Home Metabolism SREBP inhibitor - Fatty Acid Synthase inhibitor Fatostatin HBr For research use only.

Fatostatin HBr

Synonyms: 125B11 HBr

Fatostatin HBr is an inhibitor of sterol regulatory element binding protein (SREBP). It impairs the activation of SREBP-1 and SREBP-2.

Fatostatin HBr Chemical Structure

Fatostatin HBr Chemical Structure

CAS: 298197-04-3

Selleck's Fatostatin HBr has been cited by 12 publications

Purity & Quality Control

Batch: Purity: 99.71%
99.71

Fatostatin HBr Related Products

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Cell Data

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
CHO-K1 cells Function assay 20 h Inhibition of SREBP2 activation expressed in CHO-K1 cells co-transfected with pSRE-Luc plasmid assessed as inhibition of luciferase expression after 20 hrs by luciferase reporter gene assay, IC50=5.6 μM 21561152
mouse hepatocytes Function assay 1 uM 90 mins Metabolic stability in mouse hepatocytes at 1 uM after 90 mins by LC-MS/MS analysis 21561152
InhA cells Antimicrobial assay Antimicrobial activity against Mycobacterium tuberculosis H37Rv over-expressing InhA cells assessed as upshift of MIC relative to wild type 24967731
Click to View More Cell Line Experimental Data

Biological Activity

Description Fatostatin HBr is an inhibitor of sterol regulatory element binding protein (SREBP). It impairs the activation of SREBP-1 and SREBP-2.
Targets
SREBPs [1]
In vitro
In vitro Fatostatin inhibits the insulin-induced adipogenesis of 3T3-L1 cells and the serum-independent growth of human androgen-independent prostate cancer (DU145) cells. Fatostatin blocks the activation of SREBPs in cells in tissue culture[1]. Fatostatin suppresses cell proliferation and anchorage-independent colony formation in both androgen-responsive LNCaP and androgen-insensitive C4-2B prostate cancer cells. Fatostatin also reduced in vitro invasion and migration in both cell lines. Further, fatostatin causes G2/M cell cycle arrest and induces apoptosis by increasing caspase-3/7 activity and the cleavages of caspase-3 and PARP[2].
Cell Research Cell lines CHO-K1 cells
Concentrations 20 μM
Incubation Time 20 h
Method On day 0, CHO-K1 cells are plated out onto a 96-well plate in medium A. On day 2, the cells are transiently cotransfected with pCMV-PLAP-BP2(513–1141), pCMV-SCAP, and pAc-β-gal, using Lipofectamine reagent. After incubation for 5 hr, the cells are washed with PBS and then incubated in medium B, in the absence or presence of fatostatin (20 μM) or sterols (10 μg/mL cholesterol and 1 μg/mL 25-hydroxycholesterol). After 20 hr of incubation, an aliquot of the medium is assayed for secreted alkaline phosphatase activity. The cells in each well are lysed and used for measurement of β-galactosidase activities. The alkaline phosphatase activity is normalized by the activity of β-galactosidase.
Experimental Result Images Methods Biomarkers Images PMID
Western blot p-SREBP-1 / N-SREBP-1 / p-SREBP-2 / N-SREBP-2 / FASN / HMGCR AR / PSA Cyclin B / PH3 24493696
Immunofluorescence α-tubulin / centromere 27378817
Growth inhibition assay Cell viability 24493696
In Vivo
In vivo Fatostatin blocks increases in body weight, blood glucose, and hepatic fat accumulation in obese ob/ob mice, even under uncontrolled food intake[1]. Fatostatin significantly inhibits subcutaneous C4-2B tumor growth and markedly decreases serum PSA level compared to the control group[2].
Animal Research Animal Models Obese (ob/ob) mice (C57BL/6J background)
Dosages 30 mg/kg
Administration i.p.

Chemical Information & Solubility

Molecular Weight 375.33 Formula

C18H18N2S·HBr
CAS No. 298197-04-3 SDF Download Fatostatin HBr SDF
Smiles CCCC1=NC=CC(=C1)C2=NC(=CS2)C3=CC=C(C=C3)C.Br
Storage (From the date of receipt)

In vitro
Batch:

Ethanol : 58 mg/mL

DMSO : 7 mg/mL ( (18.65 mM)； Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Water : Insoluble


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In vivo
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