Fatostatin is an inhibitor of SREBP that directly binds SCAP (SREBP cleavage-activating protein) and blocks its ER-to-Golgi transport with IC50 of 2.5 and 10 μM in mammalian cells. Fatostatin blocked increases in body weight, blood glucose, and hepatic fat accumulation in obese ob/ob mice, even under uncontrolled food intake[3]. In vitro analysis revealed that fatostatin significantly inhibited the secretion of inflammatory cytokines from cells activated with lipopolysaccharide, without affecting cell viability[4]. Fatostatin inhibited tubulin polymerization, arrested cells in mitosis, activated the spindle assembly checkpoint, and triggered mitotic catastrophe and reduced cell viability[5]. Fatostatin, an inhibitor of SREBP1, could increase the sensitivity of endometrial cancer to progesterone and reverse progesterone resistance by inhibiting SREBP1 both in vitro and in vivo[6].
Fatostatin/脂肪抑制素 细胞实验
Cell Line
Concentration
Treated Time
Description
References
RD cells
0.01 - 1 µM
48 hours
Inhibited cell growth and migration
Mol Metab. 2025 Feb;92:102085.
RH30 cells
0.01 - 1 µM
48 hours
Inhibited cell growth and migration
Mol Metab. 2025 Feb;92:102085.
RD cells
1 mM
48 hours
Increased cell death
Mol Metab. 2025 Feb;92:102085.
BT20 cells
5 µM
48 hours
Fatostatin had no significant effect on the growth of ER- cells.
Oncogenesis. 2018 Aug 24;7(8):66.
RS4;11 and ALL-PO cells
1 µM
48 hours
Sequential administration of AZD1775 in conjunction with several of these drugs effectively inhibited the recovery of RS4;11 and ALL-PO cells.
Genome Biol. 2024 May 31;25(1):143.
MCF-7 cells
5 µM
48 hours
Fatostatin inhibited the growth of ER+ cells, leading to cell cycle arrest and apoptosis.
Oncogenesis. 2018 Aug 24;7(8):66.
T47D cells
5 µM
48 hours
Fatostatin inhibited the growth of ER+ cells, leading to cell cycle arrest and apoptosis.
Oncogenesis. 2018 Aug 24;7(8):66.
MDA-MB-231 cells
5 µM
48 hours
Fatostatin had no significant effect on the growth of ER- cells.
Oncogenesis. 2018 Aug 24;7(8):66.
U87R cells
3.93 µM
5 days
To test the inhibitory effect of Fatostatin on TMZ-resistant cells, the results showed that the IC50 of Fatostatin for U87R cells was 3.93 µM, significantly lower than the IC50 of TMZ.
Acta Pharmacol Sin. 2023 Mar;44(3):670-679.
U87 cells
8.69 µM
5 days
To test the inhibitory effect of Fatostatin on TMZ-sensitive cells, the results showed that the IC50 of Fatostatin for U87 cells was 8.69 µM.
Acta Pharmacol Sin. 2023 Mar;44(3):670-679.
Fatostatin/脂肪抑制素 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
NOD/SCID mice
RD cell xenograft model
Oral
10 mg/kg
3 times a week for 3 weeks
Reduced tumor growth
Mol Metab. 2025 Feb;92:102085.
Mice
Patient-derived xenograft (PDX) model
Intravenous injection
120 mg/kg
5 days a week for 21 days
To assess the in vivo efficacy of AZD1775 in treating ALL; results indicated effectiveness in the PDX model.
Genome Biol. 2024 May 31;25(1):143.
Mice
Subcutaneous C4-2B xenograft mouse model
Intraperitoneal injection
15 mg/kg
42 days
Fatostatin significantly reduced tumor growth and serum PSA levels.
Mol Cancer Ther. 2014 Apr;13(4):855-66
Mice
Ptenpc−/−; Pmlpc−/− mouse model
Intraperitoneal (i.p.) injections
15 mg/kg
Every other day for 2 months
Fatostatin inhibited both prostate tumor growth and distant lymph node metastasis, significantly reduced the expression of SREBP-regulated enzymes for synthesis of FA and cholesterol, decreased the frequency of Ki-67 positive cells, and induced apoptosis.
Nat Genet. 2018 Feb;50(2):206-218
Mice
MCF-7 cell xenograft model
Intraperitoneal injection
30 mg/kg/day
Once daily for 16 days
Fatostatin significantly reduced the growth of MCF-7 xenograft tumors and induced endoplasmic reticulum stress and apoptosis.
搜索
