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Catalog No. T0984   CAS 51-21-8
Synonyms: 5-Fluoracil, NSC 19893, 5-FU, Fluorouracil

Fluorouracil interrupts nucleotide synthetic by inhibiting thymidylate synthase (TS) in tumor cells.

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5-Fluorouracil, CAS 51-21-8
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Purity: 98%
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Biological Description
Chemical Properties
Storage & Solubility Information
Description Fluorouracil interrupts nucleotide synthetic by inhibiting thymidylate synthase (TS) in tumor cells.
In vitro Sulforaphane and 5-Fluorouracil (5-FU) treatment sequentially have a synergistic effect, which led to a significant reduction in the cell growth of the breast cancer MDA-MB-231 cell line. 24 h after the sequential treatment with sulforaphane and 5-FU, early apoptotic cells were dominant, while after 48 h and 72 h both early and late apoptotic cells occurred. The largest number of apoptotic cells was reported after 72 h [1]. 5-Fu and doxorubicin (Dox) show synergistic anticancer efficacy. The IC50 value of 5-Fu/Dox-DNM toward MDA-MB-231 cells is 0.25 μg/mL, presenting an 11.2-fold and 6.1-fold increase in cytotoxicity compared to Dox-DNM and 5-Fu-DNM, respectively [2].
In vivo After 5 days of tail vein injections of 40 mg/kg/day 5-FU in female BALB/c mice, the mice were given oral elemental diet group (ED group) or dextrin with the same number of calories (control group). Although body weight decreased after 5-FU treatment, ED group mice weighed more than control group mice. Additionally, although control mice developed diarrhea after 5-FU treatment, the ED group showed only loose stools. The control group saliva volume was approximately one-sixth of the vehicle group volume after 5-FU treatment; this was improved to approximately half in the ED group. The area ratio of PAS-positive cells in the colonic mucosa was reduced by 5-FU treatment, with the ratio being higher in the ED group than that in the control group. Similar tumor growth suppression was observed in the 5-FU and ED groups [3].
Cell Research After a 7-day habituation period, the mice were divided into three groups (vehicle group, dextrin group, and ED group; n = 6 mice per group) that had the same mean body weight (time of grouping was designated as day 0). Then, mice were treated by tail vein injections from day 0 to 4; mice in the dextrin and ED groups received 40 mg/kg/day of 5- fluorouracil (5-FU) injection 250 mg, while mice in the vehicle group received 10 mL/kg/day physiological saline, which was equivalent to the dose of 5-FU. Additionally, twice a day from day 0 to 6, ED group mice received 1.6 kcal/0.8 mL/day ED administered orally, while mice in the vehicle and dextrin groups received dextrin containing the same amount of calories. Body weight and food consumption were measured before administration of 5-FU and ED on days 0 and 7. Food consumption was measured with respect to each group. Mice were accommodated individually in specially prepared polycarbonate cages, and two or more fresh stools per mouse were scored as follows: 0, the stools were not crushed when pushed by human fingers; 1, the stools were crushed, but the core remained when pushed by human fingers; 2, the stools were crushed and the core did not remain when pushed by human fingers; 3, the stools were crushed and stuck to the fingers when pushed by human fingers; 4, the stools lost their shape just from being touched. Autopsies were conducted on day 7. After bleeding, the large intestine (the colon and rectum) was taken, and the length was measured. The lumen was washed with physiological saline, the excess water was wiped off, and specimens were weighed. Section 3 cm distal from the center of the large intestine was fixed with formalin for histological evaluation. Salivary glands (the submandibular gland and sublingual gland) were collected and weighed. The collected salivary glands were fixed with formalin, and after the tissue sections were prepared, they were stained with hematoxylin and eosin [3].
Synonyms 5-Fluoracil, NSC 19893, 5-FU, Fluorouracil
Molecular Weight 130.08
Formula C4H3FN2O2
CAS No. 51-21-8


Powder: -20°C for 3 years

In solvent: -80°C for 2 years

Solubility Information

Ethanol: 1.3 mg/mL (10 mM)

DMSO: 13 mg/mL (100 mM)

( < 1 mg/ml refers to the product slightly soluble or insoluble )

References and Literature

1. Milczarek M, et al. Autophagic cell death and premature senescence: New mechanism of 5-fluorouracil and sulforaphane synergistic anticancer effect in MDA-MB-231 triple negative breast cancer cell line. Food Chem Toxicol. 2018 Jan;111:1-8. 2. Han R, et al. Amphiphilic dendritic nanomicelle-mediated co-delivery of 5-fluorouracil and doxorubicin for enhanced therapeutic efficacy. J Drug Target. 2017 Feb;25(2):140-148. 3. Kawashima R, et al. Influence of an elemental diet on 5-fluorouracil-induced morphological changes in the mouse salivary gland and colon. Support Care Cancer. 2016 Apr;24(4):1609-16. 6. Yin L, et al. Antitumor effects of oncolytic herpes simplex virus type 2 against colorectal cancer in vitro and in vivo. Ther Clin Risk Manag. 2017 Feb 7;13:117-130. 7. Kim W, Park C, Park J, et al. Pine needle hexane extract promote cell cycle arrest and premature senescence via p27 KIP1 upregulation gastric cancer cells[J]. Food Science and Biotechnology. 2020: 1-9. 8. Liu L, Liu S, Deng P, et al. Targeting the IRAK1-S100A9 Axis Overcomes Resistance to Paclitaxel in Nasopharyngeal Carcinoma[J]. Cancer Research.


1. Ouyang S, Li H, Lou L, et al. Inhibition of STAT3-ferroptosis negative regulatory axis suppresses tumor growth and alleviates chemoresistance in gastric cancer. Redox Biology. 2022: 102317 2. Liu L, Liu S, Deng P, et al. Targeting the IRAK1-S100A9 Axis Overcomes Resistance to Paclitaxel in Nasopharyngeal Carcinoma. Cancer Research. 2021 Mar 1;81(5):1413-1425. doi: 10.1158/0008-5472.CAN-20-2125. Epub 2021 Jan 5. 3. Liu L, Liu S, Deng P, et al. Targeting the IRAK1–S100A9 Axis Overcomes Resistance to Paclitaxel in Nasopharyngeal Carcinoma. Cancer Research. 2021, 81(5): 1413-1425. 4. Luo X, Cai G, Guo Y, et al. Exploring Marine-Derived Ascochlorins as Novel Human Dihydroorotate Dehydrogenase Inhibitors for Treatment of Triple-Negative Breast Cancer. Journal of Medicinal Chemistry.. 5. Lü Z, Li X, Li K, et al. Nitazoxanide and related thiazolides induce cell death in cancer cells by targeting the 20S proteasome with novel binding modes. Biochemical Pharmacology. 2022: 114913. 6. Li Q, Lai Q, He C, et al. RUNX1 regulates the proliferation and chemoresistance of colorectal cancer through the Hedgehog signaling pathway. Journal of Cancer. 2021, 12(21): 6363-6371. 7. Xu X, Zhang S, Wang Y, et al. Virtual Screening Inhibitors of Ubiquitin-specific Protease 7 combining Pharmacophore Modeling and Molecular Docking. Molecular Informatics. 2022 8. Zhao F, Huang Y, Zhang Y, et al. SQLE inhibition suppresses the development of pancreatic ductal adenocarcinoma and enhances its sensitivity to chemotherapeutic agents in vitro. Molecular Biology Reports. 2022: 1-9

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5-Fluorouracil 51-21-8 Apoptosis Cell Cycle/Checkpoint DNA Damage/DNA Repair Metabolism Microbiology/Virology Proteases/Proteasome Nucleoside Antimetabolite/Analog Endogenous Metabolite DNA/RNA Synthesis HIV Protease 5 Fluorouracil inhibit 5-Fluoracil NSC 19893 Inhibitor 5Fluorouracil Human immunodeficiency virus 5-FU Fluorouracil HIV inhibitor