SML4194
PRI-724
≥98% (HPLC)
别名:
4-(((6S,9S,9aS)-1-(Benzylcarbamoyl)-2,9-dimethyl-4,7-dioxo-8-(quinolin-8-ylmethyl)octahydro-2H-pyrazino[2,1-c][1,2,4]triazin-6-yl)methyl)phenyl dihydrogen phosphate, 4-(((6S,9S,9aS)-1-(Benzylcarbamoyl)-2,9-dimethyl-4,7-dioxo-8-(quinolin-8-ylmethyl)octahydro-1H-pyrazino[2,1-c][1,2,4]triazin-6-yl)methyl)phenyldihydrogen phosphate, Foscenvivint, PO 724, OP-724, OP724, PRI 724, PRI724, Phosphorylated C-82
质量水平
方案
≥98% (HPLC)
表单
powder
颜色
white to beige
溶解性
DMSO: 2 mg/mL, clear
储存温度
-10 to -25°C
SMILES字符串
O=C(NCC1=CC=CC=C1)N(N(CC2=O)C)[C@]([C@@H](N(C3=O)CC4=CC=CC5=C4N=CC=C5)C)([H])N2[C@H]3CC6=CC=C(C=C6)OP(O)(O)=O
生化/生理作用
Precursor form of the ICG-001 analog C-82, a selective inhibitor against β-catenin interaction with CREB-binding protein (CBP; CREBBP), but not p300.
PRI-724 (Foscenvivint; OP-724) is a phosphorylated predrug that is hydrolyzed to the ICG-001 analog C-82, a selective inhibitor against β-catenin interaction with CREB-binding protein (CBP; CREBBP), but not p300, resulting in upregulated p300/β-catenin complex. PRI-724 treatment reduces the fibrosis induced by CCl4 (1:4 v/v in mineral oil, 1mL/kg 2x per wk) or bile duct ligation (BDL) in mice in vivo (0.4 mg in PBS/kg i.p. 4x per wk). PRI-724 active metabolite C-829 (10 µM) inhibits β-catenin signaling in isolated primary hepatic stellate cells (HSCs) from mice in cultures.
PRI-724 (Foscenvivint; OP-724) is a phosphorylated predrug that is hydrolyzed to the ICG-001 analog C-82, a selective inhibitor against β-catenin interaction with CREB-binding protein (CBP; CREBBP), but not p300, resulting in upregulated p300/β-catenin complex. PRI-724 treatment reduces the fibrosis induced by CCl4 (1:4 v/v in mineral oil, 1mL/kg 2x per wk) or bile duct ligation (BDL) in mice in vivo (0.4 mg in PBS/kg i.p. 4x per wk). PRI-724 active metabolite C-829 (10 µM) inhibits β-catenin signaling in isolated primary hepatic stellate cells (HSCs) from mice in cultures.
法规信息
新产品
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Hiroyasu Okazaki et al.
Experimental lung research, 45(7), 188-199 (2019-07-13)
Purpose/Aim of the Study: Wnt/β-catenin signaling was reported to be activated in pulmonary fibrosis, and was focused on as a target for antifibrotic therapy. However, the mechanism how the inhibition of Wnt/β-catenin signaling ameliorate pulmonary fibrosis has not been fully
Yosuke Osawa et al.
EBioMedicine, 2(11), 1751-1758 (2016-02-13)
Wnt/β-catenin is involved in every aspect of embryonic development and in the pathogenesis of many human diseases, and is also implicated in organ fibrosis. However, the role of β-catenin-mediated signaling on liver fibrosis remains unclear. To explore this issue, the
Xuejie Jiang et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 24(10), 2417-2429 (2018-02-22)
Purpose: Wnt/β-catenin signaling is required for leukemic stem cell function. FLT3 mutations are frequently observed in acute myeloid leukemia (AML). Anomalous FLT3 signaling increases β-catenin nuclear localization and transcriptional activity. FLT3 tyrosine kinase inhibitors (TKI) are used clinically to treat
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