AC-4-130 |
| Catalog No.GC62272 |
AC-4-130은 강력한 STAT5 SH2 도메인 억제제입니다. AC-4-130은 STAT5에 직접 결합하여 STAT5 활성화, 이량체화, 핵 전위 및 STAT5 의존성 유전자 전사를 방해합니다. AC-4-130은 FLT3-ITD로 구동되는 백혈병 세포에서 세포 주기 정지 및 세포자멸사를 유도합니다. AC-4-130은 항암 활성을 가지며 급성 골수성 백혈병(AML)에서 병리학적 수준의 STAT5 활성을 효율적으로 차단할 수 있습니다.
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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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