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How to Cite 1. For In-Text Citation (Materials & Methods): 2. For Key Resources Table: |
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| Formula | C6H12O5 |
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| Molecular Weight | 164.16 | CAS No. | 154-17-6 | ||||
| Solubility (25°C)* | In vitro | DMSO | 33 mg/mL (201.02 mM) | ||||
| Water | 33 mg/mL (201.02 mM) | ||||||
| Ethanol | Insoluble | ||||||
| In vivo (Add solvents to the product individually and in order) |
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* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.) |
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| Description | An analog of glucose, 2-Deoxy-D-glucose (2-DG) is a glycolytic inhibitor with antiviral activity. It induces apoptosis and inhibits Herpes Simplex Virus type-1 (HSV-1) receptor expression. | |
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| In vitro | 2-Deoxy-D-glucose (2-DG) activates AKT function through phosphatidylinositol 3-kinase (PI3K) and is independent of glycolysis or mTOR inhibition. Its treatments disrupt the binding between insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 (IGFBP3) so that the free form of IGF-1 could be released from the IGF-1·IGFBP3 complex to activate IGF-1 receptor (IGF1R) signaling. 2-DG-induced activation of many survival pathways can be jointly attenuated through IGF1R inhibition. This compound also induces time- and dose-dependent ERK phosphorylation[1]. It is readily transported into cells and is phosphorylated by hexokinase, but cannot be metabolized further and accumulates in the cell. This leads to ATP depletion and the induction of cell-death[2]. 2DG significantly suppresses proliferation, causes apoptosis and reduces migration of murine endothelial cells, inhibiting formation of lamellipodia and filopodia and causing disorganization of F-actin filaments in murine endothelial cell[5]. | |
| In vivo | Treatment of cancer patients with relatively high doses of 2-Deoxy-D-glucose (2-DG) (greater than 200 mg/kg) was largely ineffective in managing tumor growth. Side effects of this compound included elevated blood glucose levels, progressive weight loss with lethargy, and behavioral symptoms of hypoglycemia[2]. It enhances isoflurane-induced loss of righting reflex in mice. By reducing metabolism, 2-DG treatment can decrease body temperature in rodent, enhancing sensitivity to anesthetics[3]. A diet containing it significantly increased serum ketone body level and brain expression of enzymes required for ketone body metabolism. The 2-DG-induced maintenance of mitochondrial bioenergetics was paralleled by simultaneous reduction in oxidative stress. Further, treated mice exhibited a significant reduction of both amyloid precursor protein (APP) and amyloid beta (Aβ) oligomers, which was paralleled by significantly increased α-secretase and decreased γ-secretase expression, indicating that this compound induced a shift towards a non-amyloidogenic pathway. It increased expression of genes involved in Aβ clearance pathways, degradation, sequestering, and transport. Concomitant with increased bioenergetic capacity and reduced β-amyloid burden, 2-DG significantly increased expression of neurotrophic growth factors, BDNF and NGF, thus reduces pathology in female mouse model of Alzheimer's disease[4]. |
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Data from [ , , Int J Oncol, 2018, 52(6):1899-1911 ]
| The noncanonical function of liver-type phosphofructokinase potentiates the efficacy of HDAC inhibitors in cancer [ Signal Transduct Target Ther, 2025, 10(1):341] | PubMed: 41083431 |
| Mitochondrial-cytochrome c oxidase II promotes glutaminolysis to sustain tumor cell survival upon glucose deprivation [ Nat Commun, 2025, 16(1):212] | PubMed: 39747079 |
| Simvastatin overcomes the pPCK1-pLDHA-SPRINGlac axis-mediated ferroptosis and chemo-immunotherapy resistance in AKT-hyperactivated intrahepatic cholangiocarcinoma [ Cancer Commun (Lond), 2025, 10.1002/cac2.70036] | PubMed: 40443016 |
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| Glycolysis Induces Abnormal Transcription Through Histone Lactylation in T-lineage Acute Lymphoblastic Leukemia [ Genomics Proteomics Bioinformatics, 2025, qzaf029] | PubMed: 40193528 |
| HIF-1-mediated macrophage metabolic reprogramming promotes AKI to CKD transition [ Int J Biol Sci, 2025, 21(13):5936-5955] | PubMed: 41079928 |
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