱ trial of blosozumab in postmenopausal women with low bone mineral density showed that blosozumab treatment resulted in a significant dose-dependent increase in bone mineral density, which further supports the conclusion that blosozumab is a potential anabolic therapy for osteoporosis. In September of the same year, women who had completed treatment were followed up to evaluate the effect of discontinuation of blosozumab. It was found that there were no adverse events related to the treatment one year after the cessation of treatment, and the anti-drug antibodies in the patients generally decreased.
• SOST/Sclerostin impairs the osteogenesis and angiogesis in glucocorticoid-associated osteonecrosis of femoral head., PMID:39342093
• SOST/sclerostin, an osteocyte-derived negative regulator of bone formation., PMID:15869900
• Suppression of Sost/Sclerostin and Dickkopf-1 Augment Intervertebral Disc Structure in Mice., PMID:35278242
• Sclerostin and Cardiovascular Disease., PMID:37490188
• SOST/Sclerostin Improves Posttraumatic Osteoarthritis and Inhibits MMP2/3 Expression After Injury., PMID:29377313
• Methylation of the Sclerostin (SOST) Gene in Serum Free DNA: A New Bone Biomarker?, PMID:33372860
• Sclerostin: clinical insights in muscle-bone crosstalk., PMID:37632438
• The Effects of Sclerostin on the Immune System., PMID:31970653
• Sclerostin: from bench to bedside., PMID:33206222
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| Note | For research use only. Not suitable for clinical or therapeutic use. |
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