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Merck
CN

SML2664

Sigma-Aldrich

GNF-4877

≥98% (HPLC)

别名:

(3R)-1-[3-[[[3-Amino-6-[2-fluoro-5-(1-methylethoxy)phenyl]-2-pyrazinyl]carbonyl]amino]-4-pyridinyl]-3-piperidinecarboxylic acid, GNF 4877

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About This Item

经验公式(希尔记法):
C25H27FN6O4
分子量:
494.52
UNSPSC代码:
12352200
NACRES:
NA.77

方案

≥98% (HPLC)

表单

powder

颜色

faint yellow to dark orange

溶解性

DMSO: 2 mg/mL, clear

储存温度

2-8°C

SMILES字符串

NC1=NC=C(C2=CC(OC(C)C)=CC=C2F)N=C1C(NC3=CN=CC=C3N4C[C@H](C(O)=O)CCC4)=O

InChI

1S/C25H27FN6O4/c1-14(2)36-16-5-6-18(26)17(10-16)19-12-29-23(27)22(30-19)24(33)31-20-11-28-8-7-21(20)32-9-3-4-15(13-32)25(34)35/h5-8,10-12,14-15H,3-4,9,13H2,1-2H3,(H2,27,29)(H,31,33)(H,34,35)/t15-/m1/s1

InChI key

UZIATSFXNVOVFE-OAHLLOKOSA-N

生化/生理作用

GNF-4877 is an orally available dual inhibitor of Dyrk1a and Gsk3b that induces proliferation of functional primary human and rodent β-cells. GNF4877 reduces non-fasting blood glucose levels in a mouse model of T1D.
orally available dual inhibitor of Dyrk1a and Gsk3b that induces proliferation of functional primary human and rodent β-cells

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

新产品

历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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J Shirakawa et al.
Diabetes, obesity & metabolism, 18 Suppl 1, 71-77 (2016-09-13)
β-Cell dysfunction in type 1 and type 2 diabetes is accompanied by a progressive loss of β-cells, and an understanding of the cellular mechanism(s) that regulate β-cell mass will enable approaches to enhance hormone secretion. It is becoming increasingly recognized
Weijun Shen et al.
Nature communications, 6, 8372-8372 (2015-10-27)
Insufficient pancreatic β-cell mass or function results in diabetes mellitus. While significant progress has been made in regulating insulin secretion from β-cells in diabetic patients, no pharmacological agents have been described that increase β-cell replication in humans. Here we report
Timothy M Horton et al.
Cell chemical biology, 26(2), 213-222 (2018-12-12)
Diabetes is a hyperglycemic condition characterized by pancreatic β-cell dysfunction and depletion. Whereas methods for monitoring β-cell function in vivo exist, methods to deliver therapeutics to β cells are lacking. We leveraged the rare ability of β cells to concentrate zinc to

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