Catalog No.S1156 Synonyms: RO 09-1978
Molecular Weight(MW): 359.35
Capecitabine is a tumor-selective fluoropyrimidine carbamate, which achieves higher intratumoral 5-FU level with lower toxicity than 5-FU.
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2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.
|Description||Capecitabine is a tumor-selective fluoropyrimidine carbamate, which achieves higher intratumoral 5-FU level with lower toxicity than 5-FU.|
|Features||A tumor-selective fluoropyrimidine carbamate.|
Both LS174T WT and LS174T-c2 cells show significantly greater sensitivity to Capecitabine when cultivated in the same plates as HepG2 hepatoma with IC50 values of 890 and 630 μM in LS174T WT alone and cultivated with HepG2, respectively. In addition, for the LS174T-C2 subline, the IC50 falls from 330 ± 4 down to 89 ± 6 μm when cultivated in the same plates as hepatoma cells. Furthermore, Capecitabine induces apoptosis in a Fas-dependent manner, and shows a 7-fold higher cytotoxicity and markedly stronger apoptotic potential in thymidine phosphorylase (TP)-transfected LS174T-c2 cells. 
|In vivo||In the human cancer xenograft models studied, Capecitabine is more effective in a wider dose range and has a broader spectrum of antitumor activity than 5-FU, UFT or its intermediate metabolite 5'-DFUR, which can be correlated with tumor dThdPase levels.  Capecitabine inhibits tumor growth and metastatic recurrence after resection of human hepatocellular carcinoma (HCC) in highly metastatic nude mice model which is attributed to the high expression of platelet-derived endothelial cell growth factor in tumors. |
|In vitro||DMSO||72 mg/mL (200.36 mM)|
|Ethanol||72 mg/mL (200.36 mM)|
|Water||6 mg/mL (16.69 mM)|
* 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.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02767752||Not yet recruiting||Pancreatic Cancer||Herlev Hospital|GENIS||September 2016||Phase 2|
|NCT00960544||Not yet recruiting||Breast Cancer||M.D. Anderson Cancer Center|Myriad Genetic Laboratories, Inc.||September 2016||Phase 2|
|NCT02831179||Not yet recruiting||Functional Pancreatic Neuroendocrine Tumor|Malignant Somatostatinoma|Merkel Cell Carcinoma|Metastatic Adrenal Gland Pheochromocytoma|Metastatic Carcinoid Tumor|Multiple Endocrine Neoplasia Type 1|Multiple Endocrine Neoplasia Type 2A|Multiple Endocrine Neoplasia Type 2B|Neuroendocrine Neoplasm|Non-Functional Pancreatic Neuroendocrine Tumor|Pancreatic Glucagonoma|Pancreatic Insulinoma|Recurrent Adrenal Cortex Carcinoma|Recurrent Adrenal Gland Pheochromocytoma|Recurrent Merkel Cell Carcinoma|Somatostatin-Producing Neuroendocrine Tumor|Stage III Adrenal Cortex Carcinoma|Stage III Thyroid Gland Medullary Carcinoma|Stage IIIA Merkel Cell Carcinoma|Stage IIIB Merkel Cell Carcinoma|Stage IV Adrenal Cortex Carcinoma|Stage IV Merkel Cell Carcinoma|Stage IVA Thyroid Gland Medullary Carcinoma|Stage IVB Thyroid Gland Medullary Carcinoma|Stage IVC Thyroid Gland Medullary Carcinoma|Thymic Carcinoid Tumor|VIP-Producing Neuroendocrine Tumor|Well Differentiated Adrenal Cortex Carcinoma|Zollinger Ellison Syndrome||Vanderbilt-Ingram Cancer Center|National Cancer Institute (NCI)||August 2016||Phase 1|
|NCT02795988||Not yet recruiting||Gastrointestinal Neoplasms|Adenocarcinoma||Imugene Limited||August 2016||Phase 1|Phase 2|
|NCT02574455||Not yet recruiting||Breast Cancer||Immunomedics, Inc.||July 2016||Phase 3|
|NCT02830139||Not yet recruiting||Malignant Neoplasm of Colorectum||Wuhan University||July 2016||Phase 2|
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