148 results about "Urokinase Plasminogen Activator" patented technology

The invention concerns a marker for low-grade inflammation and metabolic syndrome (MS) and MS-related diseases and/or low-grade inflammation-related diseases such as cardiovasculardisease, ischemic heart disease and type 2 diabetes. More particularly it concerns the measurement of the concentration of soluble urokinase plasminogen activator receptor (suPAR) in human biological fluids (sputum, cystic fluid, ascites, serum, plasma, urine) as a tool of diagnosing and/or prognosticating low-grade inflammation and metabolic syndrome and the risk of development of the related diseases such as cancer, cardiovascular disease, ischemic heart disease and type 2 diabetes.

A monoclonal or polyclonal antibody directed against urokinase plasminogen activator receptor (u-PAR), or a subsequence, analogue or glycosylation variant thereof. Antibodies are disclosed which react with free u-PAR or with complexes between u-PA and u-PAR and which are capable of 1) catching u-PAR in ELISA, or 2) detecting u-PAR, e.g. in blotting, or 3) in radioimmunoprecipitation assay precipitate purified u-PAR in intact or fragment form, or 4) is useful for immunohistochemical detection of u-PAR, e.g. in immunostaining of cancer cells, such as in tissue sections at the invasive front, or 5) inhibits the binding of pro-u-PA and active u-PA and thereby inhibits cell surface plasminogen activation. Methods are disclosed 1) for detecting or quantifying u-PAR, 2) for targeting a diagnostic to a cell containing a u-PAR on the surface, 3) for preventing or counteracting proteolytic activity in a mammal. Methods for for selecting a substance suitable for inhibiting u-PA/u-PAR interaction, for preventing or counteracting localized proteolytical activity in a mammal, for inhibiting the invasion and/or metastasis comprise the use of the antibodies and of nude mice inoculated with human cancer cells which are known to invade and/or metastasize in mice and having a distinct color, f.x. obtained by means of an enzyme and a chromogenic substrate for the enzyme, the color being different from the cells of the mouse.

A process for inhibiting vascular proliferation separately introduces components into the eye to generate plasmin in the eye in amounts to induce complete posterior vitreous detachment where the vitreoretinal interface is devoid of cortical vitreous remnants. The process administers a combination of lysine-plasminogen, at least one recombinant plasminogen activator selected from the group consisting of urokinase, streptokinase, tissue plasminogen activator, chondroitinase, pro-urokinase, retavase, metaloproteinase, and thermolysin and a gaseous adjuvant to form a cavity in the vitreous. The composition is introduced into the vitreous in an amount effective to induce crosslinking of the vitreous and to induce substantially complete posterior vitreous detachment from the retina without causing inflammation of the retina. The gaseous adjuvant material is introduced into the vitreous simultaneously with or after the lysine-plasminogen and recombinant plasminogen activator such as recombinant urokinase to compress the vitreous against the retina while the composition induces the complete posterior vitreous detachment.

The present invention relates to novel compounds for inhibiting the urokinase plasminogen activator (uPA), which have high bioavailability and oral administerability, and also to the use thereof as therapeutic active compounds for the treatment of urokinase- or/and urokinase receptor-associated disorders such as, for example, tumors and metastasizing. The invention relates in particular to compounds containing hydroxyamidine or hydroxyguanidine groups.

The invention is about a method to purify the recombined human urokinase by the chromatography. The invention relates to recovery the gene engineering production from the mammal cell culture using the Streamline-SP, Sephacryl S-200, Sepharose Fast Flow and DEAE-Sepharose Fast Flow method. The recombined human urokinase can meet the SFDA standard and the percent recovery is above 70%, the purity is above 99% by using the method.

The present invention relates to the use of uPAR-binding molecule-drug conjugates capable of specifically binding a urokinase plasminogen activator receptor (uPAR) as therapeutic and diagnostic reagents for the treatment and monitoring of metastases. The present invention provides methods of treatment of metastases, comprising administering to a subject a uPAR-binding molecule-chemotherapeutic conjugate that is capable of binding to and internalizing into uPAR-expressing cells. The present invention further provides pharmaceutical compositions and kits comprising such conjugates. The present invention further provides methods and compositions relating to combination therapy for cancer involving or mediated by uPAR-expressing cells using uPAR-binding molecule-drug conjugates of the invention.

The invention relates to a urine protein enriching method. In the method, urine protein in urine is absorbed directly by an adsorbent in a urinal or a pee hopper, and the adsorbent for adsorbing the urine protein is conveyed to a working point for follow-up treatment; and based on the isoelectric point properties of specific urine protein, the urine protein such as urinary trypsin inhibitor, human urinary kininogenase, urokinase and the like is adsorbed directly and effectively by using the specific adsorbent such as ion exchange resin, and thus, the step of collecting the urine is avoided. The method does not influence sanitation of toilets obviously, reduces the cost of urine transportation substantially and solves a series of environmental problems.

The present invention relates to compositions of the polypeptide EEIIMID and one or more fibrinolytic agents selected from the group consisting of scuPA, tPA, uPA, tcuPA, streptokinase, rt-PA, alteplase, rt-PA derivatives, reteplase, lanoteplase, TNK-rt-PA, anisoylated plasminogen streptokinase complex, anistreplase, or a streptokinase derivative. The invention further relates to methods of enhancing the fibrinolytic activity, reducing the side effects due to vasoactivity caused by the fibrinolytic agents, or prolonging the half lives of the fibrinolytic agents by adding EEIIMD.

The invneiton relates to expression, purification and crystallization of urokinase catalytic domain mutant, relating to the field of medicine, biotechnique, and structural biology. And the invention provides a techical method of expression, purification and crystallization of urokinase catalytic domain mutant in Pichia pastoris. And the cultured urokinase catalytic domain mutant has crystallographic space group R3, and unit cell parameters: a=b=120.48, c=42.45, alpha=beta=90.0deg, and gama=120.0 deg. And this protein has serine proteinase activity, appliable to high flux screening of urokinase inhibitor; and its high resolution crystal provides a research and development platform for design and development of urokinase inhibitor.

A specific purified high-molecular urokinase chromatography media is characterized by having a structure as follows: HOOC-(CH2)4(NH)C-O-R-O-C(NH)NH(CH2)4-CO-X,X=NHC6H5C(NH)NH2, wherein R represents cross-linked agarose substrate. The specific purified high-molecular urokinase chromatography media has the advantages of being simple in preparation process and mild for reaction conditions, being applicable to high-efficiency separation of high-molecular urokinase media and low-molecular urokinase media, and being capable of implementing industrial production of high-purification and high-molecular urokinase.

A thrombus target fusion mA5UKB with both anticoagulating and thrombolytic functions is prepared from the mutant mAnxA5 of AnnexinA5 having anti-coagulating function and the urokinase B chain (UKB) having thrombolytic function through fusing. It can be used to prepare the thrombolytic medicine.

In the field of biological medicines, a use of prourokinase (proUK) and variants thereof in facilitated percutaneous coronary intervention (PCI) in patients with acute myocardial infarction is provided. The use includes: within 6 hrs after a patient is afflicted with accurate myocardial infarction (AMI), firstly, performing thrombolytic therapy with proUK or variants thereof, and then, performing a PCI operation, to dredge the infarction related artery (IRA) as soon as possible, and re-establish an effective forward blood flow, such that an ischemic myocardium is reperfused. According to the present invention, the facilitated PCI for treatment of AMI with the proUK or variants thereof has an effect superior to that of direct PCI.

The invention relates to waterless self-circulating urine flushing equipment with a function of collecting raw urokinase. The equipment comprises a water incoming tank, urinals and a pipeline. The water incoming tank is an overhead purified water tank providing the urinals with water through the pipeline. A human body sensor is arranged over a water inlet of each urinal and is in control connection with an electromagnetic valve which controls the water incoming tank to supply water. A drain pipe under every urinal is communicated with a liquid storage tank. A water level sensor in control connection with a booster pump switch is arranged inside the liquid storage tank. A liquid outlet of a booster pump is communicated with a liquid filter system. The liquid filter system comprises a plurality of filter elements; each filter element is arranged inside a cylinder; the liquid discharged from the liquid storage tank by the booster pump passes the filter elements in order, and a purified water outlet is communicated with the overhead purified water tank. The waterless self-circulating urine flushing equipment is applicable to urinals, especially applicable to water-deficient areas, and has the advantages such that application and maintenance costs are lower, less water is consumed, the environment is protected, recycling efficiency of waste water and filtrate is high, and the equipment can be used normally in cold areas.

There is provided a 177-Lu labelled peptide for site-specific targeting of the Urokinase Plasminogen Activator Receptor (uPAR) thereby enabling treatment of a cancer disease associated with high uPAR expression; e.g. treatment of colorectal cancer by administering to a patient an effective amount of the 177-Lu labelled peptide.

The invention provides an extraction method of clotting genomic DNA (deoxyribonucleic acid), which comprises the following steps that: nattokinase is added to a sample before extraction, and fibrin can be quickly decomposed by utilizing the thrombolytic force of the nattokinase several times more than that of a thrombolytic agent UK (urokinase), and further blood clots are separated, so that the blood clots become a homogeneous solution; and the obstacle of blood DNA extraction caused by sludged blood is removed, thereby the extraction speed of blood DNA is obviously improved, and simultaneously the purity and the yield of DNA product are greatly increased. The method provided by the invention is applicable to the extraction of DNA from sludged blood from a crime scene or dead bodies, the extraction of high-throughput blood gDNA and the extraction of blood gDNA in an antibody analysis experiment.

Hepatic cirrhosis is considered a severe health problem in Mexico, since it is the third mortality cause in working-age people and there is no 100% effective treatment. Cirrhosis is characterized by an exacerbated increase of collagen in liver parenchyma, replacing the hepatocytes and thus provoking liver failure. This is one of the reasons why we have used a gene therapy through specific delivery to cirrhotic livers of the gene of human urokinase plasminogen activator (huPA), which activates mechanisms that induce the degradation of excess cellular matrix and stimulate hepatocyte proliferation, obtaining thus a fast re-establishment of the liver function. In the instant invention, the modified human uPA gene was inserted in the adenoviral vector (pAd-DeltahuPA), because it is not secreted and does not provoke hypercoagulation or spontaneous internal bleedings. Moreover, data from the bio-distribution essay with an adenoviral vector with reporter gene beta-gal have shown liver specificity as the target organ of the vector. Using ELISA, huPa protein was detected in liver homogenates (4500 pg/ml) in animals treated with pAd-DeltahuPA and was also intracellularly detected through immunochemistry in liver cuts (80% positive cells). huPa induced a dramatic fibrosis reduction (85%) on day 10 of vector administration, compared to control cirrhotic rats and 55% hepatocyte proliferation increase. Liver function tests (ALT, AST, alkaline phosphatase and bilirubin) dropped to nearly normal levels and hepatocyte proliferation was observed. Because of the two beneficial event cascades, gene therapy with modified huPA can be developed as a definite potential treatment for patients with liver cirrhosis.

The present invention discloses the expression method of natto kinase and its special expression vector and engineering bacterium. The expression vector is lactic acid bacteria constitutive expression vector containing constitutive expression promoter, natto kinase leading peptide and its mature peptide coding sequence; or lactic acid bacteria inducing expression vector containing inducing expression promoter, transmembrane signaling peptide coding sequence, natto kinase leading peptide and its mature peptide coding sequence. Experiment shows that the expressed product of the engineering bacterium has relatively high fibrinolysis activity up to 41.7 urokinase unit each milliliter of the fermented supernatant, eating safety, no toxic side effect on human body and high stability, is suitable for direct oral taking and may be added to various kinds of food. The present invention lays foundation for developing orally taken thrombolytic functional health food of natto kinase.

The invention discloses a manufacturing method of an adjustable liver damage animal model and a special DNA fragment thereof; a DNA fragment I is formed by sequentially connecting liver super promoters and antisense tetracycline activator coding genes of a Tet-on gene expression system from upstream to downstream; an DNI fragment II is formed by sequentially connecting tetracycline reaction factors, promoters and prourokinase activator coding genes of the Tet-off/Tet-on gene expression system from upstream to downstream; a recombination expression vector carrying the DNI fragment II is used for converting mammalian cells, the cells are cultivated to obtain recombinant adenovirus. The DNA fragment I is led in the animal to obtain a transgenosis first-construction animal; the transgenosis first-construction animal and scid/bg animal are back-crossed to obtain the animal carrying the DNA fragment I with the scid/bg background; the recombinant adenovirus is used for injecting the animal carrying the DNA fragment I with the scid/bg background, so as to obtain the adjustable liver damage animal model; in the model, the prourokinase activator expression is activated by doxycycline, the expression intensity is changed along with the change of dosage, the specificity is very high.

The present invention features pharmaceutical compositions and methods to inhibit angiogenesis, with implications to cancer therapy. These methods are based on the discovery that activated thrombin has antiangiogenic activity and that this antiangiogenic activity is at least in part, mediated through the activation of a class of thrombin receptors termed, Protease Activated Receptor (PAR). Pharmaceutical compositions and methods are also directed to a class of proteases which mediate this activation, particularly the urokinase plasminogen activator (uPA) polypeptide.