U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

Details

Stereochemistry ACHIRAL
Molecular Formula C2H8O7P2
Molecular Weight 206.0282
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of ETIDRONIC ACID

SMILES

CC(O)(P(O)(O)=O)P(O)(O)=O

InChI

InChIKey=DBVJJBKOTRCVKF-UHFFFAOYSA-N
InChI=1S/C2H8O7P2/c1-2(3,10(4,5)6)11(7,8)9/h3H,1H3,(H2,4,5,6)(H2,7,8,9)

HIDE SMILES / InChI

Molecular Formula C2H8O7P2
Molecular Weight 206.0282
Charge 0
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.

Approval Year

Targets

Targets

Primary TargetPharmacologyConditionPotency
Target ID: CHEMBL2366048
Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
DIDRONEL

Approved Use

Didronel 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 Date

2.4192E11
Preventing
DIDRONEL

Approved Use

Didronel 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 Date

2.4192E11
PubMed

PubMed

TitleDatePubMed
Possibility of "distraction arthrogenesis": first report in rabbit model.
2001
Effect of menatetrenone on bone mineral density and incidence of vertebral fractures in postmenopausal women with osteoporosis: a comparison with the effect of etidronate.
2001
Effect of intermittent cyclical treatment with etidronate disodium (HEBP) and calcium plus alphacalcidol in postmenopausal osteoporosis.
2001
Initiation of osteoporosis treatment after bone mineral density testing.
2001
Inhibition of bone resorption by alendronate and risedronate does not require osteoclast apoptosis.
2001 Dec
[Therapy of osteoporosis. Risk factors alone are not an indication].
2001 Dec 6
Risedronate pharmacokinetics and intra- and inter-subject variability upon single-dose intravenous and oral administration.
2001 Feb
Treatment of osteoporosis with bisphosphonates.
2001 Feb
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
[Bisphosphonate treatment prevents hip fractures in 70-79 year old women with osteoporotic vertebral fractures].
2001 Jul 14
Prevention of corticosteroid induced osteoporosis in inpatients recently discharged from a tertiary teaching hospital.
2001 Mar
Evidence-based medicine: putting theory into practice.
2001 Mar
Once-a-week alendronate (Fosamax).
2001 Mar 19
Prevention and treatment of osteoporosis.
2001 Mar-Apr
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
Risedronate: clinical usage.
2001 May
Effect of combined risedronate and hormone replacement therapies on bone mineral density in postmenopausal women.
2001 May
The role of combination treatment for osteoporosis.
2001 May
Visualization of bisphosphonate-induced caspase-3 activity in apoptotic osteoclasts in vitro.
2001 May
[Therapy of osteoporosis from the viewpoint of evidence-based medicine].
2001 May 15
The effect of risedronate on the risk of hip fracture in elderly women.
2001 May 31
[Alternatives to hormonal treatment for the prevention of postmenopausal osteoporosis: the bisphosphonates].
2001 Nov
Familial fibrodysplasia ossificans progressiva: trial with etidronate disodium.
2001 Nov
Role of alendronate and risedronate in preventing and treating osteoporosis.
2001 Nov
Extracellular signal-regulated kinases and calcium channels are involved in the proliferative effect of bisphosphonates on osteoblastic cells in vitro.
2001 Nov
Conventional treatment of hypercalcemia of malignancy.
2001 Nov 15
A method to assess the proportion of treatment effect explained by a surrogate endpoint.
2001 Nov 15
Risedronate treatment and extended fracture protection in postmenopausal women.
2001 Nov-Dec
Treatment of osteoporosis in men with fluoride alone or in combination with bisphosphonates.
2001 Oct
Risedronate increases bone density and reduces vertebral fracture risk within one year in men on corticosteroid therapy.
2001 Oct
Alendronate for the treatment of osteoporosis in men.
2001 Oct
Comparative efficacy and safety study of etidronate and alendronate in postmenopausal osteoporosis. effect of adding hormone replacement therapy.
2001 Oct
Maintenance of cancellous bone in ovariectomized, human parathyroid hormone [hPTH(1-84)]-treated rats by estrogen, risedronate, or reduced hPTH.
2001 Oct
Painful multifocal arthritis: therapy with rhenium 186 hydroxyethylidenediphosphonate ((186)Re HEDP) after failed treatment with medication--initial results of a prospective study.
2001 Oct
[Osteoporosis. Fracture as alarm signal].
2001 Oct 11
Bisphosphonates for osteoporosis.
2001 Sep
Effects of high-dose etidronate treatment on microdamage accumulation and biomechanical properties in beagle bone before occurrence of spontaneous fractures.
2001 Sep
Alendronate does not interfere with 99mTc-methylene diphosphonate bone scanning.
2001 Sep
Pharmacologic therapy for the treatment and prevention of osteoporosis.
2001 Sep
[Risedronate now also approved for hip fractures. Study discloses significant risk reduction in proximal femoral neck fractures].
2001 Sep 6
[Optimizing treatment of osteoporosis. Rapidly effective therapy lowers fracture risk in 1 year up to 70%].
2001 Sep 6
Discovery of a high molecular weight complex of calcium, phosphate, fetuin, and matrix gamma-carboxyglutamic acid protein in the serum of etidronate-treated rats.
2002 Feb 8
Patents

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 Sat Dec 16 17:53:39 UTC 2023
Edited
by admin
on Sat Dec 16 17:53:39 UTC 2023
Record UNII
M2F465ROXU
Record Status Validated (UNII)
Record Version
  • Download
Name Type Language
ETIDRONIC ACID
HSDB   INCI   INN   MART.   MI   USAN   WHO-DD  
INCI   INN   USAN  
Official Name English
ETIDRONATE
VANDF  
Common Name English
ETIDRONIC ACID [INCI]
Common Name English
M05BA01
Code English
(1-Hydroxyethylidene)diphosphonic acid
Systematic Name English
HYDROXYETHYLIDENE-1,1-DIPHOSPHONIC ACID
Systematic Name English
etidronic acid [INN]
Common Name English
ETIDRONIC ACID [HSDB]
Common Name English
(1-HYDROXY-ETHYLIDENE)DIPHOSPHONIC ACID
Systematic Name English
NSC-227995
Code English
PHOSPHONIC ACID, (1-HYDROXYETHYLIDENE)BIS-
Common Name English
ETIDRONIC ACID [USAN]
Common Name English
PHOSPHONIC ACID, P,P'-(1-HYDROXYETHYLIDENE)BIS-
Systematic Name English
ETIDRONATE [VANDF]
Common Name English
Etidronic acid [WHO-DD]
Common Name English
1-HYDROXYETHANE-1,1-BISPHOSPHONIC ACID
Systematic Name English
ETIDRONIC ACID [MART.]
Common Name English
OEDP
Common Name English
ETIDRONIC ACID [MI]
Common Name English
Classification Tree Code System Code
Food Contact Sustance Notif, (FCN No.) FCN NO. 1096
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 699
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1144
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 691
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1247
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
WHO-ATC M05BB01
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
WHO-VATC QM05BA01
Created by admin on Sat Dec 16 17:53:42 UTC 2023 , Edited by admin on Sat Dec 16 17:53:42 UTC 2023
LIVERTOX 386
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
NDF-RT N0000175579
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 561
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1081
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1082
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
NCI_THESAURUS C443
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1094
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 625
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 951
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 724
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 670
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 908
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1089
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 641
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 993
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1236
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
WHO-ATC M05BA01
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 921
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1035
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1132
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 801
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 323
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 1093
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 728
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 447
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
WHO-VATC QM05BB01
Created by admin on Sat Dec 16 17:53:42 UTC 2023 , Edited by admin on Sat Dec 16 17:53:42 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 880
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 887
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
NCI_THESAURUS C67439
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 140
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
NDF-RT N0000007707
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Food Contact Sustance Notif, (FCN No.) FCN NO. 911
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
Code System Code Type Description
ECHA (EC/EINECS)
220-552-8
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
NSC
227995
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
PUBCHEM
3305
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
INN
2758
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
FDA UNII
M2F465ROXU
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
MERCK INDEX
m5182
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY Merck Index
DRUG BANK
DB01077
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
MESH
D012968
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
LACTMED
Etidronate
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
EPA CompTox
DTXSID6023028
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
DRUG CENTRAL
1098
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
HSDB
5898
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
DAILYMED
M2F465ROXU
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
CHEBI
4907
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
IUPHAR
7184
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
NCI_THESAURUS
C1332
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
SMS_ID
100000082093
Created by admin on Sat Dec 16 17:53:42 UTC 2023 , Edited by admin on Sat Dec 16 17:53:42 UTC 2023
PRIMARY
RXCUI
1356715
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
WIKIPEDIA
Etidronic acid
Created by admin on Sat Dec 16 17:53:42 UTC 2023 , Edited by admin on Sat Dec 16 17:53:42 UTC 2023
PRIMARY
ChEMBL
CHEMBL871
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
CAS
2809-21-4
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
RXCUI
42682
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
ALTERNATIVE
EVMPD
SUB07299MIG
Created by admin on Sat Dec 16 17:53:41 UTC 2023 , Edited by admin on Sat Dec 16 17:53:41 UTC 2023
PRIMARY
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