Denosumab
Denosumab injection
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| Monoclonal antibody | |
|---|---|
| Type | Whole antibody |
| Source | Human |
| Target | RANK ligand |
| Clinical data | |
| Trade names | Prolia, Xgeva |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a610023 |
| License data | |
| Pregnancy category |
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| Routes of administration |
Subcutaneous injection, every six months |
| ATC code | |
| Legal status | |
| Legal status | |
| Pharmacokinetic data | |
| Bioavailability | N/A |
| Metabolism | proteolysis |
| Identifiers | |
| Synonyms | AMG 162 |
| CAS Number | |
| ChemSpider |
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| UNII | |
| KEGG | |
| ChEMBL | |
| Chemical and physical data | |
| Formula | C6404H9912N1724O2004S50 |
| Molar mass | 144.7 kg/mol |
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Denosumab (trade names Prolia and Xgeva) is a human monoclonal antibody for the treatment of osteoporosis, treatment-induced bone loss, metastases to bone, and giant cell tumor of bone.
Denosumab is contraindicated in people with low blood calcium levels.
The most common side effects are joint and muscle pain in the arms or legs.
Denosumab is a RANKL inhibitor, which works by preventing the development of osteoclasts which are cells that break down bone. It was developed by the biotechnology company Amgen.
Denosumab is used for those with osteoporosis at high risk for fractures, bone loss due to certain medications, and in those with bone metastases.
A 2012 meta-analysis found that denosumab was better than placebo, zoledronic acid and pamidronate in reducing the risk of fractures in those with cancer.
In those with postmenopausal osteoporosis it decreases the risk of fractures but increases the risk of infection. A 2013 review concluded that it is a reasonable treatment for this condition.
The most common side effects are joint and muscle pain in the arms or legs. There is an increased risk of infections such as cellulitis, hypocalcemia (low blood calcium), hypersensitivity allergy reactions, and osteonecrosis of the jaw and atypical hip fractures. Another trial showed significantly increased rates of eczema and hospitalization due to infections of the skin. It has been proposed that the increase in infections under denosumab treatment might be connected to the role of RANKL in the immune system. RANKL is expressed by T helper cells, and is thought to be involved in dendritic cell maturation.
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