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DMOG
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
DMOG图片
CAS NO:89464-63-1
规格:98%
分子量:175.14
包装与价格:
包装价格(元)
50mg电议
100mg电议
200mg电议

产品介绍
Competitive HIF-PH inhibitor, cell-permeable
CAS:89464-63-1
分子式:C6H9NO5
分子量:175.14
纯度:98%
存储:Store at -20°C

Background:

IC50: 9.3 and 3.7 μM for hydroxyproline synthesis inhibition of embryonic chicken lung extracted from tissue and culture medium [1].


Dimethyloxalylglycine (DMOG) is an inhibitor of prolyl-4-hydroxylase domain (PHD) enzymes that regulate the stability of hypoxia-inducible factor (HIF). Localized tissue hypoxia is a feature of infection and inflammation, leading to the upregulation of the transcription factors HIF-1α and NF-κB via inhibition of oxygen sensing hydroxylase enzymes.


In vitro: DMOG acts to stabilize HIF-1a expression under normal oxygen tension in cultured cells at concentrations from 0.1 to 1 mmol/L [2].


In vivo: Pre-treatment with DMOG attenuates systemic LPS-induced activation of the NF-κB pathway. Furthermore, mice treated with DMOG had significantly increased survival in LPS-induced shock. In addition, in vivo DMOG treatment upregulates the expression of IL-10, specifically in the peritoneal B-1 cell population [3].


Clinical trial: Currently no clinical data are available.


参考文献:
[1] Baader E, Tschank G, Baringhaus KH, Burghard H, Günzler V.  Inhibition of prolyl 4-hydroxylase by oxalyl amino acid derivatives in vitro, in isolated microsomes and in embryonic chicken tissues. Biochem J. 1994 Jun 1;300 ( Pt 2):525-30.
[2] Jaakkola P, Mole DR, Tian YM, Wilson MI, Gielbert J, Gaskell SJ, von Kriegsheim A, Hebestreit HF, Mukherji M, Schofield CJ, Maxwell PH, Pugh CW, Ratcliffe PJ.  Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation. Science. 2001 Apr 20;292(5516):468-72.
[3] Hams E, Saunders SP, Cummins EP, O'Connor A, Tambuwala MT, Gallagher WM, Byrne A, Campos-Torres A, Moynagh PM, Jobin C, Taylor CT, Fallon PG.  The hydroxylase inhibitor dimethyloxallyl glycine attenuates endotoxic shock via alternative activation of macrophages and IL-10 production by B1 cells. Shock. 2011 Sep;36(3):295-302.