There will be a HazMat fee per item when shipping a dangerous goods. The HazMat fee will be charged to your UPS/DHL/FedEx collect account or added to the invoice unless the package is shipped via Ground service. Ship by air in Excepted Quantity (each bottle), which is up to 1g/1mL for class 6.1 packing group I or II, and up to 25g/25ml for all other HazMat items.

Type	HazMat fee for 500 gram (Estimated)
Excepted Quantity	USD 0.00
Limited Quantity	USD 15-60
Inaccessible (Haz class 6.1), Domestic	USD 80+
Inaccessible (Haz class 6.1), International	USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic	USD 100+
Accessible (Haz class 3, 4, 5 or 8), International	USD 200+

Structure of 5-Fluorouracil
CAS No.: 51-21-8

*Storage: {[sel_prStorage]}

*Shipping: {[sel_prShipping]}

5-Fluorouracil is a potent antitumor agent that affects pyrimidine synthesis by inhibiting thymidylate synthetase thus depleting intracellular dTTP pools.

Synonyms: 5-FU; NSC 19893

4.5 *For Research Use Only !

{[proInfo.pro_purity]}

Cat. No.: {[proInfo.prAm]} Purity: {[proInfo.pro_purity]}

Change View

Size

Price

VIP Price

DE Stock

US Stock

Asia Stock

Global Stock

In Stock

{[ item.pr_size ]}

Inquiry {[ getRatePrice(item.pr_usd,item.pr_rate,item.mem_rate,item.pr_is_large_size_no_price, item.vip_usd) ]}

{[ item.pr_size ]}

In Stock

- +

Please Login or Create an Account to: See VIP prices and availability

Quality Control of 5-Fluorouracil Purity: 98% SDS Specification

COA

Search for reports by entering the product batch number.
Batch number can be found on the product's label following the word 'Batch'.

NMR

Search for reports by entering the product batch number.
Batch number can be found on the product's label following the word 'Batch'.

CNMR

Search for reports by entering the product batch number.
Batch number can be found on the product's label following the word 'Batch'.

HPLC

Search for reports by entering the product batch number.
Batch number can be found on the product's label following the word 'Batch'.

LC-MS

Search for reports by entering the product batch number.
Batch number can be found on the product's label following the word 'Batch'.

1-2 Day Shipping
High Quality
Technical Support

Product Citations Show More

Discovery of KDX1381, a Bivalent CK2α Inhibitor for the Treatment of Solid Tumors as a Single Agent or in Combination

Marlhoux, Léna ; Arnaud, Alexandre ; Hervieu, Céline ; Makulyte, Gabriela ; Martinasso, Charlotte ; Mularoni, Angélique , et al.

DOI: 10.1021/acs.jmedchem.5c00695 PubMed ID: 40493957 JMC,2025,68(12):12819-12844.

Abstract: Casein kinase 2 (CK2) has emerged as a promising therapeutic target across a broad spectrum of malignancies, including pediatric and orphan cancers. The identification of a ligandable allosteric αD pocket on the CK2α subunit has enabled the development of bivalent inhibitors, which bind simultaneously to both the adenosine triphosphate (ATP) site and the allosteric pocket. Here, we report the discovery and pharmacological characterization of KDX1381, a structure-guided bivalent CK2α inhibitor with low-nanomolar potency and high selectivity, confirmed by cocrystal structures. In mice, KDX1381 suppressed CK2-driven tumor growth as a monotherapy and enhanced therapeutic efficacy when combined with vascular endothelial growth factor receptor (VEGFR) inhibitors or DNA-damaging agents in hepatocellular carcinoma and glioma models. These findings support bivalent CK2α inhibition as a differentiated therapeutic strategy with broad applicability in CK2-dependent cancers.

Purchased from AmBeed: 61825-94-3 ; 1009820-21-6 ; 444731-52-6 ; 85622-93-1 ; 557795-19-4 ; 755037-03-7 ; 849217-68-1 ; 15663-27-1 ; 284461-73-0 ; 417716-92-8 ; 51-21-8

Synergistic Anticancer Effects of Silibinin and Sulforaphane: Targeting Gastric Cancer via PI3K/AKT and ERK1/2 MAPK Pathway Inhibition and Molecular Docking Insights

Liu, Yanfeng ; Zhang, Ming ;

DOI: 10.1002/jbt.70237 PubMed ID: 40152010 J. Biochem. Mol. Toxicol.,2025,39(4):e70237.

Abstract: In the current period of pharmaceutical discovery, herbal remedies have shown to be an unmatched supply of anticancer medications. By changing the tumor microenvironment and several signaling pathways, plants and their byproducts through analogs have an important part in the therapy for carcinoma. The current investigation assessed the effectiveness of inhibiting the development of gastric cancer cells in HGC-27 cells by attenuating the PI3K/AKT and ERK 1/2 MAPK signaling pathways using the natural medicines silibinin (SIL) and sulforaphane (SFN) complemented by molecular docking analysis. After being exposed to various doses of SIL and SFN (SIL+SFN) for 24 h (0–50 µM), the cells were evaluated for multiple studies. The MTT assay was used to examine the combo that SIL+SFN induced cytotoxicity. ROS was assessed by DCFH-DA staining. Apoptotic changes were investigated, and MMP levels in HGC-27 cells were investigated utilizing the proper fluorescent staining techniques. Flow cytometry and western blot analysis were used to evaluate the protein profiles of cell survival, cell cycle, proliferation, and apoptosis. The molecular docking was conducted with Autodock Vina (v1.5.6). The docking results were analyzed using BIOVIA Discovery Studio Visualizer to identify key interactions. The relative cytotoxicity of SIL and SFN was found to be approximately 24.96 and 28.79 μM, correspondingly, according to the findings. After a 24-h incubation period, the combination of SIL and SFN generates significant cytotoxicity in HGC-27 cells, with an IC₅₀ of 15.43 μM. Furthermore, HGC-27 cells administered SIL and SFN simultaneously exhibited elevated apoptotic signals and significant ROS production. Molecular docking demonstrated strong binding affinities between the compounds and the target proteins, supporting their potential mechanisms of action. Therefore, the combination usage of SIL + SFN has been viewed as a chemotherapeutic drug since it prevents the synthesis of PI3K/AKT and ERK 1/2 MAPK mediated control of cell growth and cell cycle-regulating proteins. To utilize them commercially conducting more in vivo research in the near future will be necessary to ascertain how well the co-treatment triggers apoptosis.

Keywords: cell proliferation ; cytotoxicity ; gastric cancer ; PI3K/AKT signalling pathway ; silibinin ; sulforaphane

Purchased from AmBeed: 51-21-8

MCM8 Promotes NSCLC Progression by Competitively Inhibiting HRD1-Mediated CDC42 Ubiquitination and Degradation

Qian, Siyi ; Zeng, Longwu ; Chen, Fuxin ; Tian, Yuxuan ; Zhao, Binjie ; Liu, Qiang , et al.

DOI: 10.21203/rs.3.rs-7116246/v1 Central South University,2025.

Abstract: Colon cancer ranks among the top three in both the incidence and mortality rates of malignant tumors worldwide. Moreover, radical surgery is difficult for patients with advanced colon cancer, and chemotherapy drugs are prone to drug resistance. The five-year survival rate is only 13.1%. Therefore, an in-depth analysis of the occurrence, development and drug resistance mechanism of colon cancer is of great clinical significance for optimizing the treatment plan of patients and improving prognosis. As one of the homologous recombination repair proteins, micrormosomal maintenance protein 8 (MCM8) plays an important role in the normal physiological process of cells. In recent years, the research on its role in tumorigenesis and development has gradually deepened, but the role of MCM8 in the malignant progression of colon cancer still remains to be explored. MCM8 is abnormally highly expressed in colon cancer cells and tissues, and is positively correlated with the pathological stage progression and poor prognosis of patients. Our study indicated that MCM8 promotes the transition of the cell cycle from the G1 phase to the S phase. Moreover, our study showed that MCM8 interacted with Cdc42 and promoted its protein stability by competitively inhibiting the ubiquitination modification of Cdc42's E3 ubiquitin ligase HRD1. The rescue experiment showed that MCM8 promoted the proliferation, cell cycle progression, invasion, tumor-forming ability in vivo and resistance to 5-FU of colon cancer cells through Cdc42, while inhibiting cell apoptosis. Collectively, MCM8 is abnormally highly expressed in colon cancer and stabilizes Cdc42 protein by competitively inhibiting HRD1, thereby promoting the occurrence and development of colon cancer and the formation of 5-FU resistance.

Purchased from AmBeed: 51-21-8

MeCP2 confers 5-fluorouracil resistance in gastric cancer via upregulating the NOX4/PKM2 pathway

Qin, Yannan ; Ma, Xiaoping ; Guo, Chen ; Cai, Shuang ; Ma, Hailin ; Zhao, Lingyu

DOI: 10.1186/s12935-022-02489-y PubMed ID: 35180871 Cancer Cell Int.,2022,22,86.

Abstract: Background: Increasing evidence suggests that aberrant methylation is involved in 5-fluorouracil (5-FU) resistance in gastric cancer (GC). Our previous work has identified that Methyl-CpG binding protein 2 (MeCP2) promotes GC progression by binding to the methylation sites of promoter regions of specific genes to affect the downstream signaling pathways. However, the function and molecular mechanisms of MeCP2 in GC 5-FU resistance remain unclear. Methods: We detected the expression of MeCP2 in 5-FU-resistant GC cells and examined cell behaviors when MeCP2 was silenced. The molecular mechanisms were explored through chromatin immunoprecipitation (ChIP)-qRT-PCR, luciferase reporter assay, clinical tissue samples analysis, and in vivo tumorigenicity assay. Results: MeCP2 was up-regulated in 5-FU-resistant GC cells. Knockdown of MeCP2 enhanced the sensitivity of the cells to 5-FU. Moreover, MeCP2 promoted NOX4 transcription in the cells by binding to the promoter of NOX4. Silencing NOX4 rescued the inductive effect of MeCP2 overexpression on 5-FU sensitivity of GC cells and reduced the expression of NOX4 and PKM2 in MeCP2 overexpressed 5-FU-resistant GC cells. In addition, our in vivo experiments demonstrated that MeCP2 knockdown enhanced 5-FU sensitivity in tumors. Conclusion: MeCP2 confers 5-FU resistance in GC cells via upregulating the NOX4/PKM2 pathway, which may lead to a promising therapeutic strategy for GC.

Keywords: MeCP2 ; Gastric cancer ; 5-Fluorouracil resistance ; NOX4

Purchased from AmBeed: 51-21-8

Bcl-xL DNAzymes promote radiosensitivity and chemosensitivity in colorectal cancer cells via enhancing apoptosis

Yu, Zhen ; Guo, Jun ; Meng, Tao ; Ge, Lei ; Liu, Lin ; Wang, Haijiang , et al.

DOI: 10.1186/s40360-022-00553-x PubMed ID: 35123593 BMC Pharmacol. Toxicol.,2022,23,13.

Abstract: Background: RNA-cleaving deoxyribozymes (DNAzymes) are catalytic deoxyribonucleic acid molecules that have become a promising new class of gene suppressors by binding and cleaving target mRNA. This study investigated whether DNAzymes targeting Bcl-xL enhanced the effectiveness of radiotherapy and chemotherapy in colorectal cancer (CRC) cells. Methods: Two types of CRC cells, SW480 and SW837, were transfected with five DNAzymes. Cell viability, Bcl-xL expression and apoptosis were examined. SW480 xenograft model was used to examine the combined effects of Bcl-xL DNAzymes and 5-FU (or X-rays) on tumor growth. Results: Three Bcl-xL DNAzymes, DT882, DT883, and DT884 were identified to be effective in suppressing Bcl-xL expression and causing cell apoptosis. Furthermore, DT882 combined with 5-FU or radiotherapy addictively promoted cell apoptosis and significantly inhibited the growth of SW480 xenografts in vivo. Conclusions: These results suggest that Bcl-xL DNAzymes can enhance the radiosensitivity and chemosensitivity in CRC cells via inducing apoptosis.

Keywords: DNAzyme ; Bcl-xL ; Radiotherapy ; 5-fluorouracil ; Colorectal cancer cells

Purchased from AmBeed: 51-21-8

Britannin stabilizes T cell activity and inhibits proliferation and angiogenesis by targeting PD-L1 via abrogation of the crosstalk between Myc and HIF-1α in cancer

Zhang, Yu Fan ; Zhang, Zhi Hong ; Li, Ming Yue ; Wang, Jing Ying ; Xing, Yue ; Ri, MyongHak , et al.

DOI: 10.1016/j.phymed.2020.153425 PubMed ID: 33310309 Phytomedicine,2021,81,153425.

Abstract: Background: Programmed cell death-ligand 1 (PD-L1) is overexpressed in tumor cells, which causes tumor cells to escape T cell killing, and promotes tumor cell survival, cell proliferation, migration, invasion, and angiogenesis. Britannin is a natural product with anticancer pharmacological effects. Purpose: In this work, we studied the anticancer potential of britannin and explored whether britannin mediated its effect by inhibiting the expression of PD-L1 in tumor cells. Methods: In vitro, the mechanisms underlying the inhibition of PD-L1 expression by britannin were investigated by MTT assay, homology modeling and molecular docking, RT-PCR, western blotting, co-immunoprecipitation, and immunofluorescence. The changes in tumor killing activity, cell proliferation, cell cycle, migration, invasion, and angiogenesis were analyzed by T cell killing assays, EdU labeling, colony formation, flow cytometry, wound healing, matrigel transwell invasion, and tube formation, respectively. In vivo, the antitumor activity of britannin was evaluated in the HCT116 cell xenograft model. Results: Britannin reduced the expression of PD-L1 in tumor cells by inhibiting the synthesis of the PD-L1 protein but did not affect the degradation of the PD-L1 protein. Britannin also inhibited HIF-1α expression through the mTOR/P70S6K/4EBP1 pathway and Myc activation through the Ras/RAF/MEK/ERK pathway. Mechanistically, britannin inhibited the expression of PD-L1 by blocking the interaction between HIF-1α and Myc. In addition, britannin could enhance the activity of cytotoxic T lymphocytes and inhibit tumor cell proliferation and angiogenesis by inhibiting PD-L1. Finally, in vivo observations were confirmed by demonstrating the antitumor activity of britannin in a murine xenograft model. Conclusion: Britannin inhibits the expression of PD-L1 by blocking the interaction between HIF-1α and Myc. Moreover, britannin stabilizes T cell activity and inhibits proliferation and angiogenesis by inhibiting PD-L1 in cancer. The current work highlights the anti-tumor effect of britannin, providing insights into the development of cancer therapeutics via PD-L1 inhibition.

Keywords: Britannin ; PD-L1 ; Myc ; HIF-1α ; Antitumor

Purchased from AmBeed: 51-21-8

LncRNA SNHG7 regulates mesenchymal stem cell through the Notch1/Jagged1/Hes-1 signaling pathway and influences Folfirinox resistance in pancreatic Cancer

Cheng, Dongfeng ; Fan, Juanjuan ; Qin, Kai ; Zhou, Yiran ; Yang, Jingrui ; Ma, Yang , et al.

DOI: 10.3389/fonc.2021.719855 PubMed ID: 34631547 Front. Oncol., 2021,11,719855.

Abstract: Pancreatic cancer (PC) is one of the deadliest gastrointestinal cancers, accounting for the fourth highest number of cancer-related fatalities. Increasing data suggests that mesenchymal stem cells (MSCs) might influence the drug resistance of GC cells in the tumor microenvironment and play essential roles in drug resistance development. However, the precise underlying process remains a mystery. The purpose of this study was to look at the control of MSC-induced SNHG7 in pancreatic cancer. In vitro and in vivo sphere formation, colony formation, and flow cytometry investigations revealed the stemness and Folfirinox resistance in pancreatic cancer cells. To confirm the direct connections between SNHG7 and other related targets, RNA pulldown and immunoprecipitation tests were performed. MSC co-culture enhanced the stemness and Folfirinox resistance in pancreatic cancer cells according to the findings. MSC coculture increased SNHG7 expression in pancreatic cancer cells, contributing to the stemness and Folfirinox resistance. We demonstrated that Notch1 interacted with SNHG7 and could reverse the facilitative effect of SNHG7 on the stemness and Folfirinox resistance in pancreatic cancer cells. Finally, our findings showed that MSCs increased SNHG7 expression in pancreatic cancer cells, promoting the stemness and Folfirinox resistance via the Notch1/Jagged1/Hes-1 signaling pathway. These findings could provide a novel approach and therapeutic target for pancreatic cancer patients.

Keywords: SNHG7 ; Notch1 ; pancreatic cancer ; stemness ; resistance

Purchased from AmBeed: 61825-94-3 ; 1492-18-8 ; 97682-44-5 ; 51-21-8

Lidocaine suppresses the malignant behavior of gastric cancer cells via the c-Met/c-Src pathway

Zeng, Wei ; Xing, Ze Ting ; Tan, Mei Yun ; Wu, Yan Wen ; Zhang, Chun Yuan ;

DOI: 10.3892/etm.2021.9868 PubMed ID: 33747163 Exp. Ther. Med.,2021,21(5):424.

Abstract: The present study was designed to investigate the role and mechanism of action behind the action of lidocaine in gastric cancer cells. Lidocaine was tested for its potential role in affecting the viability of cells using Cell Counting Kit-8 (CCK-8) assays. It was found that there was a decreased MKN45 cell viability upon lidocaine treatment in a dose-dependent manner. Phosphorylated c-Met, phosphorylated c-Src, c-Met and c-Src levels were detected using western blotting following lidocaine or hepatocyte growth factor (HGF) intervention. It was found that the phosphorylation levels of c-Met and c-Src were markedly reduced by lidocaine treatment, with this effect being further relieved by the addition of HGF. Subsequently, whether lidocaine repressed the malignant biological properties of gastric cancer cells through the c-Met/c-Src axis was further investigated through the detection of epithelial-mesenchymal transition markers (N-caderin and vimentin), wound healing and transwell assay analysis. In addition, cell apoptosis and the levels of apoptosis-related proteins were determined using TUNEL and western blot assays, respectively. The results demonstrated that the malignant behavior of cells were notably repressed upon lidocaine treatment, but the addition of HGF markedly reversed these effects, indicating that the effects of lidocaine on supressing the malignant behaviour of cells could be mediated through the c-Met/c-Src axis. Subsequently, whether lidocaine affected the sensitivity of cells to cisplatin or 5-FU was analyzed using a CCK-8 assay. Enhanced sensitivity of cells to cisplatin or 5-FU was observed when treated in combination with lidocaine. The present study concluded that the involvement of the c-Met/c-Src pathway in the biological behaviour of MKN45 cells was mediated by lidocaine. Therefore, lidocaine may have the potential to suppress the malignant behaviour and proliferation of gastric cancer cells.

Keywords: lidocaine ; gastric cancer ; c-Met ; c-Src ; proliferation ; epithelial-mesenchymal transition

Purchased from AmBeed: 51-21-8

MSC-induced lncRNA HCP5 drove fatty acid oxidation through miR-3619-5p/AMPK/PGC1α/CEBPB axis to promote stemness and chemo-resistance of gastric cancer

Wu, Honglei ; Liu, Bin ; Chen, Zhaosheng ; Li, Guangchun ; Zhang, Zhen ;

DOI: 10.1038/s41419-020-2426-z PubMed ID: 32300102 Cell Death Dis.,2020,11,233.

Abstract: Chemotherapy is the first-tier treatment regime for gastric cancer (GC) patients at advance stages. Mesenchymal stem cell (MSC) cam affect drug-resistance of GC cells in tumor microenvironment, but the detailed mechanism remains poorly understood. Present study aimed to investigate the regulation of MSC-induced long non-coding RNA (lncRNA) in GC. Dysregulated lncRNAs in GC were analyzed based on GEO data. Stemness and drug-resistance of GC cells were detected by sphere formation, colony formation, CCK-8, and flow cytometry analyses. MicroRNA (miRNA)-related pathways were analyzed by online KEGG analysis tool DAVID6.8. Molecular interactions were determined by luciferase reporter assay, pulldown, RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), and co-immunoprecipitation (CoIP). Results revealed that MSC co-culture improved stemness and drug-resistance of GC cells. LncRNA histocompatibility leukocyte antigen complex P5 (HCP5) was induced in GC cells by MSC co-culture, contributing to stemness and drug-resistance. Mechanistically, HCP5 sequestered miR-3619-5p and upregulated PPARG coactivator 1 alpha (PPARGC1A), increasing transcription complex Peroxisome proliferator activated receptor (PPAR) coactivator‐1α (PGC1α)/CEBPB and transcriptionally inducing carnitine palmitoyltransferase 1 (CPT1), which prompted the fatty acid oxidation (FAO) in GC cells. In conclusion, MSC-induced lncRNA HCP5 drove FAO through miR-3619-5p/AMPK/PGC1α/CEBPB axis to promote stemness and chemo-resistance of GC, indicating that targeting HCP5 was a novel approach to enhancing the efficacy of chemotherapy in GC.

Purchased from AmBeed: 61825-94-3 ; 51-21-8 ; 124083-20-1

Convallatoxin promotes apoptosis and inhibits proliferation and angiogenesis through crosstalk between JAK2/STAT3 (T705) and mTOR/STAT3 (S727) signaling pathways in colorectal cancer

Zhang, Zhi Hong ; Li, Ming Yue ; Wang, Zhe ; Zuo, Hong Xiang ; Wang, Jing Ying ; Xing, Yue , et al.

DOI: 10.1016/j.phymed.2020.153172 PubMed ID: 32004989 Phytomedicine,2020,68,153172.

Abstract: Background: Aberrant activation of STAT3 is frequently encountered and promotes survival, cellular proliferation, migration, invasion and angiogenesis in tumor cell. Convallatoxin, triterpenoid ingredient, exhibits anticancer pharmacological properties. Purpose: In this work, we investigated the anticancer potential of convallatoxin and explored whether convallatoxin mediates its effect through interference with the STAT3 activation in colorectal cancer cells. Methods: In vitro, the underlying mechanisms of convallatoxin at inhibiting STAT3 activation were investigated by homology modeling and molecular docking, luciferase reporter assay, MTT assay, RT-PCR, Western blotting and immunofluorescence assays. Changes in cellular proliferation, apoptosis, migration, invasion and angiogenesis were analyzed by EdU labeling assay, colony formation assay, flow cytometry assay, wound-healing assay, matrigel transwell invasion assay and tube formation assays. And in vivo, antitumor activity of convallatoxin was assessed in a murine xenograft model of HCT116 cells. Results: Convallatoxin decreased the viability of colorectal cancer lines. Moreover, convallatoxin reduced the P-STAT3 (T705) via the JAK1, JAK2, and Src pathways and inhibited serine-727 phosphorylation of STAT3 via the PI3K-AKT-mTOR-STAT3 pathways in colorectal cancer cells. Interestingly, we discovered the crosstalk between mTOR and JAK2 in mTOR/STAT3 and JAK/STAT3 pathways, which collaboratively regulated STAT3 activation and convallatoxin play a role in it. Convallatoxin also downregulated the expression of target genes involved cell survival (e.g., Survivin, Bcl-xl, Bcl-2), proliferation (e.g., Cyclin D1), metastasis (e.g., MMP-9), and angiogenesis (e.g., VEGF). Indeed, we found that convallatoxin inhibited tube formation, migration, and invasion of endothelial cells, and inhibited the proliferation. Finally, in vivo observations were confirmed by showing antitumor activity of convallatoxin in a murine xenograft model. Conclusion: The result of the current study show that convallatoxin promotes apoptosis and inhibits proliferation and angiogenesis through crosstalk between JAK2/STAT3 (T705) and mTOR/STAT3 (S727) signaling pathways in colorectal cancer cells and indicate that convallatoxin could be a valuable candidate for the development of colorectal cancer therapeutic.

Keywords: Convallatoxin ; STAT3 ; Survival ; Proliferation ; Angiogenesis ; Colorectal cancer

Purchased from AmBeed: 51-21-8

Product Details of 5-Fluorouracil

CAS No. :	51-21-8
Formula :	C₄H₃FN₂O₂
M.W :	130.08
SMILES Code :	O=C(N1)NC=C(F)C1=O
Synonyms :	5-FU; NSC 19893
MDL No. :	MFCD00006018
InChI Key :	GHASVSINZRGABV-UHFFFAOYSA-N
Pubchem ID :	3385

Safety of 5-Fluorouracil

GHS Pictogram:
Signal Word:	Danger
Hazard Statements:	H301-H351
Precautionary Statements:	P201-P202-P264-P270-P280-P301+P310+P330-P308+P313-P405-P501
Class:	6.1
UN#:	2811
Packing Group:	Ⅲ

Related Pathways of 5-Fluorouracil

DNA

RTK

Isoform Comparison

Biological Activity

In Vitro:

Cell Line WiDr cells RKO cells Hct116 cells Detroit562 HUVECs MCF-7 cells Yeast cells (Saccharomyces cerevisiae) Yeast cells (Saccharomyces cerevisiae)	Concentration	Treated Time	Description	References

WiDr cells	0–115.2 μM	48 hours	To test the effect of SQLE knockdown on 5-FU sensitivity, results showed that SQLE knockdown increased the sensitivity of tumor cells to 5-FU treatment.	Cell Commun Signal. 2024 May 18;22(1):278.
RKO cells	0–115.2 μM	48 hours	To test the effect of SQLE knockdown on 5-FU sensitivity, results showed that SQLE knockdown increased the sensitivity of tumor cells to 5-FU treatment.	Cell Commun Signal. 2024 May 18;22(1):278.
Hct116 cells	20 ×10−6M	24 hours	To evaluate the effect of 5-FU on Hct116 cell growth, showing remarkable dose-dependent growth inhibition.	Adv Sci (Weinh). 2022 Oct;9(30):e2200717.
Detroit562	0.5–50 µM	72 h	To evaluate the resistance of CD10-positive subpopulation to 5-Fluorouracil, the results showed that the CD10-positive subpopulation was significantly more refractory to 5-Fluorouracil than the CD10-negative subpopulation.	Br J Cancer. 2014 Jul 29;111(3):506-14.
HUVECs	1 µg/mL	48 h	5-FU was used as a functional inhibitor of endothelial cells, cocultured with PD-MSCs and WKYMVm to evaluate its effect on endothelial cell activity and angiogenesis.	Cells. 2022 Jan 11;11(2):232.
MCF-7 cells	1, 2, 3, 4, 5, 6 µg/mL	24 h	To detect the sensitivity of MCF-7 cells to 5-fluorouracil, the results showed that EVs-treated cells had reduced sensitivity to 5-fluorouracil and significantly increased IC50.	Cell Biosci. 2021 Apr 5;11(1):68.
Yeast cells (Saccharomyces cerevisiae)	5 μg/ml	5 h	To investigate the effect of 5-FU on tRNAValAAC stability in trm4 trm8 double mutants. Results showed that 5-FU significantly reduced tRNAValAAC levels even at 30°C, and this effect was suppressed in met22 or xrn1 mutants.	Nucleic Acids Res. 2024 Jun 10;52(10):5841-5851
Yeast cells (Saccharomyces cerevisiae)	10 μg/ml	5 h	To investigate the effect of 5-FU on tRNAValAAC stability in yeast cells lacking specific tRNA methylations. Results showed that 5-FU significantly reduced tRNAValAAC levels in trm8 mutants, and this effect was suppressed in met22 or xrn1 mutants.	Nucleic Acids Res. 2024 Jun 10;52(10):5841-5851

In Vivo:

Species Mice Mice Mice Mice	Animal Model Wild-type, Hoxa9-deficient, and miR-155-deficient mice APCmin/þ mouse model Primary myelofibrosis model Chronic Myeloid Leukemia Model	Administration	Dosage	Frequency	Description	References

Mice	Wild-type, Hoxa9-deficient, and miR-155-deficient mice	Intraperitoneal injection	150 mg/kg	Single injection, lasting 4 days	To study the function of HOXA9 in bone marrow cells	Nucleic Acids Res. 2010 Sep;38(16):5472-8
Mice	APCmin/þ mouse model	Intravenous injection	50 mg/kg	Once daily for 8 weeks	To evaluate the anti-tumor effect of 5-FU in APCmin/t mice, the results showed that 5-FU significantly reduced the number and size of adenomas.	Nat Commun. 2017 Jan 4;8:14058
Mice	Primary myelofibrosis model	Intravenous injection	150 mg/kg	Single injection	Used to pre-treat donor mice for bone marrow cell collection	Nat Cell Biol. 2017 Jun;19(6):677-688
Mice	Chronic Myeloid Leukemia Model		200 mg/kg	Single dose	To construct a chronic myeloid leukemia model for studying the role of RalA in leukemia.	Int J Biol Sci. 2023 Feb 13;19(4):1211-1227

Clinical Trial:

NCT Number	Conditions	Phases	Recruitment	Completion Date	Locations

NCT00943137	Cancer (Advanced Stage)	PHASE2	UNKNOWN	2025-06-17	National University Hospital, ... More >>Singapore, 119074, Singapore Less <<
NCT04812626	Scar Keloid		COMPLETED	2021-09-14	B.P. Koirala Institute of Heal... More >>th Sciences, Dharān Bāzār, Province No. 1, 025, Nepal Less <<
NCT01525329	Actinic Keratosis\|Organ or Tis... More >>sue Transplant; Complications Less <<	PHASE3	TERMINATED	2025-12-16	Cleveland Clinic, Cleveland, O... More >>hio, 44195, United States Less <<
NCT04269369	Colon Cancer\|Stomach Tumor\|Ana... More >>l Tumor\|Pancreas Cancer\|Esophageal Cancer Less <<	PHASE4	UNKNOWN	2021-09-30	-
NCT00000122	Glaucoma	PHASE3	COMPLETED	1988-06-01	-
NCT00000758	HIV Infections\|Cervix, Dysplas... More >>ia Less <<	PHASE3	COMPLETED	1998-04-01	Usc La Nichd Crs, Los Angeles,... More >> California, 90033, United States\|Univ. of Miami AIDS CRS, Miami, Florida, 33136, United States\|Northwestern University CRS, Chicago, Illinois, 60611, United States\|Cook County Hosp. CORE Ctr., Chicago, Illinois, 60612, United States\|Univ. of Chicago - Dept. of Peds., Div. of Infectious Disease, Chicago, Illinois, 60637, United States\|Tulane/LSU Maternal/Child CRS, New Orleans, Louisiana, 70112, United States\|Johns Hopkins Adult AIDS CRS, Baltimore, Maryland, 21287, United States\|Bmc Actg Crs, Boston, Massachusetts, 02118, United States\|Beth Israel Deaconess Med. Ctr., ACTG CRS, Boston, Massachusetts, 02215, United States\|Children's Hospital of Michigan NICHD CRS, Detroit, Michigan, 48201, United States\|NJ Med. School CRS, Newark, New Jersey, 07103, United States\|Bronx-Lebanon Hosp. IMPAACT CRS, Bronx, New York, 10457, United States\|SUNY - Buffalo, Erie County Medical Ctr., Buffalo, New York, 14215, United States\|Memorial Sloan-Kettering Cancer Ctr., New York, New York, 10021, United States\|Univ. of Rochester ACTG CRS, Rochester, New York, 14642, United States\|SUNY Upstate Med. Univ., Dept. of Peds., Syracuse, New York, 13210, United States\|Unc Aids Crs, Chapel Hill, North Carolina, 27599, United States\|Univ. of Cincinnati CRS, Cincinnati, Ohio, 45267, United States\|UW School of Medicine - CHRMC, Seattle, Washington, 98122, United States\|Puerto Rico-AIDS CRS, San Juan, 00936, Puerto Rico\|San Juan City Hosp. PR NICHD CRS, San Juan, 00936, Puerto Rico Less <<

Protocol

Bio Calculators

Preparing Stock Solutions

1mg

5mg

10mg

1 mM

5 mM

10 mM

7.69mL

1.54mL

0.77mL

38.44mL

7.69mL

3.84mL

76.88mL

15.38mL

7.69mL

References

[1]Longley DB, Harkin DP, et al. 5-fluorouracil: mechanisms of action and clinical strategies. Nat Rev Cancer. 2003 May;3(5):330-8.

[2]Diasio RB, Harris BE, et al. Clinical pharmacology of 5-fluorouracil. Clin Pharmacokinet. 1989 Apr;16(4):215-37.

[3]Santi DV, McHenry CS, et al. Mechanism of interaction of thymidylate synthetase with 5-fluorodeoxyuridylate. Biochemistry. 1974 Jan 29;13(3):471-81.

[4]Glazer RI, Lloyd LS, et al. Association of cell lethality with incorporation of 5-fluorouracil and 5-fluorouridine into nuclear RNA in human colon carcinoma cells in culture. Mol Pharmacol. 1982 Mar;21(2):468-73.

[5]Cao Z, Zhang Z, et al. Antitumor and immunomodulatory effects of low-dose 5-FU on hepatoma 22 tumor-bearing mice. Oncol Lett. 2014 Apr;7(4):1260-1264. Epub 2014 Feb 6.

[6]Song MK, Park MY, et al. 5-Fluorouracil-induced changes of intestinal integrity biomarkers in BALB/c mice. J Cancer Prev. 2013 Dec;18(4):322-9.

[7]Li J, Chen Y, et al. Simultaneous determination of the novel anti-tumor candidate drug MDH-7 and 5-fluorouracil in rat plasma by LC-MS/MS: Application to pharmacokinetic interactions. J Chromatogr B Analyt Technol Biomed Life Sci. 2018 Sep 15;1095:235-240.

Precautionary Statements-General
Code	Phrase
P101	If medical advice is needed,have product container or label at hand.
P102	Keep out of reach of children.
P103	Read label before use
Prevention
Code	Phrase
P201	Obtain special instructions before use.
P202	Do not handle until all safety precautions have been read and understood.
P210	Keep away from heat/sparks/open flames/hot surfaces. - No smoking.
P211	Do not spray on an open flame or other ignition source.
P220	Keep/Store away from clothing/combustible materials.
P221	Take any precaution to avoid mixing with combustibles
P222	Do not allow contact with air.
P223	Keep away from any possible contact with water, because of violent reaction and possible flash fire.
P230	Keep wetted
P231	Handle under inert gas.
P232	Protect from moisture.
P233	Keep container tightly closed.
P234	Keep only in original container.
P235	Keep cool
P240	Ground/bond container and receiving equipment.
P241	Use explosion-proof electrical/ventilating/lighting/equipment.
P242	Use only non-sparking tools.
P243	Take precautionary measures against static discharge.
P244	Keep reduction valves free from grease and oil.
P250	Do not subject to grinding/shock/friction.
P251	Pressurized container: Do not pierce or burn, even after use.
P260	Do not breathe dust/fume/gas/mist/vapours/spray.
P261	Avoid breathing dust/fume/gas/mist/vapours/spray.
P262	Do not get in eyes, on skin, or on clothing.
P263	Avoid contact during pregnancy/while nursing.
P264	Wash hands thoroughly after handling.
P265	Wash skin thouroughly after handling.
P270	Do not eat, drink or smoke when using this product.
P271	Use only outdoors or in a well-ventilated area.
P272	Contaminated work clothing should not be allowed out of the workplace.
P273	Avoid release to the environment.
P280	Wear protective gloves/protective clothing/eye protection/face protection.
P281	Use personal protective equipment as required.
P282	Wear cold insulating gloves/face shield/eye protection.
P283	Wear fire/flame resistant/retardant clothing.
P284	Wear respiratory protection.
P285	In case of inadequate ventilation wear respiratory protection.
P231 + P232	Handle under inert gas. Protect from moisture.
P235 + P410	Keep cool. Protect from sunlight.
Response
Code	Phrase
P301	IF SWALLOWED:
P304	IF INHALED:
P305	IF IN EYES:
P306	IF ON CLOTHING:
P307	IF exposed:
P308	IF exposed or concerned:
P309	IF exposed or if you feel unwell:
P310	Immediately call a POISON CENTER or doctor/physician.
P311	Call a POISON CENTER or doctor/physician.
P312	Call a POISON CENTER or doctor/physician if you feel unwell.
P313	Get medical advice/attention.
P314	Get medical advice/attention if you feel unwell.
P315	Get immediate medical advice/attention.
P320
P302 + P352	IF ON SKIN: wash with plenty of soap and water.
P321
P322
P330	Rinse mouth.
P331	Do NOT induce vomiting.
P332	IF SKIN irritation occurs:
P333	If skin irritation or rash occurs:
P334	Immerse in cool water/wrap n wet bandages.
P335	Brush off loose particles from skin.
P336	Thaw frosted parts with lukewarm water. Do not rub affected area.
P337	If eye irritation persists:
P338	Remove contact lenses, if present and easy to do. Continue rinsing.
P340	Remove victim to fresh air and keep at rest in a position comfortable for breathing.
P341	If breathing is difficult, remove victim to fresh air and keep at rest in a position comfortable for breathing.
P342	If experiencing respiratory symptoms:
P350	Gently wash with plenty of soap and water.
P351	Rinse cautiously with water for several minutes.
P352	Wash with plenty of soap and water.
P353	Rinse skin with water/shower.
P360	Rinse immediately contaminated clothing and skin with plenty of water before removing clothes.
P361	Remove/Take off immediately all contaminated clothing.
P362	Take off contaminated clothing and wash before reuse.
P363	Wash contaminated clothing before reuse.
P370	In case of fire:
P371	In case of major fire and large quantities:
P372	Explosion risk in case of fire.
P373	DO NOT fight fire when fire reaches explosives.
P374	Fight fire with normal precautions from a reasonable distance.
P376	Stop leak if safe to do so. Oxidising gases (section 2.4) 1
P377	Leaking gas fire: Do not extinguish, unless leak can be stopped safely.
P378
P380	Evacuate area.
P381	Eliminate all ignition sources if safe to do so.
P390	Absorb spillage to prevent material damage.
P391	Collect spillage. Hazardous to the aquatic environment
P301 + P310	IF SWALLOWED: Immediately call a POISON CENTER or doctor/physician.
P301 + P312	IF SWALLOWED: call a POISON CENTER or doctor/physician IF you feel unwell.
P301 + P330 + P331	IF SWALLOWED: Rinse mouth. Do NOT induce vomiting.
P302 + P334	IF ON SKIN: Immerse in cool water/wrap in wet bandages.
P302 + P350	IF ON SKIN: Gently wash with plenty of soap and water.
P303 + P361 + P353	IF ON SKIN (or hair): Remove/Take off Immediately all contaminated clothing. Rinse SKIN with water/shower.
P304 + P312	IF INHALED: Call a POISON CENTER or doctor/physician if you feel unwell.
P304 + P340	IF INHALED: Remove victim to fresh air and Keep at rest in a position comfortable for breathing.
P304 + P341	IF INHALED: If breathing is difficult, remove victim to fresh air and keep at rest in a position comfortable for breathing.
P305 + P351 + P338	IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing.
P306 + P360	IF ON CLOTHING: Rinse Immediately contaminated CLOTHING and SKIN with plenty of water before removing clothes.
P307 + P311	IF exposed: call a POISON CENTER or doctor/physician.
P308 + P313	IF exposed or concerned: Get medical advice/attention.
P309 + P311	IF exposed or if you feel unwell: call a POISON CENTER or doctor/physician.
P332 + P313	IF SKIN irritation occurs: Get medical advice/attention.
P333 + P313	IF SKIN irritation or rash occurs: Get medical advice/attention.
P335 + P334	Brush off loose particles from skin. Immerse in cool water/wrap in wet bandages.
P337 + P313	IF eye irritation persists: Get medical advice/attention.
P342 + P311	IF experiencing respiratory symptoms: call a POISON CENTER or doctor/physician.
P370 + P376	In case of fire: Stop leak if safe to Do so.
P370 + P378	In case of fire:
P370 + P380	In case of fire: Evacuate area.
P370 + P380 + P375	In case of fire: Evacuate area. Fight fire remotely due to the risk of explosion.
P371 + P380 + P375	In case of major fire and large quantities: Evacuate area. Fight fire remotely due to the risk of explosion.
Storage
Code	Phrase
P401
P402	Store in a dry place.
P403	Store in a well-ventilated place.
P404	Store in a closed container.
P405	Store locked up.
P406	Store in corrosive resistant/ container with a resistant inner liner.
P407	Maintain air gap between stacks/pallets.
P410	Protect from sunlight.
P411
P412	Do not expose to temperatures exceeding 50 oC/ 122 oF.
P413
P420	Store away from other materials.
P422
P402 + P404	Store in a dry place. Store in a closed container.
P403 + P233	Store in a well-ventilated place. Keep container tightly closed.
P403 + P235	Store in a well-ventilated place. Keep cool.
P410 + P403	Protect from sunlight. Store in a well-ventilated place.
P410 + P412	Protect from sunlight. Do not expose to temperatures exceeding 50 oC/122oF.
P411 + P235	Keep cool.
Disposal
Code	Phrase
P501	Dispose of contents/container to ...
P502	Refer to manufacturer/supplier for information on recovery/recycling

Physical hazards
Code	Phrase
H200	Unstable explosive
H201	Explosive; mass explosion hazard
H202	Explosive; severe projection hazard
H203	Explosive; fire, blast or projection hazard
H204	Fire or projection hazard
H205	May mass explode in fire
H220	Extremely flammable gas
H221	Flammable gas
H222	Extremely flammable aerosol
H223	Flammable aerosol
H224	Extremely flammable liquid and vapour
H225	Highly flammable liquid and vapour
H226	Flammable liquid and vapour
H227	Combustible liquid
H228	Flammable solid
H229	Pressurized container: may burst if heated
H230	May react explosively even in the absence of air
H231	May react explosively even in the absence of air at elevated pressure and/or temperature
H240	Heating may cause an explosion
H241	Heating may cause a fire or explosion
H242	Heating may cause a fire
H250	Catches fire spontaneously if exposed to air
H251	Self-heating; may catch fire
H252	Self-heating in large quantities; may catch fire
H260	In contact with water releases flammable gases which may ignite spontaneously
H261	In contact with water releases flammable gas
H270	May cause or intensify fire; oxidizer
H271	May cause fire or explosion; strong oxidizer
H272	May intensify fire; oxidizer
H280	Contains gas under pressure; may explode if heated
H281	Contains refrigerated gas; may cause cryogenic burns or injury
H290	May be corrosive to metals
Health hazards
Code	Phrase
H300	Fatal if swallowed
H301	Toxic if swallowed
H302	Harmful if swallowed
H303	May be harmful if swallowed
H304	May be fatal if swallowed and enters airways
H305	May be harmful if swallowed and enters airways
H310	Fatal in contact with skin
H311	Toxic in contact with skin
H312	Harmful in contact with skin
H313	May be harmful in contact with skin
H314	Causes severe skin burns and eye damage
H315	Causes skin irritation
H316	Causes mild skin irritation
H317	May cause an allergic skin reaction
H318	Causes serious eye damage
H319	Causes serious eye irritation
H320	Causes eye irritation
H330	Fatal if inhaled
H331	Toxic if inhaled
H332	Harmful if inhaled
H333	May be harmful if inhaled
H334	May cause allergy or asthma symptoms or breathing difficulties if inhaled
H335	May cause respiratory irritation
H336	May cause drowsiness or dizziness
H340	May cause genetic defects
H341	Suspected of causing genetic defects
H350	May cause cancer
H351	Suspected of causing cancer
H360	May damage fertility or the unborn child
H361	Suspected of damaging fertility or the unborn child
H361d	Suspected of damaging the unborn child
H362	May cause harm to breast-fed children
H370	Causes damage to organs
H371	May cause damage to organs
H372	Causes damage to organs through prolonged or repeated exposure
H373	May cause damage to organs through prolonged or repeated exposure
Environmental hazards
Code	Phrase
H400	Very toxic to aquatic life
H401	Toxic to aquatic life
H402	Harmful to aquatic life
H410	Very toxic to aquatic life with long-lasting effects
H411	Toxic to aquatic life with long-lasting effects
H412	Harmful to aquatic life with long-lasting effects
H413	May cause long-lasting harmful effects to aquatic life
H420	Harms public health and the environment by destroying ozone in the upper atmosphere

{[proInfo.proName]}

CAS No.: 51-21-8

{[proInfo.proName]}

CAS No.: 51-21-8

Product Citations Show More

Alternative Products

Product Details of 5-Fluorouracil

Safety of 5-Fluorouracil

Related Pathways of 5-Fluorouracil

Isoform Comparison

Biological Activity

Protocol

References

Historical Records

Categories

Precautionary Statements-General

Prevention

Response

Storage

Disposal

Physical hazards

Health hazards

Environmental hazards

Inquiry

Molarity Calculator

Total Compounds Calculator

Dissolution Calculator