Glucose metabolism; glycolysis; hexokinase; HSV-1; Antimetabolites; Antiviral Agents； 2 - DG targets hexokinase. It can be phosphorylated by hexokinase to form 2 - DG - 6 - phosphate, which accumulates in cells and inhibits hexokinase activity, thus blocking glycolysis. It also competitively inhibits phosphoglucose isomerase as 2 - DG - 6 - phosphate can compete with fructose - 6 - phosphate for phosphoglucose isomerase.

在 MCF-7 细胞中，4、8 或 16 mM 2-脱氧-D-葡萄糖 (2-DG) 以剂量和时间依赖性方式显着降低 ATP 水平，与 2-DG 的效果相当关于细胞生长。暴露于 4、8 或 16 mM 2-脱氧-D-葡萄糖 1、3 或 5 天，具体方式取决于剂量和时间 [1]。当施用 2-DG 时，戊糖磷酸途径 (PPP) 反应者上调，并且 6-磷酸终点脱氢酶产生更多的 NADPH。由于 NADPH 增加和谷胱甘肽合成酶表达上调，2-DG 还原型谷胱甘肽在 NB4 细胞中升高 [3]。

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在乳腺肿瘤细胞中，2 - DG以剂量和时间依赖的方式抑制细胞生长。它降低细胞活力，将细胞周期阻滞在G1/S期，并诱导细胞凋亡。其机制可能与抑制糖酵解有关，糖酵解受抑制导致ATP生成减少，活性氧（ROS）水平升高[1]
在白血病细胞中，2 - DG破坏代谢平衡，导致葡萄糖消耗和乳酸生成减少。它还会引起细胞内ATP水平下降和ROS增加，进而可能导致细胞死亡[3]

2-脱氧-D-葡萄糖（0.03%，w/w）推迟了乳腺癌可能的发生，并导致最终体重显着降低了 7% [1]。 2. 在提取过程中，2-脱氧-D-葡萄糖（3 mmol/kg，静脉注射）以剂量依赖性方式降低[2]。
注：尽管进行了大量的临床前和临床研究，2-DG在癌症和病毒治疗中的应用仍然有限。其快速代谢和短半衰期（根据Hansen等人的说法，在输注50 mg/kg2 DG后，其血浆半衰期仅为48分钟），使2-DG成为一种相对较差的候选药物。此外，必须以相对较高的浓度（≥5 mmol/L）给予2-DG，以与血糖竞争。根据Stein等人，在第1-14天口服45 mg/kg的剂量被定义为安全的，因为患者没有经历任何剂量限制毒性。值得注意的是，在60 mg/kg的剂量下，两名患者出现了3级剂量限制毒性——无症状QTc延长。根据Burckhardt等人和Stalder等人先前发表的研究，在暴露于2-DG的患者中，出现非特异性T波变平和QT延长，没有任何严重心律失常事件。[4]

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在脂多糖/右旋半乳糖（LPS/D - Gal）诱导的致死性肝损伤小鼠模型中，2 - DG处理可抑制血浆转氨酶升高，减轻组织病理学异常，提高小鼠存活率。它还能抑制促凋亡细胞因子TNF - α的产生、JNK的磷酸化、半胱天冬酶级联反应的激活以及TUNEL阳性凋亡肝细胞的数量[4]

ATP测定。使用ENLITEN ATP测定试剂盒（Promega Corporation，Kadison，WI）测定2-DG对细胞中ATP水平的影响，使用TD 20/20光度计（Turner Biosystem，Sunnyvale，CA）检测生物发光，并通过上述结晶紫法估计的细胞数标准化每个孔的ATP量。[1]

用MCF-7人癌症细胞研究葡萄糖代谢紊乱的信号通路，2-DG以剂量和时间依赖的方式降低细胞生长和细胞内ATP（P<0.01）。2-DG处理增加了磷酸化AMP活化蛋白激酶和Sirt-1的水平，并降低了磷酸化Akt（P<0.05）。这些研究支持这样一种假设，即DER在一定程度上通过限制葡萄糖的可用性来抑制致癌作用，并且能量代谢是ERMA用于化学预防的靶点。[1]

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对于乳腺肿瘤细胞，将不同浓度的2 - DG加入细胞培养基中，培养不同时间（如24h、48h、72h）。然后，通过MTT法检测细胞活力，利用碘化丙啶染色结合流式细胞术分析细胞周期。通过Annexin V - FITC/PI双染和流式细胞术检测细胞凋亡。通过基于荧光素酶的方法测量细胞内ATP水平，利用荧光探针检测ROS水平[1]
对于白血病细胞，将其在2 - DG存在下培养，定期测量培养基中的葡萄糖消耗量和乳酸生成量。通过基于荧光素酶的方法检测细胞内ATP水平，利用荧光探针检测ROS水平[3]

For the carcinogenesis study, ninety 21-day-old female Sprague-Dawley rats were injected i.p. with 50 mg of 1-methyl-1-nitrosourea per kilogram of body weight. Following injection, animals were ad libitum fed AIN-93G diet containing 0.00%, 0.02%, or 0.03% (w/w) 2-DG for 5 weeks. 2-DG decreased the incidence and multiplicity of mammary carcinomas and prolonged cancer latency (P < 0.05). The 0.02% dose of 2-DG had no effect on circulating levels of glucose, insulin, insulin-like growth factor-I, IGF binding protein-3, leptin, or body weight gain. [1]

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In the LPS/D - Gal - induced liver injury mouse model, 2 - DG is dissolved in normal saline. Mice are intraperitoneally injected with 2 - DG at a dose of 200 mg/kg once a day for 7 consecutive days. The control group is injected with the same volume of normal saline. Then, the plasma aminotransferase levels are measured, and the liver tissue is used for histopathological examination and TUNEL staining to detect apoptosis [4]

Absorption, Distribution and Excretion
WHEN THE RENAL EXCRETION OF 2-DEOXYGLUCOSE WAS STUDIED IN DOGS AND RATS BY CONVENTIONAL CLEARANCE AND STOP-FLOW TECHNIQUES, IT WAS REABSORBED BY THE RENAL TUBULES AT AN AVG OF 68-89% OF THE FILTERED LOADS AND THE REABSORPTION SITE WAS IN THE PROXIMAL TUBULES.

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Metabolism / Metabolites
2-DEOXY-D-GLUCOSE WAS CONVERTED TO THE 6-PHOSPHATE IN MOUSE TESTIS AND LIVER AFTER IP INJECTION OF 50 MG/KG BODY WT DAILY FOR 7 DAYS.

Interactions
2-DEOXYGLUCOSE INJECTED INTRAPERITONEALLY IN RATS IN LARGE DOSES CAUSED CHANGES IN THE ELECTRORETINOGRAM CONSISTING OF A DECR IN BOTH ALPHA- AND BETA-WAVES. THE EFFECT WAS ANTAGONIZED BY D-GLUCOSE. Grant, W. M. Toxicology of the Eye. 2nd ed. Springfield, Illinois: Charles C. Thomas, 1974., p. 353

SIMULTANEOUS ADMIN OF GLUCOSE @ DOSE EXCEEDING ITS MAX TUBULAR TRANSPORT CAPACITY INHIBITED TUBULAR REABSORPTION OF 2-DEOXYGLUCOSE. THUS, THE PROCESS OF TUBULAR REABSORPTION IS PROBABLY THE SAME AS THAT FOR GLUCOSE. WOOSLEY RL ET AL; RENAL TUBULAR TRANSPORT OF 2-DEOXY-D-GLUCOSE IN DOGS AND RATS; J PHARMACOL EXP THER 173(1) 13 (1970)

IN ANESTROUS SHEEP, 2-DEOXYGLUCOSE INFUSION INHIBITED LH RELEASE INDUCED BY ESTRADIOL BUT NOT BY LH-RH. CRUMP AD ET AL; ESTRADIOL-INDUCED LUTEINIZING HORMONE (LH) RELEASE IS INHIBITED BY 2-DEOXYGLUCOSE INFUSION IN SHEEP; J PHYSIOL (LONDON) 330: 93P (1982)

2-DEOXY-D-GLUCOSE INHIBITED REPAIR OF POTENTIALLY LETHAL DAMAGE INDUCED BY X-RAYS IN MOUSE EHRLICH ASCITES TUMOR CELLS.

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Non-Human Toxicity Excerpts
2-DEOXYGLUCOSE INJECTED INTRAPERITONEALLY IN RATS IN LARGE DOSES CAUSED CHANGES IN THE ELECTRORETINOGRAM CONSISTING OF A DECR IN BOTH ALPHA- AND BETA-WAVES. Grant, W. M. Toxicology of the Eye. 2nd ed. Springfield, Illinois: Charles C. Thomas, 1974., p. 353
...120 MG/DAY /GIVEN TO RAT/ FROM THE 9TH THROUGH THE 20TH GESTATIONAL DAY... RESORPTIONS WERE 69% AND THE SURVIVING FETUSES WERE ALL MALFORMED. ANOPHTHALMIA, CLEFT LIP AND PALATE AND LESIONS OF THE EXTREMITIES WERE OBSERVED. ...GAVE 1 G/KG ON DAYS 8, 9, 10 OR 11 & FOUND NO MALFORMATIONS IN SURVIVING RAT FETUSES.

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Interactions
2-DEOXYGLUCOSE INJECTED INTRAPERITONEALLY IN RATS IN LARGE DOSES CAUSED CHANGES IN THE ELECTRORETINOGRAM CONSISTING OF A DECR IN BOTH ALPHA- AND BETA-WAVES. THE EFFECT WAS ANTAGONIZED BY D-GLUCOSE.
SIMULTANEOUS ADMIN OF GLUCOSE @ DOSE EXCEEDING ITS MAX TUBULAR TRANSPORT CAPACITY INHIBITED TUBULAR REABSORPTION OF 2-DEOXYGLUCOSE. THUS, THE PROCESS OF TUBULAR REABSORPTION IS PROBABLY THE SAME AS THAT FOR GLUCOSE.
IN ANESTROUS SHEEP, 2-DEOXYGLUCOSE INFUSION INHIBITED LH RELEASE INDUCED BY ESTRADIOL BUT NOT BY LH-RH.
2-DEOXY-D-GLUCOSE INHIBITED REPAIR OF POTENTIALLY LETHAL DAMAGE INDUCED BY X-RAYS IN MOUSE EHRLICH ASCITES TUMOR CELLS.
For more Interactions (Complete) data for 2-DEOXY-D-GLUCOSE (6 total), please visit the HSDB record page.

[1]. Zhu Z, et al. 2-Deoxyglucose as an energy restriction mimetic agent: effects on mammary carcinogenesis and on mammary tumor cell growth in vitro. Cancer Res. 2005 Aug 1;65(15):7023-30.
[2]. Ueyama A, et al. Nonradioisotope assay of glucose uptake activity in rat skeletal muscle using enzymatic measurement of 2-deoxyglucose 6-phosphate in vitro and in vivo. Biol Signals Recept. 2000 Sep-Oct;9(5):267-74.
[3]. Miwa H, et al. Leukemia cells demonstrate a different metabolic perturbation provoked by 2-deoxyglucose. Oncol Rep. 2013 May;29(5):2053-7
[4]. Int J Mol Sci. 2020 Jan; 21(1): 234.

2-deoxy-D-glucose has been reported in Streptomyces nigra with data available.
2-Deoxy-D-glucose is a non-metabolizable glucose analog in which the hydroxyl group at position 2 of glucose is replaced by hydrogen, with potential glycolysis inhibiting and antineoplastic activities. Although the exact mechanism of action has yet to be fully elucidated, upon administration of 2-deoxy-D-glucose (2-DG), this agent competes with glucose for uptake by proliferating cells, such as tumor cells. 2-DG inhibits the first step of glycolysis and therefore prevents cellular energy production, which may result in decreased tumor cell proliferation.
2-deoxy-D-glucose is a metabolite found in or produced by Saccharomyces cerevisiae.
2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.

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Therapeutic Uses
Antimetabolites; Antiviral Agents
MEDICATION (VET): TOPICAL TREATMENT OF HERPES GENITALIS IN FEMALE GUINEA PIGS WITH 2-DEOXY-D-GLUCOSE IN EITHER AGAROSE GELS OR MICONAZOLE NITRATE OINTMENT FAILED TO PREVENT DEVELOPMENT OF GENITAL LESIONS OR TO REDUCE THE MEAN TITERS OF RECOVERABLE VIRUS IN VAGINAL SWABS FROM INFECTED ANIMALS.

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2 - DG is a glucose analog, which is the first - proposed calorie restriction mimetic. By blocking glycolysis, it can mimic the metabolic, hormonal, and physiological effects of calorie restriction, and has a beneficial effect on chronic pathological processes such as cancer, Alzheimer 's disease, and Parkinson 's disease. It can also protect against acute ischemia injury in rats. Its role in inhibiting glycolysis is of great significance for the study of tumor cell metabolism and the development of anti - cancer strategies [4]

C6H12O5

164.1565

164.068

C, 43.90; H, 7.37; O, 48.73

154-17-6

2-Deoxy-D-glucose-d;188004-07-1;2-Deoxy-D-glucose-13C;201612-55-7;2-Deoxy-D-glucose-13C-1;119897-50-6

108223

White to off-white solid powder

1.4±0.1 g/cm3

456.7±45.0 °C at 760 mmHg

146-147ºC

244.1±25.2 °C

0.0±2.5 mmHg at 25°C

1.534

Endogenous metabolite

-3.07

97.99

4

5

5

11

116

3

O([H])[C@]([H])([C@@]([H])(C([H])([H])O[H])O[H])[C@@]([H])(C([H])([H])C([H])=O)O[H]

VRYALKFFQXWPIH-PBXRRBTRSA-N

InChI=1S/C6H12O5/c7-2-1-4(9)6(11)5(10)3-8/h2,4-6,8-11H,1,3H2/t4-,5-,6+/m1/s1

2-Deoxy-D-arabinohexose

2-deoxy-D-glucose; Deoxyglucose; 154-17-6; 2-Deoxy-D-arabino-hexose; 2-Desoxy-D-glucose; 2-DG; (3R,4S,5R)-3,4,5,6-tetrahydroxyhexanal; 2-Deoxy-D-mannose;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ≥ 24 mg/mL (~146.20 mM)

配方 1 中的溶解度: 130 mg/mL (791.91 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶。

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配方 2 中的溶解度: ~130 mg/mL (~792 mM) in PBS

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。