61626-91-3Relevant articles and documents
APPLICATIONS OF N6-SUBSTITUTED ADENOSINE DERIVATIVE AND N6-SUBSTITUTED ADENINE DERIVATIVE TO CALMING, HYPNOSES, CONVULSION RESISTANCE, EPILEPTIC RESISTANCE, PARKINSON DISEASE RESISTANCE, AND DEMENTIA PREVENTION AND TREATMENT
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Paragraph 0095, (2018/10/27)
PROBLEM TO BE SOLVED: To prepare analgesics, hypnotic agents, anticonvulsant agents, antiepileptics, antiparkinson drugs, dementia prophylactics, and health care food. SOLUTION: The present invention relates to an N6-substituted adenosine derivative and an N6-substituted adenine derivative selected from the group consisting of specific compounds. The present invention also relates to a pharmaceutical composition at least comprising a therapeutically effective amount of the compounds and a pharmaceutically acceptable carrier. The invention further relates to the compounds used in preparation of analgesics, hypnotic agents, anticonvulsant agents, antiepileptics, antiparkinson drugs, dementia prophylactics, and health care food. COPYRIGHT: (C)2016,JPO&INPIT
N6-SUBSTITUTED ADENOSINE DERIVATIVES AND N6-SUBSTITUTED ADENINE DERIVATIVES AND USES THEREOF
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Paragraph 0089, (2013/03/26)
The present invention provides N6-substituted adenosine derivatives and N6-substituted adenine derivatives, manufacturing methods thereof, a pharmaceutical composition comprising the said compounds above, and uses of these compounds in manufacturing medicaments and health-care products for treating insomnia, convulsion, epilepsy, and Parkinson's diseases, and preventing and treating dementia.
Characterization of scavengers of γ-ketoaldehydes that do not inhibit prostaglandin biosynthesis
Zagol-Ikapitte, Irene,Amarnath, Venkataraman,Bala, Manju,Roberts II, L. Jackson,Oates, John A.,Boutaud, Olivier
experimental part, p. 240 - 250 (2011/02/22)
Expression of cyclooxygenase-2 (COX-2) is associated with the development of many pathologic conditions. The product of COX-2, prostaglandin H2 (PGH2), can spontaneously rearrange to form reactive γ-ketoaldehydes called levuglandins (LGs). This γ-ketoaldehyde structure confers a high degree of reactivity on the LGs, which rapidly form covalent adducts with primary amines of protein residues. Formation of LG adducts of proteins has been demonstrated in pathologic conditions (e.g., increased levels in the hippocampus in Alzheimer's disease) and during physiologic function (platelet activation). On the basis of knowledge that lipid modification of proteins is known to cause their translocation and to alter their function, we hypothesize that modification of proteins by LG could have functional consequences. Testing this hypothesis requires an experimental approach that discriminates between the effects of protein modification by LG and the effects of cyclooxygenase-derived prostanoids acting through their G-protein coupled receptors. To achieve this goal, we have synthesized and evaluated a series of scavengers that react with LG with a potency more than 2 orders of magnitude greater than that with the ε-amine of lysine. A subset of these scavengers are shown to block the formation of LG adducts of proteins in cells without inhibiting the catalytic activity of the cyclooxygenases. Ten of these selective scavengers did not produce cytotoxicity. These results demonstrate that small molecules can scavenge LGs in cells without interfering with the formation of prostaglandins. They also provide a working hypothesis for the development of pharmacologic agents that could be used in experimental animals in vivo to assess the pathophysiological contribution of levuglandins in diseases associated with cyclooxygenase up-regulation.
