ホームページ Metabolism Carbohydrate Metabolism modulator - Apoptosis related activator - HSV inhibitor 2-DG (2-Deoxy-D-glucose) For research use only.

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

別名：2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose

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.

2-DG (2-Deoxy-D-glucose)化学構造

CAS No. 154-17-6

サイズ 価格(税別) 在庫状況
10mM (1mL in DMSO) JPY 29500 国内在庫あり
JPY 22000 国内在庫あり
JPY 38500 国内在庫あり
JPY 100500 国内在庫なし(納期7~10日)
JPY 445500 国内在庫なし(納期7~10日)

代表番号: 045-509-1970|電子メール：[email protected]
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2-DG (2-Deoxy-D-glucose)と併用されることが多い化合物

Albendazole

2-Deoxy-D-glucose and Albendazole combination use exhibits high efficiency in treating human echinococcosis.

Xin Q, et al. PLoS Negl Trop Dis. 2022 Jul 18;16(7):e0010618.

Fenofibrate

2-Deoxy-D-glucose and Fenofibrate induce necrotic and apoptotic cell death in different tumor cell lines.

Liu H, et al. Oncotarget. 2016 Jun 14;7(24):36461-36473.

Venetoclax (ABT-199)

2-Deoxy-D-glucose and Venetoclax induce apoptosis in multiple myeloma cell lines.

Halliez M, et al. Blood (2013) 122 (21): 1921.

Metformin

2-Deoxy-D-glucose and Metformin enhance tumor cell ablation upon Cobalt60 radiation treatment in breast cancer cell lines.

Chatterjee S, et al. Breast Cancer (Dove Med Press). 2015 Aug 31;7:251-65.

Doxorubicin

2-DG and Doxorubicin lower glutathione, increase oxidation, lipid peroxidation, and cytotoxicity in T47D breast cancer cells.

Mustafa EH, et al. Asian Pac J Cancer Prev. 2015;16(8):3213-3222.

2-DG (2-Deoxy-D-glucose)関連製品

Carbohydrate Metabolism阻害剤の選択性比較

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.
Targets
glycolysis [1]
In Vitro
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].
細胞実験 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.
In Vivo
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].
動物実験 動物モデル Adult C57BL/6J mice
投与量 1000 mg/kg
投与経路 i.p.
NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02558140 Completed
Neoplasms
Hoffmann-La Roche
 October 11 2015 Phase 1
NCT01998841 Completed
Alzheimer''s Disease
Genentech Inc.|Banner Alzheimer''s Institute|National Institute on Aging (NIA)
 December 20 2013 Phase 2

化学情報

分子量 164.16 化学式

C6H12O5
CAS No. 154-17-6 SDF Download 2-DG (2-Deoxy-D-glucose) SDFをダウンロードする
Smiles C(C=O)C(C(C(CO)O)O)O
保管

In vitro
Batch:

DMSO : 33 mg/mL ( (201.02 mM)； 吸湿したDMSOは溶解度を減少させます。新しいDMSOをご使用ください。)

Water : 33 mg/mL

Ethanol : 5.5 mg/mL

モル濃度計算器

in vivo
Batch:

Add solvents to the product individually and in order.

投与溶液組成計算機

実験計算

モル濃度計算器

質量 濃度 体積 分子量

投与溶液組成計算機(クリア溶液)

ステップ１：実験データを入力してください。（実験操作によるロスを考慮し、動物数を1匹分多くして計算・調製することを推奨します）

mg/kg g μL 匹

ステップ２：投与溶媒の組成を入力してください。（ロット毎に適した溶解組成が異なる場合があります。詳細については弊社までお問い合わせください）

% DMSO % % Tween 80 % ddH2O
%DMSO %

計算結果：

投与溶媒濃度： mg/ml;

DMSOストック溶液調製方法： mg 試薬を μL DMSOに溶解する（濃度 mg/mL, 注：濃度が当該ロットのDMSO溶解度を超える場合はご連絡ください。 )

投与溶媒調製方法：Take μL DMSOストック溶液に μL PEG300，を加え、完全溶解後μL Tween 80，を加えて完全溶解させた後 μL ddH2O，を加え完全に溶解させます。

投与溶媒調製方法：μL DMSOストック溶液に μL Corn oil，を加え、完全溶解。

注意：１.ストック溶液に沈殿、混濁などがないことをご確認ください；
２.順番通りに溶剤を加えてください。次のステップに進む前に溶液に沈殿、混濁などがないことを確認してから加えてください。ボルテックス、ソニケーション、水浴加熱など物理的な方法で溶解を早めることは可能です。

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