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SML2664

Sigma-Aldrich

GNF-4877

≥98% (HPLC)

Synonym(s):

(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

Empirical Formula (Hill Notation):
C25H27FN6O4
CAS Number:
2041073-22-5
Molecular Weight:
494.52
UNSPSC Code:
12352200
NACRES:
NA.77

Assay

≥98% (HPLC)

form

powder

color

faint yellow to dark orange

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

SMILES string

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

Biochem/physiol Actions

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.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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
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
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

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