Perindopril

Manufactured by Merck Group

Sourced in United States

Perindopril is a laboratory instrument used for analyzing and measuring various chemical and biochemical compounds. It functions as a high-performance liquid chromatography (HPLC) system, which is a widely used analytical technique for the separation, identification, and quantification of complex mixtures. The core function of Perindopril is to provide accurate and reliable data on the composition and properties of the samples being analyzed.

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Perindopril erbumine (2 citations)

9 protocols using perindopril

Phytochemical Interventions in ICR Mice

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After stabilization, the ICR mice were randomly assigned to a control group (n = 8), three groups treated with phytochemicals including Curcumin (n = 8), quercetin (n = 8), and saponin (n = 8), respectively. A positive control group was also established (n = 8). Curcumin, quercetin, and saponin were orally administered daily at a dose of 50 mg/kg body weight regularly. In the positive control group, perindopril was orally administered daily at a dose of 1 mg/kg body weight, under similar conditions as the phytochemical-treated groups. The test materials, quercetin (95%), saponin (8–25%), Curcumin (Curcuma longa L., 65%) and perindopril were purchased from Sigma (Sigma Aldrich, St. Louis, MO, USA). Curcumin, quercetin, saponin and perindopril were dissolved in 0.1% Tween 80 (Sigma-Aldrich Co., St. Louis, MO, USA) according to the daily dose immediately prior to administration. The control group was treated with the same amount of physiological saline.

Kim H.L., Kim W.K, & Ha A.W. (2019). Effects of Phytochemicals on Blood Pressure and Neuroprotection Mediated Via Brain Renin-Angiotensin System. Nutrients, 11(11), 2761.

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Sensitive HPLC-MS/MS Quantification of Pharmaceuticals

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Methanol (MEOH), acetonitrile (ACN), acetic acid (AcOH), and ammonium acetate (AmAc) were supplied by Merck (Darmstadt, Germany) and all the mobile phase solvents and reagents were high-performance liquid chromatographic (HPLC)-grade with ≥99% purity. Ultra-pure water was prepared from a Milli-Q water purification system (MA, USA). Standard pharmaceuticals (metformin, ibuprofen, mefenamic acid, simvastatin, caffeine, diclofenac, perindopril, and nifedipine) were purchased from Sigma-Aldrich (Schnelldorf, Germany). The acetaminophen reference standard material was purchased from Sigma-Aldrich (St. Louis, MO, USA). The purity of all standards used in this study was ≥98%. A 1000 mg L⁻¹ stock standard solution was prepared for each pharmaceutical by dissolving an appropriate amount of each analytical standard of pharmaceuticals in methanol. Working solutions (5 mg L⁻¹) were prepared from the 1000 mg L⁻¹ stock solutions by adding 50 μL of each stock solution to a 10 mL volumetric flask and then methanol was used to fill it up to the mark. A series of standard solutions for the calibration was conducted using the working solution and diluting with water: methanol (2 : 1 v/v) at pH 10. The mixture was adjusted to pH 10 using ammonium hydroxide, 1 M.

Kafeenah H.I., Osman R, & Bakar N.K. (2018). Disk solid-phase extraction of multi-class pharmaceutical residues in tap water and hospital wastewater, prior to ultra-performance liquid chromatographic-tandem mass spectrometry (UPLC-MS/MS) analyses. RSC Advances, 8(70), 40358-40368.

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Regulation of VEGF/VEGFR in Human Retinal Endothelial Cells

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Cell culture: hRECs purchased from Angio-Proteomie (Boston, MA) were cultured in a Human Microvascular Endothelial Cell Medium (Cell Applications, Inc., San Diego, CA, Cat. No. 111–500). Experiments were performed between cell passages 3 and 8. Cells were maintained in an incubator at 37 °C under a humidified 5% CO₂: 95% air atmosphere. The media were changed twice a week. For HG experiments, hRECs were seeded in 12-well plates at 1.5 × 10⁵ cells/well and cultured either in physiologic (5 mmol/l) for 72 h or in 5.5 mM for 24 h and then challenged with HG (33 mmol/l) for 48 h. The HG-mediated induction of VEGF/VEGFR, which was conducted independently of Ang II, was investigated by treating cells with angiotensin converting enzyme (ACE) inhibitor perindopril (10 µmol/l, Sigma-Aldrich, St. Louis, MO) for 24 h. This was followed by stimulation with HG for 48 h. Then, siRNAs (20 nM) and miRNAs (20 nM mimics or 50 nM antagomirs) were transfected using the Lipofectamine 2000 reagent (Invitrogen, Carlsbad, CA) according to the manufacturer’s instructions.

Haque R., Hur E.H., Farrell A.N., Iuvone P.M, & Howell J.C. (2015). MicroRNA-152 represses VEGF and TGFβ1 expressions through post-transcriptional inhibition of (Pro)renin receptor in human retinal endothelial cells. Molecular Vision, 21, 224-235.

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Combination Therapy in D2-mdx Mice

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D2-mdx mice were randomised into four treatment groups (n = 8/group) as follows: (1) Vehicle control (phosphate-buffered saline (PBS)+Debio-025 carrier), (2) Perindopril (2 mg/kg/day; P0094, Sigma-Aldrich, St. Louis, MO, USA), (3) Debio-025 (20 mg/kg/day; Alisporivir; Debiopharm Research & Manufacturing SA, Martigny, Switzerland), and (4) Perindopril (2 mg/kg/day)+Debio-025 (20 mg/kg/day). Treatments were delivered via oral gavage as a volume of 0.1 mL. Treatment began at 12 weeks of age for six weeks.

Hayes H.M., Angerosa J., Piers A.T., White J.D., Koleff J., Thurgood M., Moody J., Cheung M.M, & Pepe S. (2022). Preserved Left Ventricular Function despite Myocardial Fibrosis and Myopathy in the Dystrophin-Deficient D2.B10-Dmdmdx/J Mouse. Oxidative Medicine and Cellular Longevity, 2022, 5362115.

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ARPE-19 Cells Glucose Response Assay

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ARPE-19 cells were purchased from the American Type Culture Collection (Manassas, VA, USA). ARPE-19 cell line was authenticated by a short tandem repeat (STR) analysis as shown in Supplementary Appendix 1. ARPE-19 cells were grown in Dulbecco’s Modified Eagle’s medium (DMEM): F12 supplemented with 10% (v/v) fetal calf serum (FCS) and a mixture of streptomycin (100 µg/mL)-penicillin (100 IU/mL) (LONZA), and passaged twice a week. ARPE-19 cells were incubated at 37 °C, and 5% CO₂ and 90% relative humidity. For glucose treatment, cells were exposed to 5.5 mM (normoglycemia, NG) as control or 33 mM d-glucose (hyperglycemia or high glucose, HG) and cultured for 48 h. To study HG-mediated induction of PRR signaling independently of Ang II, cells were treated with angiotensin converting enzyme (ACE) inhibitor perindopril (10 µmol/L, Sigma-Aldrich, St. Louis, MO, USA) for 24 h, followed by stimulation with human prorenin (Cayman Chemical, Ann Arbor, MI, USA, Item # 10007599) at a final concentration of 10 nmol/l and HG for 48 h. Specificity of ROS generation by Nox was assessed by treating hyperglycemic cells with the inhibitors of NADPH oxidase [diphenyleneiodonium, (DPI), 10 µM], nitric oxide synthase [NG-nitro-l-arginine methyl ester (l-NAME), 500 µM], mitochondrial O₂ synthesis (Rotenone, 10 µM), and xanthine oxidase (Allopurinol, 100 µM) for 24 h.

Haque R., Iuvone P.M., He L., Hur E.H., Chung Choi K.S., Park D., Farrell A.N., Ngo A., Gokhale S., Aseem M, & Kumar B. (2017). Prorenin receptor (PRR)-mediated NADPH oxidase (Nox) signaling regulates VEGF synthesis under hyperglycemic condition in ARPE-19 cells. Journal of receptor and signal transduction research, 37(6), 560-568.

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Development and Validation of HPTLC Methods for Antihypertensive Drugs

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Chromatographic glass plates, HPTLC silica gel 60 F₂₅₄, HPTLC silica gel 60 RP-18 F₂₅₄, HPTLC diol F₂₅₄, HPTLC CN F₂₅₄, and TLC cellulose were obtained from Merck (Darmstadt, Germany). Methanol, toluene, ethyl acetate, acetone, isopropyl, and acetonitrile of analytical grade were from Avantor (Gliwice, Poland). Deionized water was produced in the laboratory with the demineralizer HLP 5 from Hydrolab (Straszyn, Poland). The reagents used to prepare the acidic and basic mobile phases were as follows: formic acid (99.5%) and ammonia (25%) were also purchased from Avantor (Gliwice, Poland). Methanol and formic acid LC–MS grade were purchased from Merck (Darmstadt, Germany). Antihypertensive drugs (hydrochlorothiazide, indapamide, lercanidipine, nebivolol, telmisartan, valsartan) were donated from the Cardiology Clinic of the Independent Public Clinical Hospital No. 4 in Lublin (Lublin, Poland). Perindopril and ramipril were bought from Sigma–Aldrich (St. Louis, MO, USA). Albumin bovine fraction V (BSA) was from NzyTech–Genes & Enzymes (Lisbon, Portugal).

Jaglińska K., Polak B., Klimek-Turek A., Błaszczyk R., Wysokiński A, & Dzido T.H. (2021). Preparation of Antihypertensive Drugs in Biological Matrix with Solvent Front Position Extraction for LC–MS/MS Analysis. Molecules, 27(1), 205.

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Antihypertensive Drugs Analysis by HPTLC

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Antihypertensive drugs: ramipril, lercanidipine, valsartan, hydrochlorothiazide, telmisartan, perindopril, and nebivolol were purchased from Sigma-Aldrich (St. Louis, MO, USA). The structures, physicochemical properties and drug classes (pharmacological properties) of investigated substances are presented in Table 5. Chromatographic glass plates, HPTLC silica gel 60 F254 and HPTLC diol F254 were supplied by Merck (Darmstadt, Germany). Acetonitrile and methanol (both MS purity) were purchased from Fisher Chemical (Waltham, MA, USA). Ethanol, toluene and formic acid (98–100%) LC-MS grades were supplied by Merck (Darmstadt, Germany). The ultra-pure water was obtained from the Millipore Direct-Q3-UV purification system (Merck, Darmstadt, Germany). The plasma samples (also a reference sample) were kindly provided by the Cardiology Clinic of the Independent Public Clinical Hospital No. 4 in Lublin (Lublin, Poland).

Jaglińska K., Polak B., Klimek-Turek A., Fornal E., Stachniuk A., Trzpil A., Błaszczyk R, & Wysokiński A. (2023). Comparison of the Determination of Some Antihypertensive Drugs in Clinical Human Plasma Samples by Solvent Front Position Extraction and Precipitation Modes. Molecules, 28(5), 2213.

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Evaluating Neuroprotective Potential of Perindopril and Azilsartan

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Perindopril and azilsartan were procured from Sigma Aldrich, (CO., Saint Louis, MO, USA). Sodium- Carboxymethyl cellulose (Na-CMC) was obtained from the faculty of pharmacy at King Abdulaziz University. Aluminum chloride (AlCl₃) was obtained from KFCMR at King Abdulaziz University. Rat ELISA kits for the determination of beta-amyloid Peptide - 42 (Aβ-42) and Nitric Oxide (NO) were bought from (SunLong Biotech Co. China). Tumor necrosis factor (TNF-α), Malondialdehyde (MDA) and Acetylcholinesterase (AChE) were purchased from (Elabscience Co. USA)

Alzahrani Y.M., Alim A. Sattar M.A., Kamel F.O., Ramadan W.S, & Alzahrani Y.A. (2020). Possible combined effect of perindopril and Azilsartan in an experimental model of dementia in rats. Saudi Pharmaceutical Journal : SPJ, 28(5), 574-581.

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Drug Efficacy on Stroke Pathology

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Animals used in the drug study were individually housed and fed with the drugs mixed in with highly palatable baby food daily from the age of 5 weeks, after pathology first appears, to the age of 12 weeks. Animals were treated in five batches, with each batch containing one animal randomly assigned to each treatment group. Analysis suggested a minimum of five animals per treatment group to detect an effect size of 35% with 80% power (67) . One animal, which died before the age of 12 weeks without stroke pathology, was not included in the final analysis. Drugs were administered at doses based on previously published data demonstrating their efficacy at either lowering blood pressure or improving endothelial dysfunction when administered orally in rats: simvastatin (2 mg/kg per day; Sigma) (32, 33) , perindopril (2 mg/kg per day; Sigma) (68) , cilostazol (60 mg/kg per day; Sigma) (69) , and H+H (16 mg/kg per day; Sigma) (70) (table S2). Blood pressure was measured before treatment, and weekly after treatment started, by tail-cuff plethysmography. Myelin rarefaction was ranked blind to group from Luxol fast blue/cresyl violet-stained sections.

Rajani R.M., Quick S., Ruigrok S.R., Graham D., Harris S.E., Verhaaren B.F.J., Fornage M., Seshadri S., Atanur S.S., Dominiczak A.F., Smith C., Wardlaw J.M, & Williams A. (2018). Reversal of endothelial dysfunction reduces white matter vulnerability in cerebral small vessel disease in rats. Science translational medicine, 10(448).

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