1. Membrane Transporter/Ion Channel
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  3. Fasentin

Fasentin 

Cat. No.: HY-101849
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Fasentin, a potent glucose transport inhibitor, inhibits GLUT-1 and GLUT-4 transporters. Fasentin is a chemical sensitizer to the death receptor stimuli FAS and tumor necrosis factor (TNF) apoptosis-inducing ligand. Fasentin blocks glucose uptake in cancer cell lines and has anti-angiogenic activity.

For research use only. We do not sell to patients.

Fasentin Chemical Structure

Fasentin Chemical Structure

CAS No. : 392721-37-8

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Description

Fasentin, a potent glucose transport inhibitor, inhibits GLUT-1 and GLUT-4 transporters. Fasentin is a chemical sensitizer to the death receptor stimuli FAS and tumor necrosis factor (TNF) apoptosis-inducing ligand. Fasentin blocks glucose uptake in cancer cell lines and has anti-angiogenic activity[1][2].

IC50 & Target[1][2]

GLUT1

 

GLUT4

 

In Vitro

Fasentin (0.1-1000 μM; 72 hours) inhibits endothelial, tumour and fibroblast cell growth without inducing cell death[1].
Fasentin (25, 50, 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[1].
Fasentin (50 μM; 16 hours) alters expression of genes associated with glucose deprivation such as AspSyn and PCK-2[2].
Fasentin (40 μM; 16 hours) arrests cells in the G0/G1 phase of the cell cycle in U937 cells. Fasentin (15, 30, 80 μM; pretreatment 1 hour) induces glucose deprivation, partially blocks glucose uptake in PPC-1, DU145, and U937 cells[2].
Fasentin (100 μM; 16 hours) does not affect the migratory capability of endothelial cells[1].
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 was not statistically significant. Fasentin does not inhibit the tyrosine kinase activity of VEGFR2[1].

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

Cell Viability Assay[1]

Cell Line: Three types of endothelial cells ECs (HMEC, human microvascular endothelial cells; HUVEC, human umbilical vein endothelial cells; and BAEC, bovine aortic endothelial cells), three human tumour cell lines (MDA-MB-231 and MCF7 breast carcinoma cells, and HeLa cervix adenocarcinoma cells), and human gingival fibroblasts (HGF)
Concentration: 0.1, 1, 10, 100, 1000 μM
Incubation Time: 72 hours
Result: Inhibited endothelial, tumour and fibroblast cell growth (IC50=26.3-111.2 μM) without inducing cell death.

Cell Cycle Analysis[1]

Cell Line: HMECs
Concentration: 25, 50, 100 μM
Incubation Time: 16, 24 hours
Result: Induced a cell cycle arrest in G0/G1 phase and reduced the cell number in S phase in a dose-dependent manner.
Did not increase the subG1 population.

RT-PCR[2]

Cell Line: PPC-1 cells[2]
Concentration: 50 μM
Incubation Time: 16 hours
Result: Altered expression of genes associated with glucose deprivation such as AspSyn and PCK-2 not FLIP mRNA expression.
Molecular Weight

279.64

Formula

C₁₁H₉ClF₃NO₂

CAS No.

392721-37-8

SMILES

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

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

References
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Keywords:

FasentinGLUTGlucose transporterglucosetransportFAStumornecrosisfactoranti-angiogenicInhibitorinhibitorinhibit

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