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AC-4-130, a powerful inhibitor of the SH2 domain of STAT5, effectively hinders STAT5 activation, dimerization, nuclear translocation, and transcription of genes reliant on STAT5. This compound directly binds to STAT5, ultimately leading to cell cycle arrest and apoptosis in FLT3-ITD-driven leukemic cells. AC-4-130 exhibits notable anti-cancer properties and effectively suppresses abnormal STAT5 activity in acute myeloid leukemia (AML), making it a promising therapeutic option [1].
Pack Size | Price | Availability | Quantity |
---|---|---|---|
25 mg | $767 | 4-6 weeks | |
50 mg | $997 | 4-6 weeks | |
100 mg | $1,860 | 4-6 weeks |
Description | AC-4-130, a powerful inhibitor of the SH2 domain of STAT5, effectively hinders STAT5 activation, dimerization, nuclear translocation, and transcription of genes reliant on STAT5. This compound directly binds to STAT5, ultimately leading to cell cycle arrest and apoptosis in FLT3-ITD-driven leukemic cells. AC-4-130 exhibits notable anti-cancer properties and effectively suppresses abnormal STAT5 activity in acute myeloid leukemia (AML), making it a promising therapeutic option [1]. |
In vitro | AC-4-130 (0.1-100 μM; 72 hours) significantly increases apoptosis in MV4-11 or MOLM-13 cells in a dose- and time-dependent manner. AC-4-130 (2, 5 μM; 72 hours) induces cell cycle arrest with more G0/G1 cells and fewer in S or G2/M. AC-4-130 (0.5-2 μM; 24 hours) reduces pY-STAT5 levels in both cytoplasm and nucleus. AC-4-130-mediated STAT5 inhibition effectively blocks proliferation and clonogenic growth of primary human AML cells, with healthy CD34+ cells being less sensitive[1]. |
Molecular Weight | 751.2 |
Formula | C37H36ClF5N2O5S |
Cas No. | 1834571-82-2 |
Relative Density. | 1.362 g/cm3 (Predicted) |
Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
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