Ramipril - CAS 87333-19-5
Catalog number: B0084-140017
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C23H32N2O5
Molecular Weight:
416.51
COA:
Inquire
Targets:
Angiotensin-converting Enzyme (ACE)
Description:
Ramipril is a second generation angiotensin-converting enzyme (ACE) inhibitor that acts as a prodrug, which is hydrolyzed in vivo to the active metabolite ramiprilat. It is used in treatment of congestive heart failure, hypertension and heart attacks. It is also useful in preventing renal and retinal complications in diabetes. It was developed by Pfizer and has been listed.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-140017 10 g $399 In stock
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Purity:
>99%
Appearance:
White Solid
Synonyms:
(2s-(1(r*(r*)),2-alpha,3a-beta,6a-beta))-henylpropyl)amino)-1-oxopropyl;cyclopenta(b)pyrrole-2-carboxylicacid,octahydro-1-(2-((1-(ethoxycarbonyl)-3-p;Tritace;Altace;Carasel;Ramace;(2S,3aS,6aS)-1-[(2S)-2-[[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-3,3a,4,5,6,6a-hexahydro-2H-cyclopenta[b]pyrrole-2-carboxylic acid
Solubility:
DMSO 83.3 mg/mL; Water <1 mg/mL
Storage:
-20°C Freezer
MSDS:
Inquire
Application:
Ramipril is used in treatment of congestive heart failure, hypertension and heart attacks. It is also useful in preventing renal and retinal complications in diabetes.
Quality Standard:
EP standard
Shelf Life:
2 month in rt, long time
Quantity:
Kilogram to ton
Boiling Point:
616.2±55.0 °C | Condition: Press: 760 Torr
Melting Point:
109 °C
Density:
1.200±0.06 g/cm3 | Condition: Temp: 20 °C Press: 760 Torr
InChIKey:
HDACQVRGBOVJII-JBDAPHQKSA-N
InChI:
InChI=1S/C23H32N2O5/c1-3-30-23(29)18(13-12-16-8-5-4-6-9-16)24-15(2)21(26)25-19-11-7-10-17(19)14-20(25)22(27)28/h4-6,8-9,15,17-20,24H,3,7,10-14H2,1-2H3,(H,27,28)/t15-,17-,18-,19-,20-/m0/s1
Canonical SMILES:
CCOC(=O)C(CCC1=CC=CC=C1)NC(C)C(=O)N2C3CCCC3CC2C(=O)O
Current Developer:
Ramipril was developed by Pfizer and has been listed.
1.Naringin Reduces Hyperglycemia-Induced Cardiac Fibrosis by Relieving Oxidative Stress.
Adebiyi OA1, Adebiyi OO1, Owira PM1. PLoS One. 2016 Mar 11;11(3):e0149890. doi: 10.1371/journal.pone.0149890. eCollection 2016.
INTRODUCTION: Hyperglycemia promotes myocardial fibrotic lesions through upregulation of PKC and p38 in response to redox changes. The effects of naringin on hyperglycemia-induced myocardial fibrotic changes and its putative effects on PKC-β and p38 protein expression in type 1 rat model of diabetes are hereby investigated.
2.Ramipril and Losartan Exert a Similar Long-Term Effect upon Markers of Heart Failure, Endogenous Fibrinolysis, and Platelet Aggregation in Survivors of ST-Elevation Myocardial Infarction: A Single C
Marinšek M1, Sinkovič A1. Biomed Res Int. 2016;2016:9040457. doi: 10.1155/2016/9040457. Epub 2016 Mar 15.
Introduction. Blocking the renin-angiotensin-aldosterone system in ST-elevation myocardial infarction (STEMI) patients prevents heart failure and recurrent thrombosis. Our aim was to compare the effects of ramipril and losartan upon the markers of heart failure, endogenous fibrinolysis, and platelet aggregation in STEMI patients over the long term. Methods. After primary percutaneous coronary intervention (PPCI), 28 STEMI patients were randomly assigned ramipril and 27 losartan, receiving therapy for six months with dual antiplatelet therapy (DAPT). We measured N-terminal proBNP (NT-proBNP), ejection fraction (EF), plasminogen-activator-inhibitor type 1 (PAI-1), and platelet aggregation by closure times (CT) at the baseline and after six months. Results. Baseline NT-proBNP ≥ 200 pmol/mL was observed in 48.1% of the patients, EF < 55% in 49.1%, and PAI-1 ≥ 3.5 U/mL in 32.7%. Six-month treatment with ramipril or losartan resulted in a similar effect upon PAI-1, NT-proBNP, EF, and CT levels in survivors of STEMI, but in comparison to control group, receiving DAPT alone, ramipril or losartan treatment with DAPT significantly increased mean CT (226.
3.Effects of renin-angiotensin system inhibitors on fibrosis in patients with alcoholic chronic pancreatitis.
Madro A1, Kurzepa J2, Celinski K3, Slomka M1, Czechowska G1, Kurzepa J4, Kazmierak W1, Buszewicz G5, Ciesielka M5, Madro R5. J Physiol Pharmacol. 2016 Feb;67(1):103-10.
Chronic pancreatitis (CP) results in impairment of exocrine as well as endocrine functions and progressive fibrosis. Previous studies, have demonstrated the presence of renin-angiotensin system receptors within different pancreatic cells. The aim of the present study was to assess the effects of renin-angiotensin system (RAS) inhibitors on serum levels of fibrosis biomarkers (matrix metalloproteinase 2 and 9 (MMP-2, MMP-9), tissue inhibitor of MMP (TIMP- 1, TIMP-2), hyaluronic acid (HA)) and fasting glucose levels in patients with alcoholic CP. Seventy seven outpatients (mean age 43 years, 62 males) with diagnosed alcoholic CP were randomly enrolled into 5 study groups depending on the RAS inhibitors administered and their doses (2.5 or 5 mg and 12.5 or 25 mg for ramipril or losartan, respectively). Venous blood was sampled monthly for a period of one year to monitor serum drug levels. MMP-2, -9, TIMP-1, TIMP-2 and HA were measured with ELISA method on the onset and at the end of the study.
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CAS 87333-19-5 Ramipril

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