| Bioactivity | 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]. | ||||||||||||
| Invitro | 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]. | ||||||||||||
| Name | AC-4-130 | ||||||||||||
| CAS | 1834571-82-2 | ||||||||||||
| Formula | C37H36ClF5N2O5S | ||||||||||||
| Molar Mass | 751.20 | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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AC-4-130
CAS: 1834571-82-2 F: C37H36ClF5N2O5S W: 751.20
AC-4-130 is a potent STAT5 SH2 domain inhibitor. AC-4-130 directly binds to STAT5 and disrupts STAT5 activation, dimeriz
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