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.

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In DMSO USD 134 In stock
USD 147 In stock
USD 220 In stock
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Cited by 13 Publications

3 Customer Reviews

  • Quantitative RT-PCR analysis for mTOR levels in ASZ001 cells treated with ITRA, VISMO, or 5-FU. Data represent the mean ± SD of three independent experiments. * p < 0.05, compared to nontreated controls; ns, statistically not significant.

    J Invest Dermatol, 2018, 138(8):1716-1725. Fluorouracil (5-Fluoracil, 5-FU) purchased from Selleck.

    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 NFrqc4dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVG3NuKhcMLi NHLxcFBKSzVyPUKwJO69\y:vTB?= NEm0bJIzPDB7NUG3Oi=>
HT-29 M2m0cmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoXsO|LDqGkEoB?= M3\ITmlEPTB-IEK1JO69\y:vTB?= NH\KZWMzPDB7NUG3Oi=>
HL-60 M1TBdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoXpO|LDqGkEoB?= MX\JR|UxRThwNkCxJO69\y:vTB?= NHHVTngzPDB7NUG3Oi=>
NCI-H292 M3zX[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1SyWFczyqCqwrC= M1XKb2lEPTB-IEK1JO69\y:vTB?= Mn\ENlQxQTVzN{[=

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
p53 / PUMA / c-PARP; 

PubMed: 25965911     


(A) HCT-116 cells were treated with various doses of 5-FU for 24 hours (B) HCT-116 cells were treated with 200 uM 5-FU, then harvested at different time points after stimulation. The expression of p53, PUMA, cleaved PARP and P-Akt(S473) were detected by western blotting in different conditions.

25965911
Immunofluorescence
caveolin-3; 

PubMed: 23646193     


Cells were stained with an antibody against caveolin-3 (green) and with DAPI (blue). (A) control cells (top images), 10 mM 5-FU (middle images), 50 mM 5-FU (bottom images). Merged images are shown at the right of each panel.

phospho-histone H3 ; 

PubMed: 23646193     


Cells were grown for 24 h, treated with 5-FU and stained with an anti-phospho-histone H3 antibody (red) and with DAPI (blue). (A) control cells, (B) 0.1 mM 5-FU and (C) 1 mM 5-FU. 

p65 / p-p65(Ser536) / p53 / p-p53(Ser15); 

PubMed: 24587255     


E–H, Immunocytochemistry of p65 and p53 induction and localization by 5-FU treatment for the indicated cell lines. p65 (red), phosphor-p65 (Ser536; red), p53 (green), phospho-p53 (Ser15; red), and DAPI (blue) staining of the nucleus without (control) and with 5-FU treatment. 

Sox2 / Oct4 / Nanog / ABCG2; 

PubMed: 27009861     


(A) Immunofluorescence staining of Sox2, Oct4 and Nanog in HBE cells with or without 5-FU treatment. In untreated HBE cells, few Sox2, Oct4 or Nanog-positive cells were observed. After 5-FU treatment, the number of Sox2, Oct4 or Nanog-positive cells increased remarkably. Nuclei were counterstained with DAPI (blue). (B) Immunofluorescence staining of ABCG2 in HBE cells with or without 5-FU treatment. 

β-catenin; 

PubMed: 30111797     


Immunofluorescence detection of β-catenin in HCT-8 cells. Scale bar, 20 μm.

non-phospho β-catenin; 

PubMed: 28588704     


Effect of enhanced WNT signaling in Ell3 OE cells. Localization of non-phosphorylated β-catenin was analyzed by immunocytochemical staining in (A) control MCF-7 and (B) Ell3 OE treated with various 5-FU concentrations.

23646193 24587255 27009861 30111797 28588704
Growth inhibition assay
Cell viability; 

PubMed: 25965911     


Cells viability was analyzed using Cell Counting Kit-8 at 0, 3, 6, 12 and 24 hours after (A) 50, 100, 200, or 400 uM 5-FU treatment in HCT116 cells.

Cell proliferation; 

PubMed: 30250641     


(A) Cell proliferation assay with resveratrol in HCT116. Cells were treated with resveratrol at 0 ~ 200 μM for 72 hours and applied to MTS assay. (B) HCT116 cells were treated with 5-FU at 0~200 μM for 72 hours. (C)HCT116 cells were treated with resveratrol at 0 ~ 200 μM combined with 5-FU at 10 μM for 72 hours and applied to MTS assay. (D) DLD1 cell proliferation assay with resveratrol at 0 ~ 200 μM for 72 hours. (E) DLD1 cells were treated with 5-FU at 0~ 200 μM for 72 hours. (F) DLD1 cells were treated with resveratrol combined with 5-FU at 10 μM for 72 hours. Error bars represent standard deviation.

25965911 30250641
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(Data is from Selleck tests instead of citations):
saline (warming)
For best results, use promptly after mixing.
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
in solvent
Synonyms NSC 19893

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03196180 Not yet recruiting High Grade Cervical Intraepithelial Neoplasia|p16 Positive Neoplastic Cells Present National Cancer Institute (NCI) July 31 2019 Phase 1
NCT03196180 Not yet recruiting High Grade Cervical Intraepithelial Neoplasia|p16 Positive Neoplastic Cells Present National Cancer Institute (NCI) July 31 2019 Phase 1
NCT03883919 Not yet recruiting Pancreatic Cancer|Pancreas Cancer|Cancer of the Pancreas Washington University School of Medicine|Ipsen June 30 2019 Phase 1
NCT03883919 Not yet recruiting Pancreatic Cancer|Pancreas Cancer|Cancer of the Pancreas Washington University School of Medicine|Ipsen June 30 2019 Phase 1
NCT03784326 Not yet recruiting Clinical Stage II Esophageal Adenocarcinoma AJCC v8|Clinical Stage II Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IIA Esophageal Adenocarcinoma AJCC v8|Clinical Stage IIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IIB Esophageal Adenocarcinoma AJCC v8|Clinical Stage IIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage III Esophageal Adenocarcinoma AJCC v8|Clinical Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IC Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IC Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage II Esophageal Adenocarcinoma AJCC v8|Pathologic Stage II Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIA Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage III Esophageal Adenocarcinoma AJCC v8|Pathologic Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIA Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIB Esophageal Adenocarcinoma AJCC v8|Pathologic Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8 M.D. Anderson Cancer Center|National Cancer Institute (NCI) May 31 2019 Early Phase 1
NCT03775265 Not yet recruiting Bladder Carcinoma Infiltrating the Muscle of the Bladder Wall|Bladder Urothelial Carcinoma|Stage II Bladder Cancer AJCC v8|Stage III Bladder Cancer AJCC v8|Stage IIIA Bladder Cancer AJCC v8 National Cancer Institute (NCI) May 9 2019 Phase 3

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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.

DNA/RNA Synthesis Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID