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
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
Indication TypeIndicationCombined Product DetailsApproval LevelAge GroupPatient CharacteristicsDose Form
Adjunct therapy in treatment ofAdenocarcinomas of the pancreas•••••••••••••••••••••••
Used in combination to treatAdvanced or metastatic breast cancerRegimen in combination with: Docetaxel (DB01248)••••••••••••••••••• ••••••••••• ••••• ••••••••••••• •••••••• ••••••••••••• •••••••••••••••
Treatment ofAdvanced or metastatic breast cancer•••••••••••••••••••••••••• ••••••• •••••••••••••••
Treatment ofCarcinoma of gallbladder••• •••••••••••
Treatment ofCholangiocarcinoma••• •••••••••••
Associated Therapies
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

TargetActionsOrganism
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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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
PathwayCategory
Capecitabine Action PathwayDrug action
Capecitabine Metabolism PathwayDrug metabolism
Pharmacogenomic Effects/ADRs
Interacting Gene/EnzymeAllele nameGenotype(s)Defining Change(s)Type(s)DescriptionDetails
Dihydropyrimidine dehydrogenase [NADP(+)]DPYD*2A(A;A) / (A;G)G > AADR Directly StudiedThe 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 > CADR Directly StudiedThe 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 > AADR Directly StudiedThe 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 > AADR Directly StudiedThe 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 > GADR Directly StudiedThe 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 > AADR Directly StudiedThe 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 > CADR Directly StudiedThe 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.
DrugInteraction
AbacavirAbacavir may decrease the excretion rate of Capecitabine which could result in a higher serum level.
AbataceptThe metabolism of Capecitabine can be increased when combined with Abatacept.
AbciximabThe risk or severity of bleeding can be increased when Abciximab is combined with Capecitabine.
AbrocitinibThe serum concentration of Abrocitinib can be increased when it is combined with Capecitabine.
AceclofenacCapecitabine may increase the nephrotoxic activities of Aceclofenac.
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.

Products

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Active Moieties
NameKindUNIICASInChI Key
FluorouracilprodrugU3P01618RT51-21-8GHASVSINZRGABV-UHFFFAOYSA-N
Product Images
Brand Name Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImage
CapecitabineTablet150 mgOralSivem Pharmaceuticals UlcNot applicableNot applicableCanada flag
CapecitabineTablet500 mgOralSanis Health Inc2021-10-22Not applicableCanada flag
CapecitabineTablet500 mgOralJamp Pharma Corporation2022-06-16Not applicableCanada flag
CapecitabineTablet150 mgOralSanis Health Inc2021-10-22Not applicableCanada flag
CapecitabineTablet500 mgOralSivem Pharmaceuticals UlcNot applicableNot applicableCanada flag
Generic Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImage
Ach-capecitabineTablet500 mgOralAccord Healthcare Inc2014-09-19Not applicableCanada flag
Ach-capecitabineTablet150 mgOralAccord Healthcare Inc2014-09-19Not applicableCanada flag
Apo-capecitabineTablet150 mgOralApotex CorporationNot applicableNot applicableCanada flag
Apo-capecitabineTablet500 mgOralApotex CorporationNot applicableNot applicableCanada flag
CapecitabineTablet150 mg/1OralChartwell Rx, Llc2020-04-27Not applicableUS flag

Categories

ATC Codes
L01BC06 — Capecitabine
Drug Categories
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
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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
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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
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  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]
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
PhaseStatusPurposeConditionsCount
4CompletedBasic SciencePancreatic Adenocarcinoma1
4CompletedDiagnosticBreast Cancer / Colorectal Cancer1
4CompletedOtherHER2/Neu-negative Carcinoma of Breast / Hormone Receptor Positive Malignant Neoplasm of Breast / Recurrent Breast Cancer1
4CompletedTreatmentBreast Cancer2
4CompletedTreatmentColorectal Cancer5

Pharmacoeconomics

Manufacturers
Not Available
Packagers
  • Dept Health Central Pharmacy
  • F Hoffmann-La Roche Ltd.
  • Physicians Total Care Inc.
Dosage Forms
FormRouteStrength
Tablet, film coatedOral300 MG
Tablet, film coatedOral
Tablet, film coatedOral150 MG
TabletOral150 mg/1
TabletOral500 mg/1
Tablet, coatedOral50000000 mg
TabletOral150.00 mg
TabletOral500.00 mg
Tablet, coatedOral15000000 mg
Tablet, film coatedOral150.000 mg
Tablet, film coatedOral500.000 mg
Tablet, delayed releaseOral500 mg
TabletOral500.000 mg
TabletOral150 mg
TabletOral500 mg
Tablet, film coatedOral150 mg/1
Tablet, film coatedOral500 mg/1
Tablet, film coatedOral500 mg
Tablet, coatedOral150 mg
Tablet, coatedOral500 mg
Prices
Unit descriptionCostUnit
Xeloda 500 mg tablet28.97USD tablet
Xeloda 150 mg tablet8.69USD tablet
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)Region
US5472949No1995-12-052013-12-14US flag
US4966891No1990-10-302011-01-13US flag
CA2103324No1997-12-232013-11-17Canada flag
CA1327358No1994-03-012011-03-01Canada flag

Properties

State
Solid
Experimental Properties
PropertyValueSource
melting point (°C)110-121 °CNot Available
water solubility26 mg/mLNot Available
logP0.4Not Available
Predicted Properties
PropertyValueSource
Water Solubility0.248 mg/mLALOGPS
logP1.17ALOGPS
logP0.77Chemaxon
logS-3.2ALOGPS
pKa (Strongest Acidic)8.63Chemaxon
pKa (Strongest Basic)0.073Chemaxon
Physiological Charge0Chemaxon
Hydrogen Acceptor Count6Chemaxon
Hydrogen Donor Count3Chemaxon
Polar Surface Area120.69 Å2Chemaxon
Rotatable Bond Count7Chemaxon
Refractivity82.75 m3·mol-1Chemaxon
Polarizability35.94 Å3Chemaxon
Number of Rings2Chemaxon
Bioavailability1Chemaxon
Rule of FiveYesChemaxon
Ghose FilterYesChemaxon
Veber's RuleNoChemaxon
MDDR-like RuleNoChemaxon
Predicted ADMET Features
PropertyValueProbability
Human Intestinal Absorption+0.9513
Blood Brain Barrier+0.6064
Caco-2 permeable-0.7096
P-glycoprotein substrateSubstrate0.5106
P-glycoprotein inhibitor INon-inhibitor0.8234
P-glycoprotein inhibitor IINon-inhibitor0.7514
Renal organic cation transporterNon-inhibitor0.9654
CYP450 2C9 substrateNon-substrate0.7999
CYP450 2D6 substrateNon-substrate0.864
CYP450 3A4 substrateNon-substrate0.5
CYP450 1A2 substrateNon-inhibitor0.7523
CYP450 2C9 inhibitorNon-inhibitor0.7673
CYP450 2D6 inhibitorNon-inhibitor0.8612
CYP450 2C19 inhibitorNon-inhibitor0.6569
CYP450 3A4 inhibitorNon-inhibitor0.7404
CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.8484
Ames testNon AMES toxic0.6521
CarcinogenicityNon-carcinogens0.8754
BiodegradationNot ready biodegradable0.9964
Rat acute toxicity2.4690 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.9759
hERG inhibition (predictor II)Non-inhibitor0.7124
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)
Not Available
Spectra
SpectrumSpectrum TypeSplash Key
Predicted GC-MS Spectrum - GC-MSPredicted GC-MSsplash10-0ab9-9112000000-35a3e944454fc6eca103
LC-MS/MS Spectrum - LC-ESI-QFT , negativeLC-MS/MSsplash10-0a4i-0109000000-c0c4de3c4233af3f34d4
LC-MS/MS Spectrum - LC-ESI-QFT , negativeLC-MS/MSsplash10-0udi-0901000000-676f6925c6c255f4dd24
LC-MS/MS Spectrum - LC-ESI-QFT , negativeLC-MS/MSsplash10-0udi-0900000000-236cb917e50b215b9bd1
LC-MS/MS Spectrum - LC-ESI-QFT , negativeLC-MS/MSsplash10-0udi-1900000000-f06b7309e7a2ebfb3bde
LC-MS/MS Spectrum - LC-ESI-QFT , negativeLC-MS/MSsplash10-0ufr-3900000000-6bb1981f61b4205a9991
LC-MS/MS Spectrum - LC-ESI-QFT , negativeLC-MS/MSsplash10-0kdi-6900000000-ac9a56401938b72ae4f1
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-0a4i-0309000000-feac9f5163221adf2a7d
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-0udj-0912000000-258b837e7c98d16aafbf
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-0udi-0900000000-db3e2d6a5526611d6a6e
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-0udi-0900000000-b792e6750d1eaccca7aa
LC-MS/MS Spectrum - LC-ESI-QFT , negativeLC-MS/MSsplash10-0pb9-0609000000-cd05885e7f4f8d1853ec
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-0006-0090000000-8029f6bc09ef7062240e
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-006x-0590000000-8cea6a9f156f58ccb593
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-00e9-0920000000-e942daf2b25f1829bec1
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-0089-0900000000-2a5dcf8bb6ff7ae6d72f
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-001i-0900000000-460a3e3f1f8b25687c86
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-0006-0090000000-6105bf5c619fbe72100a
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-001i-0900000000-af842efa254483370f53
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-001i-1900000000-61c84595e7254f9493c9
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-001i-0900000000-25912e0277815dec7dfc
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-001i-0900000000-f992985efa9f7da2dbba
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-0006-0090000000-6ec0fa0ed4f779ff959a
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-0006-0090000000-3be9f054ad6d351dfcda
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-007o-0960000000-eeaa7c678c405b7f7e1f
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSsplash10-0006-0091000000-d66db3143fe8919802fa
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSsplash10-0kml-0396000000-1faaa2c7f8457fba3067
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSsplash10-0ab9-0960000000-b4f5bb5cc4385c1862ca
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSsplash10-0zfu-5981000000-b2c7c436223825e1a26f
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSsplash10-0c29-1941000000-76a7307ca821af1b9a1b
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSsplash10-0006-5790000000-92e0dcd90c8cb5d06a8b
Predicted 1H NMR Spectrum1D NMRNot Applicable
Predicted 13C NMR Spectrum1D NMRNot Applicable
Chromatographic Properties
Collision Cross Sections (CCS)
AdductCCS Value (Å2)Source typeSource
[M-H]-187.1072468
predicted
DarkChem Lite v0.1.0
[M-H]-197.0932468
predicted
DarkChem Lite v0.1.0
[M-H]-185.2666
predicted
DeepCCS 1.0 (2019)
[M+H]+187.0995468
predicted
DarkChem Lite v0.1.0
[M+H]+197.6482468
predicted
DarkChem Lite v0.1.0
[M+H]+187.66216
predicted
DeepCCS 1.0 (2019)
[M+Na]+186.5208468
predicted
DarkChem Lite v0.1.0
[M+Na]+197.5562468
predicted
DarkChem Lite v0.1.0
[M+Na]+194.50374
predicted
DeepCCS 1.0 (2019)

Targets

Build, predict & validate machine-learning models
Use our structured and evidence-based datasets to unlock new
insights and accelerate drug research.
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Use our structured and evidence-based datasets to unlock new insights and accelerate drug research.
Learn more
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]
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]
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]

Enzymes

Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Substrate
General Function
Transferase activity, transferring pentosyl groups
Specific Function
May have a role in maintaining the integrity of the blood vessels. Has growth promoting activity on endothelial cells, angiogenic activity in vivo and chemotactic activity on endothelial cells in v...
Gene Name
TYMP
Uniprot ID
P19971
Uniprot Name
Thymidine phosphorylase
Molecular Weight
49954.965 Da
References
  1. de Bono JS, Twelves CJ: The oral fluorinated pyrimidines. Invest New Drugs. 2001;19(1):41-59. [Article]
  2. Tsukamoto Y, Kato Y, Ura M, Horii I, Ishitsuka H, Kusuhara H, Sugiyama Y: A physiologically based pharmacokinetic analysis of capecitabine, a triple prodrug of 5-FU, in humans: the mechanism for tumor-selective accumulation of 5-FU. Pharm Res. 2001 Aug;18(8):1190-202. [Article]
  3. Blanquicett C, Gillespie GY, Nabors LB, Miller CR, Bharara S, Buchsbaum DJ, Diasio RB, Johnson MR: Induction of thymidine phosphorylase in both irradiated and shielded, contralateral human U87MG glioma xenografts: implications for a dual modality treatment using capecitabine and irradiation. Mol Cancer Ther. 2002 Oct;1(12):1139-45. [Article]
  4. Ishitsuka H, Shimma N, Horii I: [Discovery and development of novel anticancer drug capecitabine]. Yakugaku Zasshi. 1999 Dec;119(12):881-97. [Article]
  5. Ishitsuka H: Capecitabine: preclinical pharmacology studies. Invest New Drugs. 2000 Nov;18(4):343-54. [Article]
  6. Endo M, Miwa M, Eda H, Ura M, Tanimura H, Ishikawa T, Miyazaki-Nose T, Hattori K, Shimma N, Yamada-Okabe H, Ishitsuka H: Augmentation of the antitumor activity of capecitabine by a tumor selective dihydropyrimidine dehydrogenase inhibitor, RO0094889. Int J Cancer. 2003 Sep 20;106(5):799-805. [Article]
  7. Schuller J, Cassidy J, Dumont E, Roos B, Durston S, Banken L, Utoh M, Mori K, Weidekamm E, Reigner B: Preferential activation of capecitabine in tumor following oral administration to colorectal cancer patients. Cancer Chemother Pharmacol. 2000;45(4):291-7. [Article]
  8. 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]
  9. Eliason JF, Megyeri A: Potential for predicting toxicity and response of fluoropyrimidines in patients. Curr Drug Targets. 2004 May;5(4):383-8. [Article]
  10. 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]
  11. Walko CM, Lindley C: Capecitabine: a review. Clin Ther. 2005 Jan;27(1):23-44. [Article]
  12. Ranieri G, Roccaro AM, Vacca A, Ribatti D: Thymidine phosphorylase (platelet-derived endothelial cell growth factor) as a target for capecitabine: from biology to the bedside. Recent Pat Anticancer Drug Discov. 2006 Jun;1(2):171-83. [Article]
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Substrate
General Function
Triglyceride lipase activity
Specific Function
Involved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs. Hydrolyzes aromatic and aliphatic esters, but has no catalytic activity toward amides or a fatty acy...
Gene Name
CES1
Uniprot ID
P23141
Uniprot Name
Liver carboxylesterase 1
Molecular Weight
62520.62 Da
References
  1. de Bono JS, Twelves CJ: The oral fluorinated pyrimidines. Invest New Drugs. 2001;19(1):41-59. [Article]
  2. Tsukamoto Y, Kato Y, Ura M, Horii I, Ishitsuka H, Kusuhara H, Sugiyama Y: A physiologically based pharmacokinetic analysis of capecitabine, a triple prodrug of 5-FU, in humans: the mechanism for tumor-selective accumulation of 5-FU. Pharm Res. 2001 Aug;18(8):1190-202. [Article]
  3. Ishitsuka H, Shimma N, Horii I: [Discovery and development of novel anticancer drug capecitabine]. Yakugaku Zasshi. 1999 Dec;119(12):881-97. [Article]
  4. Ishitsuka H: Capecitabine: preclinical pharmacology studies. Invest New Drugs. 2000 Nov;18(4):343-54. [Article]
  5. Endo M, Miwa M, Eda H, Ura M, Tanimura H, Ishikawa T, Miyazaki-Nose T, Hattori K, Shimma N, Yamada-Okabe H, Ishitsuka H: Augmentation of the antitumor activity of capecitabine by a tumor selective dihydropyrimidine dehydrogenase inhibitor, RO0094889. Int J Cancer. 2003 Sep 20;106(5):799-805. [Article]
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Substrate
General Function
Zinc ion binding
Specific Function
This enzyme scavenges exogenous and endogenous cytidine and 2'-deoxycytidine for UMP synthesis.
Gene Name
CDA
Uniprot ID
P32320
Uniprot Name
Cytidine deaminase
Molecular Weight
16184.545 Da
References
  1. de Bono JS, Twelves CJ: The oral fluorinated pyrimidines. Invest New Drugs. 2001;19(1):41-59. [Article]
  2. Tsukamoto Y, Kato Y, Ura M, Horii I, Ishitsuka H, Kusuhara H, Sugiyama Y: A physiologically based pharmacokinetic analysis of capecitabine, a triple prodrug of 5-FU, in humans: the mechanism for tumor-selective accumulation of 5-FU. Pharm Res. 2001 Aug;18(8):1190-202. [Article]
  3. Ishitsuka H, Shimma N, Horii I: [Discovery and development of novel anticancer drug capecitabine]. Yakugaku Zasshi. 1999 Dec;119(12):881-97. [Article]
  4. Ishitsuka H: Capecitabine: preclinical pharmacology studies. Invest New Drugs. 2000 Nov;18(4):343-54. [Article]
  5. Endo M, Miwa M, Eda H, Ura M, Tanimura H, Ishikawa T, Miyazaki-Nose T, Hattori K, Shimma N, Yamada-Okabe H, Ishitsuka H: Augmentation of the antitumor activity of capecitabine by a tumor selective dihydropyrimidine dehydrogenase inhibitor, RO0094889. Int J Cancer. 2003 Sep 20;106(5):799-805. [Article]
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Downregulator
General Function
Steroid hydroxylase activity
Specific Function
Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...
Gene Name
CYP2C9
Uniprot ID
P11712
Uniprot Name
Cytochrome P450 2C9
Molecular Weight
55627.365 Da
References
  1. Janney LM, Waterbury NV: Capecitabine-warfarin interaction. Ann Pharmacother. 2005 Sep;39(9):1546-51. doi: 10.1345/aph.1G153. Epub 2005 Jul 12. [Article]
  2. Seredina TA, Goreva OB, Talaban VO, Grishanova AY, Lyakhovich VV: Association of cytochrome P450 genetic polymorphisms with neoadjuvant chemotherapy efficacy in breast cancer patients. BMC Med Genet. 2012 Jun 15;13:45. doi: 10.1186/1471-2350-13-45. [Article]
  3. Ramirez J, House LK, Karrison TG, Janisch LA, Turcich M, Salgia R, Ratain MJ, Sharma MR: Prolonged Pharmacokinetic Interaction Between Capecitabine and a CYP2C9 Substrate, Celecoxib. J Clin Pharmacol. 2019 Dec;59(12):1632-1640. doi: 10.1002/jcph.1476. Epub 2019 Jul 5. [Article]
  4. Capecitabine FDA label [File]
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Substrate
General Function
Uridine phosphorylase activity
Specific Function
Catalyzes the reversible phosphorylytic cleavage of uridine and deoxyuridine to uracil and ribose- or deoxyribose-1-phosphate (PubMed:7488099). The produced molecules are then utilized as carbon an...
Gene Name
UPP1
Uniprot ID
Q16831
Uniprot Name
Uridine phosphorylase 1
Molecular Weight
33934.005 Da
References
  1. Roosild TP, Castronovo S, Villoso A, Ziemba A, Pizzorno G: A novel structural mechanism for redox regulation of uridine phosphorylase 2 activity. J Struct Biol. 2011 Nov;176(2):229-37. doi: 10.1016/j.jsb.2011.08.002. Epub 2011 Aug 10. [Article]
  2. Roosild TP, Castronovo S: Active site conformational dynamics in human uridine phosphorylase 1. PLoS One. 2010 Sep 14;5(9):e12741. doi: 10.1371/journal.pone.0012741. [Article]
  3. Hamzic S, Kummer D, Milesi S, Mueller D, Joerger M, Aebi S, Amstutz U, Largiader CR: Novel Genetic Variants in Carboxylesterase 1 Predict Severe Early-Onset Capecitabine-Related Toxicity. Clin Pharmacol Ther. 2017 Nov;102(5):796-804. doi: 10.1002/cpt.641. Epub 2017 May 30. [Article]
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Substrate
General Function
Uridine phosphorylase activity
Specific Function
Catalyzes the reversible phosphorylytic cleavage of uridine and deoxyuridine to uracil and ribose- or deoxyribose-1-phosphate. The produced molecules are then utilized as carbon and energy sources ...
Gene Name
UPP2
Uniprot ID
O95045
Uniprot Name
Uridine phosphorylase 2
Molecular Weight
35526.93 Da
References
  1. Hamzic S, Kummer D, Milesi S, Mueller D, Joerger M, Aebi S, Amstutz U, Largiader CR: Novel Genetic Variants in Carboxylesterase 1 Predict Severe Early-Onset Capecitabine-Related Toxicity. Clin Pharmacol Ther. 2017 Nov;102(5):796-804. doi: 10.1002/cpt.641. Epub 2017 May 30. [Article]
  2. Roosild TP, Castronovo S: Active site conformational dynamics in human uridine phosphorylase 1. PLoS One. 2010 Sep 14;5(9):e12741. doi: 10.1371/journal.pone.0012741. [Article]
  3. Roosild TP, Castronovo S, Villoso A, Ziemba A, Pizzorno G: A novel structural mechanism for redox regulation of uridine phosphorylase 2 activity. J Struct Biol. 2011 Nov;176(2):229-37. doi: 10.1016/j.jsb.2011.08.002. Epub 2011 Aug 10. [Article]

Carriers

Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Binder
General Function
Toxic substance binding
Specific Function
Serum albumin, the main protein of plasma, has a good binding capacity for water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs. Its main function is the regulation of the colloid...
Gene Name
ALB
Uniprot ID
P02768
Uniprot Name
Serum albumin
Molecular Weight
69365.94 Da
References
  1. FDA Approved Drug Products: XELODA® (capecitabine) tablets, for oral use Jan 2023 [Link]

Drug created at June 13, 2005 13:24 / Updated at March 18, 2024 16:48