序号 专利名 申请号 申请日 公开(公告)号 公开(公告)日 发明人
1 一种提高尿激酶纯度的方法 CN201611197215.2 2016-12-22 CN106701722A 2017-05-24 刘乃山; 王小凤; 迟培升
发明公开了一种提高尿激酶纯度的方法。其特征在于采用了D160阳离子树脂交换法、亲和膜色谱法及亲和层析法相结合,以尿激酶粗品为原料制备尿激酶。所得到的尿激酶质量优于现有国内平,尿激酶比活可达到150,000IU/mg.pr以上,高分子尿激酶相对含量可达到90%以上,尿激酶生物活性回收率可达到65%。本方法解决了现有尿激酶制备方法普遍存在的操作繁琐、产品质量差,收率低和生产成本高等问题。
2 一种制备尿激酶的方法 CN201710197822.7 2017-03-29 CN106676088A 2017-05-17 王海瑶; 靳海宁; 熊祖应
申请属于生物技术领域,具体涉及一种制备尿激酶的方法。该方法表达尿激酶的产量高、易纯化,表达的尿激酶蛋白糖基化和人体自身表达的尿激酶结构相似,功能相同。并且,该方法不受自然资源的限制,可根据市场需求不限量生产和人体相同结构的尿激酶,投入少、产出高,溶栓效果好,无毒副作用
3 一种亲和层析纯化尿激酶的方法 CN201611197428.5 2016-12-22 CN106520739A 2017-03-22 刘乃山; 李先英; 迟培升
发明公开了一种亲和层析纯化尿激酶的方法。具体的说,就是以健康成年男性新鲜尿液为原料,经过甲壳质吸附、吸附柱层析以及亲和层析等现代蛋白质高端生化分离技术来制备高纯度的尿激酶,可以将总收率提高到80%以上,总效价不低于40000iu/mg。
4 一种提高尿激酶收率的方法 CN201611077802.8 2016-11-30 CN106520738A 2017-03-22 刘乃山; 张晓
发明公开了一种提高尿激酶收率的方法。该方法利用尿激酶蛋白质在等电点溶解度最低的特性,通过调节尿液PH值,然后加入甲壳质吸附、过滤、洗脱、离心、沉淀、干燥步骤来实现从尿液中提取尿激酶。尿激酶的产品收率达到0.02%以上。
5 一种树脂再生提高柱效纯化尿激酶的方法 CN201611077795.1 2016-11-30 CN106520737A 2017-03-22 刘乃山; 张晓
发明公开了一种树脂再生提高柱效纯化尿激酶的方法。具体的说,就是以健康成年男性新鲜尿液为原料,经过甲壳质吸附洗脱、硫酸铵盐析、吸附柱层析以及亲和层析等现代蛋白质高端生化分离技术来制备高纯度的尿激酶,可以将总收率提高到75%以上,总效价不低于50000iu/mg,柱效提升约55%。
6 一种制备尿激酶的方法 CN201510549397.4 2015-09-01 CN105087531A 2015-11-25 郑少亮; 王旭; 肖益热; 田友军
发明涉及一种直接在小便池或便斗中用装改性胶的滤布吸附尿液中的尿蛋白,并将吸附尿蛋白的滤布袋运至加工点进行后续处理的尿蛋白富集方法。本方法利用特定尿蛋白的等电点性质,通过使用包括改性硅胶,大孔树脂,甲壳素,离子树脂等;对尿胰蛋白酶抑制剂、人尿激肽原酶、尿激酶等尿蛋白直接有效吸附,避免了尿液的收集步骤。该方法对厕所的卫生状况无明显影响,并大幅度降低了尿液运输的成本以及带来的一系列环境问题。
7 聚乙二醇修饰的低分子量尿激酶及其制备方法和应用 CN201510499115.4 2015-08-14 CN105087530A 2015-11-25 苗丕渠; 韩大雄; 厉道娟; 耿春晨; 王筱蒙; 池正昌; 沈小宁
发明提供一种聚乙二醇修饰的低分子量尿激酶及其制备方法和应用。本发明采用聚乙二醇(PEG)修饰低分子量尿激酶(LMW-UK),聚乙二醇与LMW-UK的N-末端通过共价键方式连接,获得LMW-UK的聚乙二醇修饰产物。修饰产物均一性好、分离纯化工艺简单、活性回收率高,同时,显著延长了体内半衰期,具有有效治疗纤维蛋白原血症和预防动脉粥样硬化(AS)、血栓栓塞并发症、糖尿病血管并发症、糖尿病肾病等功效。
8 一种纯化尿激酶的方法 CN201410222057.6 2014-05-21 CN104031901A 2014-09-10 郭国岭; 扈会平; 徐晓; 曹延琴; 王伟梅; 邱伟
一种纯化尿激酶的方法。本发明将尿激酶粗品中2个主要分子量区域的蛋白分开处理,通过调节pH值等手段进一步去除粗品中的杂质、热源和细胞内毒素,得到了尿激酶精品。
9 一种制备尿激酶粗品的方法 CN201310643507.4 2013-11-30 CN103740687A 2014-04-23 刘乃山; 张晓涵; 安迪; 张元泽
发明公开了一种制备尿激酶粗品的方法。本发明的技术方案是利用吸附工序、脱附工序、盐析工序从合格尿液中制备尿激酶粗品的方法。本发明操作简单且有较高的收率。
10 Lung volume reduction using glue composition US11008782 2004-12-08 US07553810B2 2009-06-30 Glen Gong; Ronald Dieck
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.
11 Lung volume reduction using glue composition US11008782 2004-12-08 US20050281802A1 2005-12-22 Glen Gong; Ronald Dieck
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.
12 Long-acting composition US507154 1983-06-23 US4609546A 1986-09-02 Hajime Hiratani
A composition wherein a physiologically active polypeptide or a glycoprotein of human origin, for instance, urokinase, kallikrein or leukocyte interferon, is coupled to a polyoxyethylene-polyoxypropylene copolymer. The composition is effective in the human body for a prolonged period of time.
13 DRUG REGIMEN FOR TREATMENT OF CEREBRAL ISCHEMIA US15859075 2017-12-29 US20180185475A1 2018-07-05 Lawrence M. KAUVAR; Damir JANIGRO
Treatment of subjects experiencing cerebral ischemia is improved when the treatment employs a thrombolytic and an inhibitor against vascular endothelial growth factor receptor signal transduction (VEGF-RST) at a reduced, low dosage compared to that used to treat cancer patients. The treatment is also improved to permit point-of-care use by formulating protein drugs for long term stability at room temperature, providing doses appropriate for the method, and by combining the therapeutic agents with a point-of-care diagnostic for blood brain barrier integrity.
14 Method of treating fibrosis in skeletal muscle tissue US14763367 2015-07-24 US09901626B2 2018-02-27 G. Blair Lamb
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.
15 METHODS AND KITS FOR REVERSIBLE ADHESION OF IMPLANTS TO AN EYE SCLERA US14583946 2014-12-29 US20150182659A1 2015-07-02 Ido Didi Fabian
Methods and kits are provided for reversibly affixing an implant to a sclera of an eye of a subject. The methods and kits are based on applying a composition comprising at least one fibrin-based tissue adhesive to at least one of said implant and said sclera, thereby affixing said implant to the sclera, and applying a composition comprising at least one plasminogen activator to at least one of said implant and said sclera following a desired time-period, thereby detaching said implant from said sclera, and removing said implant from said eye.
16 METHOD OF TREATING FIBROSIS IN SKELETAL MUSCLE TISSUE US14763367 2014-01-28 US20150359860A1 2015-12-17 Blair G Lamb
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.
17 PEPTIDE DIRECTED PROTEIN KNOCKDOWN US14431060 2013-09-27 US20150266935A1 2015-09-24 Yu Tian Wang; Shelly Xuelai Lan; Wuyang Jin Jin
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.
18 Fibrinolytic/Proteolytic Treatment of Myofacial and Neuropathic Pain and Related Conditions US13751673 2013-01-28 US20140212405A1 2014-07-31 Blair Lamb
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.
19 C-1 Inhibitor prevents non-specific plasminogen activation by a prourokinase mutant without impeding fibrin-specific fibrinolysis US12215966 2008-07-01 US20090010916A1 2009-01-08 Victor Gurewich; Ralph Pannell
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 C1-inhibitor, which was the principal inhibitor of tcM5 in plasma. The effect of supplemental additions of C1-inhibitor on fibrinolysis and fibrinogenolysis by M5 was determined. Supplemental C1-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 C1-inhibitor, the rate of fibrin-specific lysis reached that achievable by nonspecific fibrinolysis, which is the maximum possible for a plasminogen activator. Plasma C1-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 C1-inhibitor are disclosed.
20 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 JP5957085B2 2016-07-27 高橋 健一; 余田 英士
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