Size | Price | Stock | Qty |
---|---|---|---|
5g |
|
||
10g |
|
||
Other Sizes |
|
Purity: ≥98%
Targets |
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.
|
---|---|
ln Vitro |
In MCF-7 cells, 2-Deoxy-D-glucose (2-DG), 4, 8, or 16 mM, dramatically decreased ATP levels in a dose- and time-dependent manner that was comparable to the effect of 2-DG on cell growth. exposure to 4, 8 or 16 mM 2-Deoxy-D-glucose 1, 3 or for 5 days in a way that depends on the dose and the amount of time [1]. When 2-DG is administered, pentose phosphate pathway (PPP) responders are upregulated, and 6-phosphate endpoint dehydrogenase produces more NADPH. The 2-DG reduced form of glutathione is elevated in NB4 cells due to an increase in NADPH and an upregulation of glutathione synthetase expression [3].
In mammary tumor cells, 2 - DG inhibits cell growth in a dose - and time - dependent manner. It reduces cell viability, blocks cell cycle progression at the G1/S phase, and induces apoptosis. The mechanism may be related to the inhibition of glycolysis, which leads to a decrease in ATP production and an increase in reactive oxygen species (ROS) levels [1] In leukemia cells, 2 - DG disrupts the metabolic balance, leading to a decrease in glucose consumption and lactate production. It also causes a decrease in intracellular ATP levels and an increase in ROS, which may lead to cell death [3] |
ln Vivo |
2-Deoxy-D-glucose (0.03%, w/w) postponed the possible beginning of breast cancer and led to a statistically significant 7% reduction in final body weight [1]. 2. During extraction, 2-Deoxy-D-glucose (3 mmol/kg, iv) is lowered in a dose-dependent manner [2].
Note: Despite the numerous preclinical and clinical studies, the use of 2-DG in cancer and viral treatment has been limited. Its rapid metabolism and short half-life (according to Hansen et al., after treatment with infusion of 50 mg/kg2-DG, its plasma half-life was only 48 min), make 2-DG a relatively poor drug candidate. Moreover, 2-DG must be given at relatively high concentrations (≥5 mmol/L) to compete with blood glucose. According to Stein et al., the dose of 45 mg/kg received orally on days 1–14 was defined as safe because patients did not experience any dose-limiting toxicities. Notably, at the dose of 60 mg/kg, two patients experienced dose-limiting toxicity of grade 3–asymptomatic QTc prolongation. According to former studies published by Burckhardt et al. and Stalder et al., among patients exposed to 2-DG, non-specific T wave flattening and QT prolongation, without any event of severe arrhythmia, developed.[4] In lipopolysaccharide/d - galactosamine (LPS/D - Gal) - induced lethal liver injury mouse models, 2 - DG treatment suppresses the elevation of plasma aminotransferases, alleviates histopathological abnormalities, and improves the survival rate of mice. It also suppresses the production of pro - apoptotic cytokine TNF - α, the phosphorylation of JNK, the activation of the caspase cascade, and the number of TUNEL - positive apoptotic hepatocytes [4] |
Enzyme Assay |
ATP assay. The effect of 2-DG on ATP level in the cells was determined using an ENLITEN ATP assay kit (Promega Corporation, Kadison, WI), the bioluminescence was detected using a TD 20/20 luminometer (Turner Biosystem, Sunnyvale, CA), and the amount of ATP per well was standardized by the cell number estimated by crystal violet method described above.[1]
|
Cell Assay |
Using MCF-7 human breast cancer cells to investigate the signaling pathways perturbed by disruption of glucose metabolism, 2-DG reduced cell growth and intracellular ATP in a dose- and time-dependent manner (P < 0.01). Treatment with 2-DG increased levels of phosphorylated AMP-activated protein kinase and Sirt-1 and reduced phosphorylated Akt (P < 0.05). These studies support the hypothesis that DER inhibits carcinogenesis, in part, by limiting glucose availability and that energy metabolism is a target for the development of ERMA for chemoprevention.[1]
For mammary tumor cells, different concentrations of 2 - DG are added to the cell culture medium, and the cells are cultured for different time periods (such as 24h, 48h, 72h). Then, the cell viability is detected by the MTT method, and the cell cycle is analyzed by flow cytometry using propidium iodide staining. Apoptosis is detected by Annexin V - FITC/PI double - staining and flow cytometry. Intracellular ATP levels are measured by a luciferase - based assay, and ROS levels are detected by fluorescent probes [1] For leukemia cells, they are cultured in the presence of 2 - DG, and the glucose consumption and lactate production in the culture medium are measured at regular intervals. Intracellular ATP levels are detected by a luciferase - based assay, and ROS levels are detected by fluorescent probes [3] |
Animal Protocol |
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]
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] |
ADME/Pharmacokinetics |
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. 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. |
Toxicity/Toxicokinetics |
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. 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. 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. |
References |
[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. |
Additional Infomation |
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. 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. 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] |
Molecular Formula |
C6H12O5
|
---|---|
Molecular Weight |
164.1565
|
Exact Mass |
164.068
|
Elemental Analysis |
C, 43.90; H, 7.37; O, 48.73
|
CAS # |
154-17-6
|
Related CAS # |
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
|
PubChem CID |
108223
|
Appearance |
White to off-white solid powder
|
Density |
1.4±0.1 g/cm3
|
Boiling Point |
456.7±45.0 °C at 760 mmHg
|
Melting Point |
146-147ºC
|
Flash Point |
244.1±25.2 °C
|
Vapour Pressure |
0.0±2.5 mmHg at 25°C
|
Index of Refraction |
1.534
|
Source |
Endogenous metabolite
|
LogP |
-3.07
|
Hydrogen Bond Donor Count |
4
|
Hydrogen Bond Acceptor Count |
5
|
Rotatable Bond Count |
5
|
Heavy Atom Count |
11
|
Complexity |
116
|
Defined Atom Stereocenter Count |
3
|
SMILES |
O([H])[C@]([H])([C@@]([H])(C([H])([H])O[H])O[H])[C@@]([H])(C([H])([H])C([H])=O)O[H]
|
InChi Key |
VRYALKFFQXWPIH-PBXRRBTRSA-N
|
InChi Code |
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
|
Chemical Name |
2-Deoxy-D-arabinohexose
|
Synonyms |
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;
|
HS Tariff Code |
2934.99.9001
|
Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
Solubility (In Vitro) |
H2O : ≥ 24 mg/mL (~146.20 mM)
|
---|---|
Solubility (In Vivo) |
Solubility in Formulation 1: 130 mg/mL (791.91 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
Solubility in Formulation 2: ~130 mg/mL (~792 mM) in PBS  (Please use freshly prepared in vivo formulations for optimal results.) |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 6.0916 mL | 30.4581 mL | 60.9162 mL | |
5 mM | 1.2183 mL | 6.0916 mL | 12.1832 mL | |
10 mM | 0.6092 mL | 3.0458 mL | 6.0916 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
NCT05314933 | COMPLETED | Drug: 2-Deoxyglucose Other: Placebo |
Acute Nasopharyngitis | G.ST Antivirals GmbH | 2022-03-03 | Phase 1 |
NCT02765204 | COMPLETED | Drug: Dapagliflozin Drug: Saxagliptin Drug: Glucose |
Diabetes Mellitus, Type 2 | Uppsala University | 2016-03 | Phase 4 |
NCT01778218 | COMPLETED | Radiation: Radiolabeled (99Tc) EC-DG (ethylenedicysteine-deoxyglucose |
Coronary Artery Disease | Cell>Point LLC | 2013-01 | Phase 2 |
NCT00865319 | COMPLETED | Radiation: Radiolabeled (99Tc) EC-DG (ethylenedicysteine-deoxyglucose) Radiation: 18 F fluorodeoxyglucose |
Non Small Cell Lung Cancer | Cell>Point LLC | 2009-06 | Phase 2 |
NCT02077699 | COMPLETED | Dietary Supplement: Lactobacillus casei DG | Irritable Bowel Syndrome | SOFAR S.p.A. | 2012-03 | Phase 4 |