DMOG (Synonyms: Dimethyloxallyl Glycine) |
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Catalog No.GC16973
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DMOG is a competitive and cell-permeable hypoxia-inducible factor prolyl hydroxylase (HIF-PH) inhibitor, as well as an activator of hypoxia-inducible factor-1α (HIF-1α).
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 89464-63-1
Sample solution is provided at 25 µL, 10mM.
DMOG is a competitive and cell-permeable hypoxia-inducible factor prolyl hydroxylase (HIF-PH) inhibitor, as well as an activator of hypoxia-inducible factor-1α (HIF-1α)[1]. DMOG stabilizes HIF-1α and prevents its prolyl hydroxylation-mediated degradation by inhibiting HIF-PH enzymatic activity, thereby stabilizing HIF-1α and activating downstream target gene expression at both the cellular and animal levels[2]. DMOG is commonly used in research areas including HIF signaling pathway regulation, ischemia-reperfusion injury protection, angiogenesis, and neuroprotection[3,4].
In vitro, treatment of rat bone marrow mesenchymal stromal cells (BM-MSCs) with DMOG (500, 1000μM) for 72h significantly upregulated C-X-C chemokine receptor type 4 (CXCR4) protein expression compared with the control group[5]. DMOG (0.5mM) pretreatment of PC12 and HCT116 cells for 0.5h significantly inhibited mitochondrial respiration and activated glycolytic activity[6].
In vivo, Sprague-Dawley rats exposed to chronic hypoxia (10% O2) and treated with DMOG (100mg/kg; once daily; i.p.) for 4 weeks showed significant stabilization of myocardial HIF-1α protein levels[7]. In BALB/c mice pretreated with DMOG (8mg/mouse; i.p.) 2h prior to lipopolysaccharide (LPS)-induced endotoxic shock, DMOG significantly improved survival rate, decreased serum TNF-α levels, and increased IL-10 levels[8].
References:
[1] Zhang Y, Cai W, Ren Z, et al. Chiral supramolecular hydrogel loaded with dimethyloxalyglycine to accelerate chronic diabetic wound healing by promoting cell proliferation and angiogenesis[J]. Gels, 2022, 8(7): 437.
[2] Ding H, Gao Y S, Wang Y, et al. Dimethyloxaloylglycine increases the bone healing capacity of adipose-derived stem cells by promoting osteogenic differentiation and angiogenic potential[J]. Stem cells and development, 2014, 23(9): 990-1000.
[3] Sen T, Sen N. Treatment with an activator of hypoxia-inducible factor 1, DMOG provides neuroprotection after traumatic brain injury[J]. Neuropharmacology, 2016, 107: 79-88.
[4] Ockaili R, Natarajan R, Salloum F, et al. HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation[J]. American Journal of Physiology-Heart and Circulatory Physiology, 2005, 289(2): H542-H548.
[5] Yinfei W, Aiping J, Chao F, et al. DFO and DMOG up-regulate the expression of CXCR4 in bone marrow mesenchymal stromal cells[J]. Die Pharmazie-An International Journal of Pharmaceutical Sciences, 2013, 68(10): 835-838.
[6] Zhdanov A V. HIF-independent inhibition of mitochondrial function by DMOG: Immediate–early effects and long-term consequences[J]. Biochimica et Biophysica Acta (BBA)-Bioenergetics, 2014.
[7] Zhang S, Ma K, Liu Y, et al. Stabilization of Hypoxia-inducible Factor by DMOG Inhibits Development of Chronic Hypoxia–Induced Right Ventricular Remodeling[J]. Journal of cardiovascular pharmacology, 2016, 67(1): 68-75.
[8] Hams E, Saunders S P, Cummins E P, et al. The hydroxylase inhibitor dimethyloxallyl glycine attenuates endotoxic shock via alternative activation of macrophages and IL-10 production by B1 cells[J]. Shock, 2011, 36(3): 295-302.
| Cell experiment [1]: | |
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Cell lines |
BM-MSCs |
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Preparation Method |
BM-MSCs were treated with DMOG (500, 1000μM) for 72h, then cells were collected and subjected to Western blot analysis using anti-CXCR4 antibodies. |
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Reaction Conditions |
500, 1000μM; 72h |
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Applications |
Treatment wtih DMOG significantly upregulated CXCR4 protein expression levels in BM-MSCs. |
| Animal experiment [2]: | |
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Animal models |
BALB/c mice |
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Preparation Method |
BALB/c mice were pretreated with DMOG (8mg/mouse; i.p.) for 2h, followed by LPS (10mg/kg; i.p.) injection to induce endotoxic shock. Survival was monitored, and serum levels of TNF-α and IL-10 were measured at 3h after LPS treatment by MSD multiplex cytokine array and ELISA, respectively. |
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Dosage form |
8mg/mouse; i.p. |
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Applications |
Treatment with DMOG significantly improved the survival rate of mice with endotoxin shock, reduced serum TNF-α, and increased IL-10 levels. |
References: [1] Yinfei W, Aiping J, Chao F, et al. DFO and DMOG up-regulate the expression of CXCR4 in bone marrow mesenchymal stromal cells[J]. Die Pharmazie-An International Journal of Pharmaceutical Sciences, 2013, 68(10): 835-838. [2] Hams E, Saunders S P, Cummins E P, et al. The hydroxylase inhibitor dimethyloxallyl glycine attenuates endotoxic shock via alternative activation of macrophages and IL-10 production by B1 cells[J]. Shock, 2011, 36(3): 295-302. | |
| Cas No. | 89464-63-1 | SDF | |
| Synonyms | Dimethyloxallyl Glycine | ||
| Chemical Name | methyl 2-[(2-methoxy-2-oxoethyl)amino]-2-oxoacetate | ||
| Canonical SMILES | COC(=O)CNC(=O)C(=O)OC | ||
| Formula | C6H9NO5 | M.Wt | 175.14 |
| Solubility | DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 30 mg/ml,PBS (pH 7.2): 10 mg/ml | Storage | Store at -20°C |
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.7097 mL | 28.5486 mL | 57.0972 mL |
| 5 mM | 1.1419 mL | 5.7097 mL | 11.4194 mL |
| 10 mM | 571 μL | 2.8549 mL | 5.7097 mL |
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Quality Control & SDS
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- Purity: >98.00% Appearance: A solid
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Average Rating: 5 (Based on Reviews and 30 reference(s) in Google Scholar.)