Clodronate

244.89

244.89

234-212-1

0813BZ6866

DTXSID8046959|DTXSID40237035|DTXSID4042670

C61685

M05BA02|M - Musculo-skeletal system

2931900090

115

-2.1

Solid

2.306±0.06 g/cm3(Predicted)

250 °C

474.7±55.0 °C(Predicted)

240.9±31.5 °C

1.598

7.47e+00 g/L

2.55E-10mmHg at 25°C

Patients experiencing an overdose may present with hypocalcemia, while severe overdoses can present with kidney failure, liver damage, and unconsciousness. Overdose can be managed through symptomatic and supportive care, including monitoring and administration of electrolytes including calcium. Gastric lavage may remove unabsorbed drug in the gastrointestinal tract.

Clodronic acid is 36% protein bound in plasma.

Clodronic acid is indicated as an adjunct in the management of osteolysis from bone metastases of malignant tumors and for management of hypercalcemia of malignancy.

Clodronic acid is a first generation bisphosphonate that inhibits osteoclast mediated bone resorption. It has a wide therapeutic index as a large overdose is required for significant toxicity and a long duration of action due to the slow release from bone. Patients should be counselled regarding the risk of hypocalcemia, hypovolemia, renal insufficiency, transient hyperphosphatemia, and transient hyperparathyroidism.

Agents that inhibit BONE RESORPTION and/or favor BONE MINERALIZATION and BONE REGENERATION. They are used to heal BONE FRACTURES and to treat METABOLIC BONE DISEASES such as OSTEOPOROSIS. (See all compounds classified as Bone Density Conservation Agents.)

Oral clodronic acid has a bioavailability of 1-2%. A 200mg intravenous dose reaches a C_max of 16.1mg/L with an AUC of 44.2mg\*h/L. A 200mg intramuscular dose reaches a C_max of 12.8mg/L with an AUC of 47.5mg\*h/L. Further pharmacokinetic data for clodronic acid are not readily available.|Clodronate is eliminated unchanged in the urine.|The renal clearance of clodronate is approximately 90mL/min.

Clodronate is not metabolized in humans.

The mean plasma half life of clodronate is 5.6h.

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. First generation bisphosphonates closely mimic the structure of pyrophosphate, which can be incorporated into ATP anologues that cannot be hydrolyzed, disrupting all ATP mediated actions of osteoclasts.

Acid, Clodronic

Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients