Fluorouracil (5-Fluoracil, 5-FU)

Catalog No.S1209 Synonyms: NSC 19893

Fluorouracil (5-Fluoracil, 5-FU) Chemical Structure

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.

Size Price Stock Quantity  
In DMSO USD 134 In stock
USD 147 In stock
USD 220 In stock
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2 Customer Reviews

  • 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.

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Biological Activity

Description Fluorouracil (5-Fluoracil, 5-FU) is a DNA/RNA synthesis inhibitor, which interrupts nucleotide synthetic by inhibiting thymidylate synthase (TS) in tumor cells.
Targets
Thymidylate synthase [1]
(Tumor cells)
In vitro

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. [1] 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 [2], pancreatic cancer cell lines Capan-1 [3], and human colon carcinoma cell line HT-29 [4] with IC50 of 9 μg/mL, 3 μg/mL, 0.22 μM, 2.5 μM, respectively.

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MCF-7 MnjPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVe3NuKhcMLi NUGzNJFjUUN3ME2yNEDPxGdxbVy= M37UeFI1ODl3MUe2
HT-29 NF;IUGdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVfSXZU2PzMEoHlCpC=> MVnJR|UxRiB{NTFOwIcwdUx? M2PGOVI1ODl3MUe2
HL-60 NX7QW2pXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M13LclczyqCqwrC= M2rIcmlEPTB;OD62NFEh|rypL33M M1fTTlI1ODl3MUe2
NCI-H292 NYHwT4t5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmX1O|LDqGkEoB?= NV62dVFMUUN3ME6gNlUh|rypL33M MlSzNlQxQTVzN{[=

... Click to View More Cell Line Experimental Data

In vivo Adrucil is widely used in the treatment of a range of cancers, including colorectal and breast cancers. [1] 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%. [5]

Protocol

Cell Research:[4]
+ Expand
  • Cell lines: Human colon carcinoma cell line HT-29
  • Concentrations: ~25 μM
  • Incubation Time: 7 days
  • Method: Growth inhibition is measured after treatment of cells with Adrucil for 7 days in 96-well plates (4000 HT-29 cells/well in RPMI 1640 medium with 10% dialyzed fetal bovine serum); increasing concentrations of Adrucil are added after allowing for cell attachment overnight. At the end of incubation, cells are rinsed three times with phosphate-buffered saline (pH 7.4), fixed with 10% trichloroacetic acid for 60 min at 4 ℃, washed five times with deionized water, and stained with 0.4% sulforhoda-mine B solution for 15 min at room temperature. Unstained sulforhodamine B is removed by rinsing with 1% glacial acetic acid. Afterwards, stained cell proteins are dried and dissolved with 10 mM Tris-HCl. The optical density value is measured using a detector at 540 nm wavelength.
    (Only for Reference)
Animal Research:[5]
+ Expand
  • Animal Models: Murine colon carcinomas Colon 38
  • Formulation: PBS
  • Dosages: 100 mg/kg
  • Administration: i.p. weekly
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 26 mg/mL (199.87 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order:
saline (warming)
10mg/mL

* 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.

Chemical Information

Molecular Weight 130.08
Formula

C4H3FN2O2

CAS No. 51-21-8
Storage powder
Synonyms NSC 19893

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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

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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

  • Question 1:

    I was wondering if the product #s1209 (5-fluorouracil) is suitable to inject into mice ?

  • Answer:

    S1209 is suitable to inject (I.P.) into mice as indicating in this paper: http://www.ncbi.nlm.nih.gov/pubmed/8995503.

Related Antibodies

DNA/RNA Synthesis Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID