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1. 发明授权

EP1758562B1 COMPOSITIONS AND METHODS FOR BONE FORMATION AND REMODELING 有权
标题翻译：骨形成和重塑的组合物和方法
公开(公告)号：EP1758562B1
公开(公告)日：2012-12-05
申请号：EP05751764.1
申请日：2005-05-18
申请人： ENZO THERAPEUTICS, INC. , Zhang, Yazhou , Liu, Peng , Li, Xiaofeng , Zhang, Jie , Shan, Jufang , Engelhardt, Dean
发明人： WU, Dianqing , ZHANG, Yazhou , LIU, Peng , LI, Xiaofeng , ZHANG, Jie , SHAN, Jufang , ENGELHARDT, Dean
IPC分类号： A61P19/00 , A61P19/08 , A61P19/10 , A61K31/00 , G01N33/68
CPC分类号： G01N33/6893 , A61K38/00 , G01N33/6887 , G01N2500/00 , G01N2800/10 , G01N2800/108

2. 发明公开

EP3717100A1 DOUBLE-LAYERED CELLULOSE NANOFIBER MATERIAL, METHOD OF MANUFACTURING, MEMBRANES, AND USE THEREOF 有权转让
公开(公告)号：EP3717100A1
公开(公告)日：2020-10-07
申请号：EP18811246.0
申请日：2018-11-28
申请人： Mathew, Aji Pallikunnel , Liu, Peng
发明人： Mathew, Aji Pallikunnel , Liu, Peng
IPC分类号： B01D39/18

3. 发明授权

EP2248528B1 Use of compositions comprising Dkk2 and fragments thereof for the stimulation or enhancement of bone formation 有权转让
标题翻译：其中DKK2或其片段，对于骨形成刺激或增强组合物的使用
公开(公告)号：EP2248528B1
公开(公告)日：2013-01-02
申请号：EP10172837.6
申请日：2005-05-18
申请人： ENZO THERAPEUTICS, INC. , Li, Xiaofeng , Liu, Peng , Liu, Wenzhong , Engelhardt, Dean
发明人： Li, Xiaofeng , Liu, Peng , Liu, Wenzhong , Engelhardt, Dean , Wu, Dianqing
IPC分类号： A61K38/00 , A61P19/00 , A61P19/08 , A61P19/10
CPC分类号： A61K38/1709

4. 发明专利

CA3085128A1 DOUBLE-LAYERED CELLULOSE NANOFIBER MATERIAL, METHOD OF MANUFACTURING, MEMBRANES, AND USE THEREOF 未知
公开(公告)号：CA3085128A1
公开(公告)日：2019-06-06
申请号：CA3085128
申请日：2018-11-28
申请人： MATHEW AJI PALLIKUNNEL , LIU PENG
发明人： MATHEW AJI PALLIKUNNEL , LIU PENG
IPC分类号： B01D39/18
摘要： A double-layered material consisting of a cellulose nanofibrous (CNF) layer and a graphene oxide (GO) nanolayer coating, wherein the material comprises 0.5-4 wt.% of GO, preferably 1- 2 wt.% of GO, in relation to the total weight of the material is disclosed, as well as methods for producing said material, membranes comprising said material, and uses of said material and membranes. Thus, the present invention provides a cellulose nanofiber material with a high flux, a good separation performance and a strong mechanical and structural stability in solution.

5. 发明专利

IL179366D0 COMPOSITIONS AND METHODS FOR THE STIMULATION OR ENHANCEMENT OF BONE FORMATION AND THE SELF-RENEWAL OF CELLS 未知
公开(公告)号：IL179366D0
公开(公告)日：2007-03-08
申请号：IL17936606
申请日：2006-11-16
申请人： ENZO THERAPEUTICS INC , LI XIAOFENG , LIU PENG , LIU WENZHONG , ENGELHARDT DEAN , WU DIANQING
IPC分类号： A61K20100101

6. 发明授权

EP2409732B1 Compositions and methods for bone formation and remodeling 有权
标题翻译：成分和骨形成，并形成行业方法
公开(公告)号：EP2409732B1
公开(公告)日：2016-04-06
申请号：EP11184755.4
申请日：2005-05-18
申请人： Enzo Therapeutics, Inc. , Zhang, Yazhou , Liu, Peng , Li, Xiaofeng , Zhang, Jie , Shan, Jufang , Engelhardt, Dean
发明人： Zhang, Yazhou , Liu, Peng , Li, Xiaofeng , Zheng, Jie , Shan, Jufang , Engelhardt, Dean
IPC分类号： A61P19/00 , A61P19/08 , A61P19/10 , A61K31/00 , G01N33/68
CPC分类号： G01N33/6893 , A61K38/00 , G01N33/6887 , G01N2500/00 , G01N2800/10 , G01N2800/108

7. 发明公开

EP2248528A1 Use of compositions comprising Dkk2 and fragments thereof for the stimulation or enhancement of bone formation 有权转让
标题翻译：其中DKK2或其片段，对于骨形成刺激或增强组合物的使用
公开(公告)号：EP2248528A1
公开(公告)日：2010-11-10
申请号：EP10172837.6
申请日：2005-05-18
申请人： ENZO THERAPEUTICS, INC. , Li, Xiaofeng , Liu, Peng , Liu, Wenzhong , Engelhardt, Dean
发明人： Li, Xiaofeng , Liu, Peng , Liu, Wenzhong , Engelhardt, Dean , Wu, Dianqing
IPC分类号： A61K38/00 , A61P19/00 , A61P19/08 , A61P19/10
CPC分类号： A61K38/1709
摘要： Compositions and methods for the treatment of bone diseases, bone fractures, bone injuries and other bone abnormalities involving the use of Dkk protein, a Wnt antagonist, a Wnt inhibitor, or any other related protein for the stimulation or enhancement of mineralization and for stimulating the renewal of cells. One Dkk protein, Dickkopf-2 (Dkk-2), acts to stimulate bone formation independently of Wnt proteins which may be inhibited and/or antagonized by Dkk-2. Dkk-2 displayed enhanced specific targeting ability and enhanced biological activity in stimulating or enhancing mineralization. Dkk-2 also played a role in the differentiation and self-renewal of hematopoietic stem cells and mesenchymal stem cells, particularly in osteoblastogenesis and osteoclastogenesis.
摘要翻译：组合物和骨疾病，骨折，骨损伤及其它骨异常涉及使用Dkk蛋白，Wnt拮抗剂，Wnt抑制剂，或用于刺激或增强矿化的任何其它相关蛋白的治疗和用于刺激方法细胞的更新。一种Dkk蛋白，顽固-2（DKK-2）的作用是刺激骨形成unabhängig哪可以被Dkk-2来抑制和/或拮抗的Wnt蛋白。 DKK-2中显示增强的特异性靶向能力和在刺激或增强矿化增强的生物活性。 DKK-2因而在分化及造血干细胞和间充质干细胞的自我更新中发挥了作用，特别是在成骨细胞和破骨细胞形成。

8. 发明公开

EP1755643A4 COMPOSITIONS AND METHODS FOR THE STIMULATION OR ENHANCEMENT OF BONE FORMATION AND THE SELF-RENEWAL OF CELLS 审中-公开
标题翻译：组合物和方法刺激或增加骨形成和细胞的自我更新
公开(公告)号：EP1755643A4
公开(公告)日：2009-08-19
申请号：EP05758035
申请日：2005-05-18
申请人： ENZO THERAPEUTICS INC , LI XIAOFENG , LIU PENG , LIU WENZHONG , ENGELHARDT DEAN
发明人： WU DIANQING , LI XIAOFENG , LIU PENG , LIU WENZHONG , ENGELHARDT DEAN
IPC分类号： A61K38/00 , A61K38/17 , A61P19/00 , A61P19/08 , A61P19/10
CPC分类号： A61K38/1709

9. 发明公开

EP1758562A2 COMPOSITIONS AND METHODS FOR BONE FORMATION AND REMODELING 有权
标题翻译：组合物和骨形成和重塑方法
公开(公告)号：EP1758562A2
公开(公告)日：2007-03-07
申请号：EP05751764.1
申请日：2005-05-18
申请人： ENZO THERAPEUTICS, INC. , Zhang, Yazhou , Liu, Peng , Li, Xiaofeng , Zhang, Jie , Shan, Jufang , Engelhardt, Dean
发明人： WU, Dianqing , ZHANG, Yazhou , LIU, Peng , LI, Xiaofeng , ZHANG, Jie , SHAN, Jufang , ENGELHARDT, Dean
IPC分类号： A61K9/68
CPC分类号： G01N33/6893 , A61K38/00 , G01N33/6887 , G01N2500/00 , G01N2800/10 , G01N2800/108
摘要： The mechanism by which the high bone mass (HBM) mutation (G171V) of the Wnt coreceptor LRP5 regulates the canonical Wnt signaling was investigated. The mutation was previously shown to reduce Dkk protein-1-mediated antagonism, suggesting that the first YWTD repeat domain where G171 is located may be responsible for Dkk protein-mediated antagonism. However, we found that the third YWTD repeat, but not the first repeat domain, is required for DKK1-mediated antagonism. Instead, we found that the G171V mutation disrupted the interaction of LRP5 with Mesd, a chaperon protein for LRP5/6 molecules on the cell surface. Although the reduction in the level of cell surface LRP5 molecules led to a reduction in Wnt signaling in a paracrine paradigm, the mutation did not appear to affect the activity of coexpressed Wnt in an autocrine paradigm. Together with the observation that osteoblast cells produce autocrine canonical Wnt, Wnt7b, and that osteocytes produce paracrine Dkk1, we believe that the G171V mutation may cause an increase in Wnt activity in osteoblastls by reducing the numnber of targets for paracrine Dkk1 to antagonize without affecting the activity of autocrine Wnt.

10. 发明公开

EP3150255A1 COMPOSITIONS AND METHODS FOR BONE FORMATION AND REMODELING 审中-公开
标题翻译： ZUSAMMENSETZUNGEN UND VERFAHREN ZUR KNOCHENBILDUNG UND -UMFORMUNG
公开(公告)号：EP3150255A1
公开(公告)日：2017-04-05
申请号：EP16000780.3
申请日：2005-05-18
申请人： Enzo Therapeutics, Inc. , Zhang, Yazhou , Liu, Peng , Li, Xiaofeng , Zhang, Jie , Shan, Jufang , Engelhardt, Dean
发明人： Enzo Therapeutics, Inc. , Zhang, Yazhou , Liu, Peng , Li, Xiaofeng , Zhang, Jie , Shan, Jufang , Engelhardt, Dean
IPC分类号： A61P19/00 , A61P19/08 , A61P19/10 , A61K31/00 , G01N33/68 , A61K38/16
CPC分类号： G01N33/6893 , A61K38/00 , G01N33/6887 , G01N2500/00 , G01N2800/10 , G01N2800/108
摘要： The mechanism by which the high bone mass (HBM) mutation (G171V) of the Wnt coreceptor LRP5 regulates the canonical Wnt signaling was investigated. The mutation was previously shown to reduce Dkk protein-1-mediated antagonism, suggesting that the first YWTD repeat domain where G171 is located may be responsible for Dkk protein-mediated antagonism. However, we found that the third YWTD repeat, but not the first repeat domain, is required for DKK1-mediated antagonism. Instead, we found that the G171V mutation disrupted the interaction of LRP5 with Mesd, a chaperon protein for LRP5/6 molecules on the cell surface. Although the reduction in the level of cell surface LRP5 molecules led to a reduction in Wnt signaling in a paracrine paradigm, the mutation did not appear to affect the activity of coexpressed Wnt in an autocrine paradigm. Together with the observation that osteoblast cells produce autocrine canonical Wnt, Wnt7b, and that osteocytes produce paracrine Dkkl, we believe that the G171V mutation may cause an increase in Wnt activity in osteoblastls by reducing the numnber of targets for paracrine Dkkl to antagonize without affecting the activity of autocrine Wnt.
摘要翻译：研究了Wnt共同受体LRP5的高骨量（HBM）突变（G171V）调节规范Wnt信号传导的机制。以前显示突变以减少Dkk蛋白-1介导的拮抗作用，表明G171位于第一个YWTD重复结构域可能是Dkk蛋白介导的拮抗作用的原因。然而，我们发现第三个YWTD重复，但不是第一个重复结构域，是DKK1介导的拮抗作用所必需的。相反，我们发现G171V突变破坏了LRP5与Mesd的相互作用，Mesd是细胞表面上LRP5 / 6分子的伴侣蛋白。尽管细胞表面LRP5分子水平的降低导致旁分泌范例中Wnt信号传导的降低，但突变似乎并不影响共表达的Wnt在自分泌范式中的活性。连同观察到成骨细胞产生自分泌标准Wnt，Wnt7b，并且该骨细胞产生旁分泌Dkk1，我们认为G171V突变可能通过减少旁分泌Dkk1靶向拮抗的目标数量而引起成骨细胞中Wnt活性的增加，而不影响成骨细胞自分泌Wnt的活性。

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