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Uracil

C4H4N2O2 organic

Properties

StateSolid (white crystalline powder)
ColorWhite
SolubilitySlightly soluble in water (3.6 g/L at 25°C); soluble in hot water and dilute bases
Melting Point335°C (decomposes)
Boiling PointDecomposes before boiling

About Uracil

Uracil is the pyrimidine base that distinguishes RNA from DNA, pairing with adenine through two hydrogen bonds (N3-H...N1 and C4=O...H-N6) where the corresponding A-T pair in DNA is identical except for a methyl group at C5. That methyl group is not a structural decoration — it is an evolutionary error-correction system. Cytosine in DNA spontaneously deaminates to uracil at a rate of around 100 events per cell per day, so if DNA used uracil normally, cells would have no way to distinguish damaged C from legitimate U. By using thymine (5-methyluracil), the cell flags any uracil in DNA as damage, and uracil DNA glycosylase (UDG) snips it out for the base excision repair pathway to fix. RNA, with a turnover measured in minutes to hours instead of decades, doesn't need this insurance. Pharmacologically, uracil is the chemical scaffold for 5-fluorouracil (5-FU), one of the oldest and still most widely deployed cytotoxic chemotherapy agents — first synthesized by Charles Heidelberger at Wisconsin in 1957, now consumed at the rate of thousands of kilograms per year for colorectal, breast, head/neck, and pancreatic cancers. The active metabolite FdUMP irreversibly inhibits thymidylate synthase, starving rapidly dividing cells of dTMP for DNA replication. Capecitabine (Xeloda) is the oral prodrug version that liberates 5-FU preferentially in tumor tissue.

Where you'll encounter it

If you have ever run a urea-PAGE gel of an RNA prep and stained with SYBR Gold, the bands you see depend on uracil's stacking and Watson-Crick pairing. In a molecular biology lab, the practical encounter with uracil chemistry is UNG (uracil-N-glycosylase) carryover prevention in qPCR — by replacing dTTP with dUTP in your reaction mix and adding UNG to the next cycle, any aerosol contamination from previous reactions gets cleaved before amplification can start, virtually eliminating false positives in clinical assays like RT-qPCR for HIV viral load. On the oncology floor, the standard FOLFOX regimen for stage III colon cancer infuses 5-FU at 400 mg/m^2 bolus plus 2400 mg/m^2 over 46 hours every two weeks, and patients with DPYD gene variants that slow 5-FU catabolism need dose reduction or they accumulate toxic metabolite levels — DPYD genotyping has become standard of care in many EU centers since 2020.

Common Uses

  • Pyrimidine nucleobase in RNA, pairing with adenine through two hydrogen bonds
  • Chemical scaffold for the cytotoxic chemotherapy agent 5-fluorouracil (5-FU) in colorectal and breast cancer
  • Substrate in dUTP/UNG carryover prevention systems for qPCR and RT-qPCR clinical assays
  • Synthetic precursor for capecitabine (Xeloda), the oral 5-FU prodrug
  • Reference standard in HPLC and LC-MS analysis of nucleobases and nucleotide degradation products
  • Diagnostic substrate for assays of uracil DNA glycosylase activity in DNA repair research
  • Building block in nucleoside analog synthesis for antiviral and anticancer drug discovery
  • Reagent in solid-phase synthesis of synthetic oligonucleotides for primer and probe manufacturing

Safety Information

Free uracil itself is not classified as hazardous under GHS for laboratory or research use, with no established OSHA PEL. The clinically derived 5-fluorouracil is an entirely different story: cytotoxic, reproductive toxicant Category 1B, and a USP <800> hazardous drug requiring closed-system transfer devices, chemo-rated PPE, and dedicated biosafety cabinets for compounding in oncology pharmacies. Spill response for 5-FU follows hospital cytotoxic spill kit protocols. Uracil itself is non-mutagenic but its incorporation into DNA in dUTP-imbalanced cells (e.g., methotrexate-treated or thymidylate-synthase-inhibited) creates lethal abasic sites after UDG processing. Standard lab handling of uracil powder uses nitrile gloves and a dust mask; no special engineering controls are required for ordinary research-scale work.

This safety summary is for educational reference only and may not be complete. It is not a substitute for Safety Data Sheets (SDS), medical advice, or professional chemical safety guidance. Always consult appropriate SDS and qualified professionals before handling chemicals.

Constituent Elements

Frequently Asked Questions

What is the molar mass of uracil?
Uracil (C4H4N2O2) has a molar mass of 112.087 g/mol: 4 carbon (48.044) + 4 hydrogen (4.032) + 2 nitrogen (28.014) + 2 oxygen (31.998). For ribosylated uracil (uridine, C9H12N2O6) the mass is 244.20, for the 5'-monophosphate UMP it is 324.18, and for UTP it is 484.14 — these are the masses you use when balancing in vitro transcription reactions.
Why is uracil found in RNA but not DNA?
DNA has to last for the cell's lifetime (years to decades) and through every replication. Cytosine spontaneously deaminates to uracil at about 100 events per cell per day, so if DNA contained uracil normally, the repair machinery couldn't distinguish damage from intact bases. By using thymine (5-methyluracil), any uracil that appears in DNA is automatically flagged as damage and excised by uracil DNA glycosylase. RNA molecules turn over in minutes to hours, so the deamination rate is irrelevant and the cell saves the metabolic cost of methylating every U.
How does 5-fluorouracil work as a chemotherapy drug?
5-FU enters cells through nucleobase transporters and gets phosphorylated to FdUMP, which forms a covalent ternary complex with thymidylate synthase and the cofactor methylene-THF. This irreversibly blocks the conversion of dUMP to dTMP, starving the cell of thymidine for DNA replication. Rapidly dividing cells (tumor, GI epithelium, bone marrow) are most affected, which is also why the dose-limiting toxicities are mucositis, diarrhea, and myelosuppression. About 5% of the population carries DPYD variants that slow 5-FU catabolism and dramatically raise toxicity risk; preemptive DPYD genotyping is now standard of care in much of Europe.