Biomedcode has recently incorporated in its collection of unique animal models of human disease a mouse model spontaneously developing osteoporosis pathology due to the overexpression of human RANKL. An efficacy evaluation platform is standardized to allow the evaluation of anti-osteoporosis therapeutics.

Osteoporosis is a metabolic disease characterized by decreased bone mass and density which can lead to increased risk of fractures. The underlying mechanism is an imbalance between bone resorption and bone formation. Bone resorption is the process by which osteoclasts break down bone. The activation of osteoclasts is regulated by various molecular signals, of which the receptor activator for nuclear factor κB ligand (RANKL) is one of best studied.

Osteoporosis is estimated to affect 200 million women worldwide, offering a huge, constantly rising market. Currently, the market is dominated by the bisphosphonate class of therapeutics, with the recent entrance of Amgen's Prolia (denosumab)  a fully human IGg monoclonal antibody specifically blocking human RANKL, drastically changing the landscape.

However, the size and the importance of the market push the pharmaceutical industry to strive to develop new agents for osteoporosis prevention and intervention, making  the need for reliable animal models more pressing than ever.