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Fludrocortisone acetate (9α-Fludrocortisone acetate) Sale

(Synonyms: 醋酸氟氢可的松; 9α-Fludrocortisone acetate; 9α-Fluorcortisol acetate) 目录号 : GC33848

A mineralocorticoid agonist

Fludrocortisone acetate (9α-Fludrocortisone acetate) Chemical Structure

Cas No.:514-36-3

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10mM (in 1mL DMSO)
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100mg
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产品描述

Fludrocortisone acetate is the acetate form of the synthetic corticosteroid fludrocortisone, which is a mineralocorticoid receptor agonist.1 Fludrocortisone acetate (0.1-5 ?g/animal) promotes sodium retention in rats in a dose-dependent manner with 37% of sodium excreted compared with control when used at a dose of 5 ?g/animal.2 Formulations containing fludrocortisone acetate have been used in the treatment of Addison’s disease.

1.Agarwal, M.K., Coupry, F., and Philippe, M.Physiological activity and receptor binding of 9α fluorohydrocortisoneBiochem. Biophys. Res. Commun.78(2)747-753(1977) 2.Stafford, R.O., Barnes, L.E., Bowman, B.J., et al.Glucocorticoid and mineralocorticoids activities of Delta1-fluorohydrocortisoneProc. Soc. Exp. Biol. Med.89(3)371-374(1955)

Chemical Properties

Cas No. 514-36-3 SDF
别名 醋酸氟氢可的松; 9α-Fludrocortisone acetate; 9α-Fluorcortisol acetate
Canonical SMILES C[C@@]12[C@](C(COC(C)=O)=O)(O)CC[C@@]1([H])[C@]3([H])CCC4=CC(CC[C@]4(C)[C@@]3(F)[C@@H](O)C2)=O
分子式 C23H31FO6 分子量 422.49
溶解度 DMSO : ≥ 45 mg/mL (106.51 mM) 储存条件 Store at -20°C
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1 mM 2.3669 mL 11.8346 mL 23.6692 mL
5 mM 0.4734 mL 2.3669 mL 4.7338 mL
10 mM 0.2367 mL 1.1835 mL 2.3669 mL
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Research Update

Stability of Fludrocortisone acetate solutions prepared from tablets and powder

Eur J Pharm Biopharm 2003 Mar;55(2):209-13.PMID:12637099DOI:10.1016/s0939-6411(02)00159-5.

To assess the stability of Fludrocortisone acetate oral solutions prepared from tablets and powder at three temperatures over a 60-days period. Solutions of Fludrocortisone acetate 40 microg/ml were prepared from commercially available 0.05-mg tablets and powder in ethanol 17% v/v. They stored in an amber glass prescription bottles at +4, +23 and +40 degrees C shielded from light. The concentrations of Fludrocortisone acetate were determined in duplicate by high-performance liquid chromatography at 0, 1, 7, 14, 30, 50 and 60 days. The initial and final pH of solutions were compared. The recovery of Fludrocortisone acetate from tablets was determined. The times (t(90)) needed for Fludrocortisone acetate to fall to 90% of it's initial concentration were calculated by a linear regression analysis to allow the determination of the expired dates. The recovery of Fludrocortisone acetate from tablets was 78 +/- 3%. The t(90) expressed with 95% confidence limits were 2 +/- 1 and 22 +/- 3 days for the solutions prepared from tablets and stored at +23 and +4 degrees C, respectively, whereas t(90) were 11 +/- 2 days and at least 60 days for the solutions prepared with the powder and stored at +23 and +4 degrees C, respectively. No color or odour changes were observed during the study period. The initial pH of the solutions prepared from tablets and powder were 7.7 and 6.9, respectively. No change of pH values was observed at the end of the 60 days. Significant degradation of Fludrocortisone acetate occurred in formulations stored at +23 degrees C. Fludrocortisone acetate 40 microg/ml solutions prepared from tablets and powder were stable 19 days and at least 60 days, respectively, when stored at +4 degrees C. The solution prepared from powder is the best in term of stability and final concentration which is independent on the Fludrocortisone acetate recovery.

Urinary aldosterone to creatinine ratio in cats before and after suppression with salt or Fludrocortisone acetate

J Vet Intern Med 2008 Nov-Dec;22(6):1283-8.PMID:18775055DOI:10.1111/j.1939-1676.2008.0166.x.

Background: The endocrine diagnosis of primary hyperaldosteronism in cats currently is based on an increased plasma aldosterone to renin ratio, which has several disadvantages for use in veterinary practice. Objectives: To establish a reference range for the urinary aldosterone to creatinine ratio (UACR) and to determine whether oral administration of either sodium chloride or Fludrocortisone acetate is effective for use in a suppression test. Animals: Forty-two healthy cats from an animal shelter and 1 cat with primary hyperaldosteronism from a veterinary teaching hospital. Methods: Morning urine samples for determination of the basal UACR were collected from 42 healthy cats. For the suppression tests, urine samples for the UACR were collected after twice daily oral administration for 4 consecutive days of either sodium chloride, 0.25 g/kg body weight (n = 22) or Fludrocortisone acetate, 0.05 mg/kg body weight (n = 15). Results: The median basal UACR was 7.2 x 10(-9) (range, 1.8-52.3 x 10(-9)), with a calculated reference range of < 46.5 x 10(-9). Administration of sodium chloride resulted in adequate salt loading in 10 of 22 cats, but without significant reduction in the UACR. Administration of fludrocortisone resulted in a significant decrease in the UACR (median, 78%; range, 44-97%; P < .001) in healthy cats. In the cat with an aldosterone-producing adrenocortical carcinoma, the basal UACR and the UACR after fludrocortisone administration were 32 x 10(-9) and 36 x 10(-9), respectively. Conclusions and clinical importance: Using the UACR for an oral fludrocortisone suppression test may be useful for the diagnosis of primary hyperaldosteronism in cats.

Fludrocortisone acetate to treat neurally mediated hypotension in chronic fatigue syndrome: a randomized controlled trial

JAMA 2001 Jan 3;285(1):52-9.PMID:11150109DOI:10.1001/jama.285.1.52.

Context: Patients with chronic fatigue syndrome (CFS) are more likely than healthy persons to develop neurally mediated hypotension (NMH) in response to prolonged orthostatic stress. Objective: To examine the efficacy of Fludrocortisone acetate as monotherapy for adults with both CFS and NMH. Design: Randomized, double-blind, placebo-controlled trial conducted between March 1996 and February 1999. Setting: Two tertiary referral centers in the United States. Patients: One hundred individuals aged 18 to 50 years who satisfied Centers for Disease Control and Prevention criteria for CFS and had NMH provoked during a 2-stage tilt-table test. Eighty-three subjects had adequate outcome data to assess efficacy. Intervention: Subjects were randomly assigned to receive Fludrocortisone acetate, titrated to 0.1 mg/d (n = 50) or matching placebo (n = 50) for 9 weeks, followed by 2 weeks of observation after discontinuation of therapy. Main outcome measure: Proportion of subjects in each group with at least a 15-point improvement on a 100-point global wellness scale. Results: Baseline demographic and illness characteristics between the groups were similar; CFS had been present for at least 3 years in 71%. Using an intention-to-treat analysis, 7 subjects (14%) treated with fludrocortisone experienced at least a 15-point improvement in their wellness scores compared with 5 (10%) among placebo recipients (P =.76). No differences were observed in several other symptom scores or in the proportion with normal follow-up tilt test results at the end of the treatment period. Conclusions: In our study of adults with CFS, fludrocortisone as monotherapy for NMH was no more efficacious than placebo for amelioration of symptoms. Failure to identify symptomatic improvement with fludrocortisone does not disprove the hypothesis that NMH could be contributing to some of the symptoms of CFS. Further studies are needed to determine whether other medications or combination therapy are more effective in treating orthostatic intolerance in patients with CFS.

Effect of Fludrocortisone acetate on chronic unexplained nausea and abdominal pain in children with orthostatic intolerance

J Pediatr Gastroenterol Nutr 2014 Jul;59(1):39-43.PMID:25222805DOI:10.1097/MPG.0000000000000305.

Background: We hypothesized that orthostatic intolerance (OI) is associated with gastric dysrhythmias, nausea, and abdominal pain, which improves using fludrocortisone to treat OI. Methods: Patients (n=16, girls) with OI completed questionnaires before and after fludrocortisone treatment (age 14.8 ± 2.8 years). Ten patients underwent electrogastrograms (EGGs) before fludrocortisone. Results: All EGGs showed gastric dysrhythmias. Fludrocortisone reduced mean scores as follows: nausea, 3.1 ± 0.8 to 2.1 ± 1.1 (P=0.016); dizziness, 3.0 ± 1.0 to 2.2 ± 1.1 (P=0.0371); abdominal pain, 2.8 ± 1.3 to 1.9 ± 1.4 (P=0.0063); flushing, 2.3 ± 1.2 to 1.5 ± 1.4 (P=0.0476); and missing school, 2.2 ± 1.5 to 1.2 ± 1.5 (P=0.0078). Conclusions: Chronic nausea and abdominal pain accompany OI and improve with OI treatment.

Effect of Fludrocortisone acetate in patients with subarachnoid hemorrhage

Stroke 1989 Sep;20(9):1156-61.PMID:2672426DOI:10.1161/01.str.20.9.1156.

In this study with randomized controls, we administered Fludrocortisone acetate to 46 of 91 patients with subarachnoid hemorrhage in an attempt to prevent excessive natriuresis and plasma volume depletion. Fludrocortisone significantly reduced the frequency of a negative sodium balance during the first 6 days (from 63% to 38%, p = 0.041). A negative sodium balance was significantly correlated with decreased plasma volume during both the first 6 days (p = 0.014) and during the entire 12-day study period (p = 0.004). Although fludrocortisone treatment tended to diminish the decrease in plasma volume, the difference was not significant (p = 0.188). More patients in the control group developed cerebral ischemia (31% vs. 22%) and, consequently, more control patients were treated with plasma volume expanders (24% vs. 15%), which may have masked the effects of fludrocortisone on plasma volume. Fludrocortisone therefore reduces natriuresis and remains of possible therapeutic benefit in the prevention of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.