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Crizotinib-d5

MCE 國(guó)際站：Crizotinib-d5

品牌：MedChemExpress (MCE)

貨號(hào)：HY-50878S

CAS：1395950-84-1

中文名稱：克唑替尼 d5

Synonyms：PF-02341066-d5

純度：≥99.0%

存儲(chǔ)條件：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

運(yùn)輸條件：美國(guó)大陸的室溫；其他地方可能有所不同。

產(chǎn)品活性：Crizotinib-d5 是 Crizotinib 的氘代物。Crizotinib (PF-02341066) 是一種具有口服活性的，ATP 競(jìng)爭(zhēng)性的 ALK 和 c-Met 抑制劑，IC50 分別為 20 和 8 nM。在細(xì)胞的實(shí)驗(yàn)中，Crizotinib 抑制 NPM-ALK 的酪氨酸磷酸化和 c-Met 的酪氨酸磷酸化，IC50 分別為 24 和 11 nM。Crizotinib 也是 ROS1 抑制劑。Crizotinib 具有有效的腫瘤生長(zhǎng)抑制作用。

生物活性：克唑替尼-d5 是氘標(biāo)記的克唑替尼。克唑替尼 (PF-02341066) 是一種口服生物可利用的 ATP 競(jìng)爭(zhēng)性 ALK 和 c-Met 抑制劑，IC50 分別為 20 和 8 nM?？诉蛱婺嵋种?NPM-ALK 的酪氨酸磷酸化和 c-Met 的酪氨酸磷酸化，在細(xì)胞測(cè)定中的 IC50 分別為 24 和 11 nM?？诉蛱婺嵋彩?ROS1 抑制劑?？诉蛱婺峋哂杏行У哪[瘤生長(zhǎng)抑制作用[1][2][3]。

體外：氫、碳和其他元素的穩(wěn)定重同位素已被整合到藥物分子中，主要用作藥物開發(fā)過程中定量的示蹤劑。氘化因其可能影響藥物的藥代動(dòng)力學(xué)和代謝特征而受到關(guān)注[1]。MCE 尚未獨(dú)立證實(shí)這些方法的準(zhǔn)確性。它們僅供參考。

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參考文獻(xiàn)：

[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Zou HY, et al. An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms. Cancer Res. 2007, 67(9), 4408-4417.
[3]. Christensen JG, et al. Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma. Mol Cancer Ther. 2007, 6(12 Pt 1), 3314-3322.
[4]. Cui JJ, et al. Structure based drug design of crizotinib (PF-02341066), a potent and selective dual inhibitor of mesenchymal-epithelial transition factor (c-MET) kinase and anaplastic lymphoma kinase (ALK). J Med Chem. 2011 Sep 22;54(18):6342-63.
[5]. Cullinane C, et al. Differential (18)F-FDG and 3'-deoxy-3'-(18)F-fluorothymidine PET responses to pharmacologic inhibition of the c-MET receptor in preclinical tumor models. J Nucl Med. 2011 Aug;52(8):1261-7
[6]. Shen A, et al. c-Myc alterations confer therapeutic response and acquired resistance to c-Met inhibitors in MET-addicted cancers. Cancer Res. 2015 Nov 1;75(21):4548-59.
[7]. Umapathy G, et al. The kinase ALK stimulates the kinase ERK5 to promote the expression of the oncogene MYCN in neuroblastoma. Sci Signal. 2014 Oct 28;7(349):ra102.
[8]. Tucker ER, et al. Immunoassays for the quantification of ALK and phosphorylated ALK support the evaluation of on-target ALK inhibitors in neuroblastoma. Mol Oncol. 2017 Aug;11(8):996-1006.
[9]. Liu H, et al. Identifying and Targeting Sporadic Oncogenic GeneticLiu H, et al. Identifying and Targeting Sporadic Oncogenic Genetic Aberrations in Mouse Models of Triple Negative Breast Cancer. Cancer Discov. 2018 Mar;8(3):354-369.