| 序号 | 专利名 | 申请号 | 申请日 | 公开（公告）号 | 公开（公告）日 | 发明人 |
|---|---|---|---|---|---|---|
| 21 | 改善されたバイオアベイラビリティーのためにＡＴＦと融合させた薬剤 | JP2014537404 | 2012-02-07 | JP2015511932A | 2015-04-23 | 高橋 健一; 健一 高橋; 英士 余田 |
| 改善されたバイオアベイラビリティーを有する薬剤,及び,薬としての活性を発揮すべき細胞内に薬物を送達するための,ウロキナーゼ型プラスミノーゲンアクティベーターのアミノ末端フラグメント(ATF)を使用する方法が開示されている。当該薬剤は,ATFの受容体結合ドメインを含むペプチドを結合させた薬理学的に活性な化合物を含んでなる。 | ||||||
| 22 | ペプチドに誘導されたタンパク質ノックダウン | JP2015533387 | 2013-09-27 | JP2015533817A | 2015-11-26 | ティアン ワング、ユー; ファン、シュエライ; ヤング ジン、ウー |
| 一態様において、本発明はシャペロン介在性オートファジー(CMA)を標的としたシグナルドメイン、標的の細胞質タンパク質に選択的に結合するタンパク質結合ドメイン、及び細胞膜透過ドメイン(CMPD)を含むペプチドを提供する。別の態様において、本発明は方法が該ペプチドの投与を含むことを特徴とする、in vitro、及び動物における、内在性の標的タンパク質の細胞内発現レベルを減少させるための方法を提供する。方法はまた動物での病態の治療のために提供されるが、前記方法は動物に対して該ペプチドを投与することを含む。一実施形態において、病態は神経変性疾患である。本発明の別の実施形態において、標的の細胞質タンパク質は、細胞死関連タンパク質キナーゼ1及びHIV-1 Tatタンパク質のタンパク質形質導入ドメインであるCMPDである。【選択図】図1 | ||||||
| 23 | Long-acting composition | EP83303636 | 1983-06-23 | EP0098110A3 | 1986-03-05 | Hiratani, Hajime |
A composition wherein a physiologically active polypeptide or a glycoprotein for instance, urokinase, kallikrein or leukocyte interferon, is coupled to a polyoxyethylene-polyoxypropylene copolymer. The composition is effective in vivo for a prolonged period of time. |
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| 24 | Long-acting composition | EP83303636.1 | 1983-06-23 | EP0098110A2 | 1984-01-11 | Hiratani, Hajime |
A composition wherein a physiologically active polypeptide or a glycoprotein for instance, urokinase, kallikrein or leukocyte interferon, is coupled to a polyoxyethylene-polyoxypropylene copolymer. The composition is effective in vivo for a prolonged period of time. |
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| 25 | METHOD OF TREATING FIBROSIS IN SKELETAL MUSCLE TISSUE | EP14743140 | 2014-01-28 | EP2948171A4 | 2017-02-22 | LAMB BLAIR G |
| A method is disclosed to dissolve protein deposited in muscle. The method includes the step of administering an effective amount of an agent selected from the group consisting of fibrinolytics, proteolytics, photolytic and magnelytic agents. | ||||||
| 26 | PHARMACEUTICAL OR COSMETIC COMPOSITION FOR THE REGENERATION AND CICATRISATION OF THE SKIN | EP14801136 | 2014-04-10 | EP3000475A4 | 2017-01-11 | GALEANO SALVADOR JOSÉ MANUEL; FERNÁNDEZ PIN JOSÉ MANUEL; LABRADOR BARRAFÓN DANIEL; KLEIN GEORGES R; GONZÁLEZ AZUARA NURIA |
| The invention relates to a pharmaceutical or cosmetic composition for the regeneration and cicatrisation of the skin, comprising the enzyme urokinase as the active substance. Said composition also comprises at least another active substance selected from active substances with a regenerative function. The invention also relates to a galenic form for the topical administration of said pharmaceutical or cosmetic composition, and also to the uses of said galenic form for the regeneration and cicatrisation of considerable alterations of the skin, with the aim of obtaining a normotrophic evolution of said alterations. | ||||||
| 27 | Long-acting composition | EP83303636.1 | 1983-06-23 | EP0098110B1 | 1989-10-18 | Hiratani, Hajime |
| 28 | PEPTIDE DIRECTED PROTEIN KNOCKDOWN | EP13841990 | 2013-09-27 | EP2900697A4 | 2016-04-20 | WANG YU TIAN; FAN XUELAI; JIN WU YANG |
| In one aspect, the invention provides a peptide comprising a chaperone-mediated autophagy (CMA)-targeting signal domain; a protein-binding domain that selectively binds to a target cytosolic protein; and a cell membrane penetrating domain (CMPD). In another aspect, the invention provides methods for reducing the intracellular expression level of an endogenous target protein in vitro and in an animal, wherein the method involves administration of the peptide. Methods are also provided for treating a pathological condition in an animal, the methods comprising administering the peptide to the animal. In one embodiment, the pathological condition is a neurodegenerative disease. In another embodiment of the invention, the target cytosolic protein is death associated protein kinase 1 and the CMPD is protein transduction domain of the HIV-1 Tat protein. | ||||||
| 29 | PHARMACEUTICAL OR COSMETIC COMPOSITION FOR THE REGENERATION AND CICATRISATION OF THE SKIN | EP14801136.4 | 2014-04-10 | EP3000475A1 | 2016-03-30 | GALEANO SALVADOR, José Manuel; FERNÁNDEZ PIN, José Manuel; LABRADOR BARRAFÓN, Daniel; KLEIN, Georges R.; GONZÁLEZ AZUARA, Nuria |
The invention relates to a pharmaceutical or cosmetic composition for the regeneration and cicatrisation of the skin, comprising the enzyme urokinase as the active substance. Said composition also comprises at least another active substance selected from active substances with a regenerative function. The invention also relates to a galenic form for the topical administration of said pharmaceutical or cosmetic composition, and also to the uses of said galenic form for the regeneration and cicatrisation of considerable alterations of the skin, with the aim of obtaining a normotrophic evolution of said alterations. |
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| 30 | METHOD OF TREATING FIBROSIS IN SKELETAL MUSCLE TISSUE | EP14743140.7 | 2014-01-28 | EP2948171A1 | 2015-12-02 | Lamb, Blair G. |
| A method is disclosed to dissolve protein deposited in muscle. The method includes the step of administering an effective amount of an agent selected from the group consisting of fibrinolytics, proteolytics, photolytic and magnelytic agents. | ||||||
| 31 | GLUE COMPOSITIONS FOR LUNG VOLUME REDUCTION | PCT/US2005020902 | 2005-06-13 | WO2006009682A2 | 2006-01-26 | GONG GLEN; DIECK RONALD |
| The present invention relates to methods and compositions for sealing localized regions of damaged lung tissue to reduce overall lung volume. The glue compositions provide a glue featuring an adhering moiety coupled to one or more other moieties including, for example, a cross-linkable moiety and/or one other adhering moiety. The methods and compositions of the invention find use, for example, in treating pulmonary conditions, such as emphysema. | ||||||
| 32 | C-1 INHIBITOR PREVENTS NON-SPECIFIC PLASMINOGEN ACTIVATION BY A PROUROKINASE MUTANT WITHOUT IMPEDING FIBRIN-SPECIFIC FIBRINOLYSIS | PCT/US2009003895 | 2009-06-30 | WO2010002453A2 | 2010-01-07 | GUREWICH VICTOR; PANNELL RALPH |
| A mutant prourokinase plasminogen activator (M5) was developed to make prouPA less subject to spontaneous conversion to tcuPA in blood at therapeutic concentrations. Two-chain M5 was shown to form complexes with C l- inhibitor, which was the principal inhiibitor of tcM5 in plasma. The effect of supplemental additions of Cl- inhibitor on fibrinolysis and fibrinogenolysis by M5 was determined. Supplemental Cl- inhibitor restored the stability of high- dose M5 and prevented fibrinogenolysis but not fibrinolysis, the rate of which was not compromised by the inhibitor.. Due to higher dose tolerance of M5 in the presence of supplemental Cl -inhibitor, the rate of fibrin-specific lysis reached that achievable by nonspecific fibrinolysis, which is the maximum possible for a plasminogen activator.. Plasma Cl-inhibitor stabilized M5 in plasma by inhibiting tcM5 which would otherwise greatly amplify non-specific plasminogen activation causing more tcM5 generation from M5.. This unusual dissociation of inhibitory effects, whereby fibrinogenolysis and not fibrinolysis is inhibited, has significant implications for improving the safety and efficacy of fibrinolysis. Methods of reducing bleeding and non-specific plasminogen activation during fibrinolysis by administering M5 along with exogenous Cl - inhibitor are disclosed. | ||||||
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