Dequest 2015

Dequest 2015 - General Information

A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover. [PubChem]


Pharmacology of Dequest 2015

Dequest 2015 is a first generation (non-nitrogenous) bisphosphonate in the same family as clodronate and tiludronate. Dequest 2015 affects calcium metabolism and inhibits bone resorption and soft tissue calcification. Of the etidronic acid that is resorbed (from oral preparation) or infused (for intravenous drugs), about 50% is excreted unchanged by the kidney. The remainder has a very high affinity for bone tissue, and is rapidly absorbed onto the bone surface. Dequest 2015 has been shown to prevent or delay skeletal-related events and decrease bone pain as well as normalize calcium levels in the presence of hypercalcemia.


Dequest 2015 for patients


Dequest 2015 Interactions

There have been isolated reports of patients experiencing increases in their prothrombin times when etidronate was added to warfarin therapy. The majority of these reports concerned variable elevations in prothrombin times without clinically significant sequelae. Although the relevance of these reports and any mechanism of coagulation alterations is unclear, patients on warfarin should have their prothrombin time monitored.


Dequest 2015 Contraindications

Didronel tablets are contraindicated in patients with known hypersensitivity to etidronate disodium or in patients with clinically overt osteomalacia.


Additional information about Dequest 2015

Dequest 2015 Indication: For the treatment of symptomatic Paget's disease of bone and in the prevention and treatment of heterotopic ossification following total hip replacement or due to spinal cord injury.
Mechanism Of Action: Bisphosphonates, when attached to bone tissue, are absorbed by osteoclasts, the bone cells that breaks down bone tissue. Although the mechanism of action of non-nitrogenous bisphosphonates has not been fully elucidated, available data suggest that they bind strongly to hydroxyapatite crystals in the bone matrix, preferentially at the sites of increased bone turnover and inhibit the formation and dissolution of the crystals. Other actions may include direct inhibition of mature osteoclast function, promotion of osteoclast apoptosis, and interference with osteoblast-mediated osteoclast activation. Dequest 2015 does not interfere with bone mineralization. In malignancy-related hypercalcemia, etidronic acid decreases serum calcium by inhibiting tumour-induced bone resorption and reducing calcium flow from the resorbing bone into the blood. Dequest 2015 also reduces morbidity of osteolytic bone metastases by inhibiting tumour-induced bone resorption. Dequest 2015 may promote osteoclast apoptosis by competing with adenosine triphosphate (ATP) in the cellular energy metabolism. The osteoclast initiates apoptosis and dies, leading to an overall decrease in the breakdown of bone.
Drug Interactions: Aluminium Formation of non-absorbable complexes
Bismuth Formation of non-absorbable complexes
Calcium Formation of non-absorbable complexes
Iron Formation of non-absorbable complexes
Magnesium oxide Formation of non-absorbable complexes
Magnesium Formation of non-absorbable complexes
Sucralfate Formation of non-absorbable complexes
Food Interactions: Take on an empty stomach.
Avoid aluminium, calcium, iron and magnesium.
Generic Name: Etidronic acid
Synonyms: Acetodiphosphonic acid; Acide etidronique [INN-French]; Acido etidronico [INN-Spanish]; Acidum etidronicum [INN-Latin]; EHDP; Etidronate Disodium; Etidronsaeure; HEDP; Hydroxyethanediphosphonic acid; Oxyethylidenediphosphonic acid; Etidronate
Drug Category: Antihypocalcemic Agents; Antineoplastic Agents; Bisphosphonates; Osteoporosis Prophylactic
Drug Type: Small Molecule; Approved

Other Brand Names containing Etidronic acid: Cintichem Technetium 99m Hedspa; Dequest 2010; Dequest 2015; Dequest Z 010; Didronel; Didronel IV; Ferrofos 510; MPI Stannous Diphosphonate; Osteoscan; Turpinal SL;
Absorption: The amount of drug absorbed after an oral dose is approximately 3%.
Toxicity (Overdose): Clinical experience with acute etidronic acid overdosage is extremely limited. Decreases in serum calcium following substantial overdosage may be expected in some patients. Signs and symptoms of hypocalcemia also may occur in some of these patients. Some patients may develop vomiting. In one event, an 18-year-old female who ingested an estimated single dose of 4800 to 6000 mg (67 to 100 mg/kg) of etidronate was reported to be mildly hypocalcemic (7 .5 2 mg/ dl) and experienced paresthesia of the fingers.
Protein Binding: Not Available
Biotransformation: Not metabolized.
Half Life: In normal subjects, plasma half-life of etidronic acid, based on non-compartmental pharmacokinetics is 1 to 6 hours.
Dosage Forms of Dequest 2015: Tablet Oral
Chemical IUPAC Name: (1-hydroxy-1-phosphonoethyl)phosphonic acid
Chemical Formula: C2H8O7P2
Etidronic acid on Wikipedia:
Organisms Affected: Humans and other mammals