CAS: 89464-63-1; Methyl 2-((2-Methoxy-2-Oxoethyl)Amino)-2-Oxoacetate

相似化合物

5262-39-5 3586-25-2 1117-77-7

上下游产品

monomethyl oxalyl chloride glycine ethyl ester hydr°Chloride dimethyl iminodiacetate Dimethyl oxalatemethyl 5-methoxy-1,3-oxazole-2-carboxylate

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参考文献:Ep1785418
标题:Ep1785418

专利信息

专利号:WO-2024170500-A1
优先权日:2023-02-13
标题:Methods of treating iron deficiency-related diseases
发明人：KAUTZ LÉON
权利人:INST NAT SANTE RECH MED; ECOLE NAT VETERINAIRE DE TOULOUSE; INSTITUT NATIONAL DE RECH POUR L’AGRICULTURE L’ALIMENTATION ET L’ENVIRONNEMENT; UNIV TOULOUSE III – PAUL SABATIER
摘要:Anemia, defined as a decreased quantity of circulating functional red blood cells, is a major source of morbidity and mortality affecting a-third of the worldwide population. As a functional component of erythrocytes hemoglobin, iron is essential for oxygen storage and transport. The liver-derived peptide hepcidin is the master regulator of iron homeostasis. During anemia, the erythroid hormone erythroferrone regulates hepcidin synthesis to ensure the proper supply of iron to the bone marrow for red blood cells synthesis. However, mounting evidence suggested that another factor may exert a similar function. Inventors identified the hepatokine FGL1 as a previously undescribed suppressor of hepcidin that is highly induced in the liver in response to hypoxia during the recovery from anemia and in thalassemic mice. Inventors demonstrated that FGL1 is a potent suppressor of hepcidin in vitro and in vivo. Deletion of Fgl1 in mice results in a blunted repression of hepcidin after bleeding. Finally, FGL1 is a BMP antagonist that directly binds BMP6 to impair the canonical BMP-SMAD signaling cascade that governs hepcidin regulation. Accordingly, the present invention relates to a FGL1 polypeptide for use in the treatment of a patient affected with an iron deficiency-related disease.

专利号:WO-2024231384-A1
优先权日:2023-05-10
标题:Compositions for treating senescence related disease
发明人：PENDE MARIO; FUMAGALLI STEFANO
权利人:INST NAT SANTE RECH MED; CENTRE NAT RECH SCIENT; UNIV PARIS CITE
摘要:Inventors have identified glycerol-3-phosphate (G3P) and phosphoethanolamine (PEtn) metabolism as potent regulators of the senescent program at the nexus of TAG and PL metabolism. They show that Glycerol kinase (GK) and Phosphate Cytidylyltransferase 2 Ethanolamine (Pcyt2) activities, which catalyse regulatory steps in TAG and PL synthesis impact G3P and PEtn levels in a homeostatic fashion controlling the senescence program. Finally, they provide evidence that pharmacological inhibitors of GK activity act senomorphic, thus suggesting a novel therapeutic target for interventions in age-related diseases and cancer. The present invention relates to a method for treating senescence related disease in a subject in need thereof comprising administering said subject with a therapeutically effective amount of a modulator of Glycerol kinase (GK), Glycerol 3 phosphate phosphatase (G3PP), Ethanolamine-Phosphate Phospho-Lyase (ETNPPL) and/or Phosphate Cytidylyltransferase 2 (PCYT2).