Etidronate (sodium salt)
(Synonyms: 依替膦酸钠,Etidronate disodium; HEDPA disodium; HEDP disodium) 目录号 : GC43642
A bisphosphonate bone resorption inhibitor
Cas No.:7414-83-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Etidronate is a first generation, non-nitrogenous diphosphonate analog of endogenous pyrophosphate. It binds to hydroxyapatite and induces osteoclast apoptosis, thereby inhibiting abnormal bone resorption. Unlike other bisphosphonates, etidronate may also prevent bone calcification.
| Cas No. | 7414-83-7 | SDF | |
| 别名 | 依替膦酸钠,Etidronate disodium; HEDPA disodium; HEDP disodium | ||
| Canonical SMILES | [O-]P(C(P([O-])(O)=O)(O)C)(O)=O.[Na+].[Na+] | ||
| 分子式 | C2H6O7P2•2Na | 分子量 | 250 |
| 溶解度 | PBS (pH 7.2): 5 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4 mL | 20 mL | 40 mL |
| 5 mM | 0.8 mL | 4 mL | 8 mL |
| 10 mM | 0.4 mL | 2 mL | 4 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Conventional treatment of hypercalcemia of malignancy
Am J Health Syst Pharm 2001 Nov 15;58 Suppl 3:S8-15.PMID:11757206DOI:10.1093/ajhp/58.suppl_3.S8.
Treatment of hypercalcemia of malignancy (HCM) is briefly reviewed, available treatments are compared, and treatment guidelines are presented. The most effective strategy is treatment of the underlying malignancy. For patients who have a poor prognosis and no viable treatment options, the most humane course may be no treatment at all since encephalopathy will cloud their consciousness. Patients with mild hypercalcemia (corrected serum calcium concentration < 12 mg/dL) may respond to oral hydration, salt restriction, and ambulation, which encourage the normal bone remodeling process. Patients with moderate (corrected serum calcium concentration 12.0-13.5 mg/dL) to severe (> 13.5 mg/dL) hypercalcemia may require rehydration with 0.9% sodium chloride injection. Furosemide may be indicated to counteract fluid overload from rehydration measures or in patients at risk of developing congestive heart failure. For patients with renal failure not caused by dehydration, dialysis with a calcium-free or low-calcium solution is the treatment of choice. The calciuric effect of rehydration lasts only two to three days, and antiresorptive therapy is indicated for patients who require a longer duration of effect. Calcitonin is useful if a rapid decrease in serum calcium is necessary, but tachyphylaxis limits its use. Corticosteroids should be used only in patients with tumors that produce 1,25-dihydroxycholecalciferol. The use of plicamycin is limited because of adverse effects. Before the availability of zolendronic acid, pamidronate disodium was the treatment of choice, because of its longer duration of action than Etidronate disodium and potential safety advantages. Zolendronic acid (discussed elsewhere in this supplement) is likely to supercede pamidronate disodium as the drug of choice for HCM, but the presence of symptoms, the rate of rise in serum calcium concentration, and the overall status of the patient are important considerations in selecting therapy.
Prediction of bioavailability of selected bisphosphonates using in silico methods towards categorization into a biopharmaceutical classification system
Acta Pol Pharm 2013 Sep-Oct;70(5):877-82.PMID:24147367doi
The physicochemical properties relevant to biological activity of selected bisphosphonates such as clodronate disodium salt, Etidronate disodium salt, pamidronate disodium salt, alendronate sodium salt, ibandronate sodium salt, risedronate sodium salt and zoledronate disodium salt were determined using in silico methods. The main aim of our research was to investigate and propose molecular determinants thataffect bioavailability of above mentioned compounds. These determinants are: stabilization energy (deltaE), free energy of solvation (deltaG(solv)), electrostatic potential, dipole moment, as well as partition and distribution coefficients estimated by the log P and log D values. Presented values indicate that selected bisphosphonates a recharacterized by high solubility and low permeability. The calculated parameters describing both solubility and permeability through biological membranes seem to be a good bioavailability indicators of bisphosphonates examined and can be a useful tool to include into Biopharmaceutical Classification System (BCS) development.
Palliation of painful bone metastases from prostate cancer using sodium Etidronate: results of a randomized, prospective, double-blind, placebo-controlled study
J Urol 1989 Jan;141(1):85-7.PMID:2462069DOI:10.1016/s0022-5347(17)40597-0.
Sodium Etidronate is a diphosphonate compound that inhibits bone resorption and mineralization. The drug has been reported to be highly effective for the palliation of painful bone metastasis from prostatic cancer. Fifty-seven patients were entered into a randomized, prospective, double-blind, placebo-controlled study of sodium Etidronate. All patients had hormone refractory metastatic prostatic cancer and bone pain requiring analgesics. No difference was seen in the symptomatic response rate or analgesic requirement between patients treated with sodium Etidronate and placebo. With the dose scheme used in this study sodium Etidronate was ineffective for palliation of bone pain from prostatic cancer.
Esophageal irritation due to alendronate sodium tablets: possible mechanisms
Dig Dis Sci 1998 Sep;43(9):1998-2002.PMID:9753265DOI:10.1023/a:1018894827961.
Animal studies were done using an in vivo dog model to examine the possible mechanism for the esophageal adverse events reported with alendronate sodium tablets. These studies showed that under low pH conditions alendronate sodium can cause esophageal irritation. No esophageal irritation occurred at pH 3.5 or higher where the drug exists primarily as the sodium salt. The animal studies also showed that alendronate sodium can exacerbate preexisting esophageal damage. Exposure of the esophageal mucosa for a prolonged period to alendronate sodium tablet can also cause mild esophageal irritation. These findings suggest that the esophageal irritation in patients taking Fosamax can be from prolonged contact with the tablet, reflux of acidic gastric contents with alendronate sodium, and exacerbation of preexisting esophageal damage. The findings also suggest that other bisphosphonates can cause esophageal injury under similar conditions.
Giant zirconium-bisphosphonate nano-ribbons and their liquid crystalline phase behaviour in water
Dalton Trans 2021 Jun 1;50(21):7314-7323.PMID:33955437DOI:10.1039/d1dt00736j.
In decimolar aqueous solutions, zirconium oxychloride octahydrate forms several micrometer long and approximately 15 nm wide thin ribbons through the reaction with excess amounts of the sodium salt of 1-hydroxyethane-1,1-diphosphonic acid (HEDP, known as etidronic acid). Primarily deduced from SAXS, TEM, EXAFS and solid-state NMR analyses, a consistent structural model enables congruous explanations for the colloidal behaviour of the purified ribbons as well as of their reaction products with ammonia and amines, respectively. Properties of the lyotropic, liquid crystalline phases are discussed in the light of potential applications in aqueous coatings.