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Submit ReviewSTF 31 is an inhibitor of GLUT1; inhibits glucose uptake in renal cell carcinoma (RCC) 4 cells. Activity causes necrotic cell death in von Hippel-Lindau (VHL)-deficient RCC cells. Also NAMPT inhibitor. Eliminates human pluripotent stem cells from culture with limited toxicity towards differentiated cells.
STF 31 is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Stem Cell Library. Find out more about compound libraries available from Tocris.
M. Wt | 423.53 |
Formula | C23H25N3O3S |
Storage | Store at RT |
Purity | ≥99% (HPLC) |
CAS Number | 724741-75-7 |
PubChem ID | 984333 |
InChI Key | NGQPRVWTFNBUHA-UHFFFAOYSA-N |
Smiles | O=C(NC2=CN=CC=C2)C1=CC=C(CNS(C3=CC=C(C(C)(C)C)C=C3)(=O)=O)C=C1 |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solvent | Max Conc. mg/mL | Max Conc. mM | |
---|---|---|---|
Solubility | |||
DMSO | 42.35 | 100 |
The following data is based on the product molecular weight 423.53. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
Concentration / Solvent Volume / Mass | 1 mg | 5 mg | 10 mg |
---|---|---|---|
1 mM | 2.36 mL | 11.81 mL | 23.61 mL |
5 mM | 0.47 mL | 2.36 mL | 4.72 mL |
10 mM | 0.24 mL | 1.18 mL | 2.36 mL |
50 mM | 0.05 mL | 0.24 mL | 0.47 mL |
References are publications that support the biological activity of the product.
Chan et al (2011) Targeting GLUT1 and the Warburg effect in renal cell carcinoma by chemical synthetic lethality. Sci.Transl.Med. 3 94ra70 PMID: 21813754
Adams et al (2014) NAMPT is the cellular target of STF-31-like small-molecule probes. ACS Chem.Biol. 9 2247 PMID: 25058389
Kropp et al (2015) Inhibition of an NAD+ salvage pathway provides efficient and selective toxicity to human pluripotent stem cells. Stem Cells Transl.Med. 4 483 PMID: 25834119
If you know of a relevant reference for STF 31, please let us know.
Keywords: STF 31, STF 31 supplier, STF31, glut1, glucose, transporters, inhibitors, inhibits, uptake, slc2a1, Glucose, Transporters, NAMPT, ESCs, and, iPSC, 4484, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for STF 31 include:
Xintaropoulou et al (2018) Expression of glycolytic enzymes in ovarian cancers and evaluation of the glycolytic pathway as a strategy for ovarian cancer treatment. BMC Cancer 18 636 PMID: 29866066
Thwe et al (2017) Cell-Intrinsic Glycogen Metabolism Supports Early Glycolytic Reprogramming Required for Dendritic Cell Immune Responses. Cell Metab 26 558 PMID: 28877459
Robert et al (2014) MYC regulates the unfolded protein response and glucose and glutamine uptake in endocrine resistant breast cancer. Mol Cancer 13 239 PMID: 25339305
Fons et al (2019) PPM1D mutations silence NAPRT gene expression and confer NAMPT inhibitor sensitivity in glioma. Nat Commun 10 3790 PMID: 31439867
Xintaropoulou et al (2015) A comparative analysis of inhibitors of the glycolysis pathway in breast and ovarian cancer cell line models. Oncotarget 6 25677 PMID: 26259240
Lei et al (2023) Pharmacological vitamin C inhibits mTOR signaling and tumor growth by degrading Rictor and inducing HMOX1 expression. PLoS Genet 19 e1010629 PMID: 36787291
Nael A et al (2017) Insulin signaling via the PI3-kinase/Akt pathway regulates airway glucose uptake and barrier function in a CFTR-dependent manner. Am J Physiol Lung Cell Mol Physiol 312 L688-L702 PMID: 28213469
Kropp et al (2015) Inhibition of an NAD+ salvage pathway provides efficient and selective toxicity to human pluripotent stem cells. Mol Cell Biol 4 483 PMID: 25834119
Do you know of a great paper that uses STF 31 from Tocris? Please let us know.
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After 72hr treatment with three different inhibitors (GPP78,STF118804, and STF31), we used 10nM to 10uM.
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This poster summarizes the main metabolic pathways in cancer cells and highlights potential targets for cancer therapeutics. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways providing potential cancer therapeutic targets.