Furazolidone

Furazolidone (50 μM; in the RTTA assay) inhibits bone marrow transformation mediated by a series of leukemia fusion proteins, including AML1-ETO, MLL-ENL, MLL-AF9, and R1A-RAR-RIIa, and shows a relatively higher IC₅₀ value for normal murine bone-marrow c-Kit positive cells compared to AML1-ETO transformed cells^[1].

Furazolidone (1-50 μM; 24 h-72 h) inhibits the proliferation of AML cell lines (Kasumi-1, NB4, MolM13, MV4-11, U937, and HL-60) in a dose-and time-dependent manner, with IC₅₀ values ranging from 10-20 μM, and also compromises the ability of leukemic cells (Kasumi-1, NB4, MolM-13) to form colonies^[1].
Furazolidone (IC₅₀ values for each cell line; 72 h) induces apoptosis in AML cells (Kasumi-1, NB4, MV4-11, MolM13), with a 2.1-fold increase in %Annexin V+/7-AAD+ in Kasumi-1, 1.7-fold in NB4, 2.0-fold in MV4-11, and 1.6-fold in MolM13 compared with the vehicle-treated control (DMSO), but has no evidence of increased apoptosis in U937 and HL-60 leukemic cells^[1].
Furazolidone (IC₅₀ values for each cell line; 72 h) induces the differentiation of AML cell lines (Kasumi-1, NB4, MV4-11), as indicated by the increased expression of the myeloid differentiation marker CD11b, evident morphologic changes characteristic of differentiation (such as the appearance of granules and condensation of the nucleus), and an increased NBT-positive rate in Kasumi-1 and NB4 cells^[1].
Furazolidone (IC₅₀ values for each cell line; 72 h) up-regulates the protein level, but not the mRNA level, of p53 in AML cells (Kasumi-1, NB4, MV4-11, MolM13)^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.