Covalent modification of surfaces with polymers to increase
biocompatibility
    1.
    发明授权
    Covalent modification of surfaces with polymers to increase biocompatibility 失效
    用聚合物共价修饰表面以增加生物相容性

    公开(公告)号:US5977252A

    公开(公告)日:1999-11-02

    申请号:US612270

    申请日:1996-03-07

    CPC分类号: A61L33/0088

    摘要: Described herein is a technique for covalently modifying tissue and cellular surfaces to inhibit cell adhesion. The process described herein is conducted under conditions tolerable in vivo and employs a biocompatible polymer having a reactive group attached to at least one end that reacts with groups present or on tissue and cellular surfaces under aqueous and mild conditions and thereby covalently attaches the polymer to the tissue or cellular surface. Preferably, the reactive group attached to the polymer reacts with amines and hydroxyls present on tissue and cellular surfaces. In one preferred embodiment, the methods described herein provide for the covalent modification of tissue and cellular surfaces using a PEG-diisocyanate solution. The methods described herein are particularly useful in impairing platelet and leukocyte deposition in blood vessels and thereby thwarting thrombosis and restenosis, a common complication of vascular procedures including PTCA and vascular surgery. Furthermore, by masking the tissue surface proteins from blood elements, the methods described herein are useful in decreasing graft thrombogenicity and reducing the complications of vascular surgery. Finally the methods described herein reduce the immunogenicity of transplanted tissues and cells and thereby reduce the need for immunosuppressive therapy.

    摘要翻译: 本文描述了共价修饰组织和细胞表面以抑制细胞粘附的技术。 本文描述的方法在体内可耐受的条件下进行,并且使用生物相容性聚合物,其具有连接至至少一个末端的反应性基团,所述反应性基团在水溶液和温和条件下与存在的或与组织和细胞表面上的基团反应,从而将聚合物共价连接到 组织或细胞表面。 优选地,连接到聚合物的反应性基团与存在于组织和细胞表面上的胺和羟基反应。 在一个优选的实施方案中,本文所述的方法使用PEG-二异氰酸酯溶液提供组织和细胞表面的共价修饰。 本文描述的方法特别可用于损害血管中的血小板和白细胞沉积,从而阻止血栓形成和再狭窄,包括PTCA和血管手术的血管手术的常见并发症。 此外,通过从血液元件掩蔽组织表面蛋白质,本文所述的方法可用于降低移植物血栓形成和减少血管手术的并发症。 最后,本文所述的方法降低了移植组织和细胞的免疫原性,从而减少了免疫抑制治疗的需要。