Uridine 5′-diphosphoglucose
Based on 9 publication(s) in Google Scholar
Uridine 5’-diphosphoglucose (UDP-glucose), secreted by cardiomyocytes during ischemia and reperfu, is a potent agonist of the proinflammatory P2Y14 receptor. It acts an important role in the regulation of inflammation and neutrophil polarization in neutrophils. Uridine 5’-diphosphoglucose is also the precursor of glucose-containing oligosaccharides, polysaccharides, glycoproteins, and glycolipids in animal tissues and in some microorganisms. Uridine 5’-diphosphoglucose is promising for research in counteracting myocardial infarction/reperfusion (MIR)-induced inflammation in the heart tissue.
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- CAS 番号: 133-89-1
- 分子式: C15H24N2O17P2
- 分子量:566.30
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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MedChemExpress（MCE）の使用を引用している文献 Uridine 5′-diphosphoglucose
More- Mol Plant. 2025 Dec 13:S1674-2052(25)00435-6. [Abstract]
- J Am Chem Soc. 2020 Sep 16;142(37):16039-16050. [Abstract]
- Cell Rep. 2025 Nov 18;44(12):116577. [Abstract]
- BMC Biotechnol. 2026 Apr 15;26(1):69. [Abstract]
- BMC Cancer. 2025 Jun 1;25(1):982. [Abstract]
- Clin Immunol. 2024 Aug:265:110300. [Abstract]
- SSRN. 2024 Jul 16.
- Evid Based Complement Alternat Med. 2022 Nov 23:2022:5227335. [Abstract]
- Research Square Preprint. 2021 Nov.
Customer Validation & Images
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WB
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RT-PCR
Endogenous Metabolite アイソフォーム固有の製品をすべて表示
MoreP2Y Receptor アイソフォーム固有の製品をすべて表示
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生物活性
製品説明
IC50 & Target
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Human Endogenous Metabolite |
P2Y14 Receptor |
Microbial Metabolite |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| COS-7 | EC50 |
0.261 μM
Compound: 1
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Agonist activity at human P2Y14 receptor expressed in human COS7 cells
Agonist activity at human P2Y14 receptor expressed in human COS7 cells
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[PMID: 19502066] |
| COS-7 | EC50 |
0.35 μM
Compound: 1
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Agonist activity at human P2Y14 expressed in COS7 cells assessed as stimulation of PLC-mediated [3H]inositol hydrolysis
Agonist activity at human P2Y14 expressed in COS7 cells assessed as stimulation of PLC-mediated [3H]inositol hydrolysis
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[PMID: 17407275] |
| COS-7 | EC50 |
354 nM
Compound: 1, UDP-glucose
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Agonist activity at human P2Y14 receptor expressed in COS7 cells assessed as stimulation of PLC
Agonist activity at human P2Y14 receptor expressed in COS7 cells assessed as stimulation of PLC
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[PMID: 17088057] |
| COS-7 | EC50 |
400 μM
Compound: 1, UDPG
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Agonist activity at recombinant human P2Y14 receptor expressed in African green monkey COS7 cells co-transfected with Galphaqi assessed as stimulation of phospholipase Cbeta
Agonist activity at recombinant human P2Y14 receptor expressed in African green monkey COS7 cells co-transfected with Galphaqi assessed as stimulation of phospholipase Cbeta
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[PMID: 25868749] |
| HEK293 | EC50 |
400 nM
Compound: 1
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Agonist activity at human P2Y14 receptor expressed in HEK293 cells coexpressing phospholipase C-activating Gi protein cells assessed as inhibition of forskolin induced [3H]cAMP production
Agonist activity at human P2Y14 receptor expressed in HEK293 cells coexpressing phospholipase C-activating Gi protein cells assessed as inhibition of forskolin induced [3H]cAMP production
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[PMID: 19902968] |
体外実験
Uridine 5’-diphosphoglucose (0-100 μM, 24 h) upregulates the expression of P2Y14 receptor, which induces neutrophil apoptos[2]. Uridine 5’-diphosphoglucose (1 μM, 24 h) and PPTN (HY-110322A) result in suppressed mRNA level of inflammatory factors including CCL3, IL1β,IL12a, TNF-α in neutrophils compared to cells treated with Uridine 5’-diphosphoglucose disodium salt alone, on the contrary, anti-inflammatory factors including IL10, TGF-β1, YM1 are upregulated upon Uridine 5’-diphosphoglucose disodium salt and PPTN (HY-110322A) in neutrophils[2]. Depletion of the pools of uridine 5’-diphosphoglucose (5 or 20 mM, incubation for 3 h) in the liver of the rat was associated with decreased glycosylation of secreted and tissue glycoproteins, influencing the rate of glomerular basement membrane (GBM) synthesis in rats[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Neutrophils
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Concentration:0-100 μM
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Incubation Time:24 h
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Result:Decreased cell viability and elevated apoptosis of neutrophils, which was blunted by PPTN (HY-110322A).
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Cell Line:Neutrophils
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Concentration:1 μM
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Incubation Time:24 h
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Result:Resulted in impaired neutrophil migration, which was inverted by PPTN (HY-110322A).
化学情報
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CAS 番号 133-89-1
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分子量 566.30
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分子式 C15H24N2O17P2
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SMILES
O[C@@H]1[C@H](O)[C@@H](COP(O)(OP(O)(O[C@@H]2[C@@H]([C@H]([C@@H]([C@H](O2)CO)O)O)O)=O)=O)O[C@H]1N3C=CC(NC3=O)=O
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別名
UDP-D-Glucose
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Structure Classification
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Initial Source
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (9)
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Journal Impact Factor
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Most Recent
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Mol Plant
2025 Dec 13:S1674-2052(25)00435-6. PMID: 41392480 -
J Am Chem Soc
2020 Sep 16;142(37):16039-16050. PMID: 32885969 -
Cell Rep
Blocking glycogen synthase 1 in white adipose tissue alleviates hypermetabolism following severe burn injury through inhibition of JAK2 by UDPG. [Abstract]2025 Nov 18;44(12):116577. PMID: 41259203 -
BMC Biotechnol
Mechanistic insights into how cichoriin inhibits P2Y14R to suppress MSU-induced gouty inflammation. [Abstract]2026 Apr 15;26(1):69. PMID: 41987170 -
BMC Cancer
Targeting INF2 with DiosMetin 7-O-β-D-Glucuronide: a new stratagem for colorectal cancer therapy. [Abstract]2025 Jun 1;25(1):982. PMID: 40452021
Uridine 5′-diphosphoglucose purchased from MedChemExpress. Usage Cited in: BMC Cancer. 2025 Jun 1;25(1):982. [Abstract]
Cellular Thermal Shift Assay was performed to detect the interactions between molecules and INF2 protein.The results demonstrated that the thermal stability of INF2 proteins was no significantly changed after treatment with Uridine 5′-diphosphoglucose disodium (10 μM; 24 h) and Alginic acid.
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Clin Immunol
Abnormal metabolism in melanocytes participates in the activation of dendritic cell in halo nevus. [Abstract]2024 Aug:265:110300. PMID: 38950722
Uridine 5′-diphosphoglucose purchased from MedChemExpress. Usage Cited in: Clin Immunol. 2024 Aug:265:110300. [Abstract]
RNA levels of inflammatory genes in Uridine 5′-diphosphoglucose disodium (UDP-G, 25–100 μM; 24) treated DC2.4 (murine DC cell line) cells. The results showed that UDP-G (25-100 μM) significantly upregulated the expression levels of Cxcl9, Cxcl10, and Il23 in treated mouse DC cells (DC2.4 cell line).
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Evid Based Complement Alternat Med
Isoschaftoside Inhibits Lipopolysaccharide-Induced Inflammation in Microglia through Regulation of HIF-1 α-Mediated Metabolic Reprogramming. [Abstract]2022 Nov 23:2022:5227335. PMID: 36467557 -
プロトコル
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
純度とドキュメンテーション
参考文献
[2]. Li K, et al. Upregulation of P2Y14 receptor in neutrophils promotes inflammation after myocardial ischemia/reperfusion injury[J]. Life Sci. 2023 Aug 1;326:121805. [Content Brief]
[3]. Cortes P, Dumler F, Levin NW. De novo pyrimidine nucleotide biosynthesis in isolated rat glomerul[J]i. Kidney Int. 1986 Jul;30(1):27-34. [Content Brief]
[4]. Das A, et al. Human P2Y(14) receptor agonists: truncation of the hexose moiety of uridine-5'-diphosphoglucose and its replacement with alkyl and aryl groups. J Med Chem. 2010 Jan 14;53(1):471-80. [Content Brief]
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
Uridine 5′-diphosphoglucose 関連分類
HY-113044 関連分類
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