DMOG (Dimethyloxallyl Glycine) is a cell permeable and competitive inhibitor of HIF-PH, which results in HIF-1α stabilisation and accmulation in vitro and in vivo^[1]. DMOG is an α-ketoglutarate analogue and inhibits α-KG-dependent hydroxylases. DMOG acts as a pro-angiogenic agent and plays a protective role in experimental model of colitis and diarrhoea via HIF-1 related signal^[2][4]. DMOG induces cell autophagy^[5].

HIF-1α prolyl hydroxylase^[1]

DMOG efficiently suppresses hydroxyproline synthesis in intact cells, but shows only weakly active in the microsomal system^[1]. DMOG reduces FGF-2-induced proliferation and cyclin A expression by inhibiting prolyl hydroxylase activity in HPASMC^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

DMOG inhibits endogenous HIF inactivation, and induces angiogenesis in ischaemic skeletal muscles of mice^[2]. Up-regulation of hypoxia-inducible factor-1α by DMOG enhances the cardioprotective effects of ischemic postconditioning in hyperlipidemic rats^[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

175.14

C₆H₉NO₅

89464-63-1

Room temperature in continental US; may vary elsewhere.

DMSO : ≥ 50 mg/mL (285.49 mM)

H₂O : 50 mg/mL (285.49 mM; Need ultrasonic)

* “≥” means soluble, but saturation unknown.

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： PBS

  Solubility: 150 mg/mL (856.46 mM); Clear solution; Need ultrasonic

• [1]. Baader E, et al. 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]. Milkiewicz M, et al. Inhibition of endogenous HIF inactivation induces angiogenesis in ischaemic skeletal muscles of mice. J Physiol. 2004 Oct 1;560(Pt 1):21-6.

  [3]. Schultz K, et al. Prolyl hydroxylase 2 deficiency limits proliferation of vascular smooth muscle cells by hypoxia-inducible factor-1{alpha}-dependent mechanisms. Am J Physiol Lung Cell Mol Physiol. 2009 Jun;296(6):L921-7.

  [4]. Li X, et al. Up-regulation of hypoxia-inducible factor-1α enhanced the cardioprotective effects of ischemic postconditioning in hyperlipidemic rats. Acta Biochim Biophys Sin (Shanghai). 2014 Feb;46(2):112-8.

  [5]. Singh A, et al. Hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitors induce autophagy and have a protective effect in an in-vitro ischaemia model.Sci Rep. 2020 Jan 31;10(1):1597.

To analyze DNA synthesis as an index of cellular proliferation, VSMC are plated in 48-well plates (5,000 per square centimeter) in growth medium, incubated overnight, and serum-deprived (1% FCS) for 24 h. Replicate wells are then stored at −70°C for baseline (day 0) cell counts, and fresh medium with or without growth factors is added to the remaining wells, which are incubated 72-96 h in 20 or 5% O₂. Days 0 and 3 or 4 cell counts are determined by lysing cells in a buffer containing a fluorescent dye, which has minimal fluorescence by itself but fluoresces when bound to DNA or RNA. Absolute cell numbers are calculated by comparing the fluorescence of specimens with that of a standard curve similarly prepared using a known number of cells.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Two groups of mice (C57Bl6) are used. One group (n=11) receives dimethyloxalylglycine (DMOG) i.p. (8 mg in 0.5 mL saline) on days 1, 3, 5, 7 and 9 while the animals in the other group are injected with sterile saline (0.5 mL) at the same intervals (n=6). A third group is treated with DMOG without ligation (n=4) and four unoperated mice serve as controls. After 11 days mice are terminally anaesthetized and the extensor digitorum longus (EDL) and tibialis anterior (TA) muscles excised.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Baader E, et al. 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]. Milkiewicz M, et al. Inhibition of endogenous HIF inactivation induces angiogenesis in ischaemic skeletal muscles of mice. J Physiol. 2004 Oct 1;560(Pt 1):21-6.

  [3]. Schultz K, et al. Prolyl hydroxylase 2 deficiency limits proliferation of vascular smooth muscle cells by hypoxia-inducible factor-1{alpha}-dependent mechanisms. Am J Physiol Lung Cell Mol Physiol. 2009 Jun;296(6):L921-7.

  [4]. Li X, et al. Up-regulation of hypoxia-inducible factor-1α enhanced the cardioprotective effects of ischemic postconditioning in hyperlipidemic rats. Acta Biochim Biophys Sin (Shanghai). 2014 Feb;46(2):112-8.

  [5]. Singh A, et al. Hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitors induce autophagy and have a protective effect in an in-vitro ischaemia model.Sci Rep. 2020 Jan 31;10(1):1597.