2-Deoxy-D-glucose - CAS 154-17-6
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
2-Deoxy-D-glucose
Catalog Number:
154-17-6
Synonyms:
2-Deoxy-D-arabino-hexose; D-Arabino-2-deoxyhexose
CAS Number:
154-17-6
Description:
2-deoxy-D-Glucose is a non-metabolizable glucose analog that inhibits phosphorylation of glucose by hexokinase, the first step of glycolysis. This results in the depletion in cellular ATP, the inhibition of protein glycosylation, and the disruption of ER quality control by inducing the unfolded protein response. 2-deoxy-D-Glucose has been shown to cause cell cycle inhibition and cell death in in vitro models of hypoxia, induce autophagy, increase reactive oxygen species production, activate AMPK, and block tumor cell growth in animal models.
Molecular Weight:
164.16
Molecular Formula:
C6H12O5
COA:
Inquire
MSDS:
Inquire
Targets:
Hexokinase
Chemical Structure
CAS 154-17-6 2-Deoxy-D-glucose

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Reference Reading


1.2-Deoxy-D-Glucose Is a Potent Inhibitor of Biofilm Growth in Escherichia coli.
Sutrina SL1, Griffith MS2, Lafeuille C3. Microbiology. 2016 Apr 5. doi: 10.1099/mic.0.000290. [Epub ahead of print]
Escherichia coli strain 15 (ATCC 9723), which forms robust biofilms, was grown under optimal biofilm conditions in NaCl-free Luria-Bertani broth (LB*) or in LB* supplemented with one of the non-metabolizable analogues 2-deoxy-D-glucose (2DG), α-methyl-D-mannopyranoside (αMM), or α-methyl-D-glucopyranoside (αMG). Biofilm growth was inhibited by mannose analogue 2DG even at very low concentration in unbuffered medium, and the maximal inhibition was enhanced in the presence of either 100 mM KPO4 or 100 mM MOPS, pH 7.5; in buffered medium, concentrations of 0.02 % (1.2 mM) or more inhibited nearly completely. In contrast, mannose analogue αMM, which should not be able to enter the cells but has been reported to inhibit biofilm growth by binding to FimH, did not exhibit strong inhibition even at concentrations up to 1.8 % (108 mM). The glucose analogue αMG inhibited biofilm growth, but much less strongly than 2DG. None of the analogues inhibited planktonic growth or caused a change in pH of the unbuffered medium.
2.Mitochondrial dysfunction in H9c2 cells during ischemia and amelioration with Tribulus terrestris L.
Reshma PL1, Sainu NS1, Mathew AK2, Raghu KG3. Life Sci. 2016 Apr 2. pii: S0024-3205(16)30201-6. doi: 10.1016/j.lfs.2016.03.055. [Epub ahead of print]
AIMS: The present study investigates the protective effect of partially characterized Tribulus terrestris L. fruit methanol extract against mitochondrial dysfunction in cell based (H9c2) myocardial ischemia model.
3.Molecular imaging of atherosclerotic lesions by positron emission tomography - can it meet the expectations?
Brammen L1, Steiner S2, Berent R3, Sinzinger H4. Vasa. 2016 Apr;45(2):125-32. doi: 10.1024/0301-1526/a000506.
Early non-invasive imaging of atherosclerosis and in particular the detection of lesions at risk with high specificity could significantly affect cardiovascular morbidity and mortality. Conventional nuclear medicine approaches, in particular using autologous radiolabeled lipoproteins, can be related to histopathological findings; however, they fail to identify lesions at risk. Positron emission tomography (PET) tracers with much better physical properties have been examined, the most detailed information being available for F-18-deoxyglucose (FDG) and F-18-sodium fluoride (NaF). These two approaches are sensitive to different biochemical mechanisms, i.e. inflammation and microcalcification. Initial enthusiasm, in particular for F-18-FDG, has disappeared, although for F-18-NaF there is some hope, but this is not a breakthrough. No tracer is available so far that is able to identify a specific characteristic of a lesion prone to rupture. Other PET tracers in the pipeline have been examined, mainly in experimental models and only a few in patients, but they failed to contribute significantly to early lesion discovery and do not support great expectations.