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受注:045-509-1970 |
技術サポート:tech@selleck.co.jp 平日9:00〜18:00 1営業日以内にご連絡を差し上げます |
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Synonyms | 2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose | Storage (From the date of receipt) |
3 years -20°C powder 1 years -80°C in solvent |
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| 化学式 | C6H12O5 |
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| 分子量 | 164.16 | CAS No. | 154-17-6 | ||||||||
| Solubility (25°C)* | 体外 | DMSO | 33 mg/mL (201.02 mM) | ||||||||
| Water | 33 mg/mL (201.02 mM) | ||||||||||
| Ethanol | 5.5 mg/mL (33.5 mM) | ||||||||||
| 体内 (毎回新しく調製した物を用意してください) |
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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. |
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| 製品説明 | 2-DG (2-Deoxy-D-glucose), an analog of glucose, is a glycolytic inhibitor with antiviral activity. 2-Deoxy-D-glucose 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. It disrupts 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]. Its diet 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 it induced a shift towards a non-amyloidogenic pathway. This compound increased expression of genes involved in Aβ clearance pathways, degradation, sequestering, and transport. Concomitant with increased bioenergetic capacity and reduced β-amyloid burden, it significantly increased expression of neurotrophic growth factors, BDNF and NGF, thus reduces pathology in female mouse model of Alzheimer's disease[4]. |
| 細胞アッセイ | 細胞株 | H460 or H157 cells |
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| 濃度 | 5 mM | |
| 反応時間 | 48 h | |
| 実験の流れ | H460 or H157 cells (2×103) are seeded in 96-well cell culture plates and treated with 5 mM 2-Deoxy-D-glucose (2-DG) only, 5 or 10 μM IGF1R inhibitor II only, or a combination of it and IGF1R inhibitor II. Cell growth inhibition is determined after 48 h by the CellTiter 96® AQueous nonradioactive cell proliferation assay. |
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| 動物実験 | 動物モデル | Adult C57BL/6J mice |
| 投薬量 | 1000 mg/kg | |
| 投与方法 | i.p. |
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Data from [Data independently produced by , , Int J Oncol, 2018, 52(6):1899-1911]
| 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 |
| Aldehyde Dehydrogenase 2 Lactylation Aggravates Mitochondrial Dysfunction by Disrupting PHB2 Mediated Mitophagy in Acute Kidney Injury [ Adv Sci (Weinh), 2025, 12(8):e2411943] | PubMed: 39737891 |
| A CD147-targeted small-molecule inhibitor potentiates gemcitabine efficacy by triggering ferroptosis in pancreatic ductal adenocarcinoma [ Cell Rep Med, 2025, 6(8):102292] | PubMed: 40834852 |
| PDK4-driven lactate accumulation facilitates LPCAT2 lactylation to exacerbate sepsis-induced acute lung injury [ Cell Death Differ, 2025, 10.1038/s41418-025-01585-6] | PubMed: 41057687 |
| 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 |
| Vitamin D impedes eosinophil chemotaxis via inhibiting glycolysis-induced CCL26 expression in eosinophilic chronic rhinosinusitis with nasal polyps [ Cell Commun Signal, 2025, 23(1):104] | PubMed: 39985085 |
| Glycolysis regulates palatal mesenchyme proliferation through Pten-Glut1 axis via Pten classical and non-classical pathways [ Cell Biol Toxicol, 2025, 41(1):53] | PubMed: 40014184 |
| MTFR1 phosphorylation-activated adaptive mitochondrial fusion is essential for colon cancer cell survival during glucose deprivation [ Neoplasia, 2025, 63:101159] | PubMed: 40121946 |
長期の保管のために-20°Cの下で製品を保ってください。
人間や獣医の診断であるか治療的な使用のためにでない。
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