KY-226

KY-226 inhibits human PTP1B activity, but does not exhibit peroxisome proliferator-activated receptor γ (PPARγ) agonist activity. In rodent preadipocytes (3T3-L1), KY-226 up to 10 μM has no effects on adipocyte differentiation. In human hepatoma-derived cells (HepG2), KY-226 (0.3-10 μM) increases the phosphorylated insulin receptor (pIR) produced by insulin.^[1]

In db/db mice, the oral administration of KY-226 (10 and 30 mg/kg/day, 4 weeks) significantly reduces plasma glucose and triglyceride levels as well as hemoglobin A1c values without increasing body weight gain. KY-226 attenuates plasma glucose elevations in the oral glucose tolerance test. KY-226 also increases pIR and phosphorylated Akt in the liver and femoral muscle. In high-fat diet-induced obese mice, the oral administration of KY-226 (30 and 60 mg/kg/day, 4 weeks) decreases body weight gain, food consumption, and fat volume gain with increases in phosphorylated STAT3 in the hypothalamus.^[1]

• Cell lines

  3T3-L1, HepG2

• Concentrations

  0.1-10 μM

• Incubation Time

  1 h

• Method

  Cells with or without the overexpression of PTP1B are seeded at a density of 1 x 10 cells/well on 6-well plates and cultured for 24 h and then for 6 h in serumfree DMEM. Cells are cultured in the presence or absence of KY226 for 1 h, followed by an incubation with insulin for 10 min.Cells are washed and then used for various assays.