fluorouracil

fluor·o·u·ra·cil

(flʊr'ō-yʊr'ə-sĭl, flôr'-, flōr'-) pronunciation

n.
An antineoplastic agent, C₄H₃FN₂O₂, used especially in the treatment of cancers of the skin, breast, and digestive system.

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Fluorouracil

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Key Terms: Cytotoxic drug, DNA, Infusion therapy.

Definition

Fluorouracil is a medication that kills cancer cells. It is also known as 5-FU or 5-fluourouracil, and as the brand name Adrucil.

Purpose 5-FU may be used in combination with other chemotherapy agents to treat cancers of the breast, stomach, colon, rectum, and pancreas.

Description 5-FU is a cytotoxic drug. This means that it kills cancer cells. 5-FU kills cells by interfering with the activities of DNA and RNA, which are molecules in the cells important in expressing genetic material.

Recommended Dosage

Most frequently, 5-FU is given as an injection into the vein (intravaneous injection or IV). Many different doses and regimens are used depending on the cancer diagnosis, and patients should discuss with their physician the dose based on the individual protocol used. A sample dose is 500 to 1,000 mg per square meter of body surface area given as a 24-hour infusion for four to five days every three weeks. A dose of 425 mg per square meter of body surface area per day for five days given along with the drug leucovorin is also common.

Precautions

Patients with allergic reaction to 5-FU should not be administered this drug. It is also inadvisable for pregnant women. 5-FU should be administered with caution to patients with impaired liver or kidney function, or in patients with a history of heart problems.

Side Effects

The amount of drug given and the duration of which it is given during a single session greatly influences the side effects seen. For example, when given as a 24-hour continuous infusion, the most common side effects are diarrhea and mouth ulcers. If 5-FU is given as a bolus infusion (a high quantity of the drug all at once), the most common side effect is bone marrow suppression; this results in a decrease of the white blood cells responsible for fighting infections, the platelets responsible for blood clotting, and the red blood cells responsible for providing oxygen to the cells of the body.

The severity of the side effects is increased when 5-FU is given with the drug leucovorin. Vomiting, diarrhea, nausea, and loss of appetite (anorexia) may occur regardless of how 5-FU is administered. The diarrhea side effect may be severe in some patients, and it is important for them to alert their doctor immediately so that appropriate medications for the diarrhea can be prescribed.

5-FU may cause rashes, increased sensitivity to sunlight, changes in skin color, changes to the fingernails, and redness and swelling in the palms of the hands and soles of the feet. Patients who have had heart disease before starting therapy with 5-FU may have problems with blood flow to the heart. Rarely, 5-FU may cause an allergic reaction, dry eyes, sleepiness, confusion, headache, changes in walking gait, involuntary rapid movement of the eyes, and difficulty speaking. When 5-FU is applied directly on the skin, there are usually no side effects except for those to the skin itself. These may include burning sensations, pain, and darkening of the skin color.

Some authorities recommend discontinuation of 5-FU therapy as soon as mild side effects are observed as a way of reducing the extent of injury to the digestive tract. Administration may then be restarted at a lower dose after the side effects have stopped.

Interactions

People taking fluorouracil should consult their doctor before taking any other prescription drug, over-thecounter drug, or herbal remedy.

—Bob Kirsch

Drug Info:

Fluorouracil, 5-FU

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Brand names: Adrucil®, Carac™, Efudex®, Fluoroplex®

Chemical formula:

Drug Forms:

Espa�ol:

Fluorouracil Topical solution

What is this medicine?

FLUOROURACIL, 5-FU (flure oh YOOR a sil) is a chemotherapy agent. It is used on the skin to treat skin cancer and skin conditions that could become cancer.

This medicine may be used for other purposes; ask your health care provider or pharmacist if you have questions.

What should I tell my health care provider before I take this medicine?

They need to know if you have any of these conditions:
•DPD enzyme deficiency
•recent or current radiation therapy
•swelling or open sores at the treatment site
•an unusual or allergic reaction to fluorouracil, other chemotherapy, other medicines, foods, dyes, or preservatives
•pregnant or trying to get pregnant
•breast-feeding

How should I use this medicine?

This medicine is only for use on the skin. Follow the directions on the prescription label. Wash hands before and after use. Wash affected area and gently pat dry. To apply this medicine use a cotton-tipped applicator, or use gloves if applying with fingertips. If applied with unprotected fingertips, it is very important to wash your hands well after you apply this medicine. Avoid applying to the eyes, nose, or mouth. Apply enough medicine to cover the affected area. You can cover the area with a light gauze dressing, but do not use tight or air-tight dressings. Finish the full course prescribed by your doctor or health care professional, even if you think your condition is better. Do not stop taking except on the advice of your doctor or health care professional.

Talk to your pediatrician regarding the use of this medicine in children. Special care may be needed.

Overdosage: If you think you have taken too much of this medicine contact a poison control center or emergency room at once.
NOTE: This medicine is only for you. Do not share this medicine with others.

What may interact with this medicine?

Interactions are not expected. Do not use any other skin products without telling your doctor or health care professional.

This list may not describe all possible interactions. Give your health care provider a list of all the medicines, herbs, non-prescription drugs, or dietary supplements you use. Also tell them if you smoke, drink alcohol, or use illegal drugs. Some items may interact with your medicine.

What should I watch for while using this medicine?

Visit your doctor or health care professional for checks on your progress. You will need to use this medicine for 2 to 6 weeks. This may be longer depending on the condition being treated. You may not see full healing for another 1 to 2 months after you stop using the medicine.

Treated areas of skin can look unsightly during and for several weeks after treatment with this medicine.

This medicine can make you more sensitive to the sun. Keep out of the sun. If you cannot avoid being in the sun, wear protective clothing and use sunscreen. Do not use sun lamps or tanning beds/booths.

What side effects may I notice from receiving this medicine?

Side effects that you should report to your doctor or health care professional as soon as possible:
•severe redness and swelling of normal skin

Side effects that usually do not require medical attention (report to your doctor or health care professional if they continue or are bothersome):
•dark colored skin
•eye irritation including burning, itching, sensitivity, stinging, or watering
•increased sensitivity of the skin to sun and ultraviolet light
•pain and burning of the affected area
•scaling or swelling of the affected area
•skin rash, itching of the affected area
•tenderness

This list may not describe all possible side effects. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.

Where should I keep my medicine?

Keep out of the reach of children.

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F). Do not freeze. Keep container tightly closed. Throw away any unused medicine after the expiration date.

Last updated: 7/1/2002

Important Disclaimer: The drug information provided here is for educational purposes only. It is intended to supplement, not substitute for, the diagnosis, treatment and advice of a medical professional. This drug information does not cover all possible uses, precautions, side effects and interactions. It should not be construed to indicate that this or any drug is safe for you. Consult your medical professional for guidance before using any prescription or over the counter drugs.

Oxford A-Z of Medicinal Drugs:

fluorouracil

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(5-fluorouracil; 5-FU)

An antimetabolite used for the treatment of solid tumours (see cancer), especially those of the gastrointestinal tract (such as cancers of the colon and rectum) and breast cancer. It is usually administered intravenously, sometimes in conjunction with folinic acid, which increases its effectiveness. It is usually given as intensive courses of several days' treatment every 3–4 weeks. Fluorouracil can also be used topically to treat certain malignant skin tumours. A prescription only medicine, it is available as a solution for injection, capsules, or a cream.

Side effects:
injections or capsules may cause bone marrow suppression, inflammation of the mucous membranes lining the mouth, stomach, and intestine, and nausea and vomiting. See cytotoxic drugs.

Precautions:
see cytotoxic drugs.

Interactions with other drugs:

Clozapine there is an increased risk of agranulocytosis (a blood disorder), and the two drugs should not be used together.
Phenytoin its adverse effects may be increased.
Temoporfin sensitivity to light is increased if fluorouracil cream is used with it.
Warfarin: its anticoagulant effect is enhanced.

Proprietary preparation:
Efudix (cream).

Previous:	fluorometholone, fluoride, fluorescein sodium
Next:	fluoxetine, flupentixol, fluphenazine decanoate

Oxford Dictionary of Biochemistry:

fluorouracil

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symbol: FUra (not FU); 5-fluorouracil; 5-fluoro-2,4(1H,3H)-pyrimidinedione; a synthetic analogue of uracil that is enzymically converted via its β-d-ribofuranoside, fluorouridine (symbol: FUrd), to fluorodeoxyuridine (symbol: FdUrd) and then to fluorodeoxyuridylate, which is a potent inhibitor of thymidylate synthase and, hence, of DNA synthesis. Thus fluorouracil is a suicide inactivator of thymidylate synthase. Fluorouracil and fluorodeoxyuridine are anticancer drugs, commonly used in combination therapy against fast-growing tumours.

Previous:	fluoroscope, fluorophor, fluorometer
Next:	fluoxetine, flush end, flux

Mosby's Dental Dictionary:

fluorouracil (topical)

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trade names: Efudex, Fluoroplex; drug class: topical antineoplastic; action: inhibits synthesis of DNA and RNA in susceptible cells; uses: keratosis, basal cell carcinoma.

Wikipedia on Answers.com:

Fluorouracil

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Fluorouracil


Systematic (IUPAC) name
5-fluoro-1H-pyrimidine-2,4-dione
Clinical data
Trade names	Carac
AHFS/Drugs.com	monograph
MedlinePlus	a682708
Pregnancy cat.	D(AU) D (intravenous), X (topical) (US)
Legal status	℞-only (US)
Routes	Intravenous (infusion or bolus) and topical
Pharmacokinetic data
Bioavailability	28 to 100%
Protein binding	8 to 12%
Metabolism	Intracellular and hepatic (CYP-mediated)
Half-life	10 to 20 minutes
Excretion	Renal
Identifiers
CAS number	51-21-8^Y
ATC code	L01BC02
PubChem	CID 3385
DrugBank	APRD00516
ChemSpider	3268^Y
UNII	U3P01618RT^Y
KEGG	D00584^Y
ChEBI	CHEBI:46345^Y
ChEMBL	CHEMBL185^Y
Chemical data
Formula	C₄H₃F N₂O₂
Mol. mass	130.077 g/mol
SMILES	eMolecules & PubChem
InChI InChI=1S/C4H3FN2O2/c5-2-1-6-4(9)7-3(2)8/h1H,(H2,6,7,8,9)^Y Key:GHASVSINZRGABV-UHFFFAOYSA-N^Y
Physical data
Melt. point	282 - 283 °C (-195 °F)
N(what is this?) (verify)

Fluorouracil (5-FU or f5U) (sold under the brand names Adrucil, Carac, Efudix, Efudex and Fluoroplex) is a drug that is a pyrimidine analog which is used in the treatment of cancer. It is a suicide inhibitor and works through irreversible inhibition of thymidylate synthase. It belongs to the family of drugs called antimetabolites. It is typically administered with leucovorin.

Contents

1 Uses
2 Synthesis
3 Mode of action
4 Adverse effects
5 History
6 Interactive pathway map
7 References
8 External links

Uses

The chemotherapy agent 5-FU, which has been used against cancer for about 40 years, acts in several ways, but principally as a thymidylate synthase inhibitor. Interrupting the action of this enzyme blocks synthesis of the pyrimidine thymidine, which is a nucleoside required for DNA replication. Thymidylate synthase methylates deoxyuridine monophosphate (dUMP) into thymidine monophosphate (dTMP). Administration of 5-FU causes a scarcity in dTMP, so rapidly dividing cancerous cells undergo cell death via thymineless death.^[1]

Like many anti-cancer drugs, 5-FU's effects are felt system wide but fall most heavily upon rapidly dividing cells that make heavy use of their nucleotide synthesis machinery, such as cancer cells, but also other cells in parts of the body that are rapidly dividing, for example, the cells lining the digestive tract.

Some of its principal uses are in colorectal cancer, and pancreatic cancer, in which it has been the established form of chemotherapy for decades (platinum-containing drugs approved for human use in the US since 1978 are also very well established). It is sometimes used in the treatment of inflammatory breast cancer, an especially aggressive form of breast cancer.

5-FU is used in ophthalmic surgery, specifically to augment trabeculectomy (an operation performed to lower the intraocular pressure in patients with glaucoma) in patients deemed to be at high risk for failure. 5-FU acts as an anti-scarring agent in this regard, since excessive scarring at the trabeculectomy site is the main cause for failure of the surgery.

Fluorouracil can be used topically (as a cream) for treating actinic (solar) keratoses and some types of basal cell carcinomas of the skin. It is often referred to by its trade names Efudex, Carac or Fluoroplex.

Due to fluorouracil's toxicity and the fact that it can be manufactured using the same reaction as uracil, its precursor, 5-fluoroorotic acid, is commonly used in laboratories to screen against organisms capable of synthesizing uracil.

It is a key component in tegafur-uracil.

Synthesis

5-FU was designed, synthesized and patented by Charles Heidelberger in 1957.^[2]^[3]^[4]

Since uracil is a normal component of RNA, the rationale behind the development of the drug was that cancer cells, with their increased genetic instability, might be more sensitive to 'decoy' molecules that mimic the natural compound than normal cells. The scientific goal in this case was to synthesize a drug which demonstrated specific uracil antagonism. The drug proved to have anti-tumor capabilities.

When elemental fluorine is reacted with uracil, 5-fluorouracil is produced. 5-Fluorouracil masquerades as uracil during the nucleic acid replication process. Because 5-fluorouracil is similar in shape to but does not perform the same chemistry as uracil, the drug inhibits RNA replication enzymes, thereby eliminating RNA synthesis and stopping the growth of cancerous cells.

Mode of action

As a pyrimidine analogue, it is transformed inside the cell into different cytotoxic metabolites which are then incorporated into DNA and RNA, finally inducing cell cycle arrest and apoptosis by inhibiting the cell's ability to synthesize DNA. It is an S-phase specific drug and only active during certain cell cycles. In addition to being incorporated in DNA and RNA, the drug has been shown to inhibit the activity of the exosome complex, an exoribonuclease complex of which the activity is essential for cell survival.

Capecitabine is a prodrug that is converted into 5-FU in the tissues. It can be administered orally.

Adverse effects

Side effects include myelosuppression, mucositis, dermatitis and diarrhea.

5-FU injection and topical even in small doses cause both acute central nervous system (CNS) damage and progressively worsening delayed degeneration of the CNS in mice. This latter effect is caused by 5-FU-induced damage to the oligodendrocytes that produce the insulating myelin sheaths.^[5]

When using a pyrimidine-based drug, users must be aware that some people have a genetic inability to metabolize them. Current theory points to nearly 8% of the population having dihydropyrimidine dehydrogenase (DPD) deficiency. There are laboratory tests to determine the relative activity of the DPD enzyme. It is expected that with a potential 500,000 people in North America using the pyrimidine-based 5-FU, this form of testing will increase.

The typical starting dose of capecitabine is 2,500 mg/m² per day in Europe and 2,000 mg/m² per day in the US. Probably the main action of 5-FU occurs when a 5-FU metabolite binds to thymidylate synthase. This binding is stable only in the presence of methylenetetrahydrofolate. It is speculated that this may explain why people in the US—a country that mandates adding folic acid to some foods—apparently require a lower dose of capecitabine than people in Europe, where countries do not mandate added folic acid.^[6]^[7]

The body converts both folic acid and leucovorin to methylenetetrahydrofolate. Each of those precursors amplified the effect of 5-FU in one animal study.^[8] However, another animal study seemed to indicate that, given the same 5-FU treatment, a special diet containing no folic acid worked better than the normal diet.^[9]

Folic acid may amplify the desired action and the toxicity of 5-FU. The exact mechanism of interaction is unknown.^[10]

When 5-FU is given intravenously, it is typically mixed with leucovorin in order to increase 5-FU activity. Folic acid may work as well as leucovorin, but the one human study performed (with a high dose of folic acid, from 40 mg/m² to 140 mg/m²) had disappointing results and concluded that further studies were needed.^[11] There is some confusion about whether the amount of folic acid in a normal diet and multivitamins is enough to interact badly with 5-FU.^[12]

One study showed that 79 percent of the patients who switched from 5-FU (with leucovorin) to Xeloda (capecitabine) had serious side effects. None of the patients who switched from Xeloda to 5-FU (with leucovorin) had serious side effects. The researchers were unsure why.^[13]

Trissel and colleagues have shown that 5-FU and leucovorin are physically incompatible when mixed in portable-pump reservoirs.^[14] Similarly, infusion of 5-FU and leucovorin via permanent indwelling catheters is complicated by catheter blockage due to calcium carbonate formation (Ardalan and Flores, 1995).^[15]

History

In 1954 Abraham Cantarow and Karl Paschkis found liver tumors absorbed radioactive uracil more readily than normal liver cells. Charles Heidelberger, who had earlier found that fluorine in fluoroacetic acid inhibited a vital enzyme, asked Robert Duschinsky and Robert Schnitzer at Hoffman-La Roche to synthesize fluorouracil.^[16] Some credit Heidelberger and Duschinsky with the discovery that 5-fluorouracil markedly inhibited tumors in mice.^[17] The original 1957 report in Nature has Heidelberger as lead author, along with N.K.Chaudhuri, Peter Danneberg, Dorothy Mooren, Louis Griesbach, Robert Duschinsky, R.J. Schnitzer, E. Pleven, and J. Scheiner.^[18]

Interactive pathway map

Click on genes, proteins and metabolites below to link to respective articles. ^[19]

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Fluorouracil (5-FU) Activity edit

References

^ Longley DB, Harkin DP, Johnston PG (May 2003). "5-fluorouracil: mechanisms of action and clinical strategies". Nat. Rev. Cancer 3 (5): 330–8. doi:10.1038/nrc1074. PMID 12724731. http://www.nature.com/nrc/journal/v3/n5/full/nrc1074.html.
^ "Awards, Appointments, Announcements". J Natl Cancer Inst 91 (15): 1278–80. 1999. doi:10.1093/jnci/91.15.1278. http://jnci.oxfordjournals.org/content/91/15/1278.full.
^ Chu E (September 2007). "Ode to 5-Fluorouracil". Clinical Colorectal Cancer 6 (9): 609. doi:10.3816/CCC.2007.n.029. http://cigjournals.metapress.com/content/b464v2u31594jj28/.
^ National Academy of Sciences, Biographical Memoirs,80:135
^ "Chemotherapy-induced Damage to the CNS as a Precursor Cell Disease" by Dr. Mark D. Noble, University of Rochester
^ Midgley R, Kerr DJ (January 2009). "Capecitabine: have we got the dose right?". Nat Clin Pract Oncol 6 (1): 17–24. doi:10.1038/ncponc1240. PMID 18936793. http://www.nature.com/nrclinonc/journal/v6/n1/full/ncponc1240.html.
^ Midgley, Rachel. "Regional Variation in Capecitabine Metabolism and Toxicity". Medscape.com. http://www.medscape.com/viewarticle/583704_3.
^ Raghunathan K, Priest DG (September 1999). "Modulation of fluorouracil antitumor activity by folic acid in a murine model system". Biochem. Pharmacol. 58 (5): 835–9. doi:10.1016/S0006-2952(99)00157-4. PMID 10449194. http://linkinghub.elsevier.com/retrieve/pii/S0006-2952(99)00157-4.
^ Tucker JM, Davis C, Kitchens ME, et al. (December 2002). "Response to 5-fluorouracil chemotherapy is modified by dietary folic acid deficiency in Apc(Min/+) mice". Cancer Lett. 187 (1–2): 153–62. doi:10.1016/S0304-3835(02)00402-0. PMID 12359363. http://linkinghub.elsevier.com/retrieve/pii/S0304383502004020.
^ "Folic-acid and Xeloda Interactions"
^ "Handbook of drug-nutrient interactions" by Joseph I. Boullata, Vincent T. Armenti, 2007, p.207, 208
^ "Xeloda and Folic acid"
^ "Switching from 5FU to Xeloda Can Cause Significant Side Effects"
^ Trissel LA, Martinez JF, Xu QA (April 1995). "Incompatibility of fluorouracil with leucovorin calcium or levoleucovorin calcium". Am J Health Syst Pharm 52 (7): 710–5. PMID 7627739.
^ Ardalan B, Flores MR (April 1995). "A new complication of chemotherapy administered via permanent indwelling central venous catheter". Cancer 75 (8): 2165–8. doi:10.1002/1097-0142(19950415)75:8<2165::AID-CNCR2820750821>3.0.CO;2-W. PMID 7697607.
^ Sneader W. (2005). Drug Discovery, p. 255.
^ Cohen, Seymour (30 January 2008). "50 years ago in cell biology: A virologist recalls his work on cell growth inhibition". The Scientist. http://www.the-scientist.com/news/display/54259/.
^ Heidelberger C, Chaudhuri NK, Danneberg P, et al. (March 1957). "Fluorinated pyrimidines, a new class of tumour-inhibitory compounds". Nature 179 (4561): 663–6. doi:10.1038/179663a0. PMID 13418758.
^ The interactive pathway map can be edited at WikiPathways: "Fluoropyrimidine_Activity_WP1601". http://www.wikipathways.org/index.php/Pathway:WP1601.

External links

Cancerbackup.org.uk – Fluorouracil's use in cancer

Intracellular chemotherapeutic agents/antineoplastic agents (L01)

SPs/MIs
(M phase)

Block microtubule assembly	Vinca alkaloids (Vinblastine, Vincristine, Vinflunine, Vindesine, Vinorelbine)

Block microtubule disassembly	Taxanes (Cabazitaxel, Docetaxel, Larotaxel, Ortataxel, Paclitaxel, Tesetaxel) • Epothilones (Ixabepilone)

DNA replication
inhibitor

DNA precursors/
antimetabolites
(S phase)

Folic acid	dihydrofolate reductase inhibitor (Aminopterin, Methotrexate, Pemetrexed, Pralatrexate) • thymidylate synthase inhibitor (Raltitrexed, Pemetrexed)

Purine	adenosine deaminase inhibitor (Pentostatin) halogenated/ribonucleotide reductase inhibitors (Cladribine, Clofarabine, Fludarabine) thiopurine (Thioguanine, Mercaptopurine)

Pyrimidine	thymidylate synthase inhibitor (Fluorouracil, Capecitabine, Tegafur, Carmofur, Floxuridine) DNA polymerase inhibitor (Cytarabine) ribonucleotide reductase inhibitor (Gemcitabine) hypomethylating agent (Azacitidine, Decitabine)

Deoxyribonucleotide	ribonucleotide reductase inhibitor (Hydroxycarbamide)

Topoisomerase inhibitors
(S phase)

I	Camptotheca (Camptothecin, Topotecan, Irinotecan, Rubitecan, Belotecan)

II	Podophyllum (Etoposide, Teniposide)

II+Intercalation	Anthracyclines (Aclarubicin, Daunorubicin, Doxorubicin, Epirubicin, Idarubicin, Amrubicin, Pirarubicin, Valrubicin, Zorubicin) • Anthracenediones (Mitoxantrone, Pixantrone)

Crosslinking of DNA
(CCNS)

Alkylating	Nitrogen mustards: Mechlorethamine • Cyclophosphamide (Ifosfamide, Trofosfamide) • Chlorambucil (Melphalan, Prednimustine) • Bendamustine • Uramustine • Estramustine Nitrosoureas: Carmustine • Lomustine (Semustine) • Fotemustine • Nimustine • Ranimustine • Streptozocin Alkyl sulfonates: Busulfan (Mannosulfan, Treosulfan) Aziridines: Carboquone • ThioTEPA • Triaziquone • Triethylenemelamine

Alkylating-like	Platinum (Carboplatin, Cisplatin, Nedaplatin, Oxaliplatin, Triplatin tetranitrate, Satraplatin)

Nonclassical	Hydrazines (Procarbazine) • Triazenes (Dacarbazine, Temozolomide) • Altretamine • Mitobronitol

Intercalation	Streptomyces (Actinomycin, Bleomycin, Mitomycin, Plicamycin)

Photosensitizers/PDT

Aminolevulinic acid/Methyl aminolevulinate • Efaproxiral • Porphyrin derivatives (Porfimer sodium, Talaporfin, Temoporfin, Verteporfin)

Other

Enzyme inhibitors	FI (Tipifarnib) • CDK inhibitors (Alvocidib, Seliciclib) • PrI (Bortezomib) • PhI (Anagrelide) • IMPDI (Tiazofurine) • LI (Masoprocol) • PARP inhibitor (Olaparib) • HDAC (Panobinostat, Vorinostat, Romidepsin)

Receptor antagonists	ERA (Atrasentan) • retinoid X receptor (Bexarotene) • sex steroid (Testolactone)

Other/ungrouped	Amsacrine • Trabectedin • retinoids (Alitretinoin, Tretinoin) • Arsenic trioxide • asparagine depleters (Asparaginase/Pegaspargase) • Celecoxib • Demecolcine • Elesclomol • Elsamitrucin • Etoglucid • Lonidamine • HAMLET (human alpha-lactalbumin made lethal to tumor cells) • Lucanthone • Mitoguazone • Mitotane • Oblimersen • Omacetaxine mepesuccinate • mTOR inhibitors (Everolimus, Temsirolimus)

M: NEO

tsoc, mrkr

tumr, epon, para

drug (L1i/1e/V03)

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