Denosumab
| Monoclonal antibody | |
|---|---|
| Type | Whole antibody |
| Source | Human |
| Target | RANK ligand |
| Clinical data | |
| Trade names | Prolia, Xgeva, others |
| Other names | AMG-162 |
| Biosimilars | denosumab-adet, denosumab-bbdz, denosumab-bmwo, denosumab-bnht, denosumab-desu, denosumab-dssb, denosumab-kyqq, denosumab-mobz, denosumab-nxxp, denosumab-qbde, Acvybra, Aukelso, Bildyos, Bilprevda, Bomyntra, Boncresa, Bosaya, Conexxence, Degevma, Denbrayce, Enoby, Enwylma, Evfraxy, Izamby, Jubbonti, Jubereq, Junod, Kefdensis, Obodence, Osenvelt, Ospomyv, Osqay, Osvyrti, Oziltus, Ponlimsi, Stoboclo, Vevzuo, Vysribli, Wyost Xbonzy, Xbryk, Xtrenbo, Yaxwer, Zadenvi, Zvogra |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a610023 |
| License data | |
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| Routes of administration | Subcutaneous |
| Drug class | Disease-modifying antirheumatic drug |
| ATC code | |
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| Legal status | |
| Pharmacokinetic data | |
| Bioavailability | N/A |
| Metabolism | Proteolysis |
| Identifiers | |
| CAS Number | |
| DrugBank | |
| ChemSpider |
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| UNII | |
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| Chemical and physical data | |
| Formula | C6404H9912N1724O2004S50 |
| Molar mass | 144722.80 g·mol−1 |
Denosumab, sold under the brand names Prolia and Xgeva among others, is a human monoclonal antibody used for the treatment of osteoporosis, treatment-induced bone loss, metastases to bone, and giant cell tumor of bone.
The most common side effects are joint and muscle pain in the arms or legs.
Denosumab is a human IgG2 monoclonal antibody that inhibits the protein RANKL (receptor activator of nuclear factor kappa-Β ligand). RANKL is essential for the formation, function and survival of decreasing the development of osteoclasts, which are cells that resorb (break down) bone. Denosumab binds to RANKL with high affinity and specificity, preventing the interaction between RANKL and RANK (receptor activator of nuclear factor-kappa B). This leads to a reduction in osteoclast numbers and function, and a decrease in bone resorption in cortical and trabecular bones, including cancer-induced bone destruction. It was developed by the biotechnology company Amgen.