Catalog No.S1507 Synonyms: BMS-186295, SR-47436
Molecular Weight(MW): 428.53
Irbesartan (SR-47436, BMS-186295) is a highly potent and specific angiotensin II type 1 (AT1) receptor antagonist with IC50 of 1.3 nM.
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Efficacy of ARBs at preventing StAR upregulation in SII-stimulated H295R cells. (A,B) Western blotting for StAR protein levels in H295R cells transfected to overexpress barr1 and treated for 6 hrs with 10 μM SII alone (SII) or in the presence of 10 μM of each of the sartans tested. Representative blots of 3 independent experiments are shown in (A), including blots for barr1 to confirm its overexpression and for GAPDH (glyceraldehyde 3-phosphate dehydrogenase) as loading control, and the StAR protein induction (as % of the SII response), as derived by densitometric quantification, is shown in (B). *, p <0.05, n=3 independent experiments/treatment. Blots shown have been cropped to fit space requirements and run under the same experimental conditions (same gel) (the full length blots are shown in Supplementary Information). (C,D) Western blotting for StAR protein levels in dominant negative barr1 mutanttransfected H295R cells and treated as in (A-B). Representative blots are shown in (C), including blots for the dominant negative barr1 mutant to confirm its overexpression and for GAPDH as loading control, and the StAR protein induction (as % of vehicle-no stimulation), as derived by densitometric quantification, is shown in (D). No significant differences were observed among treatments, nor did any treatment cause any induction in StAR levels. Blots shown have been cropped to fit space requirements and run under the same experimental conditions (same gel) (the full length blots are shown in Supplementary Information). n=3 independent experiments/treatment. LOS: Losartan-; VAL: Valsartan; CAN: Candesartan; OLM: Olmesartan; IRB: Irbesartan.
Sci Rep, 2015, 5:8116.. Irbesartan purchased from Selleck.
Immunofluorescence analysis of HBcAg expression at day 10 after irbesartan administration for HBV (genotype D) infection at MGE 200. The m47F peptide (400 nM) and ezetimibe (50 lM) were used as positive controls for HBV entry inhibition.
Antiviral Res, 2015, 120:140-6.. Irbesartan purchased from Selleck.
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|Description||Irbesartan (SR-47436, BMS-186295) is a highly potent and specific angiotensin II type 1 (AT1) receptor antagonist with IC50 of 1.3 nM.|
|Features||Irbesartan is a longer acting AT1 receptor antagonist relative to losartan and valsartan.|
Irbesartan competes with angiotensin II (AII) for binding at the AT1 receptor subtype and antagonizes AII-induced contraction in rabbit aorta ring with IC50 of 4 nM. Irbesartan has no affinity for AT2 receptors.  Irbesartan (10 μM) blocks angiotensin II induced increase in αv, β1, β3, and β5 integrins, osteopontin, and α-actinin mRNA and protein levels in rat cardiac fibroblasts, leading to the decrease of cell attachment to extracellular matrix (ECM) proteins.  Irbesartan treatment markedly induces the expression of the adipogenic marker gene adipose protein 2 (aP2) in 3T3-L1 cells in a concentration-dependent manner with EC50 of 3.5 μM and 3.3-fold induction at the concentration of 10 μM. Irbesartan (10 μM) markedly induces transcriptional activity of the peroxisome proliferator–activated receptor-γ (PPARγ) by 3.4-fold independent of its AT1 receptor blocking action.  Pretreatment with Irbesartan (~10 μM) decreases angiotensin II-induced apoptosis in rat vascular smooth muscle cells by blocking angiotensin II internalization in a concentrationdependent manner. 
|In vivo||Oral administration of Irbesartan (1 mg/kg) reduces angiotensin II (AII)-induced hypertension, equipotent with losartan in conscious normotensive rats, markedly more active than losartan (10 mg/kg) in normotensive cynomolgus monkeys.  Administration of Irbesartan (7 mg/kg/day) significantly prevents skeletal muscle apoptosis and muscle atrophy in rats with monocrotaline-induced congestive heart failure (CHF), which is involved with the decrease of TNFα level and attributed to AT1 receptor blocking. |
-  Bernhart CA, et al. J Med Chem, 1993, 36(22), 3371-3380.
-  Kawano H, et al. Hypertension, 2000, 35, 273-279.
-  Schupp M, et al. Circulation, 2004, 109(17), 2054-2057.
|In vitro||DMSO||4 mg/mL warmed (9.33 mM)|
|Ethanol||3 mg/mL (7.0 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% PEG400+0.5% Tween80+5% propylene glycol
For best results, use promptly after mixing.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03493685||Recruiting||Focal Segmental Glomerulosclerosis||Retrophin Inc.||April 3 2018||Phase 3|
|NCT03016832||Recruiting||Diabetic Kidney Disease||Jiangsu Famous Medical Technology Co. Ltd.||January 2017||Early Phase 1|
|NCT03476603||Recruiting||Obesity Morbid||Norwegian University of Science and Technology|St. Olavs Hospital|Volvat Medisinsk Senter Stokkan|Namsos Hospital|Alesund Hospital||November 2 2016||--|
|NCT02842359||Completed||Type 2 Diabetes Mellitus||Sanofi||August 23 2016||Phase 4|
|NCT03147677||Recruiting||Type 2 Diabetic Nephropathy||The Third Xiangya Hospital of Central South University||July 2016||Phase 4|
|NCT02644486||Terminated||Obesity and Glomerulopathy||Zhi-Hong Liu M.D.|Nanjing University School of Medicine||January 2016||Not Applicable|
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