FOXM1-IN-3 is a potent FOXM1 inhibitor. FOXM1-IN-3 downregulates FOXM1 expression at protein and mRNA levels, suppressing downstream effectors CCNB1 and CDC25. FOXM1-IN-3 induces G2/M cell cycle arrest and apoptosis in colorectal cancer cells. FOXM1-IN-3 inhibits colony formation and cell migration in colorectal cancer cells. FOXM1-IN-3 targets the cancer stem cell phenotype in colorectal cancer cells, reducing cancer stem cell marker expression. FOXM1-IN-3 reduces tumor growth in a zebrafish xenograft model. FOXM1-IN-3 can be used for the research of colorectal cancer [1].
In Vivo, FOXM1-IN-3 (compound 14) (5-10 μM; immersion; 72 hours) inhibits tumor growth in a zebrafish xenograft model, with the most pronounced effect in the SW620 line (80.95% tumor growth at 10 μM relative to control)[1].
In Vitro, FOXM1-IN-3 (compound 14) (6.25-100 μM; 24 h) potently inhibits proliferation in SW620 and SW480 colorectal cancer cells with IC50 values of 14.9 μM and 17.5 μM, respectively, and shows favorable selectivity over normal CCD841 cells (IC50 of 36.65 μM)[1]. FOXM1-IN-3 (0.75-3 μM; 7 days) almost completely inhibits colony formation in SW480 and SW620 cells at 3 μM, reflecting long-term antiproliferative effects[1]. FOXM1-IN-3 (6.25-25 μM; 48 h) suppresses cell migration in SW480 cells at 6.25 μM and in SW620 cells at 12.5 μM over 48 h[1]. FOXM1-IN-3 shows measurable inhibition of PI3Kβ, γ, and δ[1]. FOXM1-IN-3 (6.25-25 μM; 24 h) downregulates FOXM1 and its downstream effectors CCNB1 and CDC25 in SW480 and SW620 cells at concentrations as low as 6.25 μM[1]. FOXM1-IN-3 (6.25-25 μM; 24 h) causes G2/M phase arrest in SW480 and SW620 cells, correlating with FOXM1 downregulation[1]. FOXM1-IN-3 (6.25-25 μM; 24 h) induces apoptosis in SW480 and SW620 cells at 12.5 μM and 25 μM[1]. FOXM1-IN-3 (10 μM; 24 h, 48 h) selectively targets cancer stem cell (CSC) phenotypes in SW480 and SW620 cells at 10 μM, with mild and reversible effects on normal CCD841 cells[1]. FOXM1-IN-3 has high passive permeability, low CYP interference, notable hepatotoxicity (IC50 ~5.6 μM in HepG2), and lower neurotoxicity (IC50 ~17 μM in SH-SY5Y)[1].
References:
[1]. Kułaga D, et al. Chemical modification of STL427944 toward morpholine-based 1,3,5-triazines as anticancer agents targeting FOXM1: green synthesis, biological evaluation and ADME-Tox profiling in a colorectal cancer model. Eur J Med Chem. 2026;304:118532.
In Vivo, FOXM1-IN-3 (compound 14) (5-10 μM; immersion; 72 hours) inhibits tumor growth in a zebrafish xenograft model, with the most pronounced effect in the SW620 line (80.95% tumor growth at 10 μM relative to control)[1].
In Vitro, FOXM1-IN-3 (compound 14) (6.25-100 μM; 24 h) potently inhibits proliferation in SW620 and SW480 colorectal cancer cells with IC50 values of 14.9 μM and 17.5 μM, respectively, and shows favorable selectivity over normal CCD841 cells (IC50 of 36.65 μM)[1]. FOXM1-IN-3 (0.75-3 μM; 7 days) almost completely inhibits colony formation in SW480 and SW620 cells at 3 μM, reflecting long-term antiproliferative effects[1]. FOXM1-IN-3 (6.25-25 μM; 48 h) suppresses cell migration in SW480 cells at 6.25 μM and in SW620 cells at 12.5 μM over 48 h[1]. FOXM1-IN-3 shows measurable inhibition of PI3Kβ, γ, and δ[1]. FOXM1-IN-3 (6.25-25 μM; 24 h) downregulates FOXM1 and its downstream effectors CCNB1 and CDC25 in SW480 and SW620 cells at concentrations as low as 6.25 μM[1]. FOXM1-IN-3 (6.25-25 μM; 24 h) causes G2/M phase arrest in SW480 and SW620 cells, correlating with FOXM1 downregulation[1]. FOXM1-IN-3 (6.25-25 μM; 24 h) induces apoptosis in SW480 and SW620 cells at 12.5 μM and 25 μM[1]. FOXM1-IN-3 (10 μM; 24 h, 48 h) selectively targets cancer stem cell (CSC) phenotypes in SW480 and SW620 cells at 10 μM, with mild and reversible effects on normal CCD841 cells[1]. FOXM1-IN-3 has high passive permeability, low CYP interference, notable hepatotoxicity (IC50 ~5.6 μM in HepG2), and lower neurotoxicity (IC50 ~17 μM in SH-SY5Y)[1].
References:
[1]. Kułaga D, et al. Chemical modification of STL427944 toward morpholine-based 1,3,5-triazines as anticancer agents targeting FOXM1: green synthesis, biological evaluation and ADME-Tox profiling in a colorectal cancer model. Eur J Med Chem. 2026;304:118532.