NF 157 - CAS 104869-26-3
Category: Inhibitor
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Molecular Formula:
C49H28F2N6Na6O23S6
Molecular Weight:
1437.08
COA:
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Targets:
P2Y Receptor
Description:
NF 157 is a P2Y11 receptor antagonist with IC50 value of 463 nM. It inhibits NAD+-induced activation of human granulocytes.
Purity:
≥96% by HPLC
Synonyms:
8,8'-[Carbonylbis[imino-3,1-phenylenecarbonylimino(4-fluoro-3,1-phenylene)carbonylimino]]bis-1,3,5-naphthalenetrisulfonic acid hexasodium salt
MSDS:
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InChIKey:
QJFCMJZVZFAWGF-UHFFFAOYSA-H
InChI:
InChI=1S/C49H34F2N6O23S6.6Na/c50-33-9-7-25(47(60)54-35-11-13-40(84(70,71)72)31-19-29(82(64,65)66)21-39(43(31)35)81-80-79-63)17-37(33)56-45(58)23-3-1-5-27(15-23)52-49(62)53-28-6-2-4-24(16-28)46(59)57-38-18-26(8-10-34(38)51)48(61)55-36-12-14-41(85(73,74)75)32-20-30(83(67,68)69)22-42(44(32)36)86(76,77)78;;;;;;/h1-22,63H,(H,54,60)(H,55,61)(H,56,58)(H,57,59)(H2,52,53,62)(H,64,65,66)(H,67,68,69)(H,70,71,72)(H,73,74,75)(H,76,77,78);;;;;;/q;6*+1/p-6
Canonical SMILES:
C1=CC(=CC(=C1)NC(=O)NC2=CC=CC(=C2)C(=O)NC3=C(C=CC(=C3)C(=O)NC4=C5C(=CC(=CC5=C(C=C4)S(=O)(=O)[O-])S(=O)(=O)[O-])S(=O)(=O)[O-])F)C(=O)NC6=C(C=CC(=C6)C(=O)NC7=C8C(=CC(=CC8=C(C=C7)S(=O)(=O)[O-])S(=O)(=O)[O-])SOO[O-])F.[Na+].[Na+].[Na+].[Na+].[Na+].[Na+]
1.Icariin attenuates cerebral ischemia-reperfusion injury through inhibition of inflammatory response mediated by NF-κB, PPARα and PPARγ in rats.
Xiong D1, Deng Y1, Huang B1, Yin C1, Liu B1, Shi J1, Gong Q2. Int Immunopharmacol. 2016 Jan;30:157-62. doi: 10.1016/j.intimp.2015.11.035. Epub 2015 Dec 8.
Icariin (ICA), an active flavonoid extracted from Chinese medicinal herb Epimedii, has been reported to exhibit many pharmacological effects including alleviating brain injury. However, little is known about the protection of ICA on ischemic stroke. Hence, this study was designed to investigate the neuroprotective effect of ICA and explore its underlying mechanisms on ischemic stroke induced by cerebral ischemia-reperfusion (I/R) injury in rats. The animals were pretreated with ICA at doses of 10, 30mg/kg twice per day for 3 consecutive days followed by cerebral I/R injury induced by middle cerebral artery occlusion (MCAO) for 2h and reperfusion for 24h. Neurological function and infarct volume were observed at 24h after reperfusion, the protein expression levels of interleukin-1β (IL-1β), transforming growth factor-β1 (TGF-β1), PPARα and PPARγ, inhibitory κB-α (IκB-α) degradation and nuclear factor κB (NF-κB) p65 phosphorylation were detected by Western blot, respectively.
2.microRNA and NF-kappa B.
Yuan Y1,2, Tong L3, Wu S4,5. Adv Exp Med Biol. 2015;887:157-70. doi: 10.1007/978-3-319-22380-3_9.
Nuclear Factor kappa B (NF-κB) plays important roles in regulation of countless cellular functions, including cell cycle and apoptosis. As a versatile transcription factor, NF-κB is a target of a large amount of miRNAs. Abnormal NF-κB activity is frequently associated with an abnormal level of miRNAs, which is found to play critical roles in disease progression including cancer. While the expression and activity of NF-κB can be directly or indirectly up-regulated or downregulated by various miRNAs, NF-κB can also regulate the expression of many miRNAs. Intriguingly, reciprocal regulation between miRNAs and NF-κB, which exists in the form of positive and negative feedback loops, is often observed in various cancers. In this chapter, the mechanisms and roles of miRNA-regulated NF-κB and NF-κB-regulated miRNAs in a variety of cancers will be discussed. The potential therapeutic use of miRNAs that are up- and down-stream of NF-κB signaling pathways as targets for cancer treatment will also be accessed.
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Chemical Structure

CAS 104869-26-3 NF 157

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