Fluorouracil (5-Fluoracil, 5-FU)
Catalog No.S1209 Synonyms: NSC 19893
Molecular Weight(MW): 130.08
Fluorouracil (5-Fluoracil, 5-FU) is a DNA/RNA synthesis inhibitor, which interrupts nucleotide synthetic by inhibiting thymidylate synthase (TS) in tumor cells.
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DNA-PKcs suppression mediated ROS production and GSH content in HepG2 cells exposed to CDDP and 5-Fu. a DNA-PKcs inhibition promoted ROS production in HepG2 cells treated with indicated concentrations of CDDP and 5-Fu. DCFH-DA fluorescent analysis was performed to assess the ROS level. Data presented were mean ?SD of three independent experiments.
Mol Cell Biochem 2014 10.1007/s11010-014-2253-6. Fluorouracil (5-Fluoracil, 5-FU) purchased from Selleck.
EdU staining of RBE cells treated with OSI-027 (6.25 μM) and/or 5-FU (6.25 μg/mL) was performed by using Click-iT EdU Imaging Kit. The percentages of EdU-positive cells have been provided in the right panel.
Eur Rev Med Pharmacol Sci, 2016, 20(9):1699-706.. Fluorouracil (5-Fluoracil, 5-FU) purchased from Selleck.
Purity & Quality Control
Choose Selective DNA/RNA Synthesis Inhibitors
|Description||Fluorouracil (5-Fluoracil, 5-FU) is a DNA/RNA synthesis inhibitor, which interrupts nucleotide synthetic by inhibiting thymidylate synthase (TS) in tumor cells.|
Adrucil is an analogue of uracil with a fluorine atom at the C-5 position in place of hydrogen. It rapidly enters the cell using the same facilitated transport mechanism as uracil. Adrucil is converted intracellularly to several active metabolites: fluorodeoxyuridine monophosphate (FdUMP), fluorodeoxyuridine triphosphate (FdUTP) and fluorouridine triphosphate (FUTP). The Adrucil metabolite FdUMP binds to the nucleotide-binding site of TS, forming a stable ternary complex with the enzyme and CH2THF, thereby blocking binding of the normal substrate dUMP and inhibiting dTMP synthesis. Metabolite of Adrucil also can be misincorporated into DNA, leading to DNA strand breaks and cell death. The pro-apoptosis effects of Adrucil may be related to its activation of tumor suppressor p53. Loss of p53 function reduces cellular sensitivity to Adrucil.  Adrucil is able to inhibit the survival and induce apoptosis of a board range of cancer cells. Adrucil suppresses viabilities of the nasopharyngeal carcinoma cell line CNE2 and HONE1 , pancreatic cancer cell lines Capan-1 , and human colon carcinoma cell line HT-29  with IC50 of 9 μg/mL, 3 μg/mL, 0.22 μM, 2.5 μM, respectively.
|In vivo||Adrucil is widely used in the treatment of a range of cancers, including colorectal and breast cancers.  100mg/kg Adrucil significantly suppresses tumor growth of murine colon carcinomas Colon 38 with tumor-doubling time (TD), growth-delay factor (GDF), and T/C of 26.5 days, 4.4, and 14%. |
-  Longley DB, et al. Nat Rev Cancer, 2003, 3(5), 330-338.
-  Qin L, et al. Biochem Biophys Res Commun, 2008, 371(3), 531-535.
-  Shi X, et al. Oncology, 2002, 62(4), 354-362.
|In vitro||DMSO||26 mg/mL (199.87 mM)|
|In vivo||Add solvents to the product individually and in order:
For best results, use promptly after mixing.
* 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|
|NCT01928290||Recruiting||Stomach Neoplasms|Esophageal Neoplasms||Washington University School of Medicine||November 8, 2013||Phase 2|
|NCT00193882||Completed||Esophagus Cancer||Trans-Tasman Radiation Oncology Group (TROG)|National Health and Medical Research Council, Australia|Canadian Cancer Trials Group||July 7, 2003||Phase 3|
|NCT03050814||Not yet recruiting||Colorectal Cancer||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||February 3, 2017||Phase 2|
|NCT02997228||Not yet recruiting||Colorectal Adenocarcinoma|High-Frequency Microsatellite Instability|Stage IV Colorectal Cancer|Stage IVA Colorectal Cancer|Stage IVB Colorectal Cancer||National Cancer Institute (NCI)||November 2017||Phase 3|
|NCT02912559||Not yet recruiting||Colon Adenocarcinoma|DNA Repair Disorder|Lynch Syndrome|Microsatellite Instability|Stage IIIA Colon Cancer|Stage IIIB Colon Cancer|Stage IIIC Colon Cancer||National Cancer Institute (NCI)||September 2017||Phase 3|
|NCT03043547||Not yet recruiting||Cholangiocarcinoma Non-resectable|Cholangiocarcinoma Metastatic|Cholangiocarcinoma of the Gallbladder|Cholangiocarcinoma Advanced||AIO-Studien-gGmbH|Baxalta GmbH|Shire||May 2017||Phase 2|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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Frequently Asked Questions
I was wondering if the product #s1209 (5-fluorouracil) is suitable to inject into mice ?
S1209 is suitable to inject (I.P.) into mice as indicating in this paper: http://www.ncbi.nlm.nih.gov/pubmed/8995503.