GNF7156 

GNF7156 is a DYRK1A/GSK3B inhibitor, IC₅₀ values of 100 nM for DYRK1A and 40 nM for GSK3B. GNF7156 inhibits DYRK1A and GSK3B kinase activity and induces NFAT nuclear retention. GNF7156 stimulates beta-cell cycle entry and division and maintains insulin secretory capacity. GNF7156 can be used for the research of type 1 diabetes, and type 2 diabetes^[1][2][3].

GNF7156 (4 days) potently stimulates proliferation of reversibly immortalized mouse beta (R7T1) cells with an EC₅₀ of 2.2 μM^[1].
GNF7156 (4 days) induces DNA synthesis in 15-30% of dissociated adult primary rat pancreatic β-cells^[1].
GNF7156 (4 days) induces DNA synthesis in 3-6% of dissociated adult primary human pancreatic β-cells with an EC₅₀ of 0.76 μM^[1].
GNF7156 potently inhibits purified GSK3B enzyme activity with an IC₅₀ of 40 nM^[1].
GNF7156 induces β-catenin nuclear translocation in dispersed primary rat pancreatic β-cells, confirming cellular GSK3B inhibition^[1].
GNF7156 (4 days)-induced proliferation of dispersed primary rat pancreatic β-cells is partially inhibited by overexpression of wild-type or constitutively active GSK3B, but not kinase-dead GSK3B^[1].
GNF7156 potently inhibits purified DYRK1A enzyme activity with an IC₅₀ of 100 nM^[1].
GNF7156 (4 days)-induced proliferation of dispersed primary rat pancreatic β-cells is inhibited by overexpression of wild-type DYRK1A, but not kinase-dead DYRK1A^[1].
GNF7156 (10 min-3 h) induces nuclear localization of NFATc1-GFP in INS1E rat insulinoma cells^[1].
GNF7156 inhibits NFATc1 nuclear export in INS1E rat insulinoma cells, maintaining nuclear NFATc1 localization after calcium ionophore withdrawal^[1].
GNF7156 (6.7 μM; 7 days) increases DNA content, ATP content, and islet equivalent units in intact primary human pancreatic islets while preserving glucose-stimulated insulin secretion, despite a slight reduction in total insulin content^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

GNF7156 (p.o.; daily) improves glycemic control in diabetic mice via induction of β-cell proliferation, increased β-cell mass, and increased insulin content^[2].
GNF7156 significantly increases human β-cell proliferation in diabetic NOD-SCID mice transplanted with human islets^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

418.45

C₂₂H₂₂N₆O₃

2041071-54-7

O=C(C1CCN(CC1)C2=C(NC(C3=C(N)N=CC(C4=CC=CC=C4)=N3)=O)C=NC=C2)O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Shen W, et al. Inhibition of DYRK1A and GSK3B induces human β-cell proliferation. Nat Commun. 2015 Oct 26;6:8372.  [Content Brief]

  [2]. Liu YA, et al. Selective DYRK1A Inhibitor for the Treatment of Type 1 Diabetes: Discovery of 6-Azaindole Derivative GNF2133. J Med Chem. 2020;63(6):2958-2973.  [Content Brief]

  [3]. Shirakawa J, et al. Novel factors modulating human β-cell proliferation. Diabetes Obes Metab. 2016;18 Suppl 1(Suppl 1):71-77.