DMOG | Inhibits prolyl hydroxylase domain-containing proteins
NMR (Conforms)
Protect from light
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| Size : | Price | Quantity | |
|---|---|---|---|
| 50 mg | $60.00 | ||
| 100 mg | $110.00 |
DMOG (89464-63-1) inhibits PHD or prolyl hydroxylase domain-containing proteins, activating HIF1α1,2 and inhibiting JMJD2A (IC50 = 2.5 μM)3. Displays neuroprotective effects. Inhibits neuronal cell death caused by neurotrophin deprivation.4 DMOG prevents activation of the ATR/CHK1/p53 pathway and suppresses apoptosis induced by DNA damage.5
References/Citations:
1) Asikainen et al. (2005), Activation of hypoxia-inducible factors in hyperoxia through prolyl 4-hydroxylase blockade in cells and explants of primate lung; Proc. Natl. Acad. Sci. USA, 102 10212
2) Jaakkola et al. (2001), Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation; Science, 292 468
3) Hamada et al. (2009), Synthesis and activity of N-oxalylglycine and it’s derivatives as jumonji C-domain-containing histone lysine demethylase inhibitors; Bioorg. Med. Chem. Lett., 19 2852
4) Lomb et al. (2009), Prolyl hydroxylase inhibitors depend on extracellular glucose and hypoxia-inducible factor (HIF)-2alpha to inhibit cell death caused by nerve growth factor deprivation: evidence that HIF-2alpha has a role in NGF-promoted survival of sympathetic neurons; Mol. Pharmacol., 75 1198
5) Xie et al. (2012), PHD3-dependent hydroxylation of HCLK2 promotes the DNA damage response; J. Clin. Invest., 122 2827
NMR (Conforms)
Protect from light
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Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
DMOG (89464-63-1) inhibits PHD or prolyl hydroxylase domain-containing proteins, activating HIF1α1,2 and inhibiting JMJD2A (IC50 = 2.5 μM)3. Displays neuroprotective effects. Inhibits neuronal cell death caused by neurotrophin deprivation.4 DMOG prevents activation of the ATR/CHK1/p53 pathway and suppresses apoptosis induced by DNA damage.5
References/Citations:
1) Asikainen et al. (2005), Activation of hypoxia-inducible factors in hyperoxia through prolyl 4-hydroxylase blockade in cells and explants of primate lung; Proc. Natl. Acad. Sci. USA, 102 10212
2) Jaakkola et al. (2001), Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation; Science, 292 468
3) Hamada et al. (2009), Synthesis and activity of N-oxalylglycine and it’s derivatives as jumonji C-domain-containing histone lysine demethylase inhibitors; Bioorg. Med. Chem. Lett., 19 2852
4) Lomb et al. (2009), Prolyl hydroxylase inhibitors depend on extracellular glucose and hypoxia-inducible factor (HIF)-2alpha to inhibit cell death caused by nerve growth factor deprivation: evidence that HIF-2alpha has a role in NGF-promoted survival of sympathetic neurons; Mol. Pharmacol., 75 1198
5) Xie et al. (2012), PHD3-dependent hydroxylation of HCLK2 promotes the DNA damage response; J. Clin. Invest., 122 2827
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1-855-FOCUS21
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