5-Fluorouracil
Synonym(s):5-FU;5-Fluorouracil;5-Fluorouracil - CAS 51-21-8 - Calbiochem;2,4-Dihydroxy-5-fluoropyrimidine;5-Fluoro-2,4(1H,3H)-pyrimidinedione
- CAS NO.:51-21-8
- Empirical Formula: C4H3FN2O2
- Molecular Weight: 130.08
- MDL number: MFCD00006018
- EINECS: 200-085-6
- SAFETY DATA SHEET (SDS)
- Update Date: 2024-11-09 19:38:33
What is 5-Fluorouracil?
Absorption
28-100%
Toxicity
LD50=230mg/kg (orally in mice)
Description
5-Fluorouracil (5-FU) is a prodrug form of the thymidylate synthase inhibitor fluorodeoxyuridylate (FdUMP). It is also converted to the active metabolites FUTP and FdUTP, which induce RNA and DNA damage, respectively. In vivo, 5-FU (15 mg/kg) when administered in combination with docetaxel reduces tumor growth in B88 and CAL 27 oral squamous cell carcinoma (OSCC) mouse xenograft models. Formulations containing 5-FU have been used in the treatment of colorectal, breast, gastric, and pancreatic cancers.
Chemical properties
White or almost white, crystalline powder
Chemical properties
Fluorouracil is a white crystalline solid. Practically odorless.
Originator
Efudex, Roche, US,1962
The Uses of 5-Fluorouracil
5-Fluorouracil is used as an antitumor agent in the treatment of anal, breast, colorectal, oesophageal, stomach, pancreatic and skin cancers. It finds application as a suicide inhibitor due to its irreversible inhibition of thymidylate synthase. It is also used in the treatment of actinic keratoses and bowen's disease. Further, it serves as a potent antineoplastic agent in clinical use. In addition to this, it acts as a DNA synthesis inhibitor.
The Uses of 5-Fluorouracil
A potent antineoplastic agent in clinical use. Also an inhibitor of DNA synthesis
The Uses of 5-Fluorouracil
antineoplastic, pyrimidine antimetabolite
The Uses of 5-Fluorouracil
5-Fluoro Uracil is an active metabolite of Doxifluridine (D556750).
Indications
For the topical treatment of multiple actinic or solar keratoses. In the 5% strength it is also useful in the treatment of superficial basal cell carcinomas when conventional methods are impractical, such as with multiple lesions or difficult treatment sites. Fluorouracil injection is indicated in the palliative management of some types of cancer, including colon, esophageal, gastric, rectum, breast, biliary tract, stomach, head and neck, cervical, pancreas, renal cell, and carcinoid.
Background
5-Fluorouracil is a pyrimidine analogue that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. Fluorouracil is a DNA synthesis blocker which arrests the cell cycle in G2.
Indications
Fluorouracil (5-fluorouracil, 5-fluorouracil, Efudex,
Adrucil) is a halogenated pyrimidine analogue that
must be activated metabolically. The active metabolite
that inhibits DNA synthesis is the deoxyribonucleotide
5-fluoro-2'deoxyuridine-S'-phosphate (FdUMP). 5-
Fluorouracil is selectively toxic to proliferating rather
than non-proliferating cells and is active in both the G1-
and S-phases. The target enzyme inhibited by 5-fluorouracilfluorouracil is thymidylate synthetase.
methylenetetrahydrofolate dihydrofolate
The carbon-donating cofactor for this reaction is
N5,N10 methylenetetrahydrofolate, which is converted
to dihydrofolate. The reduced folate cofactor occupies
an allosteric site on thymidylate synthetase, which allows
for the covalent binding of 5-FdUMP to the active
site of the enzyme.
Definition
ChEBI: 5-fluorouracil is a nucleobase analogue that is uracil in which the hydrogen at position 5 is replaced by fluorine. It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deoxynucleotide, it inhibits DNA synthesis (by blocking the conversion of deoxyuridylic acid to thymidylic acid by the cellular enzyme thymidylate synthetase) and so slows tumour growth. It has a role as a xenobiotic, an environmental contaminant, a radiosensitizing agent, an antineoplastic agent, an immunosuppressive agent and an antimetabolite. It is a nucleobase analogue and an organofluorine compound. It is functionally related to a uracil.
Manufacturing Process
A mixture of 200 grams (2 mols) of dry sodium fluoroacetate and 442 grams (2.86 mols) of diethyl sulfate was refluxed for 31? hours in an oil bath. The reaction mixture was then distilled through a fractionating column, yielding 177.3 grams of crude ethyl fluoroacetate, having a boiling range of 116° to 120°C. The material was redistilled through a fractionating column, yielding purified ethyl fluoroacetate boiling at 114° to 118°C.
In a 2-liter, 3-neck, round bottom flask, provided with stirrer, dropping funnel and reflux condenser, was placed 880 ml of absolute diethyl ether, and 47.6 grams (1.22 mols) of potassium, cut into 5 mm pieces, was suspended therein. 220 ml of absolute ethanol was added dropwise, while stirring, whereby the heat of reaction produced refluxing. In order to obtain complete dissolution of the potassium, the mixture was finally refluxed on a steam bath. The reaction mixture was then cooled in an ice bath, and a mixture of 135 grams (1.22 mols) of ethyl fluoroacetate and 96.4 grams (1.3 mols) of freshly distilled ethyl formate was added dropwise, while stirring and cooling, over a period of 2? hours. Upon completion of the addition of the ethyl formate, the reaction mixture was stirred for an additional hour while cooling, and then was allowed to stand overnight at room temperature.
At the end of this time the crystalline precipitate which had formed was filtered off with suction, washed with diethyl ether, and dried in a vacuum desiccator. The product comprised essentially the potassium enolate of ethyl fluoromalonaldehydate (alternative nomenclature, the potassium salt of fluoromalonaldehydic acid ethyl ester).
A mixture of 103.6 grams (0.6 mol) of the freshly prepared potassium enolate of ethyl fluoromalonaldehydate, 83.4 grams (0.3 mol) of Smethylisothiouronium sulfate and 32.5 grams (0.6 mol) of sodium methoxide was refluxed with stirring in 1,500 ml of absolute methanol. At first the reactants dissolved to a great extent, but very shortly thereafter precipitation occurred. The reaction mixture was refluxed for 2 hours and at the end of this time was evaporated to dryness in vacuo. The residue was treated with 280 ml of water; incomplete dissolution was observed.
The mixture obtained was clarified by filtering it through charcoal. The filtrate was acidified (to a slight Congo red acid reaction) by adding concentrated aqueous hydrochloric acid, containing 37% by weight HCl (48 ml required). The material which crystallized from the acidified solution was filtered off, washed free of sulfates with water and dried at 100°C, yielding crude Smethyl ether of 2-thio-5-fluorouracil, having a melting range from 202° to 221°C. The latter material was recrystallized by dissolving it in 2,035 ml of boiling ethylacetate and cooling to -20°C, yielding S-methyl ether of 2-thio-5fluorouracil, MP 230° to 237°C, in a sufficient state of purity that it could be used directly for the next step. A sample of the material was recrystallized from water (alternatively, from ethyl acetate) thereby raising the melting point to 241° to 243°C. For analysis the material was further purified by subliming it in vacuo at 140° to 150°/0.1 mm
A solution of 10.0 grams of purified S-methyl ether of 2-thio-5-fluorouracil, MP 230° to 237°C, in 150 ml of concentrated aqueous hydrochloric acid (containing approximately 37% by weight HCl) was refluxed under nitrogen for 4 hours. The reaction mixture was then evaporated in vacuo. The crystalline brownish residue was recrystallized from water. The resulting recrystallized product was further purified by sublimation in vacuo at 190° to 200°C (bath temperature)/0.1 mm pressure. There was obtained 5fluorouracil, in the form of colorless or pinkish-tan crystals, MP 282° to 283°C (with decomposition).
brand name
Adrucil (Pharmacia & Upjohn); Adrucil (Sicor); Carac (Sanofi Aventis); Efudex (Valeant); Fluoroplex (Allergan).
Therapeutic Function
Cancer chemotherapy
Synthesis Reference(s)
Journal of Heterocyclic Chemistry, 20, p. 457, 1983 DOI: 10.1002/jhet.5570200236
Tetrahedron Letters, 21, p. 277, 1980 DOI: 10.1016/S0040-4039(00)71188-9
General Description
White to nearly white crystalline powder; practically odorless. Used as an anti neoplastic drug, chemosterilant for insects.
General Description
The drug is available in a 500-mg or 10-mL vial for IV useand as a 1% and 5% topical cream. 5-FU is used in the treatmentof several carcinoma types including breast cancer,colorectal cancer, stomach cancer, pancreatic cancer, andtopical use in basal cell cancer of the skin. The mechanism ofaction includes inhibition of the enzyme TS by the deoxyribosemonophosphate metabolite, 5-FdUMP. The triphosphatemetabolite is incorporated into DNA and the ribosetriphosphate into RNA. These incorporations into growingchains result in inhibition of synthesis and function of DNAand RNA. Resistance can occur as a result of increased expressionof TS, decreased levels of reduced folate substrate5,10-methylenetetrahydrofolate, or increased levels of dihydropyrimidinedehydrogenase. Dihydropyrimidine dehydrogenaseis the main enzyme responsible for 5-FU catabolism.
Bioavailability following oral absorption is erratic.Administration of 5-FU by IV yields high drug concentrationsin bone marrow and liver. The drug does distribute intothe central nervous system (CNS). Significant drug interactionsinclude enhanced toxicity and antitumor activity of5-FU following pretreatment with leucovorin. Toxicities includedose-limiting myelosuppression, mucositis, diarrhea,and hand–foot syndrome (numbness, pain, erythema, dryness,rash, swelling, increased pigmentation, nail changes,pruritus of the hands and feet).
Air & Water Reactions
Insoluble in water.
Reactivity Profile
5-Fluorouracil may be sensitive to prolonged exposure to light. Solutions discolor on storage. 5-Fluorouracil can react with oxidizing agents and strong bases. Incompatible with methotrexate sodium.
Hazard
Questionable carcinogen.
Health Hazard
Minimum toxic dose in humans is approximately 450 mg/kg (total dose) over 30 days for the ingested drug. Intravenous minimum toxic dose in humans is a total dose of 6 mg/kg over three days. Depression of white blood cells occurred after intravenous administrative of a total dose of 480 mg/kg over 32 days. Occasional neuropathy and cardiac toxicity have been reported. Do not use during pregnancy. Patients with impaired hepatic or renal function, with a history of high-dose pelvic irradiation or previous use of alkylating agents should be treated with extreme caution. Patients with nutritional deficiencies and protein depletion have a reduced tolerance to 5-Fluorouracil.
Fire Hazard
Emits very toxic fumes of flourides and nitrogen oxides when heated to decomposition. Avoid decomposing heat.
Biological Activity
Anticancer agent. Metabolized to form fluorodeoxyuridine monophosphate (FdUMP), fluorodeoxyuridine triphosphate (FdUTP) and fluorouridine (FUTP). FdUMP inhibits thymidylate reductase causing a reduction in dTMP synthesis. FUTP and FdUTP are misincorporated into RNA and DNA respectively.
Biochem/physiol Actions
A potent antitumor agent that affects pyrimidine synthesis by inhibiting thymidylate synthetase, thus depleting intracellular dTTP pools. It is metabolized to ribonucleotides and deoxyribonucleotides, which can be incorporated into RNA and DNA. Treatment of cells with 5-FU leads to an accumulation of cells in S-phase and has been shown to induce p53 dependent apoptosis.
Mechanism of action
5-Fluorouracil (FU) is converted intracellularly to several active metabolites: fluorodeoxyuridine monophosphate (FdUMP), fluorodeoxyuridine triphosphate (FdUTP), and fluorouridine triphosphate (FUTP). The active metabolites of 5-FU disrupt RNA synthesis (FUTP), inhibit the action of thymidylate synthase (TS)—a nucleotide synthetic enzyme (FdUMP)—and can also be directly misincorporated into DNA (FdUTP). The rate-limiting enzyme in 5-FU catabolism is dihydropyrimidine dehydrogenase (DPD), which converts 5-FU to dihydrofluorouracil (DHFU). Over 80% of administered 5-FU is normally catabolized primarily in the liver, where DPD is abundantly expressed.
5-Fluorouracil (5-FU) is converted to three major active metabolites: (1) fluorodeoxyuridine monophosphate (FdUMP), (2) fluorodeoxyuridine triphosphate (FdUTP), and (3) fluorouridine triphosphate (FUTP). The main mechanism of 5-FU activation is conversion to fluorouridine monophosphate (FUMP) either directly by orotate phosphoribosyl transferase (OPRT), or indirectly via fluorouridine (FUR) through the sequential action of uridine phosphorylase (UP) and uridine kinase (UK). FUMP is then phosporylated to fluorouridine diphosphate (FUDP), which can be either further phosphorylated to the active metabolite fluorouridine triphosphate (FUTP), or converted to fluorodeoxyuridine diphosphate (FdUDP) by ribonucleotide reductase (RR). In turn, FdUDP can either be phosphorylated or dephosphorylated to generate the active metabolites FdUTP and FdUMP respectively. An alternative activation pathway involves the thymidine phosphorylase catalyzed conversion of 5-FU to fluorodeoxyuridine (FUDR), which is then phosphorylated by thymidine kinase (TK) to the thymidylate synthase (TS) inhibitor, FdUMP. Dihydropyrimidine dehydrogenase (DPD)-mediated conversion of 5-FU to dihydrofluorouracil (DHFU) is the rate-limiting step of 5-FU catabolism in normal and tumor cells.
Mechanism of action
Another action proposed for 5-fluorouracil may involve
the incorporation of the nucleotide 5-fluorouridine
triphosphate (5-FUTP) into RNA. The cytotoxic
role of these “fraudulent” 5-fluorouracil-containing
RNAs is not well understood.
Several possible mechanisms of resistance to 5-fluorouracil
have been identified, including increased synthesis
of the target enzyme, altered affinity of thymidylate
synthetase for FdUMP, depletion of enzymes
(especially uridine kinase) that activate 5-fluorouracil
to nucleotides, an increase in the pool of the normal
metabolite deoxyuridylic acid (dUMP), and an increase
in the rate of catabolism of 5-fluorouracil.
The drug has been administered orally, but absorption
by this route is erratic. The plasma half-life of 5-
fluorouracil after intravenous injection is 10 to 20 minutes.
It readily enters CSF. Less than 20% of the parent
compound is excreted into the urine, the rest being
largely metabolized in the liver.
Pharmacology
Local inflammatory reactions characterized by erythema, edema, crusting, burning, and pain are common (and, some would argue, desirable) but may be minimized by reduced frequency of application or use in combination with a topical corticosteroid.
Clinical Use
5-Fluorouracil (FU) is widely used in the treatment of a range of cancers including breast and cancers of the aerodigestive tract, but has had the greatest impact in colorectal cancer. 5-FU-based chemotherapy improves overall and disease-free survival of patients with resected stage III colorectal cancer. Nonetheless, response rates for 5-FU-based chemotherapy as a first-line treatment for advanced colorectal cancer are only between 10 and 15%. Combination of 5-FU with newer chemotherapies, such as irinotecan and oxaliplatin, has improved the response rates for advanced colorectal cancer to between 40 and 50%.
Clinical Use
5-Fluorouracil (Efudex, Fluoroplex) is an antimetabolite used for the topical treatment of actinic keratoses. It is also useful for the treatment of superficial basal cell carcinomas when conventional surgical modalities are impractical.
Clinical Use
5-Fluorouracil is used in several combination regimens in the treatment of breast cancer. It also has palliative activity in gastrointestinal adenocarcinomas, including those originating in the stomach, pancreas, liver, colon, and rectum. Other tumors in which some antitumor effects have been reported include carcinomas of the ovary, cervix, oropharynx, bladder, and prostate. Topical 5-fluorouracil cream has been useful in the treatment of premalignant keratoses of the skin and superficial basal cell carcinomas, but it should not be used in invasive skin cancer.
Side Effects
Patients who are genetically deficient in this enzyme will experience a more pronounced effect from this drug and are at significant risk for use-limiting toxicity. In general, women clear fluorouracil faster than men do. Dosage adjustments usually are not required in hepatic or renal dysfunction. Major toxicities are related to bone marrow depression, stomatitis/esophagopharyngitis, and potential GI ulceration. Nausea and vomiting are common. Solutions of fluorouracil are light sensitive, but discolored products that have been properly stored and protected from light are still safe to use.
Safety Profile
Poison by ingestion, intraperitoneal, subcutaneous, and intravenous routes. Moderately toxic by parented and rectal routes. Experimental teratogenic and reproductive effects. Human systemic effects: EKG changes, bone marrow changes, cardiac, pulmonary, and gastrointestinal effects. Human mutation data reported. A human skin irritant. Questionable carcinogen. When heated to decomposition it emits very toxic fumes of Fand NOx.
Synthesis
Fluorouracil, 4-fluorouracil (30.1.3.3), is made by condensing the ethyl ester of fluoroacetic acid with ethylformate in the presence of potassium ethoxide, forming hydroxy-methylenfluoroacetic ester (30.3.1), which cyclizes by reacting it with S-methylisothiourea to 2-methylthio-4-hydroxy-5-fluoropyrimidine, which is subsequently hydrolyzed by hydrochloric acid to fluorouracil (30.1.3.3). An alternative method of synthesizing5-fluorouracid is direct fluorination of uracil with fluorine or trifluoromethylhypofluoride.
Potential Exposure
This material is used as an antineo plastic drug for cancer treatment and as a chemosterilant for insects.
Veterinary Drugs and Treatments
5-fluorouracil is a potent cytotoxic chemotherapeutic agent used
for the topical therapy of equine limbal and eyelid squamous cell
carcinoma. It is also used as an antimetabolite to limit fibrosis over
the body of gonioimplant devices used to artificially shunt aqueous
humor out of the eye in glaucoma as well as improve long-term
filtering performance of the implant.
1% solution applied to the affected eye three times daily.
Drug interactions
Potentially hazardous interactions with other drugs Anticoagulants: possibly enhances effect of coumarins. Antipsychotics: avoid concomitant use with clozapine, increased risk of agranulocytosis. Cytotoxics: avoid with panitumumab. Folic acid: toxicity of fluorouracil increased - avoid. Metronidazole and cimetidine inhibit metabolism (increased toxicity). Temoporfin: increased skin photosensitivity with topical fluorouracil
First aid
If this chemical gets into the eyes, remove anycontact lenses at once and irrigate immediately for at least15 min, occasionally lifting upper and lower lids. Seek medical attention immediately. If this chemical contacts theskin, remove contaminated clothing and wash immediatelywith soap and water. Seek medical attention immediately. Ifthis chemical has been inhaled, remove from exposure,begin rescue breathing (using universal precautions, including resuscitation mask) if breathing has stopped and CPR ifheart action has stopped. Transfer promptly to a medicalfacility. When this chemical has been swallowed, get medical attention. Give large quantities of water and inducevomiting. Do not make an unconscious person vomit. Keepvictim quiet and maintain normal body temperature.
Mechanism of action
Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances from becoming incorporated into DNA during the "S" phase (of the cell cycle), stopping normal development and division. Fluorouracil blocks an enzyme which converts the cytosine nucleotide into the deoxy derivative. In addition, DNA synthesis is further inhibited because Fluorouracil blocks the incorporation of the thymidine nucleotide into the DNA strand.5-FU acts in several ways, but principally as a thymidylate synthase (TS) inhibitor. Interrupting the action of this enzyme blocks the synthesis of the pyrimidine thymidylate (dTMP), a nucleotide required for DNA replication.
Metabolism
Hepatic. The catabolic metabolism of fluorouracil results in degradation products ( e.g., CO2, urea and α-fluoro-?-alanine) which are inactive.
Metabolism
After intravenous injection fluorouracil is cleared rapidly from plasma. It is distributed throughout body tissues and fluids, and disappears from the plasma within about 3 hours. Within the target cell fluorouracil is converted to 5-fluorouridine monophosphate and floxuridine monophosphate (5-fluorodeoxyuridine monophosphate), the former undergoing conversion to the triphosphate which can be incorporated into RNA while the latter inhibits thymidylate synthetase. About 15% of an intravenous dose is excreted unchanged in the urine within 6 hours. Approximately 80% is inactivated mainly in the liver and is catabolised via dihydropyrimidine dehydrogenase (DPD) similarly to endogenous uracil, 60-80% is excreted as respiratory carbon dioxide; urea and other metabolites are also produced, and 2-3% by the biliary system
Side Effects
Diarrhea was the most common adverse effect reported in patients receiving systemic fluorouracil treatment. Clinicians should withhold fluorouracil for severe diarrhea until it is resolved. Other common adverse effects include vomiting, nausea, and dehydration.
storage
Store at +4°C
Shipping
UN2811 Toxic solids, organic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poisonous materials, Technical Name Required.
Incompatibilities
Incompatible with oxidizers (chlorates, nitrates, peroxides, permanganates, perchlorates, chlorine, bromine, fluorine, etc.); contact may cause fires or explo sions. Keep away from alkaline materials, strong bases, strong acids, oxoacids, epoxides, methotrexrate sodium, sources of heat.
References
1) Schlisky (1998), Biochemical and Clinical Pharmacology of 5-Fluorouracil; Oncology, 12 13
Properties of 5-Fluorouracil
Melting point: | 282-286 °C (dec.) (lit.) |
Boiling point: | 190-200°C/0.1mmHg |
Density | 1.4593 (estimate) |
storage temp. | 2-8°C |
solubility | H2O: 10 mg/mL, clear |
form | powder |
pka | pKa 8.0±0.1 (H2O) (Uncertain);3.0±0.1(H2O) (Uncertain) |
color | white |
PH | 4.3-5.3 (10g/l, H2O, 20℃) |
Water Solubility | 12.2 g/L 20 ºC |
Sensitive | Air Sensitive |
Merck | 14,4181 |
BRN | 127172 |
Stability: | Stable. Light sensitive. Combustible. Incompatible with strong oxidizing agents, strong bases. |
CAS DataBase Reference | 51-21-8(CAS DataBase Reference) |
NIST Chemistry Reference | 2,4-Pyrimidinedione, 5-fluoro-(51-21-8) |
IARC | 3 (Vol. 26, Sup 7) 1987 |
EPA Substance Registry System | 5-Fluorouracil (51-21-8) |
Safety information for 5-Fluorouracil
Signal word | Danger |
Pictogram(s) |
Skull and Crossbones Acute Toxicity GHS06 Health Hazard GHS08 |
GHS Hazard Statements |
H301:Acute toxicity,oral H351:Carcinogenicity |
Precautionary Statement Codes |
P201:Obtain special instructions before use. P202:Do not handle until all safety precautions have been read and understood. P264:Wash hands thoroughly after handling. P264:Wash skin thouroughly after handling. P270:Do not eat, drink or smoke when using this product. P280:Wear protective gloves/protective clothing/eye protection/face protection. P301+P310:IF SWALLOWED: Immediately call a POISON CENTER or doctor/physician. |
Computed Descriptors for 5-Fluorouracil
InChIKey | GHASVSINZRGABV-UHFFFAOYSA-N |
Abamectin manufacturer
Aspen Biopharma Labs Pvt Ltd
Pallav Chemicals And Solvents Pvt Ltd
SS Reagents and Chemicals
New Products
ALUMINIUM IODIDE 100 GM BUFFER CAPSULE PH 7.0 - 10 CAP BUFFER SOLUTION PH 9.5 (BORATE) EZEE BLUE GEL STAINER BORAX CARMINE (GRENACHERS ALCOHOLIC) POTASSIUM IODATE - IODIDE SOLN 0.1 N Dabigatran Acyl-O3-D-Glucuronide Trifluoroacetic Acid Salt Isofolic Acid Dabigatran 2-O-acylglucuronide metabolite Dabigatran Acyl-?-D- glucuronide Trifluroacetic Acid Erythromycin EP Impurity A Desloratidine Related Compound ARelated products of tetrahydrofuran
You may like
-
51-21-8 98%View Details
51-21-8 -
5-Fluorouracil 51-21-8 98%View Details
51-21-8 -
Fluorouracil 99% (HPLC) CAS 51-21-8View Details
51-21-8 -
5-Fluorouracil CAS 51-21-8View Details
51-21-8 -
5-Fluorouracil CAS 51-21-8View Details
51-21-8 -
5-FLUORO URACIL Extra Pure CAS 51-21-8View Details
51-21-8 -
Fluorouracil CAS 51-21-8View Details
51-21-8 -
5-Fluorouracil CAS 51-21-8View Details
51-21-8