AC-4-130 |
| カタログ番号GC62272 |
AC-4-130 は強力な STAT5 SH2 ドメイン阻害剤です。 AC-4-130 は STAT5 に直接結合し、STAT5 の活性化、二量体化、核移行、および STAT5 依存性の遺伝子転写を妨害します。 AC-4-130 は、FLT3-ITD 駆動型白血病細胞の細胞周期停止とアポトーシスを誘導します。 AC-4-130 には抗がん作用があり、急性骨髄性白血病 (AML) における病理学的レベルの STAT5 活性を効率的にブロックできます。
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1834571-82-2
Sample solution is provided at 25 µL, 10mM.
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AC-4-130 is a potent STAT5 SH2 domain inhibitor. AC-4-130 directly binds to STAT5 and disrupts STAT5 activation, dimerization, nuclear translocation, and STAT5-dependent gene transcription. AC-4-130 induces cell cycle arrest and apoptosis in FLT3-ITD-driven leukemic cells. AC-4-130 has anti-cancer activity and can efficiently block pathological levels of STAT5 activity in acute myeloid leukemia (AML)[1].
AC-4-130 (0.1-100 µM; 72 hours) leads to a significant increase in apoptosis in a dose-dependent and time-dependent manner in MV4-11 or MOLM-13 cells[1]. AC-4-130 (2, 5 µM; 72 hours) induces cell cycle arrest with an increase in G0/G1 arrested cells and a concomitant reduction in cells in S or G2/M[1]. AC-4-130 (0.5-2; 24 hours) reveals reduced pY-STAT5 levels both in the cytoplasm and nucleus[1]. AC-4-130-mediated STAT5 inhibition efficiently blocks the proliferation and clonogenic growth of primary human AML cells, while healthy CD34+ cells are less sensitive[1].
[1]. Bettina Wingelhofer, et al. Pharmacologic inhibition of STAT5 in acute myeloid leukemia. Leukemia. 2018 May;32(5):1135-1146.
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