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Candesartan

Manufactured by Merck Group
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Candesartan is a pharmaceutical product developed by Merck Group. It is a lab equipment designed for the analysis and quantification of specific compounds in various samples. The core function of Candesartan is to provide accurate and reliable measurement capabilities for researchers and scientists.

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Lab products found in correlation

Pd123319, by Merck Group (3 mentions) Ang 1 7, by Merck Group (2 mentions) Ang 2, by Merck Group (2 mentions) Human angii, by Mimotopes (2 mentions) Cgp42112a, by Merck Group (2 mentions) Lipopolysaccharide, by Merck Group (2 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (2 mentions) Glutamate, by Merck Group (1 mentions) Folic acid, by Fujifilm (1 mentions) Quercetin, by Fujifilm (1 mentions) Methotrexate, by Fujifilm (1 mentions) Dipyridamole, by Fujifilm (1 mentions) Probenecid, by Fujifilm (1 mentions) Celecoxib, by Merck Group (1 mentions) Pgf2α, by Cayman Chemical (1 mentions) Pge2 d4, by Cayman Chemical (1 mentions) Calcium ionophore a23187, by Merck Group (1 mentions) Mk571, by Merck Group (1 mentions) Pgf3α, by Cayman Chemical (1 mentions) Txb2 d4, by Cayman Chemical (1 mentions)

Close spelling variants of this product

Candesartan cilexetil (5 citations)

19 protocols using candesartan

1

Neuroprotective Effects of Candesartan in Glutamate-Induced Excitotoxicity

Cited 2 times
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We performed microarray analysis of gene expression in four sets of rat primary neuronal cultures: controls; treated with candesartan at concentrations in the range of blood levels obtained in humans after oral administration [51 (link)]; exposed to excitotoxic glutamate concentrations [25 (link)]; and treated with candesartan before the exposure to glutamate. Excitotoxicity was induced by exposing cultures to 100 μM glutamate (Sigma-Aldrich) and pretreated for 1 h with vehicle (0.1 % saline and 0.1 N Na2CO3 at pH 7.4), or the AT1R blocker candesartan (10 μM) (Sigma-Aldrich) dissolved in 0.1 N Na2CO3, pH 7.4. After addition of candesartan, the compound was not removed and was present throughout the incubation. candesartan and glutamate concentrations and timing of the experiments were selected on the basis of prior studies demonstrating protection of cultured neurons from inflammation and glutamate-induced injury [25 (link), 27 (link)]. Figure 1 is a flow chart for data analysis.

Flow chart for data analysis. ACE angiotensin converting enzyme, AD Alzheimer’s disease, ANOVA analysis of variance, CGC cerebellar granule cell, ES enrichment score, GSEA gene set enrichment analysis, IFN interferon, IPA ingenuity pathway analysis, KEGG Kyoto encyclopedia of genes and genomes, LPS lipopolysaccharide, pval p value, TGF transforming growth factor, TNF tumor necrosis factor

Elkahloun A.G., Hafko R, & Saavedra J.M. (2016). An integrative genome-wide transcriptome reveals that candesartan is neuroprotective and a candidate therapeutic for Alzheimer’s disease. Alzheimer's Research & Therapy, 8, 5.
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2

Prostanoid and Nucleotide Quantification

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All prostanoids (PGE3, PGF3α, TXB3, PGE2, PGF2α, and TXB2), deuterated prostanoids (PGE2-d4, PGF2α-d4, and TXB2-d4), and EPA were purchased from Cayman Chemical Co. (Ann Arbor, MI). Calcium ionophore A23187 and indomethacin were purchased from Sigma Aldrich (St. Louis, MO). Adenosine 5′-triphosphate (ATP) disodium salt hydrate, 5′-adenylic acid (AMP), and sodium creatine phosphate hydrate were purchased from Tokyo Chemical Industry Co., Ltd. (Tokyo, Japan). Creatine kinase was purchased from Roche Applied Science (Tokyo, Japan). Dipyridamole, probenecid, quercetin, methotrexate, and folic acid were purchased from Wako Pure Chemical Industries (Osaka, Japan). MK571, celecoxib, candesartan, estradiol 17β-glucronide (E217βG), adenosine 3′, 5′-cyclic monophosphate (cAMP), and guanosine 3′, 5′-cyclic monophosphate (cGMP) were purchased from Sigma Aldrich (St. Louis, MO). All other chemicals were of the highest purity available.
Tanaka N., Yamaguchi H, & Mano N. (2014). Transport of Eicosapentaenoic Acid-Derived PGE3, PGF3α, and TXB3 by ABCC4. PLoS ONE, 9(10), e109270.
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3

Nob Treatment for Chronic Kidney Injury

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Six-week-old male C57BL/6J mice were purchased from the Laboratory Animal Center (NLAC), NARLabs, Taiwan, and treated under the guidance of the Laboratory Experimental Animal Center of China Medical University (CMU). Animal care and welfare, UUO administration, and the treatment protocol (plan ID: CMUIACUC-2020-263-2) were approved by the Animal Research Committee of CMU. The mice were humanely housed with food and water ad libitum in a Specific Pathogen-Free (SPF) room. The temperature was maintained at 22 ± 2 °C with a 12 h light and dark cycle. After a week of acclimation, the mice were randomly divided into sham, UUO, and Nob treatment groups (n = 8); subjected to a surgical UUO procedure to cause chronic kidney injury; and then orally treated with 50 mg/kg Nob (AdooQ BioScience, Irvine, CA, USA) for 14 days. Candesartan (5 mg/kg, Sigma-Aldrich, St. Louis, MO, USA), a RAS inhibitor, has been demonstrated as therapeutically effective for CKD and was used as the positive control [21 (link),22 (link)]. UUO administration was performed as in our previous study [21 (link),23 (link)]. After Nob treatment for adaptive time points, the mice were anesthetized with isoflurane and necropsied, and UUO and contralateral kidneys were isolated.
Lo Y.H., Yang S.F., Cheng C.C., Hsu K.C., Chen Y.S., Chen Y.Y., Wang C.W., Guan S.S, & Wu C.T. (2022). Nobiletin Alleviates Ferroptosis-Associated Renal Injury, Inflammation, and Fibrosis in a Unilateral Ureteral Obstruction Mouse Model. Biomedicines, 10(3), 595.
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4

Angiotensin Signaling Pathway Modulators

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Ang II, CGP, Ang 1-7, candesartan, PD123319, A779, and forskolin were purchased from Sigma-Aldrich (St. Louis, MO, USA).
Franco R., Lillo A., Rivas-Santisteban R., Rodríguez-Pérez A.I., Reyes-Resina I., Labandeira-García J.L, & Navarro G. (2020). Functional Complexes of Angiotensin-Converting Enzyme 2 and Renin-Angiotensin System Receptors: Expression in Adult but Not Fetal Lung Tissue. International Journal of Molecular Sciences, 21(24), 9602.
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5

Angiotensin II Receptor Modulation

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Candesartan (Cat#SML0245) was purchased from Sigma Aldrich (St. Louis, MO, USA), DIZE (Cat#18678) was purchased from Cayman Chemicals (Ann Arbor, MI, USA) and human AngII (Cat#51480) was purchased from Mimotopes (Melbourne, VIC, Australia).
Matsoukas J.M., Gadanec L.K., Zulli A., Apostolopoulos V., Kelaidonis K., Ligielli I., Moschovou K., Georgiou N., Plotas P., Chasapis C.T., Moore G., Ridgway H, & Mavromoustakos T. (2022). Diminazene Aceturate Reduces Angiotensin II Constriction and Interacts with the Spike Protein of Severe Acute Respiratory Syndrome Coronavirus 2. Biomedicines, 10(7), 1731.
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6

Signaling Pathway Modulation Assays

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Lipopolysaccharide (LPS), interferon-γ (IFN-γ), Ang II, CGP-42112A, Ang [1–7], candesartan, PD123319, and A779 were purchased from Sigma-Aldrich (St. Louis, MO, USA). Forskolin was purchased from Tocris (Bristol, UK). The concentrations of ligands used for signaling assays were selected on the basis of the dose–response experiments shown in Supplementary Figure S1.
Rivas-Santisteban R., Lillo J., Muñoz A., Rodríguez-Pérez A.I., Labandeira-García J.L., Navarro G, & Franco R. (2021). Novel Interactions Involving the Mas Receptor Show Potential of the Renin–Angiotensin system in the Regulation of Microglia Activation: Altered Expression in Parkinsonism and Dyskinesia. Neurotherapeutics, 18(2), 998-1016.
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7

Diabetic Mice Treated with Antihypertensive Drugs

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About 1 week after the diabetes was established with the confirmation of significantly increased blood glucose level, either Aliskiren (5 or 25 mg/kg/day) diluted in PBS (n = 12 in each group), olmesartan (10 mg/kg/day) (n = 6), Candesartan (20 mg/kg/day) (n = 6) or PBS alone (n = 12) were administered to the diabetic mice via an osmotic minipump (Alzet model 2006) for 6 weeks. hydralazine (2 or 10 mg/kg/day) (n = 12 in each group) was given in the drinking water. In the hydralazine-treated group, we measured the amount of the water they drank daily. The blood pressures were also measured weekly to make sure the accurate drug delivery. The doses of the drugs were chosen according to the reference [10 (link),17 (link)–20 (link)]. Aliskiren and olmesartan were kindly given from Novartis and Pfizer respectively. Candesartan and hydralazine were purchesed from Sigma.
Some diabetic mice received both Aliskiren (25 mg/kg/day) and intraperitoneal injection of anti-SDF-1 neutralizing monoclonal antibody (mAb, 50 μg; R&D) 3 times per week up to 2 weeks. Mouse IgG1 isotype was administrated as a control. The protocol of animal study was approved by the Institutional Animal Care and Use Committee (IACUC) of National Yang-Ming University, Taipei, Taiwan, ROC. The study was conducted according to European Commission guidelines. (Fig 1).
Chang T.T., Wu T.C., Huang P.H., Lin C.P., Chen J.S., Lin L.Y., Lin S.J, & Chen J.W. (2015). Direct Renin Inhibition with Aliskiren Improves Ischemia-Induced Neovasculogenesis in Diabetic Animals via the SDF-1 Related Mechanism. PLoS ONE, 10(8), e0136627.
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8

Microglia and Neuron Cell Culture Protocol

Cited 1 time
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Both mouse microglia (BV2 cells) and neuron (N2a cells) were purchased from Cell
Center, Institute of Basic Medical Sciences, CAMS and PUMC, Beijing, China. BV2
cells were cultured in DMEM medium (Gibco), which was supplemented with 10%
fetal bovine serum (Gibco), and 1% penicillin-streptomycin (Gibco). The cells
were then incubated at 37°C in a humidified atmosphere of 5% CO2. For
M1 microglia, microglial cells were stimulated with 100 ng/mL LPS + 20 ng/mL
IFN-γ (PeproTech),19 (link),20 (link) and then treated with vehicle or candesartan (Sigma). For
M2 microglia, microglial cells were induced with 20 ng/mL IL-4 (PeproTech).20 (link) After 24 h treatment, cells were harvested for testing the changes of
mRNA and protein level, and the supernatant was collected for measuring the
level of inflammatory cytokines.
Qie S., Ran Y., Lu X., Su W., Li W., Xi J., Gong W, & Liu Z. (2020). Candesartan modulates microglia activation and polarization via NF-κB signaling pathway. International Journal of Immunopathology and Pharmacology, 34, 2058738420974900.
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9

Antimicrobial Assessment of Candesartan

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Candesartan (99.5%) was purchased from Sigma Aldrich (Milan, Italy). All the other chemicals and solvents were purchased from Fluka (Saint-Quentin Fallavier, France) and were of HPLC grade and used as received. For the antimicrobial assessment, tryptic soy broth (TSB, Difco, Becton-Dickenson Labs, Heidelberg, Germany) was used. All chemicals were of analytical grade and supplied by Sigma Aldrich. Double-distilled water (Microtech, Naples, Italy) was used to prepare the dilution water and treatments. The microbial growth was measured with an automatic plate reader (Synergy HTX, BioTek Instruments, Winooski, VT, USA).
Luongo G., Saviano L., Libralato G., Guida M., Siciliano A., Previtera L., Di Fabio G, & Zarrelli A. (2021). Secondary Effects of Hypochlorite Treatment on the Emerging Pollutant Candesartan: The Formation of Degradation Byproducts and Their Toxicological Profiles. Molecules, 26(11), 3422.
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10

Endothelial Cell Isolation and Treatment

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Vascular endothelial cells were isolated from experimental mice and cultured in Minimum Essential media (Merck KGaA, Darmstadt, Germany) supplemented with 10% fetal bovine serum (Invitrogen; Thermo Fisher Scientific, Inc., Waltham, MA, USA). Vascular endothelial cells were cultured at 37°C in a humidified atmosphere of 5% CO2. Cells were treated with Candesartan and/or NF-κB activity inhibitor JSH23 (Sigma-Aldrich; Merck KGaA) for 12 h at 37°C.
Zhao X, & Wang X. (2018). Candesartan targeting of angiotensin II type 1 receptor demonstrates benefits for hypertension in pregnancy via the NF-κB signaling pathway. Molecular Medicine Reports, 18(1), 705-714.
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