5mg 克唑替尼/Crizotinib （PF-02341066|c-Met和ALK抑制劑
| 參考價 | ￥ 900 |
| 訂貨量 | ≥1 |
- 公司名稱 上海高創化學科技有限公司
- 品牌 Selleck
- 型號 5mg
- 產地 美國
- 廠商性質 代理商
- 更新時間 2017/11/21 10:34:31
- 訪問次數 1690
聯系我們時請說明是化工儀器網上看到的信息，謝謝!
| 供貨周期 | 現貨 | 規格 | 5mg |
|---|---|---|---|
| 貨號 | S1068 | 主要用途 | 科研 |
克唑替尼/Crizotinib (PF-02341066|c-Met和ALK抑制劑 現貨
Crizotinib (PF-02341066)是一種有效的c-Met和ALK抑制劑，在細胞試驗中IC50分別為11 nM 和 24 nM。
化學數據
| 分子量 | 450.34 | 穩定性 | 3年 -20°C粉狀 |
|---|---|---|---|
| 化學式 | C21H22Cl2FN5O | -- -- -- | |
| CAS號 | 877399-52-5 | 別名 | N/A |
| Solubility (25°C) * | 體外 | DMSO | 9 mg/mL (19.98 mM) |
| Water | Insoluble | ||
| Ethanol | Insoluble | ||
| 體內 | 5% DMSO+30% PEG 300+dd H2O | 5mg/mL | |
| * <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. | |||
| 化學名 | 3-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-5-(1-(piperidin-4-yl)-1H-pyrazol-4-yl)pyridin-2-amine | ||
制備儲備液
| 濃度溶劑體積(DMSO)質量 | 1 mg | 5 mg | 10 mg |
| 1 mM | 2.2205 mL | 11.1027 mL | 22.2054 mL |
| 5 mM | 0.4441 mL | 2.2205 mL | 4.4411 mL |
| 10 mM | 0.2221 mL | 1.1103 mL | 2.2205 mL |
| 50 mM | - | - | - |
生物活性
| 產品描述 | Crizotinib (PF-02341066)是一種有效的c-Met和ALK抑制劑，在細胞試驗中IC50分別為11 nM 和 24 nM。 | |||||
|---|---|---|---|---|---|---|
| 靶點 |
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| 體外研究 | PF-2341066作用于mIMCD3小鼠和MDCK犬上皮細胞，作用于c-Met磷酸化作用時具有相似效果，IC50分別為5 nM 和20 nM。PF-2341066作用于表達c-Met ATP-結合位點突變型V1092I 或H1094R或 P-環突變 M1250T 的NIH3T3 細胞，具有相似的活性，且活力增高，IC50分別為19 nM,2 nM 和15 nM,而作用于表達野生型受體的NIH3T3 細胞時，IC50為13 nM。[1] 相反, 觀察到PF-2341066作用于表達c-Met活化環突變型Y1230C 和Y1235D的細胞時，與作用于野生型受體相比，效果發生顯著改變，IC50分別為127 nM 和92 nM。PF-2341066 作用于分別表達內源性c-Met 突變體R988C和 T1010I 的NCI-H69 和HOP92 細胞，也有效抑制c-Met 磷酸化, IC50分別為13 nM 和16 nM。與作用于c-Met相比，PF-2341066作用于VEGFR2 和PDGFRβ RTKs, 選擇性高1000多倍，作用于IRK和Lck選擇性高250多倍，作用于Tie2, TrkA,和TrkB選擇性高40到60倍。PF-2341066 作用于RON和 Axl RTKs時選擇性為20到30倍。相反，PF-2341066 作用于表達ALK RTK 的核磷蛋白 (NPM)- 間變性淋巴瘤激酶(ALK) 致癌融合突變體和 KARPAS299人間變性大細胞淋巴瘤(ALCL)細胞系時具有相近的IC50值，為24 nM。PF-2341066抑制c-Met依賴的癌細胞的腫瘤表現型，和內皮細胞的血管生成表現型。PF-2341066抑制人GTL-16胃癌細胞生長，IC50為9.7 nM。PF-2341066誘導 GTL-16細胞凋亡，IC50 為8.4 nM。PF-2341066 抑制HGF刺激的人NCI-H441肺癌細胞遷移和入侵，IC50分別為11 nM 和6.1 nM。PF-2341066抑制 MDCK細胞散射，IC50為16 nM。PF-2341066 抑制HGF-刺激的c-Met磷酸化,細胞存活，和Matrigel入侵，IC50分別為11 nM, 14 nM和35 nM。此外, PF-2341066抑制纖維蛋白膠中的血清刺激的 HMVEC分支小管形成 (形成血管)。[1] PF-2341066 作用于Karpas299 或SU-DHL-1 ALCL細胞，也有效抑制 NPM-ALK磷酸化，IC50 為24 nM。PF-2341066 有效抑制細胞增殖，伴隨著使細胞周期停在G(1)-S期，且誘導 ALK陽性的 ALCL 細胞凋亡，IC50為30 nM, 但是作用于ALK陰性的淋巴瘤細胞則無效果。 [2] 此外, PF-2341066 抑制骨肉瘤的一些活動行為，及其腫瘤生長 (例如,增殖和存活)和轉移 (例如，入侵和形成克隆)。[3] | |||||
| 體內研究 | PF-2341066每天按50 mg/kg和75 mg/kg劑量處理GTL-16 模型, 引起大腫瘤 (體積大于600 mm3) 明顯衰退，且按43天處理日程處理后，平均腫瘤體積降低60%。在另一項研究中, PF-2341066處理3個月以上，*抑制GTL-16腫瘤生長，PF-2341066每天按50 mg/kg劑量處理小鼠，3個月后，只有1/12小鼠的腫瘤生長得到提高。PF-2341066每天按50 mg/kg劑量處理NCI-H441 NSCLC 模型處理周期為38天，觀察到平均腫瘤體積降低43%。PF-2341066 每天按50 mg/kg劑量作用于 Caki-1 RCC模型，處理周期為33天，觀察到平均腫瘤體積降低53%，且每種腫瘤體積降低至少30%。PF-2341066每天按 50 mg/kg劑量作用于 U87MG 惡性膠質瘤或PC-3前列腺癌移植瘤模型,幾乎*抑制腫瘤生長，在實驗zui后一天，抑制分別達97% 或84%。相反, PF-2341066每天按50 mg/kg劑量口服給藥處理 MDA-MB-231 乳腺癌模型,或 DLD-1 結腸癌模型，不會顯著抑制腫瘤生長。PF-2341066每天按12.5 mg/kg, 25 mg/kg, 和50 mg/kg劑量作用于 GTL-16 腫瘤，觀察到CD31陽性內皮細胞顯著降低，這種作用存在劑量依賴性，說明 MVD 受抑制，且具有相關的抗癌高效性，這種作用也存在劑量依賴性。PF-2341066 作用于GTL-16 和 U87MG 模型，顯著降低人VEGFA 和IL-8血漿水平，這種作用存在劑量依賴性。PF-2341066口服處理GTL-16 腫瘤，觀察到磷酸化的c-Met, Akt, Erk, PLCλ1,和 STAT5水平顯著受抑制。[1]PF-2341066 每天按100 mg/kg劑量口服處理攜帶Karpas299 ALCL 移植瘤的SCID Beige 小鼠，具有抗癌高效性，這種作用存在劑量依賴性，處理15天，所有腫瘤*衰退。此外, PF-2341066抑制關鍵NPM-ALK信號調節器, 包括磷脂酶C-γ, 信號轉導器，及轉錄因子3, 細胞外信號調節激酶, 和Akt的激活劑，這些與 NPM-ALK 磷酸化和功能受抑制相關。[2] PF-2341066 抑制骨肉瘤的一些活動行為，及其腫瘤生長(例如, 增殖和存活)和轉移 (例如，入侵和形成克隆)。PF-2341066口服飼喂裸鼠，抑制生長和相關的骨肉瘤裸鼠移植瘤的骨基質的形成。[3] PF-2341066 按50 mg/kg 劑量處理 c-MET-擴增的GTL-16移植瘤，引起腫瘤衰退，這與18F-FDG 攝取的緩慢降低相關，且降低葡糖糖轉運蛋白 1, GLUT-1的表達。[4] | |||||
| 臨床實驗 | PF-2341066治療非肺鱗癌目前處于三期臨床實驗階段。 | |||||
| 特征 | ||||||
*的實驗操作 (此*來自于公開的文獻所以Selleck并不保證其有效性)
激酶實驗：
[1]
| 生化激酶實驗 | 使用連續耦合的分光光度測定c-Met催化活性，通過分析NADH消耗率而測定c-Met誘導的ADP產量，這種作用具有時間依賴性。在 340 nm處使用分光光度法在時間點測定吸光值的降低而計算NADH的消耗量。為了測定Ki值, 在含實驗試劑的實驗孔中加入不同濃度PF-2341066，然后在37oC下溫育10分鐘。加入c-Met酶開始進行實驗反應。 |
|---|
細胞實驗：
[1]
| 細胞系 | GTL-16胃癌細胞和T47D乳腺癌細胞 |
|---|---|
| 濃度 | 0 nM-256 nM |
| 處理時間 | 1小時 |
| 方法 | GTL-16胃癌細胞和T47D乳腺癌細胞接種在96孔板上，孔中含培養基，培養基中含10% 胎牛血清(FBS)，然后轉移到無血清培養基中[含0.04%牛血清蛋白(BSA)]，處理 24小時。 在調查配體依賴的RTK 磷酸化實驗中，加入相應的生長因子，處理20分鐘。細胞和 PF-2341066和/或適當配體在時間溫育1小時，然后使用含 1 mmol/L Na3VO4的HBSS沖洗細胞一次,然后從細胞中獲得蛋白裂解物。隨后,通過夾心酶聯免疫吸附試驗法使用特定的捕獲抗體在96孔板上測定選定蛋白激酶的磷酸化，使用特點檢測抗體測定磷酸化的酪氨酸殘基。抗體包被的實驗板(a) 在蛋白裂解物存在時，在4oC下過夜;(b)在溶于PBS的1% Tween-20 中沖洗7次;(c)在辣根過氧化物酶標記的抗總磷酸（PY-20）抗體（1:500）中溫育20分鐘;(d) 再次沖洗7次;(e)在3,3′,5,5′-四甲基聯苯胺過氧化物酶底物中溫育，開始顯示反應，加入0.09 N H2SO4終止反應; (f)在450 nm 處使用分光光度計測定吸光度。 |
動物實驗：
[1]
| 動物模型 | 攜帶NCI-H441,或DLD-1,或MDA-MB-231的雌性和雄性nu/nu小鼠 |
|---|---|
| 配制 | -- |
| 劑量 | 12.5 mg/kg/day, 25 mg/kg/day, 和50 mg/kg/day |
| 給藥處理 | 口服處理 |
參考
- [1] Zou HY, et al. Cancer Res. 2007, 67(9), 4408-4417.
- [2] Christensen JG, et al. Mol Cancer Ther. 2007, 6(12 Pt 1), 3314-3322.
- [3] Sampson ER, et al. J Bone Miner Res. 2011, 26(6), 1283-1294.
- [4] Cullinane C, et al. J Nucl Med. 2011, 52(8), 1261-1267.
- [5] Gong HC, et al. Int J Proteomics. 2011, 2011, 215496.
客戶使用selleck產品的實驗數據
數據來源于[Nat Med , 2011, 17, 1116-1120]
(c) Western blot analyses of p-Akt (Ser473) and p-S6RP (Ser235 and Ser236) in two RCT-E565 transplanted tumors treated with vehicle or PF02341066. Samples were isolated 4 h after the last dose from mice treated with PF02341066 for 3 d. (d) Responses of RCT-E565 transplanted tumors in athymic mice to PF02341066 or vehicle. Data are means ±s.e.m. (each group, n = 6). *P < 0.005, **P < 0.001 (Student,s t test).
數據來源于[Cancer Cell , 2011, 19, 679–690]
Ba/F3 cells grown in the presence of IL-3, or Ba/F3 cells expressing native EML4-ALK (clone #2, #10, #101, and #155) and EML4-ALK L1196M (clone #216, #302, #303, and #355), were treated with CH5424802 or PF-02341066 for 48 hr, and then the viable cells were measured by the Cell Titer-Glo Luminescent Cell Viability Assay. IC50 values were determined by plotting the drug concentration versus percentage of cell growth inhibition. Data are shown as mean ±SD (n = 3).
Crizotinib (PF-02341066)在71個文獻中得到引用
Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors. [Wilson TR, et al. Nature, 2012, 487(7408):505-9]
PubMed: 22763448MED12 controls the response to multiple cancer drugs through regulation of TGF-β receptor signaling. [Huang S, et al. Cell, 2012, 151(5):937-50]
PubMed: 23178117Oncogenic PIK3CA-driven mammary tumors frequently recur via PI3K pathway–dependent and PI3K pathway–independent mechanisms. [Liu P, et al. Nat Med, 2011, 17(9):1116-20]
PubMed: 21822287Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET. [Peinado H, et al. Nat Med, 2012, 18(6):883-91]
PubMed: 22635005A Functional Landscape of Resistance to ALK Inhibition in Lung Cancer [Wilson FH, et al. Cancer Cell, 2015, 27(3):397-408]
PubMed: 25759024AXL Mediates Resistance to PI3Kα Inhibition by Activating the EGFR/PKC/mTOR Axis in Head and Neck and Esophageal Squamous Cell Carcinomas. [Elkabets M, et al. Cancer Cell, 2015, 27(4):533-46]
PubMed: 25873175Comprehensive genomic profiling of pancreatic acinar cell carcinomas identifies recurrent RAF fusions and frequent inactivation of DNA repair genes [Chmielecki J, et al. Cancer Discov, 2014, 4(12):1398-405]
PubMed: 25266736Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms. [Diamond EL,et al. Cancer Discov, 2015, 10.1158/2159-8290.CD-15-0913]
PubMed: 26566875SMARCE1 suppresses EGFR expression and controls responses to MET and ALK inhibitors in lung cancer. [Papadakis AI, et al. Cell Res, 2015, 10.1038/cr.2015.16]
PubMed: 25656847The molecular landscape of colorectal cancer cell lines unveils clinically actionable kinase targets. [Medico E, et al. Nat Commun, 2015, 6:7002]
PubMed: 25926053Deorphanization of the human leukocyte tyrosine kinase (LTK) receptor by a signaling screen of the extracellular proteome. [Zhang H, et al. Proc Natl Acad Sci USA, 2014, 111(44):E4706-15]
PubMed: 25331893Paracrine effect of NRG1 and HGF drives resistance to MEK inhibitors in metastatic uveal melanoma. [Cheng H, et al. Cancer Res, 2015, 10.1158/0008-5472.CAN-15-0370]
PubMed: 25952648A drug resistance screen using a selective MET inhibitor reveals a spectrum of mutations that partially overlap with activating mutations found in cancer patients. [Tiedt R, et al. Cancer Res, 2011, 71(15):5255-64]
PubMed: 21697284A kinase-independent function of AKT promotes cancer cell survival. [Vivanco I, et al. Elife, 2014, 10.7554/eLife.03751]
PubMed: 25551293ALK+ anaplastic large cell lymphoma exhibits phosphatidylinositol-3 kinase/Akt activity with retained but inactivated PTEN--a report from the Children's Oncology Group. [Heuckmann JM, et al. Clin Cancer Res, 2011, 59(3):440-7]
PubMed: 21948233Characteristics of lung cancers harboring NRAS mutations. [Ohashi K, et al. Clin Cancer Res, 2013, 19(9):2584-91]
PubMed: 23515407Monitoring reversal of MET-mediated resistance to EGFR tyrosine kinase inhibitors in non-small cell lung cancer using 3'-deoxy-3'-[18F]-fluorothymidine positron emission tomography [Iommelli F et al. Clin Cancer Res, 2014, 20(18):4806-15]
PubMed: 25052479Receptor ligand-triggered resistance to alectinib and its circumvention by Hsp90 inhibition in EML4-ALK lung cancer cells. [Tanimoto A, et al. Oncotarget, 2014, 5(13):4920-8]
PubMed: 24952482Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells [Zhou Y, et al. Mol Cancer Ther, 2014, 13(1):134-43]
PubMed: 24170771Alectinib shows potent antitumor activity against RET-rearranged non-small cell lung cancer. [Kodama T, et al. Mol Cancer Ther, 2014, 10.1158/1535-7163.MCT-14-0274 ]
PubMed: 25349307Selective ALK inhibitor alectinib with potent antitumor activity in models of crizotinib resistance. [Kodama T, et al. Cancer Lett, 2014, 351(2):215-21]
PubMed: 24887559Colloidal Drug Formulations Can Explain "Bell-Shaped" Concentration-Response Curves. [Owen SC ,et al. ACS Chem Biol, 2013, 9(3):777-84]
PubMed: 24397822Epithelial-mesenchymal transition leads to crizotinib resistance in H2228 lung cancer cells with EML4-ALK translocation. [Hyeong Ryul Kim, et al. Mol Oncol, 2013, 7(6):1093-102]
PubMed: 23993685Colloidal Aggregation Affects the Efficacy of Anticancer Drugs in Cell Culture. [Owen SC, et al. ACS Chem Biol, 2012, 7(8):1429-35]
PubMed: 22625864Tivantinib (ARQ 197) efficacy is independent of MET inhibition in non-small-cell lung cancer cell lines [Calles A, et al. Mol Oncol, 2014, 9(1):260-9]
PubMed: 25226813A Novel Mechanism of EML4-ALK Rearrangement Mediated by Chromothripsis in a Patient-Derived Cell Line [Kodama T,et al. J Thorac Oncol, 2014, 9(11):1638-46]
Triple inhibition of EGFR, Met, and VEGF suppresses regrowth of HGF-triggered, erlotinib-resistant lung cancer harboring an EGFR mutation [Nakade J, et al. J Thorac Oncol, 2014, 9(6):775-83]
PubMed: 24828661Constructing and Validating High-Performance MIEC-SVM Models in Virtual Screening for Kinases: A Better Way for Actives Discovery [Sun H, et al. Sci Rep, 2016, 10.1038/srep24817]
PubMed: 27102549Expression and clinical relevance of MET and ALK in Ewing sarcomas. [Fleuren ED, et al. Int J Cancer, 2013, 133(2):427-36]
PubMed: 23335077Overcoming erlotinib resistance with tailored treatment regimen in patient-derived xenografts from naïve Asian NSCLC patients. [Yang M, et al. Int J Cancer, 2013, 132(2):E74-84]
PubMed: 22948846Crizotinib (PF‐02341066) Reverses Multidrug Resistance in Cancer Cells by Inhibiting the function of P‐glycoprotein. [Zhou WJ, et al. Br J Pharmacol, 2012, 166(5):1669-83]
PubMed: 22233293High ALK mRNA expression has a negative prognostic significance in rhabdomyosarcoma. [Bonvini P, et al. Br J Cancer, 2013, 109(12):3084-91]
PubMed: 24149177Disturbance of Ca2+ homeostasis converts Pro-Met into non-canonical tyrosine kinase p190MetNC in response to endoplasmic reticulum stress in MHCC97 cells. [Dai R, et al. J Biol Chem, 2012, 287(18):14586-97]
PubMed: 22418436The Tyrosine Kinase c-Met Contributes to the Pro-tumorigenic Function of the p38 Kinase in Human Bile Duct Cholangiocarcinoma Cells. [Dai R, et al. J Biol Chem, 2012, 287(47):39812-23]
PubMed: 23024367Synergistic effects of crizotinib and radiotherapy in experimental EML4-ALK fusion positive lung cancer. [Dai Y, et al. Radiother Oncol, 2015, 114(2):173-81]
Synergistic effects of crizotinib and radiotherapy in experimental EML4-ALK fusion positive lung cancer. [Dai Y, et al. Radiother Oncol, 2015, 114(2):173-81]
Glycan-deficient PrP stimulates VEGFR2 signaling via glycosaminoglycan [Gao Z, et al. Cellular Signalling, 2016, 19;28(6):652-662]
PubMed: 27006333Unacylated Ghrelin Promotes Skeletal Muscle Regeneration Following Hindlimb Ischemia via SOD-2-Mediated miR-221/222 Expression. [Togliatto G, et al. J Am Heart Assoc, 2013, 2(6):e000376]
PubMed: 24308935Identification of basophils as a major source of hepatocyte growth factor in chronic myeloid leukemia: a novel mechanism of BCR-ABL1-independent disease progression. [Cerny-Reiterer S, et al. Neoplasia, 2012, 14(7):572-84]
PubMed: 22904675A Receptor Tyrosine Kinase Network Comprised of FGFRs, EGFR, ERBB2 and MET Drives Growth and Survival of Head and Neck Squamous Carcinoma Cell Lines. [Singleton KR, et al. Mol Pharmacol, 2013, 83(4):882-93]
PubMed: 23371912Cardiomyocyte-specific overexpression of human stem cell factor protects against myocardial ischemia and reperfusion injury. [Xiang FL, et al. Int J Cardiol, 2013, 168(4):3486-94]
PubMed: 23680593Nexavar/Stivarga and Viagra Interact to Kill Tumor Cells [Tavallai M, et al. J Cell Physiol, 2015, 230(9):2281-98]
PubMed: 25704960Epithelial-mesenchymal transition confers resistance to selective FGFR inhibitors in SNU-16 gastric cancer cells. [Grygielewicz P, et al. Gastric Cancer, 2014, 10.1007/s10120-014-0444-1]
PubMed: 25407459Structural and functional screening in human induced-pluripotent stem cell-derived cardiomyocytes accuray identifies cardiotoxicity of multiple drug types. [Doherty KR, et al. Toxicol Appl Pharmacol, 2015, 285(1):51-60]
PubMed: 25841593The growth inhibitory effect of 17-DMAG on ALK and MYCN double-positive neuroblastoma cell line. [Yi B, et al. Tumour Biol, 2013, 35(4):3229-35]
PubMed: 24293393Saracatinib impairs the peritoneal dissemination of diffuse-type gastric carcinoma cells resistant to Met and fibroblast growth factor receptor inhibitors. [Yamaguchi H, et al. Cancer Sci, 2014, 105(5):528-36]
PubMed: 24612061Paracrine activation of MET promotes peritoneal carcinomatosis in scirrhous gastric cancer. [Zhao L, et al. Cancer Sci, 2013, 104(12):1640-6]
PubMed: 24118504Heregulin induces resistance to lapatinib-mediated growth inhibition of HER5-amplified cancer cells. [Sato Y, et al. Cancer Sci, 2013, 104(12):1618-25]
PubMed: 24112719Phosphoproteomic analysis identifies activated MET-axis PI3K/AKT and MAPK/ERK in lapatinib-resistant cancer cell line. [Lee YY, et al. Exp Mol Med, 2013, 45:e64]
PubMed: 24263233MET and PI3K/mTOR as a Potential Combinatorial Therapeutic Target in Malignant Pleural Mesothelioma [Kanteti R,et al. PLoS One, 2014, 9(9):e105919]
PubMed: 25221930Mouse Model for ROS1-Rearranged Lung Cancer. [Arai Y, et al. PLoS One, 2013, 8(2):e56010]
PubMed: 23418494STAT3 is activated by JAK2 independent of key oncogenic driver mutations in non-small cell lung carcinoma. [Looyenga BD, et al. PLoS One, 2012, 7(2):e30820]
PubMed: 22319590Activating mutations in ALK kinase domain confer resistance to structurally unrelated ALK inhibitors in NPM-ALK-positive anaplastic large-cell lymphoma [Zdzalik D J Cancer Res Clin Oncol, 2014, 140(4):589-98]
PubMed: 24509625Crizotinib inhibits migration and expression of ID1 in MET-positive lung cancer cells: implications for MET targeting in oncology. [Stutz E Future Oncol, 2014, 10(2):211-7]
PubMed: 244906073D models of epithelial-mesenchymal transition in breast cancer metastasis: high-throughput screening assay development, validation, and pilot screen. [Li Q, et al. J Biomol Screen, 2011, 16(2):141-54]
PubMed: 21297102ALK mutations conferring differential resistance to structurally diverse ALK inhibitors. [Thakral C, et al. Pediatr Blood Cancer, 2012, 17(23):7394-401]
PubMed: 22488797Inhibition of Axl improves the targeted therapy against ALK-mutated neuroblastoma. [Xu F, et al. Biochem Biophy Res Co, 2014, 10.1016/j.bbrc.2014.10.126]
EML4-ALK induces epithelial-mesenchymal transition consistent with cancer stem cell properties in H1299 non-small cell lung cancer cells. [Guo F, et al. Biochem Biophys Res Commun, 2015, 10.1016/j.bbrc.2015.02.114]
PubMed: 25735977A New Human Lung Adenocarcinoma Cell Line Harboring the EML4-ALK Fusion Gene [Isozaki H, et al. Jpn J Clin Oncol, 2014, 44(10):963-8]
PubMed: 25170107Hepatic Slate Cell Coculture Enables Sorafenib Resistance in Huh7 Cells through HGF/c-Met/Akt and Jak2/Stat3 Pathways [Chen W, et al. Biomed Res Int, 2014, 2014:764981]
PubMed: 25057499Gefitinib Inhibits the Growth of Toxoplasma gondii in HeLa Cells [Yang Z,et al. Korean J Parasitol, 2014, 52(4):439-41]
PubMed: 25246725cMET inhibitor crizotinib impairs angiogenesis and reduces tumor burden in the C3(1)-Tag model of basal-like breast cancer. [Cozzo AJ, et al. Springerplus, 2016, 5:348]
PubMed: 27057482PI3 Kinase Pathway and MET Inhibition is Efficacious in Malignant Pleural Mesothelioma. [Kanteti R, et al. Sci Rep, 2016, 6:32992]
PubMed: 27623107Green tea polyphenol EGCG suppresses osteosarcoma cell growth through upregulating miR-1. [Zhu K, et al. Tumour Biol, 2016, 37(4):4373-82]
PubMed: 26499783Signatures of drug sensitivity in nonsmall cell lung cancer. [Gong HC, et al. Int J Proteomics, 2011, 2011:215496]
PubMed: 22091388Phenotypic drug screening and target validation for improved personalized therapy reveal the complexity of phenotype-genotype correlations in clear cell renal cell carcinoma [Schneider M, et al. Urol Oncol, 2014, 32(6):877-84]
PubMed: 24929890MET Exon 14 Skipping Mutations in Lung Adenocarcinoma: Clinicopathologic Implications and Prognostic Values. [Lee GD, et al. J Thorac Oncol, 2017, S1556-0864(17)30365-9]
PubMed: 28502721Resistance to nanoparticle albumin-bound paclitaxel is mediated by ABCB1 in urothelial cancer cells. [Vallo S, et al. Oncol Lett, 2017, 13(6):4085-4092]
PubMed: 28599410An Oncogenic ALK Fusion and an RRAS Mutation in KRAS Mutation-Negative Pancreatic Ductal Adenocarcinoma. [Shimada Y, et al. Oncologist, 2017, 22(2):158-164]
PubMed: 28167572Presence of anaplastic lymphoma kinase in inflammatory breast cancer. [Robertson FM, et al. Springerplus, 2013, 2:497]
PubMed: 24102046Epithelial-mesenchymal transition confers resistance to FGFR inhibitors in gastric cancer cell line [Paulina Grygielewicz, et al. CELON PHARMA, 2013, 2013]
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克唑替尼/Crizotinib (PF-02341066|c-Met和ALK抑制劑
克唑替尼/Crizotinib (PF-02341066|c-Met和ALK抑制劑
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