标签归档：crizotinib

Crizotinib-d5(Synonyms: PF-02341066-d5)

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

Crizotinib-d5 (Synonyms: PF-02341066-d5)

Crizotinib-d5 (PF-02341066-d5) 是 Crizotinib 的氘代物。Crizotinib (PF-02341066) 是一种具有口服活性的，ATP 竞争性的 ALK 和 c-Met 抑制剂，IC50 分别为 20 和 8 nM。在细胞的实验中，Crizotinib 抑制 NPM-ALK 的酪氨酸磷酸化和 c-Met 的酪氨酸磷酸化，IC50 分别为 24 和 11 nM。Crizotinib 也是 ROS1 抑制剂。Crizotinib 具有有效的肿瘤生长抑制作用。

Crizotinib-d5(Synonyms: PF-02341066-d5)

Crizotinib-d5 Chemical Structure

CAS No. : 1395950-84-1

规格 是否有货
100 mg   询价  
250 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

生物活性

Crizotinib-d5 (PF-02341066-d5) is the deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition[1][2][3].

体外研究
(In Vitro)

Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

455.37

Formula

C21H17D5Cl2FN5O
CAS 号

1395950-84-1
中文名称

克唑替尼 d5
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [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.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

生物活性分子抑制剂Crizotinib hydrochloride(Synonyms: PF-02341066 hydrochloride)

发表于由

生物活性分子抑制剂 特异性抑制剂 激动剂 化合物库 重组蛋白 Crizotinib hydrochloride (Synonyms: PF-02341066 hydrochloride) 纯度: 99.58%

Crizotinib hydrochloride (PF-02341066 hydrochloride) 是一种口服生物可用的，具有选择性的 ATP 竞争性双 ALK 和 c-Met 抑制剂，IC50 分别为 20 和 8 nM。在细胞的实验中，Crizotinib hydrochloride (PF-02341066 hydrochloride) 抑制 NPM-ALK 的酪氨酸磷酸化和 c-Met 的酪氨酸磷酸化，IC50 分别为 24 和 11 nM。它也是 ROS 原癌基因 1 (ROS1) 抑制剂。Crizotinib hydrochloride (PF-02341066 hydrochloride) 具有有效的肿瘤生长抑制作用。

Crizotinib hydrochloride(Synonyms: PF-02341066 hydrochloride)

Crizotinib hydrochloride Chemical Structure

CAS No. : 1415560-69-8

规格 价格 是否有货 数量
Free Sample (0.1-0.5 mg)   Apply now  
10 mM * 1 mL in DMSO ￥660 In-stock
10 mg ￥600 In-stock
50 mg ￥1200 In-stock
100 mg ￥1680 In-stock
200 mg ￥2100 In-stock
500 mg ￥2900 In-stock
1 g   询价  
5 g   询价  

* Please select Quantity before adding items.

Crizotinib hydrochloride 相关产品

•相关化合物库:

  • Drug Repurposing Compound Library Plus
  • FDA-Approved Drug Library Plus
  • FDA-Approved Drug Library Mini
  • Bioactive Compound Library Plus
  • Kinase Inhibitor Library
  • Protein Tyrosine Kinase Compound Library
  • FDA-Approved Drug Library
  • Anti-Cancer Compound Library
  • Autophagy Compound Library
  • Drug Repurposing Compound Library
  • Orally Active Compound Library
  • Glutamine Metabolism Compound Library
  • FDA Approved & Pharmacopeial Drug Library
  • Anti-Lung Cancer Compound Library
  • Anti-Blood Cancer Compound Library
  • Angiogenesis Related Compound Library
  • Anti-Liver Cancer Compound Library
  • Rare Diseases Drug Library
  • Anti-Colorectal Cancer Compound Library

生物活性

Crizotinib hydrochloride (PF-02341066 hydrochloride) is an orally bioavailable, selective, and ATP-competitive dual ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib hydrochloride (PF-02341066 hydrochloride) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. It is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib hydrochloride (PF-02341066 hydrochloride) has effective tumor growth inhibition[1][2][3].

IC50 & Target

IC50: 20 nM (ALK), 8 nM (c-Met)[3]
体外研究
(In Vitro)

PF-2341066 displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50 of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50 of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50 of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50 of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50 of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively[1].
PF-2341066 also potently inhibits NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells with an IC50 of 24 nM. PF-2341066 potently prevents cell proliferation, which is associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells with IC50 of 30 nM, but not ALK-negative lymphoma cells[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

PF-2341066 reveals the ability to cause marked regression of large established tumors (> 600 mm3) in both the 50 mg/kg/day and 75 mg/kg/day treatment cohorts, with a 60% decrease in mean tumor volume over the 43-day administration schedule in the GTL-16 model. In an another study, PF-2341066 displays the ability to completely inhibits GTL-16 tumor growth for >3 months, with only 1 of 12 mice exhibiting a significant increase in tumor growth over the 3-month treatment schedule at 50 mg/kg/day. A significant dose-dependent reduction of CD31-positive endothelial cells is observed at 12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day in GTL-16 tumors, indicating that inhibition of MVD shows a dose-dependent correlation to antitumor efficacy. PF-2341066 displays a significant dose-dependent reduction of human VEGFA and IL-8 plasma levels in both the GTL-16 and U87MG models. Marked inhibition of phosphorylated c-Met, Akt, Erk, PLCλ1, and STAT5 levels is observed in GTL-16 tumors following p.o. administration of PF-2341066[1].
Treatment of c-MET-amplified GTL-16 xenografts with 50 mg/kg PF-2341066 elicits tumor regression that is associated with a slow reduction in 18F-FDG uptake and decreases expression of the glucose transporter 1, GLUT-1[4].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial

分子量

486.80

Formula

C21H23Cl3FN5O
CAS 号

1415560-69-8
中文名称

克里唑替尼盐酸
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
溶解性数据
In Vitro: 

H2O : 50 mg/mL (102.71 mM; Need ultrasonic)

DMSO : ≥ 4.9 mg/mL (10.07 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.0542 mL 10.2712 mL 20.5423 mL
5 mM 0.4108 mL 2.0542 mL 4.1085 mL
10 mM 0.2054 mL 1.0271 mL 2.0542 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂： PBS

    Solubility: 55 mg/mL (112.98 mM); Clear solution; Need ultrasonic

*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献

  • [1]. 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.

    [2]. 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.

    [3]. 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.

    [4]. 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
Cell Assay
[1]

Tumor cells are seeded in 96-well plates at low density in media supplemented with 10% FBS (growth media) and transferred to serum-free media (0% FBS and 0.04% BSA) after 24 h. Appropriate controls or designated concentrations of PF-2341066 are added to each well, and cells are incubated for 24 to 72 h. Human umbilical vascular endothelial cells (HUVEC) are seeded in 96-well plates in EGM2 media for 5 to 6 h at > 20,000 cells per well and transferred to serum-free media overnight. The following day, appropriate controls or designated concentrations of PF-2341066 are added to each well, and after 1 h incubation, HGF is added to designated wells at 100 ng/mL. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay is done to determine the relative tumor cell or HUVEC numbers.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[1]

Athymic mice bearing xenografts (300-800 mm3) are given PF-2341066 in water by oral gavage at designated dose levels. At designated times following PF-2341066 administration, mice are humanely euthanized, and tumors are resected. Tumors are snap frozen and pulverized using a liquid nitrogen-cooled cryomortar and pestle, protein lysates are generated, and protein concentrations are determined using a BSA assay. The level of total and phosphorylated protein is determined using a capture ELISA or immunoprecipitation-immunoblotting method.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. 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.

    [2]. 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.

    [3]. 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.

    [4]. 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

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

生物活性分子抑制剂Crizotinib hydrochloride(Synonyms: PF-02341066 hydrochloride)

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域
Crizotinib hydrochloride (Synonyms: PF-02341066 hydrochloride) 纯度: 99.58%

Crizotinib hydrochloride (PF-02341066 hydrochloride) 是一种口服生物可用的，具有选择性的 ATP 竞争性双 ALK 和 c-Met 抑制剂，IC50 分别为 20 和 8 nM。在细胞的实验中，Crizotinib hydrochloride (PF-02341066 hydrochloride) 抑制 NPM-ALK 的酪氨酸磷酸化和 c-Met 的酪氨酸磷酸化，IC50 分别为 24 和 11 nM。它也是 ROS 原癌基因 1 (ROS1) 抑制剂。Crizotinib hydrochloride (PF-02341066 hydrochloride) 具有有效的肿瘤生长抑制作用。

Crizotinib hydrochloride(Synonyms: PF-02341066 hydrochloride)

Crizotinib hydrochloride Chemical Structure

CAS No. : 1415560-69-8

规格 价格 是否有货 数量
Free Sample (0.1-0.5 mg)   Apply now  
10 mM * 1 mL in DMSO ￥660 In-stock
10 mg ￥600 In-stock
50 mg ￥1200 In-stock
100 mg ￥1680 In-stock
200 mg ￥2100 In-stock
500 mg ￥2900 In-stock
1 g   询价  
5 g   询价  

* Please select Quantity before adding items.

Crizotinib hydrochloride 相关产品

•相关化合物库:

  • Drug Repurposing Compound Library Plus
  • FDA-Approved Drug Library Plus
  • FDA-Approved Drug Library Mini
  • Bioactive Compound Library Plus
  • Kinase Inhibitor Library
  • Protein Tyrosine Kinase Compound Library
  • FDA-Approved Drug Library
  • Anti-Cancer Compound Library
  • Autophagy Compound Library
  • Drug Repurposing Compound Library
  • Orally Active Compound Library
  • Glutamine Metabolism Compound Library
  • FDA Approved & Pharmacopeial Drug Library
  • Anti-Lung Cancer Compound Library
  • Anti-Blood Cancer Compound Library
  • Angiogenesis Related Compound Library
  • Anti-Liver Cancer Compound Library
  • Rare Diseases Drug Library
  • Anti-Colorectal Cancer Compound Library

生物活性

Crizotinib hydrochloride (PF-02341066 hydrochloride) is an orally bioavailable, selective, and ATP-competitive dual ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib hydrochloride (PF-02341066 hydrochloride) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. It is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib hydrochloride (PF-02341066 hydrochloride) has effective tumor growth inhibition[1][2][3].

IC50 & Target

IC50: 20 nM (ALK), 8 nM (c-Met)[3]
体外研究
(In Vitro)

PF-2341066 displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50 of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50 of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50 of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50 of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50 of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively[1].
PF-2341066 also potently inhibits NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells with an IC50 of 24 nM. PF-2341066 potently prevents cell proliferation, which is associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells with IC50 of 30 nM, but not ALK-negative lymphoma cells[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

PF-2341066 reveals the ability to cause marked regression of large established tumors (> 600 mm3) in both the 50 mg/kg/day and 75 mg/kg/day treatment cohorts, with a 60% decrease in mean tumor volume over the 43-day administration schedule in the GTL-16 model. In an another study, PF-2341066 displays the ability to completely inhibits GTL-16 tumor growth for >3 months, with only 1 of 12 mice exhibiting a significant increase in tumor growth over the 3-month treatment schedule at 50 mg/kg/day. A significant dose-dependent reduction of CD31-positive endothelial cells is observed at 12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day in GTL-16 tumors, indicating that inhibition of MVD shows a dose-dependent correlation to antitumor efficacy. PF-2341066 displays a significant dose-dependent reduction of human VEGFA and IL-8 plasma levels in both the GTL-16 and U87MG models. Marked inhibition of phosphorylated c-Met, Akt, Erk, PLCλ1, and STAT5 levels is observed in GTL-16 tumors following p.o. administration of PF-2341066[1].
Treatment of c-MET-amplified GTL-16 xenografts with 50 mg/kg PF-2341066 elicits tumor regression that is associated with a slow reduction in 18F-FDG uptake and decreases expression of the glucose transporter 1, GLUT-1[4].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial

分子量

486.80

Formula

C21H23Cl3FN5O
CAS 号

1415560-69-8
中文名称

克里唑替尼盐酸
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
溶解性数据
In Vitro: 

H2O : 50 mg/mL (102.71 mM; Need ultrasonic)

DMSO : ≥ 4.9 mg/mL (10.07 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.0542 mL 10.2712 mL 20.5423 mL
5 mM 0.4108 mL 2.0542 mL 4.1085 mL
10 mM 0.2054 mL 1.0271 mL 2.0542 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂： PBS

    Solubility: 55 mg/mL (112.98 mM); Clear solution; Need ultrasonic

*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献

  • [1]. 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.

    [2]. 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.

    [3]. 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.

    [4]. 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
Cell Assay
[1]

Tumor cells are seeded in 96-well plates at low density in media supplemented with 10% FBS (growth media) and transferred to serum-free media (0% FBS and 0.04% BSA) after 24 h. Appropriate controls or designated concentrations of PF-2341066 are added to each well, and cells are incubated for 24 to 72 h. Human umbilical vascular endothelial cells (HUVEC) are seeded in 96-well plates in EGM2 media for 5 to 6 h at > 20,000 cells per well and transferred to serum-free media overnight. The following day, appropriate controls or designated concentrations of PF-2341066 are added to each well, and after 1 h incubation, HGF is added to designated wells at 100 ng/mL. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay is done to determine the relative tumor cell or HUVEC numbers.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[1]

Athymic mice bearing xenografts (300-800 mm3) are given PF-2341066 in water by oral gavage at designated dose levels. At designated times following PF-2341066 administration, mice are humanely euthanized, and tumors are resected. Tumors are snap frozen and pulverized using a liquid nitrogen-cooled cryomortar and pestle, protein lysates are generated, and protein concentrations are determined using a BSA assay. The level of total and phosphorylated protein is determined using a capture ELISA or immunoprecipitation-immunoblotting method.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. 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.

    [2]. 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.

    [3]. 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.

    [4]. 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

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2-Keto Crizotinib(Synonyms: PF-06260182)

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上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

2-Keto Crizotinib (Synonyms: PF-06260182)

2-Keto Crizotinib (PF-06260182) 是有活性的克唑替尼的内酰胺代谢产物。

2-Keto Crizotinib(Synonyms: PF-06260182)

2-Keto Crizotinib Chemical Structure

CAS No. : 1415558-82-5

规格 是否有货
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10 mg 询价
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生物活性

2-Keto Crizotinib (PF-06260182) is an active lactam metabolite of crizotinib.

体外研究
(In Vitro)

2-Keto Crizotinib (PF-06260182) is active and considerably less potent than crizotinib, and it is not thought to contribute significantly to the in vivo activity of crizotinib.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

464.32

Formula

C21H20Cl2FN5O2
CAS 号

1415558-82-5
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [1]. Balis FM, e al. First-dose and steady-state pharmacokinetics of orally administered crizotinib in children with solid tumors: a report on ADVL0912 from the Children’s Oncology Group Phase 1/Pilot Consortium. Cancer Chemother Pharmacol. 2017 Jan;79(1):181-187.

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Crizotinib(Synonyms: 克唑替尼; PF-02341066)

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

Crizotinib (Synonyms: 克唑替尼; PF-02341066) 纯度: 99.83%

Crizotinib (PF-02341066) 是一种具有口服活性的，ATP 竞争性的 ALK 和 c-Met 抑制剂，IC50 分别为 20 和 8 nM。在细胞的实验中，Crizotinib 抑制 NPM-ALK 的酪氨酸磷酸化和 c-Met 的酪氨酸磷酸化，IC50 分别为 24 和 11 nM。Crizotinib 也是 ROS1 抑制剂。Crizotinib 具有有效的肿瘤生长抑制作用。

Crizotinib(Synonyms: 克唑替尼; PF-02341066)

Crizotinib Chemical Structure

CAS No. : 877399-52-5

规格 价格 是否有货 数量
Free Sample (0.1-0.5 mg)   Apply now  
10 mM * 1 mL in DMSO ￥550 In-stock
10 mg ￥500 In-stock
50 mg ￥700 In-stock
100 mg ￥1000 In-stock
200 mg ￥1200 In-stock
500 mg ￥1900 In-stock
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生物活性

Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition[1][2][3].

IC50 & Target

IC50: 20 nM (ALK), 8 nM (c-Met)[3]
体外研究
(In Vitro)

Crizotinib (PF-02341066) displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50 of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50 of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50 of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50 of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50 of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively[1].
Crizotinib (PF-02341066) also potently inhibits NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells with an IC50 of 24 nM. PF-2341066 potently prevents cell proliferation, which is associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells with IC50 of 30 nM, but not ALK-negative lymphoma cells[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

Crizotinib (PF-02341066) reveals the ability to cause marked regression of large established tumors (> 600 mm3) in both the 50 mg/kg/day and 75 mg/kg/day treatment cohorts, with a 60% decrease in mean tumor volume over the 43-day administration schedule in the GTL-16 model. In an another study, PF-2341066 displays the ability to completely inhibits GTL-16 tumor growth for >3 months, with only 1 of 12 mice exhibiting a significant increase in tumor growth over the 3-month treatment schedule at 50 mg/kg/day. A significant dose-dependent reduction of CD31-positive endothelial cells is observed at 12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day in GTL-16 tumors, indicating that inhibition of MVD shows a dose-dependent correlation to antitumor efficacy. PF-2341066 displays a significant dose-dependent reduction of human VEGFA and IL-8 plasma levels in both the GTL-16 and U87MG models. Marked inhibition of phosphorylated c-Met, Akt, Erk, PLCλ1, and STAT5 levels is observed in GTL-16 tumors following p.o. administration of PF-2341066[1].
Treatment of c-MET-amplified GTL-16 xenografts with 50 mg/kg PF-2341066 elicits tumor regression that is associated with a slow reduction in 18F-FDG uptake and decreases expression of the glucose transporter 1, GLUT-1[4].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial

分子量

450.34

Formula

C21H22Cl2FN5O
CAS 号

877399-52-5
中文名称

克唑替尼；可唑替尼；克卓替尼；克唑替尼；克里唑替尼
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 33.33 mg/mL (74.01 mM; Need ultrasonic)

H2O : < 0.1 mg/mL (ultrasonic) (insoluble)

配制储备液
浓度 溶剂体积 质量 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

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 1.25 mg/mL (2.78 mM); Clear solution

    此方案可获得 ≥ 1.25 mg/mL (2.78 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 1.25 mg/mL (2.78 mM); Clear solution

    此方案可获得 ≥ 1.25 mg/mL (2.78 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
  • 3.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 1.25 mg/mL (2.78 mM); Clear solution

    此方案可获得 ≥ 1.25 mg/mL (2.78 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献

  • [1]. 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.

    [2]. 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.

    [3]. 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.

    [4]. 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

    [5]. 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.

    [6]. 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.

    [7]. 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.

    [8]. 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.
Kinase Assay
[1]

Cells are seeded in 96-well plates in media supplemented with 10% fetal bovine serum (FBS) and transferred to serum-free media [with 0.04% bovine serum albumin (BSA)] after 24 h. In experiments investigating ligand-dependent RTK phosphorylation, corresponding growth factors are added for up to 20 min. After incubation of cells with PF-2341066 for 1 h and/or appropriate ligands for the designated times, cells are washed once with HBSS supplemented with 1 mM Na3VO4, and protein lysates are generated from cells. Subsequently, phosphorylation of selected protein kinases is assessed by a sandwich ELISA method using specific capture antibodies used to coat 96-well plates and a detection antibody specific for phosphorylated tyrosine residues. Antibody-coated plates are (a) incubated in the presence of protein lysates at 4°C overnight; (b) washed seven times in 1% Tween 20 in PBS; (c) incubated in a horseradish peroxidase-conjugated anti-total-phosphotyrosine (PY-20) antibody (1:500) for 30 min; (d) washed seven times again; (e) incubated in 3,3′,5,5′-tetramethyl benzidine peroxidase substrate to initiate a colorimetric reaction that is stopped by adding 0.09 N H2SO4; and (f) measured for absorbance in 450 nm using a spectrophotometer.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay
[1]

Tumor cells are seeded in 96-well plates at low density in media supplemented with 10% FBS (growth media) and transferred to serum-free media (0% FBS and 0.04% BSA) after 24 h. Appropriate controls or designated concentrations of PF-2341066 are added to each well, and cells are incubated for 24 to 72 h. Human umbilical vascular endothelial cells (HUVEC) are seeded in 96-well plates in EGM2 media for 5 to 6 h at > 20,000 cells per well and transferred to serum-free media overnight. The following day, appropriate controls or designated concentrations of PF-2341066 are added to each well, and after 1 h incubation, HGF is added to designated wells at 100 ng/mL. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay is done to determine the relative tumor cell or HUVEC numbers.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[1]

Athymic mice bearing xenografts (300-800 mm3) are given PF-2341066 in water by oral gavage at designated dose levels. At designated times following PF-2341066 administration, mice are humanely euthanized, and tumors are resected. Tumors are snap frozen and pulverized using a liquid nitrogen-cooled cryomortar and pestle, protein lysates are generated, and protein concentrations are determined using a BSA assay. The level of total and phosphorylated protein is determined using a capture ELISA or immunoprecipitation-immunoblotting method.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. 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.

    [2]. 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.

    [3]. 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.

    [4]. 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

    [5]. 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.

    [6]. 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.

    [7]. 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.

    [8]. 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.

所有产品仅用作科学研究或药证申报，我们不为任何个人用途提供产品和服务

(S)-Crizotinib

发表于由

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白，专注于信号通路和疾病研究领域。

(S)-Crizotinib  纯度: 99.61%

(S)-Crizotinib 是一种有效的选择性 MTH1 (mutT 同源物)抑制剂，IC50 为 330 nM。(S)-Crizotinib 通过抑制 MTH1 破坏核苷酸库的稳态，诱导 DNA 单链断裂的增加，激活人结肠癌细胞的 DNA 修复，并有效抑制动物模型中的肿瘤生长。

(S)-Crizotinib

(S)-Crizotinib Chemical Structure

CAS No. : 1374356-45-2

规格 价格 是否有货 数量
Free Sample (0.1-0.5 mg)   Apply now  
10 mM * 1 mL in DMSO ￥880 In-stock
5 mg ￥800 In-stock
10 mg ￥1200 In-stock
50 mg ￥2900 In-stock
100 mg ￥4500 In-stock
200 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

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  • Targeted Diversity Library

生物活性

(S)-Crizotinib is a potent and selective MTH1 (mutT homologue) inhibitor with an IC50 of 330 nM. (S)-Crizotinib disrupts nucleotide pool homeostasis via MTH1 inhibition, induces an increase in DNA single strand breaks, activates DNA repair in human colon carcinoma cells, and effectively suppresses tumour growth in animal models[1].

IC50 & Target

IC50: 330 nM (MTH1)[1]
体外研究
(In Vitro)

(S)-crizotinib (0.625-80 μM; 24 hours) 降低了 NCI-H460，H1975 和 A549 细胞的活力，IC50 值分别为 14.29、16.54 和 11.25 μM[2]。
(S)-crizotinib (10-30 μM; 24 hours) 诱导 NCI-H460，H1975 和 A549 细胞凋亡[2]。
(S)-crizotinib (10-30 μM; 24 hour

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[2]

Cell Line: NSCLC cells, NCI-H460, H1975 and A549 cells
Concentration: 0.625, 1.25, 2.5, 5, 10, 20, 40, 60, 80 μM
Incubation Time: 24 hours
Result: Decreased the viability of NCI-H460, H1975 and A549 cells with IC50 values of 14.29, 16.54 and 11.25 μM, respectively.

Apoptosis Analysis[2]

Cell Line: NSCLC cells, NCI-H460, H1975 and A549 cells
Concentration: 10, 20 or 30 μM
Incubation Time: 24 hours
Result: Induced cells apoptosis.

Western Blot Analysis[2]

Cell Line: NSCLC cells, NCI-H460, H1975 and A549 cells
Concentration: 10, 20 or 30 μM
Incubation Time: 24 hours
Result: Decreased Bcl-2: Bax ratio.

体内研究
(In Vivo)

(S)-crizotinib (7.5 或 15 mg/kg；腹腔注射；每天一次，连续10天)可显着降低肿瘤体积和肿瘤重量[2]。

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Five-week-old, athymic BALB/c nu/nu female mice (17-19 g) with NCI-H460 cells[2]
Dosage: 7.5 or 15 mg/kg
Administration: Intraperitoneal injections; once daily for 10 days
Result: Resulted in significant reductions in both tumor volume and tumor weight.

分子量

450.34

Formula

C21H22Cl2FN5O
CAS 号

1374356-45-2
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 12.5 mg/mL (27.76 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 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

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 1.25 mg/mL (2.78 mM); Clear solution

    此方案可获得 ≥ 1.25 mg/mL (2.78 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 1.25 mg/mL (2.78 mM); Clear solution

    此方案可获得 ≥ 1.25 mg/mL (2.78 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
  • 3.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 1.25 mg/mL (2.78 mM); Clear solution

    此方案可获得 ≥ 1.25 mg/mL (2.78 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献

  • [1]. Huber KV, et al. Stereospecific targeting of MTH1 by (S)-crizotinib as an anticancer strategy. Nature. 2014 Apr 10;508(7495):222-7.

    [2]. Dai X, et al. (S)-crizotinib induces apoptosis in human non-small cell lung cancer cells by activating ROS independent of MTH1. J Exp Clin Cancer Res. 2017 Sep 7;36(1):120.

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