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THERAPEUTIC AGENT FOR COGNITION DISORDER INDUCED BY AMYLOID β-PROTEIN

外国特許コード F160008820
整理番号 (S2015-0044-N0)
掲載日 2016年8月10日
出願国 世界知的所有権機関(WIPO)
国際出願番号 2015JP079120
国際公開番号 WO 2016060190
国際出願日 平成27年10月15日(2015.10.15)
国際公開日 平成28年4月21日(2016.4.21)
優先権データ
  • 特願2014-211671 (2014.10.16) JP
発明の名称 (英語) THERAPEUTIC AGENT FOR COGNITION DISORDER INDUCED BY AMYLOID β-PROTEIN
発明の概要(英語) The present invention addresses the problem of providing a therapeutic agent for cognition disorders induced by amyloid β-protein, the therapeutic agent functioning by a mechanism in which amyloid β-protein is involved but which is different from conventional mechanisms. This medicinal composition, which is for the treatment of cognition disorders induced by amyloid β-protein, comprises a pharmaceutically acceptable carrier and a therapeutically effective amount of either the peptide according to the invention or a pharmaceutically acceptable ester, amide, prodrug, or salt thereof.
従来技術、競合技術の概要(英語) BACKGROUND ART
Alzheimer's disease, cognitive decline (or remembering) the main condition that neurological disease. In particular in elderly is even though the predilection, there is no effective therapeutic, are worn out in aging society and the serious problem in developed countries. In the postmortem brain of Alzheimer's disease patients which neuritic plaques observed, this is' amyloid β protein ' aggregates with are known. Then, the amyloid β protein is the main cause of Alzheimer's disease is, by numerous studies in the widely accepted.
Amyloid β protein, a precursor thereof 'the amyloid precursor protein' generated from. The amyloid precursor protein and, present on the nerve cells in the membrane protein. In the normal brain, its extracellular domain α secretase, γ-secretase in the cell membrane and then are cut in the domain, the peptide is referred to as p3 outside of the cell production, is released. This is' non-amyloid generation path ' known as, amyloid β protein is not generated (non-patent document 1). In the normal brain, but the extracellular domain of the β-secretase is several % to truncated, secreted extracellular amyloid β protein are. However, in the brain Alzheimer's disease, amyloid β production amount of the protein will be increased, amyloid β protein aggregation high so as to produce a species are considered to be. Amyloid β protein with this property, finally Alzheimer's disease patients of senile plaques formed (amyloid aggregates), deposition is observed in the brain.
Amyloid β protein is found to have a cut, gradually aggregated, finally senile plaques (amyloid aggregates) are formed, agglomeration processes' oligomeric forms (amyloid β protein that associated with the several) ' in, known to be strong neurotoxicity. The amyloid β protein oligomeric forms is, memory, learning of the neural phenomenon essential to inhibit synaptic plasticity, in vitro, both in vivo have been reported (non-patent document 2, 3). In addition, this oligomer administered to the body in the mouse brain, storage, can be lost to the learning ability have been reported (non-patent document 4, 5). A recent study, and long-term exposure to this oligomeric forms, such as neuronal cell death was also has been reported (non-patent document 6), to cause the onset of Alzheimer's disease has been paid attention as a substance.
In this way, as the cause of the amyloid β protein Alzheimer's disease is widely recognized that regardless of the fact that, currently clinically used in the therapeutic agent is Alzheimer's disease, amyloid β protein in such a manner that this design is not. Specifically, used as a therapeutic agent Alzheimer's disease (Patent Document 1) memantine or donepezil (Patent Document 2) is, and the acetylcholinesterase inhibitor respectively act as NMDA receptor inhibitors, amyloid β protein does not interact with. Since the agent is a so-called address, a dramatic improvement in the effect for Alzheimer's disease is at present.
In response to such a background, based on the mechanism of action (amyloid protein) new Alzheimer's development of therapeutics has been promoted. 1 Is one, the amyloid precursor protein from the production of amyloid β protein and attempted to attempt, the development of secretase control agent (non-patent document 1). Among them, development of γ secretase inhibitors and the most advanced, Begacestat Semagacestat (Patent Document 3) or the like (Patent Document 4), and clinical development efforts have been performed. Another has attracted attention as a therapy is, amyloid β protein in the brain is removed and antibody-recognized, antibody therapy. Actually, solanezumab Bapineuzumab (Patent Document 5) or the like, clinical development has progressed so far is MIMIC.
However, with the center of the present development of amyloid protein Alzheimer's mechanism of action and there are problems that the therapeutic agent may be known. With respect to the γ secretase inhibitors, γ secretase substrates in the first place as well as the amyloid precursor protein, are known to be near about 100 (non-patent document 7). And includes an, important cell differentiation which may include Notch receptor (non-patent document 8), concern about side effects. Actually, as was a strong candidate for the γ secretase inhibitors Semagacestat is, developed in the year 2010 the third phase clinical trials are terminated. Anti-amyloid β antibody for the antibody therapy, vasculitis and vascular cerebral edema and the like which can occur, in fact, is promising as a therapeutic agent was also Bapineuzumab antibody, was developed in 2012 is stopped.
In addition, the stroma of the γ secretase, cut the extracellular domain of the amyloid peptide may be ejected in some known (non-patent document 9, 10). These peptides are indicative of the activity since the γ secretase, fragment was cut to a biomarker of the invention of the Alzheimer's disease are some (Patent Document 6, 7). Also, referred to as Alcadein-β is membrane protein in vivo, cleaved by γ-secretase, by may be cut by further α secretase, 37 amino acid peptide (VLSSQQFLHRGHQPPPEMAGHSLASSHRNSMIPSAAT) also known being produced in the (non-patent document 11).
  • 出願人(英語)
  • ※2012年7月以前掲載分については米国以外のすべての指定国
  • NATIONAL UNIVERSITY CORPORATION HOKKAIDO UNIVERSITY
  • NATIONAL UNIVERSITY CORPORATION OKAYAMA UNIVERSITY
  • 発明者(英語)
  • SUZUKI Toshiharu
  • BAN Saori
  • INOUE Tsuyoshi
国際特許分類(IPC)
指定国 National States: AE AG AL AM AO AT AU AZ BA BB BG BH BN BR BW BY BZ CA CH CL CN CO CR CU CZ DE DK DM DO DZ EC EE EG ES FI GB GD GE GH GM GT HN HR HU ID IL IN IR IS JP KE KG KN KP KR KZ LA LC LK LR LS LU LY MA MD ME MG MK MN MW MX MY MZ NA NG NI NO NZ OM PA PE PG PH PL PT QA RO RS RU RW SA SC SD SE SG SK SL SM ST SV SY TH TJ TM TN TR TT TZ UA UG US UZ VC VN ZA ZM ZW
ARIPO: BW GH GM KE LR LS MW MZ NA RW SD SL SZ TZ UG ZM ZW
EAPO: AM AZ BY KG KZ RU TJ TM
EPO: AL AT BE BG CH CY CZ DE DK EE ES FI FR GB GR HR HU IE IS IT LT LU LV MC MK MT NL NO PL PT RO RS SE SI SK SM TR
OAPI: BF BJ CF CG CI CM GA GN GQ GW KM ML MR NE SN ST TD TG
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