"Clickable" polymer-caged nanobins as a modular drug delivery platform.
"Clickable" polymer-caged nanobins as a modular drug delivery platform.
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DOI：
10.1021/ja9017336
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发表时间：
2009-07-08
影响因子：
15
通讯作者：
Nguyen ST
中科院分区：
文献类型：
--
作者：
Lee SM;Chen H;O'Halloran TV;Nguyen ST
模块化可点击的聚合物笼纳米蛋白（PCNs）是由脂质体模板制备的，使用降胆固醇修饰的聚丙烯酸试剂，然后与炔功能化的二胺连接剂交联，可以通过点击连接偶联叠氮修饰的靶向配体。这些pcn具有ph响应特性，可用于在轻度酸性条件下触发脂质体核心内胶囊化阿霉素（DXR）有效载荷的释放。在与叠氮修饰的叶酸作为活性靶向配体点击偶联后，得到的叶酸偶联的、装载dxr的pcn （f-PCNDXR）对叶酸受体（FR）阳性的肿瘤细胞（如KB和OvCa432）的作用强于FR阴性的MCF7细胞。f-PCNDXR作为细胞fr表达水平的函数，可以很容易地识别fr阳性肿瘤细胞，在每个细胞中表现出不同程度的增强。具有靶向功能和ph敏感的药物释放触发器，f-PCNDXR对过表达叶酸靶受体的癌细胞表现出50倍的效力增强。
Modularly clickable polymer-caged nanobins (PCNs) were prepared from liposome templates using a drop-in cholesterol-modified poly(acrylic acid) reagent followed by crosslinking with alkyne-functionalized diamine linker that can allow for the conjugation of azido-modified targeting ligands via click ligation. These PCNs possess pH-responsive characteristics that can be used to trigger the release of encapsulated doxorubicin (DXR) payload inside the liposomal core under mild acidic conditions. After click-conjugation with azide-modified folate as an active targeting ligand, the resulting folate-conjugated, DXR-loaded PCNs (f-PCNDXR) demonstrated enhanced potency to folate receptor (FR)-positive tumor cells such as KB and OvCa432 over FR-negative MCF7 cells. f-PCNDXR can readily discriminate FR-positive tumor cells as a function of the level of cellular FR-expression, showing different degrees of potentiation in each cell. With both targeting functionalities and pH-sensitive drug-releasing triggers, f-PCNDXR exhibited 50 times enhanced potency to cancer cells that overexpress the folate target receptors.
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影响因子：
3.4
作者：
Ishida, T;Kirchmeier, MJ;Allen, TM
通讯作者：
Allen, TM
影响因子：
4.7
作者：
Gabizon, A;Horowitz, AT;Zalipsky, S
通讯作者：
Zalipsky, S
影响因子：
15
作者：
Bertin, PA;Gibbs, JM;Nguyen, ST
通讯作者：
Nguyen, ST
影响因子：
5.7
作者：
Chen H;Ahn R;Van den Bossche J;Thompson DH;O'Halloran TV
通讯作者：
O'Halloran TV
影响因子：
--
作者：
Bae, Y;Jang, WD;Kataoka, K
通讯作者：
Kataoka, K