FIDAS-5 is an orally active methionine adenosyltransferase 2A (MAT2A) inhibitor with an IC50 of 2.1 μM. It can effectively compete with S-adenosylmethionine for MAT2A binding and has anticancer effects.

Mat2A:2.1 μM

METHODS: FIDAS-5 (3 μM; 36 hours) was used to treat LS174T cells, and the levels of S-adenosylmethionine (SAM) and S-adenosylhomocysteine ​​(SAH) were observed.
RESULTS FIDAS-5 reduced S-adenosylmethionine (SAM) and S-adenosylhomocysteine ​​(SAH) levels in LS174T cells.
METHODS: FIDAS-5 (3 μM; 7 days) was used to treat LS174T cells, and the proliferation of LS174T cells was observed.
RESULTS FIDAS-5 significantly inhibited the proliferation of LS174T cells.
METHODS: FIDAS-5 (3 μM) treatment inhibited LS174T colorectal cancer cells, and the expression of c-Myc and cyclinD1 in LS174T colorectal cancer cells was observed by westernBlot.
RESULTS FIDAS-5 inhibited the expression of c-Myc and cyclinD1 in LS174T colorectal cancer cells [1].
METHODS: OPM2 cells were transduced with siMAT2A or scrambled siRNA for 3 days. MAT2A-silenced and parental OPM2 cells were treated with different doses of FIDAS-5 (0.5, 1, 2 μM) to determine whether FIDAS-5 indeed impairs MM cell survival by inhibiting the enzymatic activity of MAT2A.
RESULTS The antitumor effect of FIDAS-5 on MAT2A-silenced cells was impaired compared with cells transduced with scrambled siRNA. FIDAS-5 indeed inhibited MM cell survival in part by targeting MAT2A. [2]

METHODS: Tumors were induced in athymic nude mice by subcutaneous injection of HT29 CRC cells. FIDAS-5 treatment (20 mg/kg) was administered orally via gavage. The oral efficacy of FIDAS-5 on HT29 tumor xenografts in nude mice was tested by measuring tumors twice weekly using digital calipers.
RESULTS FIDAS-5 significantly inhibited xenograft tumor growth with minimal body weight differences. [1]