For research use only.
Catalog No.S1156 Synonyms: RO 09-1978
CAS No. 154361-50-9
Capecitabine (RO 09-1978) is a tumor-selective fluoropyrimidine carbamate, which achieves higher intratumoral 5-FU level with lower toxicity than 5-FU. Capecitabine treatment of HCT-15 cells causes condensation of DNA and induces apoptosis.
Selleck's Capecitabine has been cited by 16 publications
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A452 induces apoptosis and DNA damage of CRC cells. (A) HCT116 and (B) HT29 cells were cultured with 0.1% DMSO (control) or A452 (0.5, 1, 2 uM), SAHA (5 uM), cisplatin (10 uM), irinotecan (5 uM), or capecitabine (10 uM) at the indicated concentrations for 24 h. The Western blot analysis shows PARP degradation, proapoptotic and antiapoptotic markers. α-Tubulin is shown as a loading control.
Carcinogenesis, 2018, 39(1):72-83. Capecitabine purchased from Selleck.
A, HCT116 and (B) HT29 cells were treated with 0.1% DMSO (control), A452 (2 µM), SAHA (5 µM), cisplatin (10 µM), irinotecan (5 µM), or capecitabine (10 µM) alone or in combination with these compounds at the indicated concentrations for 24 h. The total protein was analyzed by western blotting with α‐tubulin as a loading control.
Mol Carcinog, 2018, 57(10):1383-1395. Capecitabine purchased from Selleck.
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|Description||Capecitabine (RO 09-1978) is a tumor-selective fluoropyrimidine carbamate, which achieves higher intratumoral 5-FU level with lower toxicity than 5-FU. Capecitabine treatment of HCT-15 cells causes condensation of DNA and induces apoptosis.|
|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)|
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT04198727||Recruiting||Other: DPD activity assessment|Drug: Capecitabine||Breast Neoplasm Malignant Female||Centre Antoine Lacassagne|Cerbaliance||July 20 2020||Not Applicable|
|NCT04274933||Terminated||Drug: Venetoclax|Drug: Capecitabine||Breast Cancer|Cancer||AbbVie||May 21 2020||Phase 1|
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