Fasentin | Glucose uptake inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $55.00 | ||
| 25 mg | $195.00 |
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
References/Citations:
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
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
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
References/Citations:
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
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