Catalog No. Size PriceQuantity
M23862-C Contact sales@xcessbio.com for quotation $100
M23862-2 2 mg solid $90
M23862-10 10 mg solid $155
M23862-100 100 mg solid $765


Fasentin, a potent glucose uptake inhibitor, inhibits GLUT-1/GLUT-4 transporters. Fasentin preferentially inhibits GLUT4 (IC50=68 μM) over GLUT1. Fasentin is a death receptor stimuli (FAS) sensitizer and sensitizes cells to FAS-induced cell death. Fasentin is also a tumor necrosis factor (TNF) apoptosis-inducing ligand sensitizer. Fasentin blocks glucose uptake in cancer cell lines and has anti-angiogenic activity.

Product information

CAS Number: 392721-37-8

Molecular Weight: 279.64

Formula: C11H9ClF3NO2

Chemical Name: N-[4-chloro-3-(trifluoromethyl)phenyl]-3-oxobutanamide

Smiles: CC(=O)CC(=O)NC1=CC(=C(Cl)C=C1)C(F)(F)F


InChi: InChI=1S/C11H9ClF3NO2/c1-6(17)4-10(18)16-7-2-3-9(12)8(5-7)11(13,14)15/h2-3,5H,4H2,1H3,(H,16,18)

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Solubility: DMSO : 100 mg/mL (357.60 mM; Need ultrasonic).

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥12 months if stored properly.

Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

In Vitro:

Fasentin (0.1-1000 μM; 72 hours) inhibits endothelial, tumour and fibroblast cell growth without inducing cell death. Fasentin (25-100 μM; 16-24 hours) induces a cell cycle arrest in G0/G1 phase and reduces the cell number in S phase in a dose-dependent manner. Fasentin (50 μM; 16 hours) alters expression of genes associated with glucose deprivation such as AspSyn and PCK-2. Fasentin (15, 30, 80 μM; pretreatment 1 hour) induces glucose deprivation, partially blocks glucose uptake in PPC-1, DU145, and U937 cells. Fasentin (100 μM; 16 hours) does not affect the migratory capability of endothelial cells. Fasentin (25-100 μM; 16 hours) lowers levels of phospho-ERK in HMECs, indicating a partial inhibition on the ERK signalling pathway, even though the effect is not statistically significant. Fasentin does not inhibit the tyrosine kinase activity of VEGFR2. Fasentin interacts with a unique site in the intracellular channel of GLUT1.

Products are for research use only. Not for human use.

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