XIAP-Targeted Prostate Cancer Therapy
    11.
    发明申请
    XIAP-Targeted Prostate Cancer Therapy 有权
    XIAP靶向前列腺癌治疗

    公开(公告)号:US20070027169A1

    公开(公告)日:2007-02-01

    申请号:US11306241

    申请日:2005-12-20

    Abstract: A treatment for prostate cancer using cyclin-dependent kinase inhibitors is provided. The effects of cyclin-dependent kinase inhibitors on the survival of prostate cancer cells was examined. Roscovitine, R-roscovitine, and CGP74514A were shown to induce the apoptosis of LNCaP and LNCaP-Rf cells, both of which express wild-type p53. The cyclin-dependent kinase inhibitors of the present invention induce the mitochondria-mediated apoptosis of prostate cancer cells by a dual mechanism: p53 accumulation and XIAP depletion.

    Abstract translation: 提供使用细胞周期蛋白依赖性激酶抑制剂治疗前列腺癌。 检查细胞周期蛋白依赖性激酶抑制剂对前列腺癌细胞存活的影响。 显示Roscovitine,R-roscovitine和CGP74514A诱导LNCaP和LNCaP-Rf细胞的凋亡,两者都表达野生型p53。 本发明的细胞周期蛋白依赖性激酶抑制剂通过双重机制诱导线粒体介导的前列腺癌细胞凋亡:p53积累和XIAP消耗。

    SYSTEM AND METHOD OF MEASURING CELL VIABILITY AND GROWTH

    公开(公告)号:US20180045681A1

    公开(公告)日:2018-02-15

    申请号:US15682070

    申请日:2017-08-21

    Abstract: A novel SH-SAW biosensor capable of non-invasive and touch-free detection of cancer cell viability and growth or proliferation in two-dimensional (2D) and three-dimensional (3D) cell cultures as well as stem cell regeneration as it pertains to cancer cell biology and anti-cancer drug development is presented. The biosensor includes two pairs of resonators including interdigital transducers reflecting fingers to quantify mass loading by the cells in suspension as well as within a tumoroid culture platform. The biosensor can be part of a perfused 3PNS-tumoroid system that is amenable to real-time non-invasive monitoring of the cell proliferation, viability, and multiplexed detection of key physiologic and clinical biomarkers.

    PI3K-Akt Pathway Inhibitors
    17.
    发明申请
    PI3K-Akt Pathway Inhibitors 审中-公开
    PI3K-Akt途径抑制剂

    公开(公告)号:US20070238745A1

    公开(公告)日:2007-10-11

    申请号:US11733001

    申请日:2007-04-09

    CPC classification number: A61K45/06 A61K31/452 A61K31/52 A61K2300/00

    Abstract: A treatment for cancer using a combination therapy including an inhibitor of the PI3K/Akt pathway in combination with roscovitine. It is shown that the combination of roscovitine and API-2 (Triciribine) or roscovitine and LY294002 induce the apoptosis of androgen-dependent (LNCaP) and androgen-independent (PC3) prostate cancer cells. Two important results have been observed. First, cells that respond to roscovitine alone (LNCaP) initiate apoptosis sooner when co-treated. Second, cells that do not respond to roscovitine alone (PC3) apoptose when co-treated, although with delayed kinetics. In the absence of roscovitine, AKT inhibitors had no effect on LNCaP or PC3 survival, and in both cell lines, the combined treatment activated the mitochondrial pathway of apoptosis. Importantly, normal epithelial cells (RPWE) remained viable in the presence of roscovitine and AKT inhibitors. Events elicited by roscovitine (down-regulation of XIAP) and AKT inhibitors (accumulation of Bim) in LNCaP and PC3 cells are identified. Additional data show that PC3 cells apoptose when treated with AKT inhibitors and depleted of either XIAP or Cdk9. Taken together, these important results lead to improved treatments for cancers, such as prostate cancer, through the combination therapies taught herein.

    Abstract translation: 使用包括PI3K / Akt途径的抑制剂与roscovitine联合治疗的癌症治疗。 显示出roscovitine和API-2(Triciribine)或roscovitine和LY294002的组合诱导雄激素依赖性(LNCaP)和雄激素依赖性(PC3)前列腺癌细胞的凋亡。 观察到两个重要的结果。 首先,当联合治疗时,对roscovitine单独应答的细胞(LNCaP)会更早地启动细胞凋亡。 第二,当联合治疗时,对roscovitine(PC3)无反应的细胞凋亡,尽管具有延迟的动力学。 在没有roscovitine的情况下,AKT抑制剂对LNCaP或PC3存活没有影响,而在两种细胞系中,联合治疗激活线粒体凋亡途径。 重要的是,正常上皮细胞(RPWE)在存在roscovitine和AKT抑制剂的情况下保持存活。 确定由roscovitine引起的事件(XIAP的下调)和AKT抑制剂(Bim的积累)在LNCaP和PC3细胞中的活性。 另外的数据显示,当用AKT抑制剂处理并耗尽XIAP或Cdk9时,PC3细胞凋亡。 总而言之,这些重要的结果导致通过本文所教导的联合疗法改善癌症治疗,例如前列腺癌。

    Methods and compositions for reducing activity of the atrial natriuretic peptide receptor and for treatment of diseases
    20.
    发明申请
    Methods and compositions for reducing activity of the atrial natriuretic peptide receptor and for treatment of diseases 审中-公开
    用于降低心房钠尿肽受体活性和治疗疾病的方法和组合物

    公开(公告)号:US20080214437A1

    公开(公告)日:2008-09-04

    申请号:US11998792

    申请日:2007-11-30

    Abstract: Methods, compositions and devices are provided by the present invention for reducing activity of a natriuretic peptide receptor and other signals. Therapeutic treatments are provided by use of polynucleotides encoding a natriuretic peptide or by regulating the expression of natriuretic peptide receptor, such as NPRA and NPRC, or combinations of these therapies. Routes used for delivering polynucleotides encoding a natriuretic peptide, or, for example, siRNA that down regulates natriuretic peptide receptor include subcutaneous injection, oral gavage, transdermal and intranasal delivery routes. Compositions can include chitosan, chitosan derivatives, and chitosan derivative and a lipid. Transdermal delivery can use a transdermal cream. Intranasal delivery can use a dropper or an aspirator for delivery of a mist. Oral gavage delivers equivalent to oral delivery. Delivery permits cell and tissue specific targeting of gene therapies resulting in expression of a natriuretic peptide or down regulation of natriuretic peptide receptor. A variety of cancers, asthma and viral diseases can be treated therapeutically using the methods and compositions of the present invention.

    Abstract translation: 本发明提供了降低利尿钠肽受体活性和其他信号的方法,组合物和装置。 通过使用编码利尿钠肽的多核苷酸或通过调节利尿钠肽受体(如NPRA和NPRC)的表达或这些疗法的组合来提供治疗性治疗。 用于递送编码利尿钠肽的多核苷酸的路线,或例如下调调节利尿钠肽受体的siRNA包括皮下注射,口服管饲,透皮和鼻内递送途径。 组合物可以包括壳聚糖,壳聚糖衍生物和壳聚糖衍生物和脂质。 透皮给药可以使用透皮霜。 鼻内输送可以使用滴管或吸气器来传送雾。 口服管子相当于口服输送。 交付允许基因治疗的细胞和组织特异性靶向导致利尿钠肽的表达或利尿钠肽受体的下调。 可以使用本发明的方法和组合物治疗多种癌症,哮喘和病毒性疾病。

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