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| | AC-4-130 Basic information |
| Product Name: | AC-4-130 | | Synonyms: | AC-4-130;AC4130,AC 4 130;Benzoic acid, 4-[[[3,5-bis(1,1-dimethylethyl)phenyl]methyl][2-[[(4-chlorophenyl)methyl][(2,3,4,5,6-pentafluorophenyl)sulfonyl]amino]acetyl]amino]- | | CAS: | 1834571-82-2 | | MF: | C37H36ClF5N2O5S | | MW: | 751.2 | | EINECS: | | | Product Categories: | | | Mol File: | 1834571-82-2.mol |  |
| | AC-4-130 Chemical Properties |
| Boiling point | 756.3±70.0 °C(Predicted) | | density | 1.362±0.06 g/cm3(Predicted) | | storage temp. | Store at -20°C | | pka | 4.28±0.10(Predicted) | | form | Solid | | color | Off-white to brown |
| | AC-4-130 Usage And Synthesis |
| Biological Activity | 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]. | | References | [1]. Bettina Wingelhofer, et al. Pharmacologic inhibition of STAT5 in acute myeloid leukemia. Leukemia. 2018 May;32(5):1135-1146. |
| | AC-4-130 Preparation Products And Raw materials |
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