IWR-1-endo - CAS 1127442-82-3
Catalog number: B0084-262341
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C25H19N3O3
Molecular Weight:
409.44
COA:
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Targets:
Wnt
Description:
IWR-1-endo is a potent inhibitor of the Wnt response, blocking a cell-based Wnt/β-catenin pathway reporter response with an IC50 value of 180 nM.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-262341 25 mg $198 In stock
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Synonyms:
IWR-1; IWR 1; IWR1; IWR-1-endo.
MSDS:
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InChIKey:
ZGSXEXBYLJIOGF-ALFLXDJESA-N
InChI:
InChI=1S/C25H19N3O3/c29-23(27-19-5-1-3-14-4-2-12-26-22(14)19)15-8-10-18(11-9-15)28-24(30)20-16-6-7-17(13-16)21(20)25(28)31/h1-12,16-17,20-21H,13H2,(H,27,29)/t16-,17+,20-,21+
Canonical SMILES:
C1C2C=CC1C3C2C(=O)N(C3=O)C4=CC=C(C=C4)C(=O)NC5=CC=CC6=C5N=CC=C6
1.Paracrine Activation of the Wnt/β-Catenin Pathway by Bone Marrow Stem Cell Attenuates Cisplatin-Induced Kidney Injury.
Jiao X;Cai J;Yu X;Ding X Cell Physiol Biochem. 2017;44(5):1980-1994. doi: 10.1159/000485904. Epub 2017 Dec 11.
BACKGROUND/AIMS: ;Cisplatin-induced acute kidney injury (AKI) involves damage to tubular cells via excess reactive oxygen species (ROS) generation. Stem cell-based therapies have shown great promise in AKI treatment. In this study, we aimed to assess the protective effect and mechanism of bone marrow mesenchymal stem cell (BMSC)-derived conditioned medium (CM) against cisplatin-induced AKI.;METHODS: ;In vitro, NRK-52E cells were incubated with cisplatin in the presence or absence of CM, followed by the assessment of cell viability, apoptosis and cell cycle distribution. Then, ICG-001 and IWR-1 were used to inhibit the wnt/β-catenin pathway. Furthermore, intracellular and mitochondrial ROS levels were evaluated using DCFH-DA and MitoSOX, respectively. In vivo, after cisplatin injection, rats were intravenously injected with CM or BMSCs. Sera and kidney tissues were collected on day 3 after cisplatin injection to evaluate changes in renal function and histology. Western blotting and qRT-PCR were employed to determine the expression of wnt/β-catenin pathway-related genes and proteins. Immunohistochemical staining was used to evaluate tubular β-catenin expression in kidney biopsy from AKI patients.
2.GSK-3β Inhibitor CHIR-99021 Promotes Proliferation Through Upregulating β-Catenin in Neonatal Atrial Human Cardiomyocytes.
Wang S;Ye L;Li M;Liu J;Jiang C;Hong H;Zhu H;Sun Y J Cardiovasc Pharmacol. 2016 Dec;68(6):425-432.
BACKGROUND: ;The renewal capacity of neonate human cardiomyocytes provides an opportunity to manipulate endogenous cardiogenic mechanisms for supplementing the loss of cardiomyocytes caused by myocardial infarction or other cardiac diseases. GSK-3β inhibitors have been recently shown to promote cardiomyocyte proliferation in rats and mice, thus may be ideal candidates for inducing human cardiomyocyte proliferation.;METHODS: ;Human cardiomyocytes were isolated from right atrial specimens obtained during routine surgery for ventricle septal defect and cultured with either GSK-3β inhibitor (CHIR-99021) or β-catenin inhibitor (IWR-1). Immunocytochemistry was performed to visualize 5-ethynyl-2'-deoxyuridine (EdU)-positive or Ki67-positive cardiomyocytes, indicative of proliferative cardiomyocytes.;RESULTS: ;GSK-3β inhibitor significantly increased β-catenin accumulation in cell nucleus, whereas β-catenin inhibitor significantly reduced β-catenin accumulation in cell plasma. In parallel, GSK-3β inhibitor increased EdU-positive and Ki67-positive cardiomyocytes, whereas β-catenin inhibitor decreased EdU-positive and Ki67-positive cardiomyocytes.;CONCLUSIONS: ;These results indicate that GSK-3β inhibitor can promote human atrial cardiomyocyte proliferation.
3.Tissue factor induces VEGF expression via activation of the Wnt/β-catenin signaling pathway in ARPE-19 cells.
Wang Y;Sang A;Zhu M;Zhang G;Guan H;Ji M;Chen H Mol Vis. 2016 Jul 25;22:886-97. eCollection 2016.
PURPOSE: ;The purpose of the present study was to investigate the potential signal mechanism of tissue factor (TF) in the regulation of the expression of vascular endothelial growth factor (VEGF) in human retinal pigment epithelial (ARPE-19) cells.;METHODS: ;An in vitro RPE cell chemical hypoxia model was established by adding cobalt chloride (CoCl2) in the culture medium. The irritative concentration of CoCl2 was determined with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay kit. VEGF production in ARPE-19 cells was measured with enzyme-linked immunosorbent assay (ELISA) and western blotting. The Wnt signaling pathway-associated molecules, including phospho-glycogen synthase kinase 3β (p-GSK3β), GSK3β, p-β-catenin and β-catenin, were detected with western blotting. pEGFP-N3-hTF was constructed and verified with digestion of the restriction enzyme and sequencing analysis. Human TF overexpression and silencing plasmids were transfected into the ARPE-19 cells to clarify the causal relationship between TF and VEGF expression. The Transwell coculture system of ARPE-19 cells and RF/6A rhesus macaque choroid-retinal endothelial cells was performed to evaluate cell invasion and tube formation ability.
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CAS 1127442-82-3 IWR-1-endo

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