| 序号 | 专利名 | 申请号 | 申请日 | 公开（公告）号 | 公开（公告）日 | 发明人 |
|---|---|---|---|---|---|---|
| 181 | GELATINASE INHIBITORS AND PRODRUGS | US14567480 | 2014-12-11 | US20150093372A1 | 2015-04-02 | Mayland Chang; Shahriar Mobashery; Mijoon Lee |
| The invention provides compounds, compositions, and methods for the treatment of diseases, disorders, or conditions that are modulated by matrix metalloproteinases (MMPs). The disease, disorder, or condition can include, for example, stroke, neurological disorders, or ophthalmological disorders. The treatment can include administering a compound or composition described herein, thereby providing a prodrug compound that metabolizes to an active MMP inhibitor in vivo. The MMP inhibition can be selective inhibition, for example, selective inhibition of MMP-2, MMP-9, and/or MMP-14. Thus, the invention provides non-mutagenic prodrug compounds of the formulas described herein that result in the inhibition of MMPs upon in vivo administration. | ||||||
| 182 | MIRAC PROTEINS | US14483980 | 2014-09-11 | US20140378660A1 | 2014-12-25 | Jay M. Short; Hwai Wen Chang; Gerhard Frey |
| This disclosure relates to a method of generating conditionally active biologic proteins from wild type proteins, in particular therapeutic proteins, which are reversibly or irreversibly inactivated at the wild type normal physiological conditions. For example, evolved proteins are virtually inactive at body temperature, but are active at lower temperatures. | ||||||
| 183 | MIRAC PROTEINS | US14196950 | 2014-03-04 | US20140187748A1 | 2014-07-03 | Jay M. Short; Hwai Wen Chang; Gerhard Frey |
| This disclosure relates to a method of generating conditionally active biologic proteins from wild type proteins, in particular therapeutic proteins, which are reversibly or irreversibly inactivated at the wild type normal physiological conditions. For example, evolved proteins are virtually inactive at body temperature, but are active at lower temperatures. | ||||||
| 184 | Treating atherosclerosis | US12528300 | 2007-02-23 | US08507646B2 | 2013-08-13 | Jian-Ning Liu |
| The present application features methods and compositions for treating patients suffering from atherosclerosis or at risk for developing atherosclerosis. The treatment includes administering to the patient a pharmaceutical composition that includes an agent capable of blocking the interaction between uPA and its receptor uPAR, e.g., an ATF or a fragment thereof, an anti-uPA antibody, a uPAR or a fragment thereof, or an antibody that specifically binds to uPAR. | ||||||
| 185 | GELATINASE INHIBITORS AND PRODRUGS | US13582678 | 2011-03-04 | US20130052184A1 | 2013-02-28 | Mayland Chang; Shahriar Mobashery; Mijoon Lee |
| The invention provides compounds, compositions, and methods for the treatment of diseases, disorders, or conditions that are modulated by matrix metalloproteinases (MMPs). The disease, disorder, or condition can include, for example, stroke, neurological disorders, or ophthalmological disorders. The treatment can include administering a compound or composition described herein, thereby providing a prodrug compound that metabolizes to an active MMP inhibitor in vivo. The MMP inhibition can be selective inhibition, for example, selective inhibition of MMP-2, MMP-9, and/or MMP-14. Thus, the invention provides non-mutagenic prodrug compounds of the formulas described herein that result in the inhibition of MMPs upon in vivo administration. | ||||||
| 186 | MIRAC PROTEINS | US13523509 | 2012-06-14 | US20120258865A1 | 2012-10-11 | Jay M. Short; Hwai Wen Chang; Gerhard Frey |
| This disclosure relates to a method of generating conditionally active biologic proteins from wild type proteins, in particular therapeutic proteins, which are reversibly or irreversibly inactivated at the wild type normal physiological conditions. For example, evolved proteins are virtually inactive at body temperature, but are active at lower temperatures. | ||||||
| 187 | MIRAC PROTEINS | US13255676 | 2010-03-09 | US20120164127A1 | 2012-06-28 | Jay M. Short; Hwai Wen Chang; Gerhard Frey; Gregory Frost |
| This disclosure relates to a method of generating conditionally active biologic proteins from wild type proteins, in particular therapeutic proteins, which are reversibly or irreversibly inactivated at the wild type normal physiological conditions. For example, evolved proteins are virtually inactive at body temperature, but are active at lower temperatures. | ||||||
| 188 | Integrated infusion container | US11994186 | 2006-06-28 | US08128612B2 | 2012-03-06 | Gi-Bum Oh |
| The present invention relates to unitary bottle for injection, more particularly, to a unitary medicine bottle having an integral structure where a medicine container is easily connected with a plastic container including a solution at a completely sterilized state so that powdered, freeze-dried or liquid medicine is mixed with the solution with one touch for a short time. The unitary medicine bottle for injection according to the present invention comprises: a plastic container equipped with a coupling member connected with a medicine container at one end and a releasing member for releasing a liquid medicine to be at the other end; a protection cap integrally formed with the coupling member to accept the medicine container; and a flue needle which moves forward in a direction of the medicine container and perforates a stopper of the medicine container and is inserted in the coupling member connecting the plastic container with the medicine container. | ||||||
| 189 | Chimeric plasminogen activators and their pharmaceutical use | US10583785 | 2003-12-18 | US08124588B2 | 2012-02-28 | Werner Seeger; Andreas Günther; Clemens Ruppert; Philipp Markart; Viktor Magdolen; Timothy E. Weaver |
| The present invention relates to recombinant chimeric proteins comprising a surfactant protein precursor N-terminally fused to a plasminogen activator or comprising a mature surfactant protein N-terminally or C-terminally fused to a plasminogen activator. The invention is also directed to the corresponding nucleic acid molecules encoding such fusion proteins as well as to a method for their production. The invention further refers to a pharmaceutical composition comprising such a fusion protein and to pharmacological uses of an inventive fusion protein for the prevention and/or treatment of inflammatory and interstitial lung diseases. | ||||||
| 190 | USE OF MATRIX METALLOPROTEINASE-10 (MMP-10) FOR THROMBOLYTIC TREATMENTS | US12861357 | 2010-08-23 | US20110091436A1 | 2011-04-21 | Josune Orbe Lopategui; Jose Antonio Rodriguez Garcia; Jose Antonio Paramo Fernandez; Rosario Serrano Vargas |
| The present invention relates to the use of matrix metalloproteinase MMP-10 in the preparation of a pharmaceutical composition useful for thrombolytic therapy, it also being possible for said composition to contain a plasminogen activator. Additionally, the present invention relates to said pharmaceutical composition for the treatment of thrombotic disorders. | ||||||
| 191 | C-1 inhibitor prevents non-specific plasminogen activation by a prourokinase mutant without impeding fibrin-specific fibrinolysis | US11732620 | 2007-04-04 | US07837992B2 | 2010-11-23 | Victor Gurewich; Ralph Pannell |
| A mutant prourokinase plasminogen activator (M5) was developed to make prouPA less subject to spontaneous activation during fibrinolysis. C1-inhibitor complexes with tcM5. The effect of C1-inhibitor on fibrinolysis and fibrinogenolysis by M5 was determined. Supplemental C1-inhibitor restores the stability of M5 but not that of prouPA. Clot lysis by M5 with supplemental C1-inhibitor showed no attenuation of the rate of fibrinolysis, whereas fibrinogenolysis was prevented by C1-inhibitor. Due to higher dose tolerance of M5 with C1-inhibitor, the rate of fibrin-specific lysis reached that achievable by nonspecific fibrinolysis without inhibitor. Plasma C1-inhibitor stabilized M5 in plasma by inhibiting tcM5 and thereby non-specific plasminogen activation. At the same time, fibrin-specific plasminogen activation remained unimpaired. This unusual dissociation of effects 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 C1-inhibitor are disclosed. | ||||||
| 192 | Targeting vector to the urokinase plasminogen activator receptor | US11468348 | 2006-08-30 | US07786088B2 | 2010-08-31 | Michael J. Welsh; Paola T. Drapkin |
| The present invention relates to the targeted delivery of a delivery vehicle construct which specifically binds to and stimulates endocytosis into cells expressing the urokinase plasminogen activator receptor (uPAR), and particularly human airway epithelia. The delivery vehicle construct comprises a portion of uPA and a cargo linked thereto and is useful for the targeted delivery of the cargo to a cell. In one aspect of the invention, the uPA portion of the delivery vehicle construct comprises the wild-type uPA, a fragment of uPA which has the PAI-1 binding region deleted, or a uPA peptide comprising amino acids 13-19 and is useful for the targeted delivery of the cargo to cells, and in particular to airway epithelia. The present invention also provides a method for delivering the delivery vehicle construct to a cell. The method comprises the steps of (a) contacting a target cell with a delivery vehicle construct comprising a uPA portion and a cargo portion; and (b) obtaining a desired result in the target cell. | ||||||
| 193 | MATERIALS AND METHODS FOR DELIVERING COMPOSITIONS TO SELECTED TISSUES | US12668349 | 2008-07-09 | US20100196435A1 | 2010-08-05 | William R. Freeman; Michael J. Sailor; Lignyun Cheng |
| This invention relates to devices, systems and methods for delivering preprogrammed quantities of an active ingredient to a biological system over time without the need for external power or electronics. | ||||||
| 194 | TREATING ATHEROSCLEROSIS | US12528300 | 2007-02-23 | US20100143335A1 | 2010-06-10 | Jian-ning Liu |
| The present application features methods and compositions for treating patients suffering from atherosclerosis or at risk for developing atherosclerosis. The treatment includes administering to the patient a pharmaceutical composition that includes an agent capable of blocking the interaction between uPA and its receptor uPAR, e.g., an ATF or a fragment thereof, an anti-uPA antibody, a uPAR or a fragment thereof, or an antibody that specifically binds to uPAR. | ||||||
| 195 | Conjugates of soluble peptidic compounds with membrane-binding agents | US10742887 | 2003-12-23 | US07655617B2 | 2010-02-02 | Richard Anthony Godwin Smith; Ian Dodd; Danuta Ewa Irena Mossakowkska |
| The present invention provides, among other things, soluble derivatives of soluble polypeptides that incorporate membrane binding elements. Methods of making these soluble derivatives, and methods of using these soluble derivatives also are provided. | ||||||
| 196 | Methods, Devices, And Compositions For Lysis Of Occlusive Blood Clots While Sparing Wound Sealing Clots | US12165904 | 2008-07-01 | US20090226413A1 | 2009-09-10 | Victor GUREWICH; Jian-Ning LIU; Paolo SARMIENTOS |
| It has now been discovered that certain mutant forms of pro-urokinase (“pro-UK”), such as so-called pro-UK mutant “M5” (Lys.sup.300.fwdarw.His)-, perform in the manner of pro-UK in lysing “bad” blood clots (those clots that occlude blood vessels), while sparing hemostatic fibrin in the so-called “good” blood clots (those clots that seal wounds, e.g., after surgery or other tissue injury). Thus, these pro-UK mutants are excellent and safe thrombolytic agents. These advantages allow them to be used in a variety of new methods, devices, and compositions useful for thrombolysis and treating various cardiovascular disorders in clinical situations where administration of other known thrombolytic agents has been too risky or even contraindicated. | ||||||
| 197 | Protease screening methods and proteases identified thereby | US11825627 | 2007-07-05 | US20090123452A1 | 2009-05-14 | Edwin L. Madison |
| Methods for identifying modified proteases with modified substrate specificity or other properties are provided. The methods screen candidate and modified proteases by contacting them with a substrate, such as a serpin, an alpha macroglobulins or a p35 family protein or modified serpins and modified p35 family members or modified alpha macroglobulins, that, upon cleavage of the substrate, traps the protease by forming a stable complex. Also provided are modified proteases. | ||||||
| 198 | Compositions and methods for modulating muscle cell and tissue contractility | US11019448 | 2004-12-21 | US07425534B2 | 2008-09-16 | Douglas B. Cines; Abd Al-Roof Higazi |
| The present invention relates to compositions and methods comprising one or more domains of urokinase-type plasminogen activator (uPA) in an amount effective to modulate one or more of the contractility and angiogenic activity of a mammalian muscle or endothelial cell or tissue for use in the treatment of a disease or condition having as a symptom thereof one or more of abnormal muscle cell or tissue contractility and abnormal angiogenic activity. The one or more domains of uPA can be present in the inventive compositions and methods either as part of the full uPA molecule in either single chain or two chain form (scuPA or tcuPA), or as an isolated polypeptide, or a fragment of the uPA molecule (e.g., the amino terminal fragment “ATF”), or a deletion mutant of the uPA molecule. The inventive methods comprise administering to a mammal afflicted with such a disease or condition the inventive composition, and modulating one or more of the contractility and the angiogenic activity of the muscle or endothelial cell or tissue, thereby treating the disease or condition. Kits for treating such diseases are also included. | ||||||
| 199 | C-1 inhibitor prevents non-specific plasminogen activation by a prourokinase mutant without impeding fibrin-specific fibrinolysis | US11732620 | 2007-04-04 | US20070298023A1 | 2007-12-27 | Victor Gurewich; Ralph Pannell |
| A mutant prourokinase plasminogen activator (M5) was developed to make prouPA less subject to spontaneous activation during fibrinolysis. C1-inhibitor complexes with tcM5. The effect of C1-inhibitor on fibrinolysis and fibrinogenolysis by M5 was determined. Supplemental C1-inhibitor restores the stability of M5 but not that of prouPA. Clot lysis by M5 with supplemental C1-inhibitor showed no attenuation of the rate of fibrinolysis, whereas fibrinogenolysis was prevented by C1-inhibitor. Due to higher dose tolerance of M5 with C1-inhibitor, the rate of fibrin-specific lysis reached that achievable by nonspecific fibrinolysis without inhibitor. Plasma C1-inhibitor stabilized M5 in plasma by inhibiting tcM5 and thereby non-specific plasminogen activation. At the same time, fibrin-specific plasminogen activation remained unimpaired. This unusual dissociation of effects 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 C1-inhibitor are disclosed. | ||||||
| 200 | Method for increasing the serum half-life of a biologically active molecule | US11113592 | 2005-04-25 | US20070060513A9 | 2007-03-15 | Robert Drummond; Steve Rosenberg |
| A method is provided for preparing a biologically active molecule having an increased serum half-life. The method involves conjugating a polymer such as polyethylene glycol to the biologically active molecule. Also provided are polypeptide drugs having an increased serum half-life, e.g., human urokinase plasminogen activator (human “uPA” or “hUPA”) or a fragment or derivative thereof. Pharmaceutical compositions containing such molecules and methods of using them to treat uPA-mediated and uPA receptor-mediated disorders are also provided. | ||||||
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