114084-78-5

This third generation biphosphonate was launched in Austria and Germany for the treatment of bone disorders such as hypercalcemia in malignancy and ostedysis, Paget's disease and osteoporosis. It does not effect bone mineralization, therefore, the potential risk of osteomalacia is prevented. This was a problem with first generation derivatives. While the exact mode of action is not understood, they are inhibitors of osteroclast mediated bone resorption. These compounds strongly interact with hydroxyapatite crystals and have a half-life in the skeleton of several years. Despite this observation ibandronate was well tolerated and safe.

White Solid

Boehringer Mannheim (Germany)

A biphosphonate bone resorption inhibitor.

A bisphosphonate antiresorptive agent. Bone resorption inhibitor.

A labeled biphosphonate bone resorption inhibitor.

Bondronat

Bisphosphonate:

Reduction of bone damage in bone metastases in breast cancer

Hypercalcaemia of malignancy

Postmenopausal osteoporosis

Potentially hazardous interactions with other drugs
None known

After initial systemic exposure, ibandronic acid rapidly binds to bone or is excreted into urine. There is no evidence that ibandronic acid is metabolised in animals or humans. The absorbed fraction of ibandronic acid is removed from the circulation via bone absorption (estimated to be 40-50% in postmenopausal women) and the remainder is eliminated unchanged by the kidney. The unabsorbed fraction of ibandronic acid is eliminated unchanged in the faeces. Renal clearance accounts for 50-60% of total clearance and is related to creatinine clearance. The difference between the apparent total and renal clearances is considered to reflect the uptake by bone.