product name Fluorouracil (5-FU)
Description: Fluorouracil (also known as 5-Fluoracil, 5-FU, NSC 19893) is a DNA/RNA synthesis inhibitor, which interrupts nucleotide synthetic by inhibiting thymidylate synthase (TS) in tumor cells. Fluorouracil is a heterocyclic aromatic organic compound that is used as a potent anticancer agent for the treatment of solid tumors, including breast cancer, ovarian cancer, head and neck cancer, and colon cancer. As an analogue of uracil, fluorouracil has a fluorine atom replacing the hydrogen atom at the C-5 position. Due to its structure similarity to DNA and RNA, fluorouracil and metabolites exert strong anticancer activities through incorporation into DNA and RNA and inhibition of thymidylate synthase (TS).
References: Nat Rev Cancer. 2003 May;3(5):330-8.
130.08
Formula
C4H3FN2O2
CAS No.
51-21-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 26 mg/mL (199.9 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Saline: 10mg/mL
Synonyms
NSC 19893
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19413145
| In Vitro |
In vitro activity: 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. Kinase Assay: Cell Assay: 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. |
|---|---|
| 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%. |
| Animal model | Murine colon carcinomas Colon 38 |
| Formulation & Dosage | Dissolved in PBS; 100 mg/kg; i.p. injection |
| References | Nat Rev Cancer. 2003 May;3(5):330-8. |
