Fosinopril (sodium salt)
(Synonyms: 福辛普利钠; SQ28555) 目录号 : GC47370
A prodrug form of fosinoprilat
Cas No.:88889-14-9
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Fosinopril is a prodrug form of the angiotensin converting enzyme (ACE) inhibitor fosinoprilat.1 Oral administration of fosinopril inhibits angiotensin I-induced pressor responses in normotensive rats, dogs, and monkeys when administered at doses of 15, 15, and 10 µmol/kg, respectively. Fosinopril (2.5 mg/kg) reduces fractional shortening and decreases left ventricular size in a porcine model of congestive heart failure.2 Formulations containing fosinopril have been used in the treatment of hypertension and congestive heart failure.
1.DeForrest, J.M., Waldron, T.L., Harvey, C., et al.Fosinopril, a phosphinic acid inhibitor of angiotensin I converting enzyme: In vitro and preclinical in vivo pharmacologyJ. Cardiovasc. Pharmacol.14(5)730-736(1989) 2.McElmurray, J.H., III, Mukherjee, R., New, R.B., et al.Angiotensin-converting enzyme and matrix metalloproteinase inhibition with developing heart failure: Comparative effects on left ventricular function and geometryJ. Pharmacol. Exp. Ther.291(2)799-811(1999)
| Cas No. | 88889-14-9 | SDF | |
| 别名 | 福辛普利钠; SQ28555 | ||
| Canonical SMILES | O=C(N1[C@H](C([O-])=O)C[C@@H](C2CCCCC2)C1)CP(CCCCC3=CC=CC=C3)(O[C@H](OC(CC)=O)C(C)C)=O.[Na+] | ||
| 分子式 | C30H45NO7P.Na | 分子量 | 585.7 |
| 溶解度 | Methanol: 1 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.7074 mL | 8.5368 mL | 17.0736 mL |
| 5 mM | 0.3415 mL | 1.7074 mL | 3.4147 mL |
| 10 mM | 0.1707 mL | 0.8537 mL | 1.7074 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。
Gateways to Clinical Trials
Methods Find Exp Clin Pharmacol 2002 Sep;24(7):431-55.PMID:12428432doi
Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies knowledge area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: Adalimumab, aeroDose insulin inhaler, agomelatine, alendronic acid sodium salt, aliskiren fumarate, alteplase, amlodipine, aspirin, atazanavir; Bacillus Calmette-Guérin, basiliximab, BQ-788, bupropion hydrochloride; Cabergoline, caffeine citrate, carbamazepine, carvedilol, celecoxib, cyclosporine, clopidogrel hydrogensulfate, colestyramine; Dexamethasone, diclofenac sodium, digoxin, dipyridamole, docetaxel, dutasteride; Eletriptan, enfuvirtidie, eplerenone, ergotamine tartrate, esomeprazole magnesium, estramustine phosphate sodium; Finasteride, fluticasone propionate, Fosinopril sodium; Ganciclovir, GBE-761-ONC, glatiramer acetate, gliclazide, granulocyte-CSF; Heparin sodium, human isophane insulin (pyr), Hydrochlorothiazide; Ibuprofen, inhaled insulin, interferon alfa, interferon beta-1a; Laminvudine, lansoprazole, lisinopril, lonafarnib, losartan potassium, lumiracoxib; MAb G250, meloxicam methotrexate, methylprednisolone aceponate, mitomycin, mycophenolate mofetil; Naproxen sodium, natalizumab, nelfinavir mesilate, nemifitide ditriflutate, nimesulide; Omalizumab, omapatrilat, omeprazole, oxybutynin chloride; Pantoprazole sodium, paracetamol, paroxetine, pentoxifylline, pergolide mesylate, permixon, phVEGF-A165, pramipexole hydrochloride, prasterone, prednisone, probucol, propiverine hydrochloride; Rabeprazole sodium, resiniferatoxin, risedronate sodium, risperidone, rofecoxib rosiglitazone maleate, ruboxistaurin mesilate hydrate; Selegiline transdermal system, sertraline, sildenafil citrate, streptokinase; Tadalafil, tamsulosin hydrochloride, technosphere/Insulin, tegaserod maleate, tenofovir disoproxil fumarate, testosterone heptanoate, testosterone undecanoate, tipifarnib, tolterodine tartrate, topiramate, troglitazone; Ursodeoxycholic acid; Valdecoxib, valsartan, vardenafil, venlafaxine hydrochloride, VX-745.
[Protective effect of Fosinopril sodium pretreatment combined with ischemic postconditioning on rat heart underwent myocardial ischemia/reperfusion injury]
Zhonghua Xin Xue Guan Bing Za Zhi 2010 Jul;38(7):633-7.PMID:21055289doi
Objective: To investigate the effects of Fosinopril sodium pre-treatment combined with ischemic postconditioning on rat serum and myocardial oxidative stress and proinflammatory cytokines post ischemia/reperfusion. Methods: Sixty Sprague-Dawley rats were randomly divided into sham group (n = 15), ischemia/reperfusion group (30 minutes in situ occlusion of the left anterior descending artery followed by 1 hour reperfusion, n = 15), IPoC group (30 minutes occlusion of the left anterior descending artery followed by 3 cycles of 10 seconds of reperfusion/10 seconds of ischemia before 1 hour reperfusion, n = 15) and Fosinopril sodium group [pretreated with Fosinopril sodium (0.9 mg×kg(-1)×d(-1) for 14 days) followed by IPoC protocol at 2 h after the last gavage, n = 15]. The arterial blood and heart samples were extracted after 1 hour reperfusion. Serum CK-MB and cTnT levels were detected by colorimetric method, myocardial infarction size was measured by nitrotetrazolium blue chloride staining, SOD content was examined by colorimetric method, MDA content was detected using thiobarbituric acid method, serum levels of Interleukin-1α (IL-1α), Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were examined by radioimmunoassay, IL-1α, IL-6 and TNF-α levels of myocardial tissue were detected by ELISA. Results: Compared with I/R group, myocardial enzymes and infarction size were significantly decreased (P < 0.05, P < 0.01), serum SOD content was increased and MDA content was decreased (all P < 0.01), serum and myocardial levels of IL-1α, IL-6 and TNF-α were significantly reduced (P < 0.05, P < 0.05, P < 0.01) in IPoC group. Compared with IPoC group, Fosinopril sodium pretreatment further reduced infarction size and myocardial enzyme CK-MB (P < 0.05), increased SOD content (P < 0.05) while reduced serum IL-6 and myocardial tissue TNF-α (P < 0.05, P < 0.01). Conclusion: Pretreatment with Fosinopril sodium enhanced the protective effect of IPoC on rat myocardium underwent I/R injury, possibly by reducing oxidative stress and early inflammatory reaction.
Effect of valsartan and Fosinopril on catecholamine-induced cardiac hypertrophy
Acta Pharmacol Sin 2000 Sep;21(9):850-4.PMID:11501170doi
Aim: To study the influence of angiotensin (Ang) II receptor antagonist (AT1) valsartan and angiotensin-converting enzyme (ACE) inhibitor Fosinopril on the cardiac hypertrophy induced by catecholamine. Methods: A cardiac hypertrophy model was produced by i.p. norepinephrine (NE) 1.5 mg.kg-1.d-1 x 15 d. The animals were divided into four groups: 1) control (sodium chloride), 2) NE, 3) NE + Fosinopril, 4) NE + valsartan. Fosinopril ig 15 mg.kg-1.d-1 x 15 d, valsartan ig 30 mg.kg-1.d-1 x 15 d. Results: Valsartan ig 30 mg.kg-1.d-1 x 15 d and Fosinopril ig 15 mg.kg-1.d-1 x 15 d prevented left ventricular hypertrophy induced by NE and decreased the content of collagen in myocardium; valsartan and Fosinopril both elevated the myosin ATPase activity, Na+, K(+)-ATPase activity in membrane, and Ca(2+)-ATPase activity in mitochondrias. Apoptosis was induced in cardiomyocytes by catecholamine. Valsartan and Fosinopril both inhibited apoptosis, and no significant differences were found in the apoptotic index between the two treatment groups. Conclusion: Valsartan and Fosinopril prevent the remodeling of cardiac hypertrophy induced by norepinephrine. Cardiac myocyte apoptosis may play a key role in the heart remodeling.
Management of hypertension: the role of combination therapy
Am J Hypertens 1997 Oct;10(10 Pt 2):262S-271S.PMID:9366283DOI:10.1016/s0895-7061(97)00333-6.
The complementary action of angiotensin converting enzyme inhibitors and diuretics in the treatment of hypertension has been demonstrated in a number of studies of Fosinopril and hydrochlorothiazide (HCTZ). The combination provides a clinically significant reduction in blood pressure while minimizing the dose-dependent adverse effects of HCTZ, such as hypotension and its metabolic effects on plasma lipoproteins, by keeping the dose of each agent to the minimum. Fosinopril has a unique dual mechanism of elimination and can therefore be used in patients with renal impairment. The efficacy of the combination of Fosinopril and hydrochlorothiazide compared with placebo and other agents is reviewed in this article. Studies have demonstrated that the combination is effective in the elderly and in renally impaired patients, regardless of severity. In addition, in non-insulin dependent diabetes, antihypertensive effect is achieved without further affecting carbohydrate and lipid metabolism, which is often the case when thiazide diuretics alone are used. A matrix study was performed to evaluate the optimum dose combination to produce blood pressure normalization and minimize side effects. This study evaluated 17 different dose combinations and demonstrated that the lowest dose combination to produce a clinically significant effect was Fosinopril 10 mg and HCTZ 12.5 mg. However, a dose-related antihypertensive effect can be seen, giving the option for the use of 20 mg Fosinopril for moderately hypertensive patients. Both combination therapy and Fosinopril were significantly more effective than HCTZ alone or placebo. The Fosinopril/HCTZ combination has also been shown to have a comparable effect to sustained-release nifedipine and propanolol + HCTZ. The studies reviewed here demonstrate that Fosinopril/HCTZ combination treatment has a number of advantages over either agent used alone, providing blood pressure normalization in a broad range of hypertensive patients, including diabetic patients and the elderly.
Fosinopril and hydrochlorothiazide combination versus individual components: lack of a pharmacokinetic interaction
Ann Pharmacother 1999 May;33(5):525-30.PMID:10369612DOI:10.1345/aph.18228.
Objective: To evaluate the pharmacokinetic interaction and bioequivalence of a combination formulation of the angiotensin-converting enzyme inhibitor Fosinopril and the diuretic hydrochlorothiazide (HCTZ). Methods: In an open-label, balanced, randomized incomplete block, three-way crossover fashion, healthy men received single doses of three of four regimens in one of two independent studies. Regimens for study A (36 subjects): (1) Fosinopril 10-mg tablet, (2) HCTZ 12.5-mg tablet, (3) a combination tablet of Fosinopril 10 mg plus HCTZ 12.5 mg, or (4) coadministered tablets of Fosinopril 10 mg and HCTZ 12.5 mg. Study B (40 subjects) received: (1) Fosinopril 20-mg tablet, (2) HCTZ 12.5-mg tablet, (3) a combination tablet of Fosinopril 20 mg plus HCTZ 12.5 mg, or (4) coadministered tablets of Fosinopril 20 mg and HCTZ 12.5 mg. Results: There was no evidence of any significant effect of HCTZ on the pharmacokinetics of fosinoprilat, based on maximum concentration value, AUC, or cumulative urinary recovery over 24 hours. Fosinoprilat had no clinically important effect on the pharmacokinetics of HCTZ only slightly decreasing its AUC by 14% in study A. Coadministration was well tolerated; no new adverse events were reported with the combination tablet. Conclusions: Fosinopril and HCTZ in a combination tablet display pharmacokinetic profiles similar to those achieved when either drug is administered alone or when coadministered in separate tablets. When used with HCTZ, the favorable pharmacokinetic feature of Fosinopril, dual and compensatory pathways of renal and hepatic elimination, is preserved.