Boning
Boning Uses, Dosage, Side Effects, Food Interaction and all others data.
Boning is a second generation, nitrogen containing bisphosphonate similar to neridronic acid and alendronic acid. Boning was first described in the literature in 1977. The second generation bisphosphonates are less common as third generation bisphosphonates, such as ibandronic acid, zoledronic acid, minodronic acid, and risedronic acid are becoming more popular.
Boning was granted FDA approval on 31 October 1991.
Boning is a second generation, nitrogen containing bisphosphonate that inhibits osteoclast mediated bone loss It has a wide therapeutic index and a long duration of action as it can be given every 3-4 weeks for certain indications. Patients should be counselled regarding the risk of elevated blood urea nitrogen, renal tubular necrosis, and nephrotoxicity.
Trade Name | Boning |
Generic | Pamidronic acid |
Pamidronic acid Other Names | Acide pamidronique, Acido pamidronico, Acidum pamidronicum, Pamidronate, Pamidronic acid |
Type | |
Formula | C3H11NO7P2 |
Weight | Average: 235.0695 Monoisotopic: 235.001074735 |
Protein binding | Pamidronate is approximately 54% protein bound in serum. |
Groups | Approved |
Therapeutic Class | |
Manufacturer | |
Available Country | China |
Last Updated: | September 19, 2023 at 7:00 am |
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Uses
Boning is a bisphosphonate used to treat Paget's disease, to treat hypercalcemia of malignancy, and to treat osteolytic bone lesions.
Pamidronate is indicated to treat moderate to severe hypercalcemia of malignancy, moderate to severe Paget's disease of bone, osteolytic bone metastases of breast cancer, and osteolytic lesions of multiple myeloma.
Boning is also used to associated treatment for these conditions: Hypercalcemia of Malignancy, Osteolytic lesion, Paget’s Disease, Osteolytic Bone metastases
How Boning works
Bisphosphonates are taken into the bone where they bind to hydroxyapatite. Bone resorption by osteoclasts causes local acidification, releasing the bisphosphonate, which is taken into the osteoclast by fluid-phase endocytosis. Endocytic vesicles become acidified, releasing bisphosphonates into the cytosol of osteoclasts where they act.
Osteoclasts mediate resorption of bone. When osteoclasts bind to bone they form podosomes, ring structures of F-actin. Disruption of the podosomes causes osteoclasts to detach from bones, preventing bone resorption.
Nitrogen containing bisphosphonates such as pamidronate are known to induce apoptosis of hematopoietic tumor cells by inhibiting the components of the mevalonate pathway farnesyl diphosphate synthase, farnesyl diphosphate, and geranylgeranyl diphosphate. These components are essential for post-translational prenylation of GTP-binding proteins like Rap1. The lack of prenylation of these proteins interferes with their function, and in the case of Rap1, leads to apoptosis. pamidronate also activated caspases 3 and 9 which further contribute to apoptosis.
Toxicity
Patients experiencing and overdose may present with hypocalcemia, fever, hypotension, and taste perversion. Overdose can be managed by symptomatic and supportive treatment which may include the administration of steroids and intravenous calcium.
Food Interaction
No interactions found.Elimination Route
In patients with a creatinine clearance >90mL/min, a 90mg intravenous dose reached a Cmax of 1.92±1.08µg/mL, with a Tmax of 4h, and an AUC of 10.2±6.95µg*h/mL.
In patients with a creatinine clearance 61-90mL/min, a 90mg intravenous dose reached a Cmax of 1.86±0.50µg/mL, with a Tmax of 4h, and an AUC of 10.7—3.91µg*h/mL.[A203264
In patients with a creatinine clearance 30-60mL/min, a 90mg intravenous dose reached a Cmax of 1.84±0.58µg/mL, with a Tmax of 4h, and an AUC of 10.1±3.38µg*h/mL.
In patients with a creatinine clearance max of 1.93±0.53µg/mL, with a Tmax of 4h, and an AUC of 34.0±8.37µg*h/mL.
Half Life
The mean elimination half life of pamidronate is 28±7 hours.
Clearance
The mean total clearance of pamidronate is 107±50mL/min and the mean renal clearance is 49±28mL/min.
Elimination Route
Pamidronate is exclusively eliminated in the urine. By 120 hours after administration, 46±16% of the dose has been eliminated in the urine.
Innovators Monograph
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