Details
Stereochemistry | ACHIRAL |
Molecular Formula | C2H7O7P2.Na |
Molecular Weight | 228.0101 |
Optical Activity | ( + / - ) |
Defined Stereocenters | 0 / 1 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
[Na+].CC(O)(P(O)(O)=O)P(O)([O-])=O
InChI
InChIKey=MKJHAUJMSPBJTL-UHFFFAOYSA-M
InChI=1S/C2H8O7P2.Na/c1-2(3,10(4,5)6)11(7,8)9;/h3H,1H3,(H2,4,5,6)(H2,7,8,9);/q;+1/p-1
Molecular Formula | Na |
Molecular Weight | 22.9898 |
Charge | 1 |
Count |
|
Stereochemistry | ACHIRAL |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Optical Activity | NONE |
Molecular Formula | C2H7O7P2 |
Molecular Weight | 205.0203 |
Charge | -1 |
Count |
|
Stereochemistry | ACHIRAL |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Optical Activity | NONE |
Etidronate is a salt of etidronic acid (brand name Didronel, also known as EHDP) a diphosphonate, which is indicated 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. Didronel is not approved for the treatment of osteoporosis. This drugs acts primarily on bone. It can inhibit the formation, growth, and dissolution of hydroxyapatite crystals and their amorphous precursors by chemisorption to calcium phosphate surfaces. Inhibition of crystal resorption occurs at lower doses than are required to inhibit crystal growth. Both effects increase as the dose increases. Preclinical studies indicate etidronate disodium does not cross the blood-brain barrier. Didronel is not metabolized. The amount of drug absorbed after an oral dose is approximately 3 percent. 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. Etidronic acid 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.
CNS Activity
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
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Target ID: CHEMBL2363055 Sources: https://www.ncbi.nlm.nih.gov/pubmed/16046206 |
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Target ID: CHEMBL2366048 Sources: https://www.ncbi.nlm.nih.gov/pubmed/21111853 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
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Primary | DIDRONEL Approved UseDidronel is indicated 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. Didronel is not approved for the treatment of osteoporosis. Paget’s Disease: Didronel is indicated for the treatment of symptomatic Paget's disease of bone. Didronel therapy usually arrests or significantly impedes the disease process as evidenced by: --Symptomatic relief, including decreased pain and/or increased mobility (experienced by 3 out of 5 patients). --Reductions in serum alkaline phosphatase and urinary hydroxyproline levels (30 percent or more in 4 out of 5 patients). --Histomorphometry showing reduced numbers of osteoclasts and osteoblasts, and more lamellar bone formation. Bone scans showing reduced radionuclide uptake at pagetic lesions. In addition, reductions in pagetically elevated cardiac output and skin temperature have been observed in some patients. In many patients, the disease process will be suppressed for a period of at least 1 year following cessation of therapy. The upper limit of this period has not been determined. The effects of the Didronel treatment in patients with asymptomatic Paget's disease have not been studied. However, Didronel treatment of such patients may be warranted if extensive involvement threatens irreversible neurologic damage, major joints, or major weight-bearing bones. Heterotopic Ossification: Didronel is indicated in the prevention and treatment of heterotopic ossification following total hip replacement or due to spinal cord injury. Didronel reduces the incidence of clinically important heterotopic bone by about two-thirds. Among those patients who form heterotopic bone, Didronel retards the progression of immature lesions and reduces the severity by at least half. Follow-up data (at least 9 months posttherapy) suggest these benefits persist. In total hip replacement patients, Didronel does not promote loosening of the prosthesis or impede trochanteric reattachment. In spinal cord injury patients, Didronel does not inhibit fracture healing or stabilization of the spine. Launch Date2.4192E11 |
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Preventing | DIDRONEL Approved UseDidronel is indicated 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. Didronel is not approved for the treatment of osteoporosis. Paget’s Disease: Didronel is indicated for the treatment of symptomatic Paget's disease of bone. Didronel therapy usually arrests or significantly impedes the disease process as evidenced by: --Symptomatic relief, including decreased pain and/or increased mobility (experienced by 3 out of 5 patients). --Reductions in serum alkaline phosphatase and urinary hydroxyproline levels (30 percent or more in 4 out of 5 patients). --Histomorphometry showing reduced numbers of osteoclasts and osteoblasts, and more lamellar bone formation. Bone scans showing reduced radionuclide uptake at pagetic lesions. In addition, reductions in pagetically elevated cardiac output and skin temperature have been observed in some patients. In many patients, the disease process will be suppressed for a period of at least 1 year following cessation of therapy. The upper limit of this period has not been determined. The effects of the Didronel treatment in patients with asymptomatic Paget's disease have not been studied. However, Didronel treatment of such patients may be warranted if extensive involvement threatens irreversible neurologic damage, major joints, or major weight-bearing bones. Heterotopic Ossification: Didronel is indicated in the prevention and treatment of heterotopic ossification following total hip replacement or due to spinal cord injury. Didronel reduces the incidence of clinically important heterotopic bone by about two-thirds. Among those patients who form heterotopic bone, Didronel retards the progression of immature lesions and reduces the severity by at least half. Follow-up data (at least 9 months posttherapy) suggest these benefits persist. In total hip replacement patients, Didronel does not promote loosening of the prosthesis or impede trochanteric reattachment. In spinal cord injury patients, Didronel does not inhibit fracture healing or stabilization of the spine. Launch Date2.4192E11 |
PubMed
Title | Date | PubMed |
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[TNF-alpha secretion by human macrophage-like cells in response to wear particles and its modification by drugs]. | 1999 May |
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Possibility of "distraction arthrogenesis": first report in rabbit model. | 2001 |
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Etidronate for treating and preventing postmenopausal osteoporosis. | 2001 |
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Initiation of osteoporosis treatment after bone mineral density testing. | 2001 |
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A meta-analysis of etidronate for the treatment of postmenopausal osteoporosis. | 2001 |
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Subcutaneous fat necrosis of the newborn following hypothermia and complicated by pain and hypercalcaemia. | 2001 Aug |
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[Therapy of osteoporosis. Risk factors alone are not an indication]. | 2001 Dec 6 |
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Treatment of osteoporosis with bisphosphonates. | 2001 Feb |
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Skeletal uptake and soft-tissue retention of 186Re-HEDP and 153Sm-EDTMP in patients with metastatic bone disease. | 2001 Feb |
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Ulcerative esophagitis caused by etidronate. | 2001 Feb |
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Effect of risedronate on the risk of hip fracture in elderly women. Hip Intervention Program Study Group. | 2001 Feb 1 |
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Effect of high doses of oral risedronate (20 mg/day) on serum parathyroid hormone levels and urinary collagen cross-link excretion in postmenopausal women with spinal osteoporosis. | 2001 Jan |
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Oesophageal transit, disintegration and gastric emptying of a film-coated risedronate placebo tablet in gastro-oesophageal reflux disease and normal control subjects. | 2001 Jan |
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Role of bisphosphonates and calcitonin in the prevention and treatment of osteoporosis. | 2001 Jul |
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Prevalence and determinants of osteoporosis drug prescription among patients with high exposure to glucocorticoid drugs. | 2001 Jun |
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Evidence-based medicine: putting theory into practice. | 2001 Mar |
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Prevention and treatment of osteoporosis. | 2001 Mar-Apr |
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Incadronate and etidronate accelerate phosphate-primed mineralization of MC4 cells via ERK1/2-Cbfa1 signaling pathway in a Ras-independent manner: further involvement of mevalonate-pathway blockade for incadronate. | 2001 May |
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Absolute vs. relative numbers in evaluating drug therapy. | 2001 May 15 |
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[Bisphosphonates in osteoporosis. Significantly reduces risk of fracture]. | 2001 May 3 |
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The effect of risedronate on the risk of hip fracture in elderly women. | 2001 May 31 |
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Role of alendronate and risedronate in preventing and treating osteoporosis. | 2001 Nov |
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Extracellular signal-regulated kinases and calcium channels are involved in the proliferative effect of bisphosphonates on osteoblastic cells in vitro. | 2001 Nov |
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Rhenium-188 HEDP to treat painful bone metastases. | 2001 Nov |
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Advances in the biology and treatment of myeloma bone disease. | 2001 Nov 15 |
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Alendronate for the treatment of osteoporosis in men. | 2001 Oct |
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Bisphosphonates for osteoporosis. | 2001 Sep |
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Effects of high-dose etidronate treatment on microdamage accumulation and biomechanical properties in beagle bone before occurrence of spontaneous fractures. | 2001 Sep |
Patents
Sample Use Guides
should be taken as a single, oral dose. Paget’s Disease: Initial Treatment Regimens: 5 to 10 mg/kg/day, not to exceed 6 months, or 11 to 20 mg/kg/day, not to exceed 3 months. The recommended initial dose is 5 mg/kg/day for a period not to exceed 6 months. Doses above 10 mg/kg/day should be reserved for when 1) lower doses are ineffective or 2) there is an overriding need to suppress rapid bone turnover (especially when irreversible neurologic damage is possible) or reduce elevated cardiac output. Doses in excess of 20 mg/kg/day are not recommended.
Route of Administration:
Oral
In vitro cytotoxicity of etidronic acid to MCF-7 cells was estimated on the basis of clonogenicity assays, while cell cycle effects were determined by using flow cytometry. A 24-hour treatment with etidronic acid (10 mM) with or without strontium chloride was cytototoxic to MCF-7cells. Etidronic acid (1, 10 mM) caused a decrease in the S-phase population and an increase in the G2/M population. Treatment of MCF-7 human breast cancer cells with etidronic acid (10 mM) for six hours caused mutations in exons 6 and 8 of the p53 gene in MCF-7 cells.
Substance Class |
Chemical
Created
by
admin
on
Edited
Sat Dec 16 08:29:37 UTC 2023
by
admin
on
Sat Dec 16 08:29:37 UTC 2023
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Record UNII |
BCZ8ETH6PD
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Record Status |
Validated (UNII)
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Record Version |
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-
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DTXSID601031599
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23687324
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29329-71-3
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13529-88-9
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BCZ8ETH6PD
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ACTIVE MOIETY |