47576
5-Fluorouracil
≥99.0% (HPLC)
Synonym(s):
2,4-Dihydroxy-5-fluoropyrimidine, 5-FU, 5-Fluoro-2,4(1H,3H)-pyrimidinedione
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About This Item
Empirical Formula (Hill Notation):
C4H3FN2O2
CAS Number:
Molecular Weight:
130.08
EC Number:
200-085-6
UNSPSC Code:
12171500
PubChem Substance ID:
Beilstein/REAXYS Number:
127172
MDL number:
InChI key
GHASVSINZRGABV-UHFFFAOYSA-N
InChI
1S/C4H3FN2O2/c5-2-1-6-4(9)7-3(2)8/h1H,(H2,6,7,8,9)
SMILES string
FC1=CNC(=O)NC1=O
assay
≥99.0% (HPLC)
solubility
H2O: 10 mg/mL, clear
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Other Notes
Potent antineoplastic agent. Its determination in tissue with microbore HPLC and fluorescence detection; Metabolised to fluoro-2′-deoxyuridine monophosphate which inhibits DNA synthesis by blocking thymidylate synthetase
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Biochemical interactions between N-(phosphonacetyl)-L-aspartate and 5-fluorouracil.
C M Liang et al.
Molecular pharmacology, 21(1), 224-230 (1982-01-01)
C Jochheim et al.
Analytical biochemistry, 217(2), 285-291 (1994-03-01)
For the determination of the cytotoxic drug 5-fluorouracil in tissue, a sensitive and selective assay has been developed based on microbore high-performance liquid chromatography and fluorescence detection after pre-column derivatization with 4-bromomethyl-7-methoxycoumarin. 5-Chlorouracil was found to be an appropriate internal
Julia K J Ahlskog et al.
Bioorganic & medicinal chemistry letters, 19(16), 4851-4856 (2009-07-21)
We describe the synthesis and characterization of two acetazolamide derivatives containing either a charged fluorophore or an albumin-binding moiety, which restrict binding to carbonic anhydrase IX and XII present on tumor cells. In vivo studies showed the preferentially targeting of
Yuko Fujiwara et al.
EBioMedicine, 33, 33-48 (2018-07-28)
Activation of intrinsic p53 tumor-suppressor (TS) pathways is an important principle underlying cancer chemotherapy. It is necessary to elucidate the precise regulatory mechanisms of these networks to create new treatment strategies. Comprehensive analyses were carried out by microarray. Expression of
Jean-Yves Douillard et al.
The New England journal of medicine, 369(11), 1023-1034 (2013-09-13)
Patients with metastatic colorectal cancer that harbors KRAS mutations in exon 2 do not benefit from anti-epidermal growth factor receptor (EGFR) therapy. Other activating RAS mutations may also be negative predictive biomarkers for anti-EGFR therapy. In this prospective-retrospective analysis, we
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