Capecitabine

Identification

Summary

Capecitabine is a nucleoside metabolic inhibitor indicated to treat different gastrointestinal, including pancreatic cancer, and breast cancer.

Brand Names

Ecansya, Xeloda

Generic Name

Capecitabine

DrugBank Accession Number

DB01101

Background

Capecitabine is an orally-administered chemotherapeutic agent used in the treatment of metastatic breast and colorectal cancers. Capecitabine is a prodrug, that is enzymatically converted to fluorouracil (antimetabolite) in the tumor, where it inhibits DNA synthesis and slows growth of tumor tissue.

Type

Small Molecule

Groups

Approved, Investigational

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Capecitabine (DB01101)

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Weight

Average: 359.3501
Monoisotopic: 359.149263656

Chemical Formula

C₁₅H₂₂FN₃O₆

Synonyms

• (1-(5-Deoxy-beta-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-carbamic acid pentyl ester
• Capecitabin
• Capecitabina
• Capécitabine
• Capecitabine
• Capecitabinum
• Pentyl [1-(5-deoxy-β-D-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl]carbamate
• pentyl 1-(5-deoxy-β-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamate

External IDs

• R340
• RO 09-1978/000
• RO-09-1978/000

Pharmacology

Indication

Capecitabine is indicated as treatment for a variety of cancer types. For colorectal cancer, capecitabine is indicated as a single agent or a component of a combination chemotherapy regiment for the adjuvant treatment of stage III colon cancer and treatment unresectable or metastatic colorectal cancer. It can also be used as a part of a combination chemotherapy perioperative treatment of adult locally advanced rectal cancer.⁴² For breast cancer, capecitabine is indicated for advanced or metastatic breast cancer as a single agent if an anthracycline- or taxane-containing chemotherapy is not indicated or as a regimen with docetaxel after disease progression on prior anthracycline-containing chemotherapy.⁴² For gastric, esophageal, or gastroesophageal junction (GEJ) cancer, capecitabine is indicated as a component of a combination chemotherapy treatment for the treatment of adult unresectable or metastatic gastric, esophageal, or GEJ cancer or adult HER2-overexpressing metastatic gastric or GEJ adenocarcinoma who have not received prior treatment for metastatic disease.⁴² Finally, for pancreatic cancer, capecitabine is indicated as adjuvant treatment for adult pancreatic adenocarcinoma as a component of a combination chemotherapy regimen.⁴²

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Associated Conditions

• Advanced or Metastatic Breast Cancer
• Carcinoma of Gallbladder
• Cholangiocarcinoma
• Hepatocellular Carcinoma
• Locally Advanced Rectal Cancer (LARC)
• Metastatic Adenocarcinoma of the Gastroesophageal Junction
• Metastatic Gastric Cancers
• Metastatic Neuroendocrine Tumors
• Pancreatic Adenocarcinoma
• Pancreatic Cancer, Advanced or Metastatic
• Platinum-resistant Epithelial Ovarian Cancer
• Refractory Fallopian Tube Carcinoma
• Stage III Colon Cancer
• Unresectable or Metastatic Colorectal Cancer
• Metastatic pancreatic endocrine carcinoma
• Refractory peritoneal cancer
• Refractory, metastatic Colorectal carcinoma
• Unresectable, metastatic Esophageal Cancer
• Unresectable, metastatic Gastric Cancer
• Unresectable, metastatic Gastroesophageal Junction Cancer

Associated Therapies

• Chemotherapy

Contraindications & Blackbox Warnings

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Pharmacodynamics

Capecitabine is a fluoropyrimidine carbamate belonging to a group of antineoplastic agents called antimetabolites, which kill cancerous cells by interfering with DNA synthesis.^39,26 It is an orally administered systemic prodrug that has little pharmacologic activity until it is converted to 5-fluorouracil (5-FU) by enzymes that are expressed in higher concentrations in many tumors.⁴⁰ Capecitabine was designed specifically to overcome the disadvantages of 5-FU and to mimic the infusional pharmacokinetics of 5-FU without the associated complexity and complications of central venous access and infusion pumps.³⁹ Particularly, since the enzymes converting 5-FU into active metabolites exist in the gastrointestinal tract, infusion of 5-FU can have gastrointestinal toxicity while also losing efficacy.⁴¹ Since capecitabine can be transported intact across the intestinal mucosa, it can be selectively delivered 5-FU to tumor tissues through enzymatic conversion preferentially inside tumor cells.⁴¹

5-FU exerts its pharmacological action through the inhibition and interference of 3 main targets: thymidylate synthase, DNA, and RNA, leading through protein synthesis disruption and apoptosis.^26,20 Population-based exposure-effect analyses demonstrated a positive association between AUC of 5-FU and grade 3-4 hyperbilirubinemia.⁴²

Mechanism of action

Capecitabine is metabolized to 5-fluorouracil in vivo by carboxylesterases, cytidine deaminase, and thymidine phosphorylase/uridine phosphorylase sequentially.^{42,18,14,15,16} 5-fluorouracil is further metabolized through a series of enzymatic reactions into 3 main active metabolites: 5-fluorouridine triphosphate (5-FUTP), 5-fluoro-2’-deoxyuridine monophosphate (5-FdUMP), and 5-fluorodeoxyuridine triphosphate (5-FdUTP).^17,18,19. These metabolites cause cell injury by two different mechanisms. First, FdUMP and the folate cofactor, N5-10-methylenetetrahydrofolate (CH₂THF), bind to thymidylate synthase (TS) to form a covalently bound ternary complex.⁴² TS is an enzyme that catalyzes the methylation of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP).^20,19 Under normal physiological conditions, dUMP binds to TS first before CH₂THF, followed by a 1,4 or Michael addition from the pyrimidine C (6)atom to the Cys146 nucleophile.^20,21 If correctly positioned, dUMP, CH₂THF, and TS would form a ternary complex to facilitate the donation of the methyl group from CH₂THF to dUMP.²⁰ However, the substitution of dUMP with FdUMP results in a new time-dependent TS–FdUMP–CH2THF complex. Since the fluorine group prevents dissociation of FdUMP from the pyrimidine ring, the whole complex is rendered irreversibly deactivated, terming this reaction "suicide inhibition".^20,22 TS inhibition prevents the conversion of dUMP to dTMP, depleting the pool of dTMP that could be phosphorylated into dTTP to be incorporated as DNA nucleotides. This disrupts the nucleotides balance, particularly the the ATP/dTTP ratio, thus impairing DNA synthesis and repair and causing apoptosis.^23,20

5-FdUMP can also be phosphorylated into 5-FdUTP, further increasing the pool of dUTP base to potentially overwhelm the activity of dUTPase.²⁵ Coupled with the decrease in dTTP, 5-FdUMP, and 5-FdUTP increase the probability of mistakenly incorporating a uracil base into DNA strands in place of thymine. Although this mistake can often be resolved by the nucleotide excision repair enzyme uracil-DNA-glycosylase (UDG), the high (F)dUTP/dTTP ratio would result in re-incorporation of uracil into DNA, leading to a futile cycle of misincorporation, excision, and repair.^24,26 Repeated base excision repair can result in abasic sites, which can lead to DNA mutagenesis and thus protein miscoding, replication forks collapse, and DNA fragmentation through single or double strand breaks ^25,27,28,29

However, several reports have found that the incorporation of uracil in genomic DNA does not significantly affect the cytotoxicity of 5-FU, suggesting that the cytotoxic effect of 5-FU is dominated by the perturbation of RNA through 5-FUTP.^30,31 Similar to 5-dFUTP, 5-FUTP can be mistakenly incorporated into RNA in place of regular UTP and disrupt regular RNA biology through various mechanisms. 5-FUTP can be incorporated into the spliceosomal U2 snRNA at pseudouridylated sites to prevent further pseudouridylation and thus pre-mrNA splicing. 5-FUTP can also change the structure of U4 and U6 snRNA and reduce the turnover rate of U1 snrNA once incorporated.³² For tRNA, 5-FUTP can affect tRNA's post-transcriptional RNA modifications activity, particularly by inhbiting pseudouridine synthase through formation of covalent complex.^33,34 Recently, the effect of 5-FUTP on miRNAs and lncRNA was also observed through profound changes in expression, although the precise mechanism is still unknown.^35,36,37

Although the main mechanism of 5-FU cytotoxicity was thought to be attributed to DNA damages, recent reports have shown that the majority of 5-FU pharmacological action is mediated through RNA, since 5-FU is accumulated ~3000- to 15 000-fold more in RNA compared to that of DNA.³⁸

Target	Actions	Organism
ADNA	incorporation into and destabilization inhibition of synthesis	Humans
ARNA	incorporation into and destabilization	Humans
AThymidylate synthase	inhibitor	Humans

Absorption

The AUC of capecitabine and its metabolite 5’-DFCR increases proportionally over a dosage range of 500 mg/m2/day to 3,500 mg/m2/day (0.2 to 1.4 times the approved recommended dosage). The AUC of capecitabine’s metabolites 5’-DFUR and fluorouracil increased greater than proportional to the dose. The interpatient variability in the Cmax and AUC of fluorouracil was greater than 85%.⁴²

Following oral administration of capecitabine 1,255 mg/m² orally twice daily (the recommended dosage when used as a single agent), the median Tmax of capecitabine and its metabolite fluorouracil was approximately 1.5 hours and 2 hours, respectively.⁴²

Volume of distribution

In colorectal cancer patients with a mean age of 58 ± 9.5 years and ECOG Performance Status of 0–1, the volume of distribution is calculated to be 186 ± 28 L.⁷

Protein binding

Plasma protein binding of capecitabine and its metabolites is less than 60% and is not concentration dependent. Capecitabine was primarily bound to human albumin (approximately 35%).⁴²

Metabolism

Capecitabine undergoes metabolism by carboxylesterase and is hydrolyzed to 5’-DFCR. 5’-DFCR is subsequently converted to 5’-DFUR by cytidine deaminase. 5’-DFUR is then hydrolyzed by thymidine phosphorylase (dThdPase) enzymes to the active metabolite fluorouracil.⁴²

Fluorouracil is subsequently metabolized by dihydropyrimidine dehydrogenase to 5-fluoro-5, 6-dihydro-fluorouracil (FUH2). The pyrimidine ring of FUH2 is cleaved by dihydropyrimidinase to yield 5-fluoro-ureido-propionic acid (FUPA). Finally, FUPA is cleaved by β-ureido-propionase to α-fluoro-β-alanine (FBAL).⁴²

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• Capecitabine
  • 5’-Deoxy-5-fluorocytidine (5'-DFCR)
    • 5’-Deoxy-5-fluorouridine (5'DFUR)
      • 5-fluorouracil
        • 5-fluouridine (5-FUR)
          • 5-fluorouridine monophosphate (5-FUMP)
            • 5-fluorouridine diphosphate (5-FUDP)
              • 5-fluorouridine triphosphate (5-FUTP)
                • 5-FUDP-hexose
        • 5-fluorouridine monophosphate (5-FUMP)
          • 5-fluorouridine diphosphate (5-FUDP)
            • 5-fluorodeoxyuridine diphosphate (5-FdUDP)
              • 5-fluorodeoxyuridine monophosphate (5-FdUMP)
              • 5-fluorodeoxyuridine triphosphate (5-FdUTP)
                • 5-fluorodeoxyuridine monophosphate (5-FdUMP)
            • 5-fluorouridine triphosphate (5-FUTP)
              • 5-FUDP-hexose
        • 5-fluorodeoxyuridine (5-FUdR)
          • 5-fluorodeoxyuridine monophosphate (5-FdUMP)
            • 5-fluorodeoxyuridine diphosphate (5-FdUDP)
              • 5-fluorodeoxyuridine triphosphate (5-FdUTP)
                • 5-fluorodeoxyuridine monophosphate (5-FdUMP)
        • dihydrofluorouracil (DHFU)
          • β-ureidopropionic acid (FUPA)
            • Urea + fluoro-β-alanine (FBAL)

Route of elimination

Following administration of radiolabeled capecitabine, 96% of the administered capecitabine dose was recovered in urine (3% unchanged and 57% as metabolite FBAL) and 2.6% in feces.⁴²

Half-life

The elimination half-lives of capecitabine and fluorouracil were approximately 0.75 hour.⁴²

Clearance

In colorectal cancer patients with a mean age of 58 ± 9.5 years and ECOG Performance Status of 0–1, the clearance of capecitabine is calculated to be 775 ± 213 mL/min.⁷

Adverse Effects

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Toxicity

Adequate studies investigating the carcinogenic potential of capecitabine have not been conducted. Capecitabine was not mutagenic in vitro to bacteria (Ames test) or mammalian cells (Chinese hamster V79/HPRT gene mutation assay). Capecitabine was clastogenic in vitro to human peripheral blood lymphocytes but not clastogenic in vivo to mouse bone marrow (micronucleus test). Fluorouracil causes mutations in bacteria and yeast. Fluorouracil also causes chromosomal abnormalities in the mouse micronucleus test in vivo.⁴²

In studies of fertility and general reproductive performance in female mice, oral capecitabine doses of 760 mg/kg/day (about 2,300 mg/m2/day) disturbed estrus and consequently caused a decrease in fertility. In mice that became pregnant, no fetuses survived this dose. The disturbance in estrus was reversible. In males, this dose caused degenerative changes in the testes, including decreases in the number of spermatocytes and spermatids. In separate pharmacokinetic studies, this dose in mice produced 5’-DFUR AUC values about 0.7 times the corresponding values in patients administered the recommended daily dose.⁴²

Based on findings in animal reproduction studies and its mechanism of action [see Clinical Pharmacology (12.1)], XELODA can cause fetal harm when administered to a pregnant woman. Available human data on XELODA use in pregnant women is not sufficient to inform the drug-associated risk. In animal reproduction studies, administration of capecitabine to pregnant animals during the period of organogenesis caused embryo lethality and teratogenicity in mice and embryo lethality in monkeys at 0.2 and 0.6 times the exposure (AUC) in patients receiving the recommended dose of 1,250 mg/m2 twice daily, respectively. Advise pregnant women of the potential risk to a fetus.⁴²

The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively.⁴²

Administer uridine triacetate within 96 hours for management of XELODA overdose. Although no clinical experience using dialysis as a treatment for XELODA overdose has been reported, dialysis may be of benefit in reducing circulating concentrations of 5’-DFUR, a low–molecular-weight metabolite of the parent compound.⁴²

Pathways

Pathway	Category
Capecitabine Action Pathway	Drug action
Capecitabine Metabolism Pathway	Drug metabolism

Pharmacogenomic Effects/ADRs

Interacting Gene/Enzyme	Allele name	Genotype(s)	Defining Change(s)	Type(s)	Description	Details
Dihydropyrimidine dehydrogenase [NADP(+)]	DPYD*2A	(A;A) / (A;G)	G > A	ADR Directly Studied	The presence of this genotype in DPYD is associated with an increased risk of drug-related toxicity from capecitabine therapy.	Details
Dihydropyrimidine dehydrogenase [NADP(+)]	DPYD*13	(C;C) / (A;C)	A > C	ADR Directly Studied	The presence of this genotype in DPYD is associated with an increased risk of drug-related toxicity from capecitabine therapy.	Details
Dihydropyrimidine dehydrogenase [NADP(+)]	---	(A;A) / (A;T)	T > A	ADR Directly Studied	The presence of this genotype in DPYD may be associated with an increased risk of drug-related toxicity from capecitabine therapy.	Details
Dihydropyrimidine dehydrogenase [NADP(+)]	DPYD*4	(G;G) / (A:G)	G > A	ADR Directly Studied	The presence of this genotype in DPYD may be associated with an increased risk of drug-related toxicity from capecitabine therapy.	Details
Dihydropyrimidine dehydrogenase [NADP(+)]	DPYD*5	(G;G) / (A;G)	A > G	ADR Directly Studied	The presence of this genotype in DPYD may be associated with an increased risk of drug-related toxicity from capecitabine therapy.	Details
Dihydropyrimidine dehydrogenase [NADP(+)]	DPYD*6	(A;A) / (A;G)	G > A	ADR Directly Studied	The presence of this genotype in DPYD may be associated with an increased risk of drug-related toxicity from capecitabine therapy.	Details
Dihydropyrimidine dehydrogenase [NADP(+)]	DPYD*9A	(C;C) / (C;T)	T > C	ADR Directly Studied	The presence of this genotype in DPYD may be associated with an increased risk of drug-related toxicity from capecitabine therapy.	Details

Interactions

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

• Approved
• Vet approved
• Nutraceutical
• Illicit
• Withdrawn
• Investigational
• Experimental
• All Drugs

Drug	Interaction
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Abacavir	Abacavir may decrease the excretion rate of Capecitabine which could result in a higher serum level.
Abatacept	The metabolism of Capecitabine can be increased when combined with Abatacept.
Abciximab	The risk or severity of bleeding can be increased when Abciximab is combined with Capecitabine.
Abrocitinib	The serum concentration of Abrocitinib can be increased when it is combined with Capecitabine.
Aceclofenac	Capecitabine may increase the nephrotoxic activities of Aceclofenac.
Acemetacin	Capecitabine may increase the nephrotoxic activities of Acemetacin.
Acenocoumarol	The serum concentration of Acenocoumarol can be increased when it is combined with Capecitabine.
Acetaminophen	Acetaminophen may decrease the excretion rate of Capecitabine which could result in a higher serum level.
Acetazolamide	Acetazolamide may increase the excretion rate of Capecitabine which could result in a lower serum level and potentially a reduction in efficacy.
Acetohexamide	The serum concentration of Acetohexamide can be increased when it is combined with Capecitabine.

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Food Interactions

• Take at the same time every day. Take XELODA 2 times a day at the same time each day, about 12 hours apart.
• Take with food. Take XELODA within 30 minutes after finishing a meal.
• Take with plain water. Swallow XELODA tablets whole with water. Do not chew, cut, or crush XELODA tablets.

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Active Moieties

Name	Kind	UNII	CAS	InChI Key
Fluorouracil	prodrug	U3P01618RT	51-21-8	GHASVSINZRGABV-UHFFFAOYSA-N

Product Images

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Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Capecitabine	Tablet	150 mg	Oral	Sivem Pharmaceuticals Ulc	Not applicable	Not applicable
Capecitabine	Tablet	500 mg	Oral	Sanis Health Inc	2021-10-22	Not applicable
Capecitabine	Tablet	500 mg	Oral	Jamp Pharma Corporation	2022-06-16	Not applicable
Capecitabine	Tablet	150 mg	Oral	Sanis Health Inc	2021-10-22	Not applicable
Capecitabine	Tablet	500 mg	Oral	Sivem Pharmaceuticals Ulc	Not applicable	Not applicable
Capecitabine	Tablet	150 mg	Oral	Jamp Pharma Corporation	2022-06-15	Not applicable
Capecitabine Accord	Tablet, film coated	150 mg	Oral	Accord Healthcare S.L.U.	2016-09-08	Not applicable
Capecitabine Accord	Tablet, film coated	500 mg	Oral	Accord Healthcare S.L.U.	2016-09-08	Not applicable
Capecitabine Accord	Tablet, film coated	150 mg	Oral	Accord Healthcare S.L.U.	2016-09-08	Not applicable
Capecitabine Accord	Tablet, film coated	500 mg	Oral	Accord Healthcare S.L.U.	2016-09-08	Not applicable

Generic Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Ach-capecitabine	Tablet	500 mg	Oral	Accord Healthcare Inc	2014-09-19	Not applicable
Ach-capecitabine	Tablet	150 mg	Oral	Accord Healthcare Inc	2014-09-19	Not applicable
Apo-capecitabine	Tablet	150 mg	Oral	Apotex Corporation	Not applicable	Not applicable
Apo-capecitabine	Tablet	500 mg	Oral	Apotex Corporation	Not applicable	Not applicable
Capecitabine	Tablet, film coated	500 mg/1	Oral	BluePoint Laboratories	2021-02-22	Not applicable
Capecitabine	Tablet, film coated	150 mg/1	Oral	Golden State Medical Supply, Inc.	2013-09-16	Not applicable
Capecitabine	Tablet, film coated	150 mg/1	Oral	Shilpa Medicare Limited	2016-12-31	Not applicable
Capecitabine	Tablet, film coated	500 mg/1	Oral	American Health Packaging	2016-03-07	Not applicable
Capecitabine	Tablet	150 mg/1	Oral	Aurobindo Pharma Limited	2018-04-17	Not applicable
Capecitabine	Tablet, film coated	500 mg/1	Oral	Areva Pharmaceuticals	2020-03-01	Not applicable

Categories

ATC Codes

L01BC06 — Capecitabine

• L01BC — Pyrimidine analogues
• L01B — ANTIMETABOLITES
• L01 — ANTINEOPLASTIC AGENTS
• L — ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS

Drug Categories

• Antimetabolites
• Antineoplastic Agents
• Antineoplastic and Immunomodulating Agents
• Cardiotoxic antineoplastic agents
• Cytidine Deaminase Substrates
• Cytochrome P-450 CYP2C9 Inhibitors
• Cytochrome P-450 CYP2C9 Inhibitors (strong)
• Cytochrome P-450 CYP2C9 Substrates
• Cytochrome P-450 CYP2C9 Substrates with a Narrow Therapeutic Index
• Cytochrome P-450 Enzyme Inhibitors
• Cytochrome P-450 Substrates
• Drugs that are Mainly Renally Excreted
• Fluoropyrimidines
• Fluorouracil and prodrugs
• Immunosuppressive Agents
• Myelosuppressive Agents
• Narrow Therapeutic Index Drugs
• Noxae
• Nucleic Acid Synthesis Inhibitors
• Nucleic Acids, Nucleotides, and Nucleosides
• Nucleoside Metabolic Inhibitor
• Pyrimidine Analogues
• Toxic Actions

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as 5'-deoxyribonucleosides. These are nucleosides in which the oxygen atom at the 5'position of the ribose moiety has been replaced by another atom. The nucleobases here are limited to purine, pyrimidine, and pyridine derivatives.

Kingdom

Organic compounds

Super Class

Nucleosides, nucleotides, and analogues

Class

5'-deoxyribonucleosides

Sub Class

Not Available

Direct Parent

5'-deoxyribonucleosides

Alternative Parents

Glycosylamines / Pyrimidones / Halopyrimidines / Aryl fluorides / Hydropyrimidines / Tetrahydrofurans / Heteroaromatic compounds / Secondary alcohols / 1,2-diols / Propargyl-type 1,3-dipolar organic compounds / Oxacyclic compounds / Azacyclic compounds / Carboximidic acids and derivatives / Organopnictogen compounds / Organonitrogen compounds / Organofluorides / Hydrocarbon derivatives / Organic oxides

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Substituents

1,2-diol / 5'-deoxyribonucleoside / Alcohol / Aromatic heteromonocyclic compound / Aryl fluoride / Aryl halide / Azacycle / Carboximidic acid derivative / Glycosyl compound / Halopyrimidine / Heteroaromatic compound / Hydrocarbon derivative / Hydropyrimidine / N-glycosyl compound / Organic 1,3-dipolar compound / Organic nitrogen compound / Organic oxide / Organic oxygen compound / Organofluoride / Organohalogen compound / Organoheterocyclic compound / Organonitrogen compound / Organooxygen compound / Organopnictogen compound / Oxacycle / Propargyl-type 1,3-dipolar organic compound / Pyrimidine / Pyrimidone / Secondary alcohol / Tetrahydrofuran

show 20 more

Molecular Framework

Aromatic heteromonocyclic compounds

External Descriptors

organofluorine compound, carbamate ester, cytidines (CHEBI:31348)

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

6804DJ8Z9U

CAS number

154361-50-9

InChI Key

GAGWJHPBXLXJQN-UORFTKCHSA-N

InChI

InChI=1S/C15H22FN3O6/c1-3-4-5-6-24-15(23)18-12-9(16)7-19(14(22)17-12)13-11(21)10(20)8(2)25-13/h7-8,10-11,13,20-21H,3-6H2,1-2H3,(H,17,18,22,23)/t8-,10-,11-,13-/m1/s1

IUPAC Name

pentyl N-{1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-methyloxolan-2-yl]-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl}carbamate

SMILES

CCCCCOC(=O)NC1=NC(=O)N(C=C1F)[C@@H]1O[C@H](C)[C@@H](O)[C@H]1O

References

Synthesis Reference

US5472949

General References

1. Walko CM, Lindley C: Capecitabine: a review. Clin Ther. 2005 Jan;27(1):23-44. [Article]
2. Wagstaff AJ, Ibbotson T, Goa KL: Capecitabine: a review of its pharmacology and therapeutic efficacy in the management of advanced breast cancer. Drugs. 2003;63(2):217-36. [Article]
3. Koukourakis GV, Kouloulias V, Koukourakis MJ, Zacharias GA, Zabatis H, Kouvaris J: Efficacy of the oral fluorouracil pro-drug capecitabine in cancer treatment: a review. Molecules. 2008 Aug 27;13(8):1897-922. [Article]
4. Twelves C: Vision of the future: capecitabine. Oncologist. 2001;6 Suppl 4:35-9. [Article]
5. Milano G, Ferrero JM, Francois E: Comparative pharmacology of oral fluoropyrimidines: a focus on pharmacokinetics, pharmacodynamics and pharmacomodulation. Br J Cancer. 2004 Aug 16;91(4):613-7. [Article]
6. de Bono JS, Twelves CJ: The oral fluorinated pyrimidines. Invest New Drugs. 2001;19(1):41-59. [Article]
7. Alqahtani S, Alzaidi R, Alsultan A, Asiri A, Asiri Y, Alsaleh K: Clinical pharmacokinetics of capecitabine and its metabolites in colorectal cancer patients. Saudi Pharm J. 2022 May;30(5):527-531. doi: 10.1016/j.jsps.2022.02.019. Epub 2022 Mar 2. [Article]
8. Vasey PA, McMahon L, Paul J, Reed N, Kaye SB: A phase II trial of capecitabine (Xeloda) in recurrent ovarian cancer. Br J Cancer. 2003 Nov 17;89(10):1843-8. doi: 10.1038/sj.bjc.6601381. [Article]
9. Wolf JK, Bodurka DC, Verschraegen C, Sun CC, Branham D, Jenkins AD, Atkinson N, Gershenson DM: A phase II trial of oral capecitabine in patients with platinum--and taxane--refractory ovarian, fallopian tube, or peritoneal cancer. Gynecol Oncol. 2006 Sep;102(3):468-74. doi: 10.1016/j.ygyno.2005.12.040. Epub 2006 Mar 3. [Article]
10. Fine RL, Gulati AP, Krantz BA, Moss RA, Schreibman S, Tsushima DA, Mowatt KB, Dinnen RD, Mao Y, Stevens PD, Schrope B, Allendorf J, Lee JA, Sherman WH, Chabot JA: Capecitabine and temozolomide (CAPTEM) for metastatic, well-differentiated neuroendocrine cancers: The Pancreas Center at Columbia University experience. Cancer Chemother Pharmacol. 2013 Mar;71(3):663-70. doi: 10.1007/s00280-012-2055-z. Epub 2013 Jan 31. [Article]
11. Strosberg JR, Fine RL, Choi J, Nasir A, Coppola D, Chen DT, Helm J, Kvols L: First-line chemotherapy with capecitabine and temozolomide in patients with metastatic pancreatic endocrine carcinomas. Cancer. 2011 Jan 15;117(2):268-75. doi: 10.1002/cncr.25425. Epub 2010 Sep 7. [Article]
12. Cartwright TH, Cohn A, Varkey JA, Chen YM, Szatrowski TP, Cox JV, Schulz JJ: Phase II study of oral capecitabine in patients with advanced or metastatic pancreatic cancer. J Clin Oncol. 2002 Jan 1;20(1):160-4. doi: 10.1200/JCO.2002.20.1.160. [Article]
13. Patt YZ, Hassan MM, Aguayo A, Nooka AK, Lozano RD, Curley SA, Vauthey JN, Ellis LM, Schnirer II, Wolff RA, Charnsangavej C, Brown TD: Oral capecitabine for the treatment of hepatocellular carcinoma, cholangiocarcinoma, and gallbladder carcinoma. Cancer. 2004 Aug 1;101(3):578-86. doi: 10.1002/cncr.20368. [Article]
14. Andreetta C, Puppin C, Minisini A, Valent F, Pegolo E, Damante G, Di Loreto C, Pizzolitto S, Pandolfi M, Fasola G, Piga A, Puglisi F: Thymidine phosphorylase expression and benefit from capecitabine in patients with advanced breast cancer. Ann Oncol. 2009 Feb;20(2):265-71. doi: 10.1093/annonc/mdn592. Epub 2008 Sep 2. [Article]
15. Loganayagam A, Arenas Hernandez M, Corrigan A, Fairbanks L, Lewis CM, Harper P, Maisey N, Ross P, Sanderson JD, Marinaki AM: Pharmacogenetic variants in the DPYD, TYMS, CDA and MTHFR genes are clinically significant predictors of fluoropyrimidine toxicity. Br J Cancer. 2013 Jun 25;108(12):2505-15. doi: 10.1038/bjc.2013.262. Epub 2013 Jun 4. [Article]
16. Timmers L, Swart EL, Boons CC, Mangnus D, van de Ven PM, Peters GJ, Boven E, Hugtenburg JG: The use of capecitabine in daily practice: a study on adherence and patients' experiences. Patient Prefer Adherence. 2012;6:741-8. doi: 10.2147/PPA.S36757. Epub 2012 Oct 19. [Article]
17. Krauss J, Bracher F: Pharmacokinetic Enhancers (Boosters)-Escort for Drugs against Degrading Enzymes and Beyond. Sci Pharm. 2018 Sep 27;86(4):E43. doi: 10.3390/scipharm86040043. [Article]
18. Nies AT, Magdy T, Schwab M, Zanger UM: Role of ABC transporters in fluoropyrimidine-based chemotherapy response. Adv Cancer Res. 2015;125:217-43. doi: 10.1016/bs.acr.2014.10.007. Epub 2015 Jan 8. [Article]
19. Panczyk M: Pharmacogenetics research on chemotherapy resistance in colorectal cancer over the last 20 years. World J Gastroenterol. 2014 Aug 7;20(29):9775-827. doi: 10.3748/wjg.v20.i29.9775. [Article]
20. Zhang N, Yin Y, Xu SJ, Chen WS: 5-Fluorouracil: mechanisms of resistance and reversal strategies. Molecules. 2008 Aug 5;13(8):1551-69. doi: 10.3390/molecules13081551. [Article]
21. Kholodar SA, Ghosh AK, Swiderek K, Moliner V, Kohen A: Parallel reaction pathways and noncovalent intermediates in thymidylate synthase revealed by experimental and computational tools. Proc Natl Acad Sci U S A. 2018 Oct 9;115(41):10311-10314. doi: 10.1073/pnas.1811059115. Epub 2018 Sep 24. [Article]
22. Bijnsdorp IV, Comijn EM, Padron JM, Gmeiner WH, Peters GJ: Mechanisms of action of FdUMP[10]: metabolite activation and thymidylate synthase inhibition. Oncol Rep. 2007 Jul;18(1):287-91. doi: 10.3892/or.18.1.287. [Article]
23. Matuo R, Sousa FG, Escargueil AE, Grivicich I, Garcia-Santos D, Chies JA, Saffi J, Larsen AK, Henriques JA: 5-Fluorouracil and its active metabolite FdUMP cause DNA damage in human SW620 colon adenocarcinoma cell line. J Appl Toxicol. 2009 May;29(4):308-16. doi: 10.1002/jat.1411. [Article]
24. Lindahl T: An N-glycosidase from Escherichia coli that releases free uracil from DNA containing deaminated cytosine residues. Proc Natl Acad Sci U S A. 1974 Sep;71(9):3649-53. doi: 10.1073/pnas.71.9.3649. [Article]
25. Olinski R, Jurgowiak M, Zaremba T: Uracil in DNA--its biological significance. Mutat Res. 2010 Dec;705(3):239-45. doi: 10.1016/j.mrrev.2010.08.001. Epub 2010 Aug 13. [Article]
26. Longley DB, Harkin DP, Johnston PG: 5-fluorouracil: mechanisms of action and clinical strategies. Nat Rev Cancer. 2003 May;3(5):330-8. [Article]
27. Owiti N, Wei S, Bhagwat AS, Kim N: Unscheduled DNA synthesis leads to elevated uracil residues at highly transcribed genomic loci in Saccharomyces cerevisiae. PLoS Genet. 2018 Jul 17;14(7):e1007516. doi: 10.1371/journal.pgen.1007516. eCollection 2018 Jul. [Article]
28. Ubhi T, Brown GW: Exploiting DNA Replication Stress for Cancer Treatment. Cancer Res. 2019 Apr 15;79(8):1730-1739. doi: 10.1158/0008-5472.CAN-18-3631. Epub 2019 Apr 9. [Article]
29. Tinkelenberg BA, Hansbury MJ, Ladner RD: dUTPase and uracil-DNA glycosylase are central modulators of antifolate toxicity in Saccharomyces cerevisiae. Cancer Res. 2002 Sep 1;62(17):4909-15. [Article]
30. Andersen S, Heine T, Sneve R, Konig I, Krokan HE, Epe B, Nilsen H: Incorporation of dUMP into DNA is a major source of spontaneous DNA damage, while excision of uracil is not required for cytotoxicity of fluoropyrimidines in mouse embryonic fibroblasts. Carcinogenesis. 2005 Mar;26(3):547-55. doi: 10.1093/carcin/bgh347. Epub 2004 Nov 25. [Article]
31. Luo Y, Walla M, Wyatt MD: Uracil incorporation into genomic DNA does not predict toxicity caused by chemotherapeutic inhibition of thymidylate synthase. DNA Repair (Amst). 2008 Feb 1;7(2):162-9. doi: 10.1016/j.dnarep.2007.09.001. Epub 2007 Oct 17. [Article]
32. Armstrong RD, Takimoto CH, Cadman EC: Fluoropyrimidine-mediated changes in small nuclear RNA. J Biol Chem. 1986 Jan 5;261(1):21-4. [Article]
33. Huang L, Pookanjanatavip M, Gu X, Santi DV: A conserved aspartate of tRNA pseudouridine synthase is essential for activity and a probable nucleophilic catalyst. Biochemistry. 1998 Jan 6;37(1):344-51. doi: 10.1021/bi971874+. [Article]
34. Samuelsson T: Interactions of transfer RNA pseudouridine synthases with RNAs substituted with fluorouracil. Nucleic Acids Res. 1991 Nov 25;19(22):6139-44. doi: 10.1093/nar/19.22.6139. [Article]
35. Deng J, Wang Y, Lei J, Lei W, Xiong JP: Insights into the involvement of noncoding RNAs in 5-fluorouracil drug resistance. Tumour Biol. 2017 Apr;39(4):1010428317697553. doi: 10.1177/1010428317697553. [Article]
36. Shah MY, Pan X, Fix LN, Farwell MA, Zhang B: 5-Fluorouracil drug alters the microRNA expression profiles in MCF-7 breast cancer cells. J Cell Physiol. 2011 Jul;226(7):1868-78. doi: 10.1002/jcp.22517. [Article]
37. Blondy S, David V, Verdier M, Mathonnet M, Perraud A, Christou N: 5-Fluorouracil resistance mechanisms in colorectal cancer: From classical pathways to promising processes. Cancer Sci. 2020 Sep;111(9):3142-3154. doi: 10.1111/cas.14532. Epub 2020 Aug 13. [Article]
38. Pettersen HS, Visnes T, Vagbo CB, Svaasand EK, Doseth B, Slupphaug G, Kavli B, Krokan HE: UNG-initiated base excision repair is the major repair route for 5-fluorouracil in DNA, but 5-fluorouracil cytotoxicity depends mainly on RNA incorporation. Nucleic Acids Res. 2011 Oct;39(19):8430-44. doi: 10.1093/nar/gkr563. Epub 2011 Jul 10. [Article]
39. McKendrick J, Coutsouvelis J: Capecitabine: effective oral fluoropyrimidine chemotherapy. Expert Opin Pharmacother. 2005 Jun;6(7):1231-9. doi: 10.1517/14656566.6.7.1231. [Article]
40. Dean L, Kane M: Capecitabine Therapy and DPYD Genotype. . [Article]
41. Shimma N, Umeda I, Arasaki M, Murasaki C, Masubuchi K, Kohchi Y, Miwa M, Ura M, Sawada N, Tahara H, Kuruma I, Horii I, Ishitsuka H: The design and synthesis of a new tumor-selective fluoropyrimidine carbamate, capecitabine. Bioorg Med Chem. 2000 Jul;8(7):1697-706. doi: 10.1016/s0968-0896(00)00087-0. [Article]
42. FDA Approved Drug Products: XELODA® (capecitabine) tablets, for oral use Jan 2023 [Link]
43. Health Canada Approved Drug Proucts: APO-CAPECITABINE, tablets for oral use [Link]

External Links

Human Metabolome Database

HMDB0015233

KEGG Drug

D01223

KEGG Compound

C12650

PubChem Compound

60953

PubChem Substance

46508686

ChemSpider

54916

RxNav

194000

ChEBI

31348

ChEMBL

CHEMBL1773

ZINC

ZINC000003806413

Therapeutic Targets Database

DAP000761

PharmGKB

PA448771

RxList

RxList Drug Page

Drugs.com

Drugs.com Drug Page

Wikipedia

Capecitabine

FDA label

Download (133 KB)

Clinical Trials

Clinical Trials

Phase	Status	Purpose	Conditions	Count
4	Completed	Basic Science	Pancreatic Adenocarcinoma	1
4	Completed	Diagnostic	Breast Cancer / Colorectal Cancer	1
4	Completed	Other	HER2/Neu-negative Carcinoma of Breast / Hormone Receptor Positive Malignant Neoplasm of Breast / Recurrent Breast Cancer	1
4	Completed	Treatment	Breast Cancer	2
4	Completed	Treatment	Colorectal Cancer	5
4	Completed	Treatment	Colorectal Neoplasms	1
4	Completed	Treatment	Upper Gastrointestinal Tumours	1
4	Recruiting	Treatment	Metastatic Breast Cancer	1
4	Recruiting	Treatment	Pancreatic Ductal Adenocarcinoma (PDAC)	1
4	Recruiting	Treatment	Thrombotic Thrombocytopenic Purpura (TTP)	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

• Dept Health Central Pharmacy
• F Hoffmann-La Roche Ltd.
• Physicians Total Care Inc.

Dosage Forms

Form	Route	Strength
Tablet, film coated	Oral
Tablet, delayed release	Oral	500 mg
Tablet, film coated	Oral	150 MG
Tablet, film coated	Oral	300 MG
Tablet	Oral	150 mg/1
Tablet	Oral	500 mg/1
Tablet	Oral	150.00 mg
Tablet	Oral	500.00 mg
Tablet, film coated	Oral	150.000 mg
Tablet, film coated	Oral	500.000 mg
Tablet	Oral	150 mg
Tablet	Oral	500 mg
Tablet, film coated	Oral	150 mg/1
Tablet, film coated	Oral	500 mg/1
Tablet, film coated	Oral	500 mg
Tablet, coated	Oral	150 mg
Tablet, coated	Oral	500 mg

Prices

Unit description	Cost	Unit
Xeloda 500 mg tablet	28.97USD	tablet
Xeloda 150 mg tablet	8.69USD	tablet

DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US5472949	No	1995-12-05	2013-12-14
US4966891	No	1990-10-30	2011-01-13
CA2103324	No	1997-12-23	2013-11-17
CA1327358	No	1994-03-01	2011-03-01

Properties

State

Solid

Experimental Properties

Property	Value	Source
melting point (°C)	110-121 °C	Not Available
water solubility	26 mg/mL	Not Available
logP	0.4	Not Available

Predicted Properties

Property	Value	Source
Water Solubility	0.248 mg/mL	ALOGPS
logP	1.17	ALOGPS
logP	0.77	Chemaxon
logS	-3.2	ALOGPS
pKa (Strongest Acidic)	8.63	Chemaxon
pKa (Strongest Basic)	0.073	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	6	Chemaxon
Hydrogen Donor Count	3	Chemaxon
Polar Surface Area	120.69 Å2	Chemaxon
Rotatable Bond Count	7	Chemaxon
Refractivity	82.75 m3·mol-1	Chemaxon
Polarizability	35.94 Å3	Chemaxon
Number of Rings	2	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	Yes	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	No	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.9513
Blood Brain Barrier	+	0.6064
Caco-2 permeable	-	0.7096
P-glycoprotein substrate	Substrate	0.5106
P-glycoprotein inhibitor I	Non-inhibitor	0.8234
P-glycoprotein inhibitor II	Non-inhibitor	0.7514
Renal organic cation transporter	Non-inhibitor	0.9654
CYP450 2C9 substrate	Non-substrate	0.7999
CYP450 2D6 substrate	Non-substrate	0.864
CYP450 3A4 substrate	Non-substrate	0.5
CYP450 1A2 substrate	Non-inhibitor	0.7523
CYP450 2C9 inhibitor	Non-inhibitor	0.7673
CYP450 2D6 inhibitor	Non-inhibitor	0.8612
CYP450 2C19 inhibitor	Non-inhibitor	0.6569
CYP450 3A4 inhibitor	Non-inhibitor	0.7404
CYP450 inhibitory promiscuity	Low CYP Inhibitory Promiscuity	0.8484
Ames test	Non AMES toxic	0.6521
Carcinogenicity	Non-carcinogens	0.8754
Biodegradation	Not ready biodegradable	0.9964
Rat acute toxicity	2.4690 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.9759
hERG inhibition (predictor II)	Non-inhibitor	0.7124

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted GC-MS Spectrum - GC-MS	Predicted GC-MS	Not Available
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-0a4i-0109000000-c0c4de3c4233af3f34d4
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-0udi-0901000000-676f6925c6c255f4dd24
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-0udi-0900000000-236cb917e50b215b9bd1
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-0udi-1900000000-f06b7309e7a2ebfb3bde
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-0ufr-3900000000-6bb1981f61b4205a9991
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-0kdi-6900000000-ac9a56401938b72ae4f1
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0a4i-0309000000-feac9f5163221adf2a7d
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0udj-0912000000-258b837e7c98d16aafbf
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0udi-0900000000-db3e2d6a5526611d6a6e
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0udi-0900000000-b792e6750d1eaccca7aa
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-0pb9-0609000000-cd05885e7f4f8d1853ec
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0006-0090000000-8029f6bc09ef7062240e
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-006x-0590000000-8cea6a9f156f58ccb593
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-00e9-0920000000-e942daf2b25f1829bec1
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0089-0900000000-2a5dcf8bb6ff7ae6d72f
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-001i-0900000000-460a3e3f1f8b25687c86
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-0006-0090000000-6105bf5c619fbe72100a
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-001i-0900000000-af842efa254483370f53
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-001i-1900000000-61c84595e7254f9493c9
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-001i-0900000000-25912e0277815dec7dfc
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-001i-0900000000-f992985efa9f7da2dbba
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0006-0090000000-6ec0fa0ed4f779ff959a
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0006-0090000000-3be9f054ad6d351dfcda
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-007o-0960000000-eeaa7c678c405b7f7e1f

Targets

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Details1. DNA

Kind

Nucleotide

Organism

Humans

Pharmacological action

Yes

Actions

Incorporation into and destabilization

Inhibition of synthesis

DNA is the molecule of heredity, as it is responsible for the genetic propagation of most inherited traits. It is a polynucleic acid that carries genetic information on cell growth, division, and function. DNA consists of two long strands of nucleotides twisted into a double helix and held together by hydrogen bonds. The sequence of nucleotides determines hereditary characteristics. Each strand serves as the template for subsequent DNA replication and as a template for mRNA production, leading to protein synthesis via ribosomes.

References

1. Walko CM, Lindley C: Capecitabine: a review. Clin Ther. 2005 Jan;27(1):23-44. [Article]
2. Thomas DM, Zalcberg JR: 5-fluorouracil: a pharmacological paradigm in the use of cytotoxics. Clin Exp Pharmacol Physiol. 1998 Nov;25(11):887-95. [Article]
3. Wyatt MD, Wilson DM 3rd: Participation of DNA repair in the response to 5-fluorouracil. Cell Mol Life Sci. 2009 Mar;66(5):788-99. doi: 10.1007/s00018-008-8557-5. [Article]
4. Ghoshal K, Jacob ST: An alternative molecular mechanism of action of 5-fluorouracil, a potent anticancer drug. Biochem Pharmacol. 1997 Jun 1;53(11):1569-75. [Article]
5. Longley DB, Harkin DP, Johnston PG: 5-fluorouracil: mechanisms of action and clinical strategies. Nat Rev Cancer. 2003 May;3(5):330-8. [Article]
6. Petty RD, Cassidy J: Novel fluoropyrimidines: improving the efficacy and tolerability of cytotoxic therapy. Curr Cancer Drug Targets. 2004 Mar;4(2):191-204. [Article]

Details2. RNA

Kind

Nucleotide

Organism

Humans

Pharmacological action

Yes

Actions

Incorporation into and destabilization

References

1. Walko CM, Lindley C: Capecitabine: a review. Clin Ther. 2005 Jan;27(1):23-44. [Article]
2. Thomas DM, Zalcberg JR: 5-fluorouracil: a pharmacological paradigm in the use of cytotoxics. Clin Exp Pharmacol Physiol. 1998 Nov;25(11):887-95. [Article]
3. Wyatt MD, Wilson DM 3rd: Participation of DNA repair in the response to 5-fluorouracil. Cell Mol Life Sci. 2009 Mar;66(5):788-99. doi: 10.1007/s00018-008-8557-5. [Article]
4. Ghoshal K, Jacob ST: An alternative molecular mechanism of action of 5-fluorouracil, a potent anticancer drug. Biochem Pharmacol. 1997 Jun 1;53(11):1569-75. [Article]
5. Longley DB, Harkin DP, Johnston PG: 5-fluorouracil: mechanisms of action and clinical strategies. Nat Rev Cancer. 2003 May;3(5):330-8. [Article]
6. Petty RD, Cassidy J: Novel fluoropyrimidines: improving the efficacy and tolerability of cytotoxic therapy. Curr Cancer Drug Targets. 2004 Mar;4(2):191-204. [Article]

Details3. Thymidylate synthase

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

General Function

Thymidylate synthase activity

Specific Function

Contributes to the de novo mitochondrial thymidylate biosynthesis pathway.

Gene Name

TYMS

Uniprot ID

P04818

Uniprot Name

Thymidylate synthase

Molecular Weight

35715.65 Da

References

1. Patel A, Pluim T, Helms A, Bauer A, Tuttle RM, Francis GL: Enzyme expression profiles suggest the novel tumor-activated fluoropyrimidine carbamate capecitabine (Xeloda) might be effective against papillary thyroid cancers of children and young adults. Cancer Chemother Pharmacol. 2004 May;53(5):409-14. [Article]
2. Eliason JF, Megyeri A: Potential for predicting toxicity and response of fluoropyrimidines in patients. Curr Drug Targets. 2004 May;5(4):383-8. [Article]
3. Carlini LE, Meropol NJ, Bever J, Andria ML, Hill T, Gold P, Rogatko A, Wang H, Blanchard RL: UGT1A7 and UGT1A9 polymorphisms predict response and toxicity in colorectal cancer patients treated with capecitabine/irinotecan. Clin Cancer Res. 2005 Feb 1;11(3):1226-36. [Article]
4. Li KM, Rivory LP, Clarke SJ: Rapid quantitation of plasma 2'-deoxyuridine by high-performance liquid chromatography/atmospheric pressure chemical ionization mass spectrometry and its application to pharmacodynamic studies in cancer patients. J Chromatogr B Analyt Technol Biomed Life Sci. 2005 Jun 5;820(1):121-30. Epub 2005 Apr 19. [Article]
5. Fischel JL, Ciccolini J, Formento P, Ferrero JM, Milano G: Synergistic cytotoxic interaction in hormone-refractory prostate cancer with the triple combination docetaxel-erlotinib and 5-fluoro-5'-deoxyuridine. Anticancer Drugs. 2006 Aug;17(7):807-13. [Article]
6. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]

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Drug created at June 13, 2005 13:24 / Updated at February 08, 2023 20:46