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AGENT FOR PREVENTING OR IMPROVING CHRONIC LUNG ALLOGRAFT DYSFUNCTION

外国特許コード F200010071
整理番号 5989
掲載日 2020年5月15日
出願国 世界知的所有権機関(WIPO)
国際出願番号 2019JP003794
国際公開番号 WO 2019159731
国際出願日 平成31年2月4日(2019.2.4)
国際公開日 令和元年8月22日(2019.8.22)
優先権データ
  • 特願2018-027063 (2018.2.19) JP
発明の名称 (英語) AGENT FOR PREVENTING OR IMPROVING CHRONIC LUNG ALLOGRAFT DYSFUNCTION
発明の概要(英語) A purpose of the present invention is to provide an immunosuppressant that can prolong suppression of rejection after lung transplant. An agent for preventing or improving chronic lung allograft dysfunction having an MEK inhibitor as an active ingredient can prolong suppression of rejection after lung transplant and makes it possible to prevent or improve chronic lung allograft dysfunction (CLAD). The agent for preventing or improving chronic lung allograft dysfunction having an MEK inhibitor as an active ingredient is administered to a lung transplant patient who has undergone treatment for acute immune rejection.
従来技術、競合技術の概要(英語) BACKGROUND ART
Human lung transplantation is successful since the year 1983, the increase in the number of cases is increasing steadily. However, post-transplantation of the five-year survival rate remains 54% and 5, other solid organ transplantation is not satisfactory as compared with the performance. Death within one year of the 1 post-operative infection is, then a number of immunological rejection reaction is the cause of death due to the (non-patent document 1-3).
Lung transplantation rejection is acute rejection is classified as chronic rejection. Acute rejection occurs at an early stage after the surgery, and the increase in the necessity of additional immunosuppressive agents in many cases, the transition to the chronic rejection (non-patent documents 4-5) is also an example. As immunosuppressive agents, calcineurin inhibitors, mTOR inhibitors, corticosteroids, mycophenolate mofetil (MMF) or the like is used. One year from the remaining through surgical and chronic rejection found. Chronic rejection (bronchiolitis obliterans change obstructive of the bronchioles are: BO) often occur, a failure constraint (restrictive allograft syndrome: RAS) may exhibit. Also, in chronic rejection, while the slow non-reversible change in lung pathology kitashi, lung dysfunction graft (Chronic Lung Allograft Dysfunction: CLAD) that causes a condition referred to. This condition is added or increased existing immunosuppressive agents often cannot be controlled, to improve the long term prognosis of lung transplantation prevent a large barrier (non-patent document 6).
Graft (CLAD) lung dysfunction itself is causing fatal bronchiolitis, serious opportunistic infections as well as the risk factors. The use of long-term immunosuppressive agents, anti-tumor immunity through weakening of new malignant tumors increased risk of developing (non-patent document 7). Chronic rejection reaction mechanism is not known yet, a method is effective to suppress the reaction and chronic rejection are not known. Therefore, there is no countermeasure to the CLAD in the current state.
T cell immune controls the main activation path, the calcineurin pathway, mTOR pathway, 3 MAPK path type are known, heretofore, the calcineurin pathway mTOR pathway and immunosuppressive approach has been investigated. MAPK pathways, many malignant tumor can be permanently activated, malignant melanoma are listed in the insurance for the (non-patent document 8) such as MEK trametinib inhibitor has been developed as an anti-tumor agent. However, MAPK pathway itself is very important to the cell for a path, from the viewpoint of the MAPK pathway immunosuppressive approach, leads to a very small risk of adverse events were not considered.
In recent years, the MEK inhibitor, graft versus host disease after bone marrow transplantation (GVHD) antiviral immune while suppressing the effect of anti-tumor immunity and preserve (GVT) have been reported (Non-Patent Document 9 and 10). These reports, the MEK inhibitor, T-cell function in the early stage of cell differentiation (central memoryT naiveT cells and the cells) and to selectively inhibit, the function of differentiation of the T cells to the post stage can be to preserve (effector memoryT cells) are shown.
  • 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
  • KYOTO UNIVERSITY
  • 発明者(英語)
  • SHINDO, Takero
  • CHEN, Fengshi
  • TAKAHAGI, Akihiro
  • DATE, Hiroshi
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 DJ DK DM DO DZ EC EE EG ES FI GB GD GE GH GM GT HN HR HU ID IL IN IR IS JO KE KG KH KN KP KR KW 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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