N-[4-chloro-3-(trifluoromethyl)phenyl]-3-oxobutanamide Property

Boiling point:

394.2±42.0 °C(Predicted)

Density 

1.411±0.06 g/cm3(Predicted)

storage temp. 

room temp

solubility 

DMSO: >10mg/mL

form 

powder

pka

10.76±0.46(Predicted)

color 

white to off-white

Stability:

Stable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20° for up to 3 months.

Safety

Hazard Codes 

Xn

Risk Statements 

22

WGK Germany 

3

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Warning

Hazard statements

H302Harmful if swallowed

Precautionary statements

P264Wash hands thoroughly after handling.

P264Wash skin thouroughly after handling.

P270Do not eat, drink or smoke when using this product.

P301+P312IF SWALLOWED: call a POISON CENTER or doctor/physician IF you feel unwell.

P330Rinse mouth.

P501Dispose of contents/container to..…

N-[4-chloro-3-(trifluoromethyl)phenyl]-3-oxobutanamide Chemical Properties,Usage,Production

Description

Fasentin (392721-37-8) is a novel inhibitor of glucose uptake which acts via inhibition of the glucose transporter GluT1 and GluT4 (IC50=68 μM).1?Inhibition of glucose uptake is cell type specific2?and is a promising approach to new cancer therapeutics3. Rescues cardiac progenitor cell dysfunction and mitochondrial fission induced by high glucose.4?Sensitizes cells to FAS-induced cell death.5,6

Uses

Fasentin is a novel glucose transport inhibitor that blocks glucose uptake and is also a chemical sensitizer to the death receptor stimuli FAS and tumor necrosis factor apoptosis-inducing ligand.

Uses

Fasentin has been used as a glucose transporter (GLUT1) inhibitor to assess its effects on the vulnerability of a wide range of triple-negative breast cancer (TNBC) cell lines and to study its effects on cytotoxic drugs induced by hydrocortisone (HC).

Biochem/physiol Actions

Fasentin is a novel inhibitor of glucose uptake, GluT1 inhibitor. Fasentin is a novel inhibitor of glucose uptake that sensitizes cells to FAS-induced cell death. Fasentin selectively sensitized to death ligands, but did not decrease FLIP expression. It alters expression of genes associated with nutrient and glucose deprivation. Fasentin interacted with a unique site in the intracellular channel of the glucose transport protein GLUT1.

storage

Store at -20°C

References

1) Granchi?et al.?(2016),?Anticancer agents interacting with membrane glucose transporters; Med. Chem. Comm.,?7?1716 2) Kraus?et al. (2018),?Targeting glucose transport and the NAD pathway in tumor cells with STF-31: a re-evaluation; Cell. Oncol. (Dordr),?41?485 3) Adekola?et al. (2012),?Glucose transporters in cancer metabolism; Curr. Opin. Oncol.,?24?650 4) Choi?et al.?(2016),?High Glucose Causes Human Cardiac Progenitor Cell Dysfunction by Promoting Mitochondrial Fission: Role of a GLUT1 Blocker; Prog. Biomol. Ther. (Seoul),?24?363 5) Schimmer?et al.?(2006),?Identification of small molecules that sensitize resistant tumor cells to tumor necrosis factor-family death receptors; Cancer Res.,?66?2367 6) Wood?et al.?(2008),?A novel inhibitor of glucose uptake sensitizes cells to FAS-induced cell death; Mol. Cancer Ther.,?7?3546