2-DG (2-Deoxy-D-glucose)

製品コードS4701 バッチS470110

印刷

化学情報

Chemical Structure 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
化学式

C6H12O5
分子量 164.16 CAS No. 154-17-6
Solubility (25°C)* 体外 Water 100 mg/mL (609.16 mM)
DMSO 33 mg/mL (201.02 mM)
Ethanol 5 mg/mL (30.45 mM)
* <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.

溶剤液（一定の濃度）を調合する

生物活性

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.
in vitro 2-Deoxy-D-glucose(2-DG) activates AKT function through phosphatidylinositol 3-kinase (PI3K) and is independent of glycolysis or mTOR inhibition. 2-DG treatments 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. 2-DG also induces time- and dose-dependent ERK phosphorylation[1]. 2-DG 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-DG (greater than 200 mg/kg) was largely ineffective in managing tumor growth. Side effects of 2-DG included elevated blood glucose levels, progressive weight loss with lethargy, and behavioral symptoms of hypoglycemia[2]. 2-DG 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]. 2-DG 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, 2-DG 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 2-DG induced a shift towards a non-amyloidogenic pathway. 2-DG 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].

プロトコル(参考用のみ)

細胞アッセイ 細胞株 H460 or H157 cells
濃度 5 mM
反応時間 48 h
実験の流れ

2×103 H460 or H157 cells are seeded in 96-well cell culture plates. Cells are treated with 5 mM 2-DG only, 5 or 10 μM IGF1R inhibitor II only, or a combination of 2-DG and IGF1R inhibitor II. Cell growth inhibition is determined after 48 h by the CellTiter 96® AQueous nonradioactive cell proliferation assay.
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.

カスタマーフィードバック

Data from [Data independently produced by , , Int J Oncol, 2018, 52(6):1899-1911]

Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

Tumor-derived Exosomal ENO2 Modulates Polarization of Tumor-associated Macrophages through Reprogramming Glycolysis to Promote Progression of Diffuse Large B-cell Lymphoma [ Int J Biol Sci, 2024, 20(3):848-863] PubMed: 38250157
Enhanced glycolysis-mediated energy production in alveolar stem cells is required for alveolar regeneration [ Cell Stem Cell, 2023, 30(8):1028-1042.e7] PubMed: 37541209
PD-1 instructs a tumor-suppressive metabolic program that restricts glycolysis and restrains AP-1 activity in T cell lymphoma [ Nat Cancer, 2023, 4(10):1508-1525] PubMed: 37723306
Xanthine dehydrogenase rewires metabolism and the survival of nutrient deprived lung adenocarcinoma cells by facilitating UPR and autophagic degradation [ Int J Biol Sci, 2023, 19(3):772-788] PubMed: 36778128
Targeting Aurora-A inhibits tumor progression and sensitizes thyroid carcinoma to Sorafenib by decreasing PFKFB3-mediated glycolysis [ Cell Death Dis, 2023, 14(3):224] PubMed: 36990998
Allosterically inhibited PFKL via prostaglandin E2 withholds glucose metabolism and ovarian cancer invasiveness [ Cell Rep, 2023, 42(10):113246] PubMed: 37831605
Targeting mitochondrial energetics reverses panobinostat- and marizomib-induced resistance in pediatric and adult high-grade gliomas [ Mol Oncol, 2023, 17(9):1821-1843] PubMed: 37014128
PDK4 rescues high-glucose-induced senescent fibroblasts and promotes diabetic wound healing through enhancing glycolysis and regulating YAP and JNK pathway [ Cell Death Discov, 2023, 9(1):424] PubMed: 38001078
Targeting mitochondrial energetics reverses panobinostat- and marizomib-induced resistance in pediatric and adult high-grade gliomas [ Mol Oncol, 2023, 17(9):1821-1843] PubMed: 37014128
Metabolic reprogramming of cancer-associated fibroblasts in pancreatic cancer contributes to the intratumor heterogeneity of PET-CT [ Comput Struct Biotechnol J, 2023, 21:2631-2639] PubMed: 37153537

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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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