Capecitabine
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MedKoo CAT#: 100120

CAS#: 154361-50-9

Description: Capecitabine is a fluoropyrimidine carbamate belonging to the class of antineoplastic agents called antimetabolites. As a prodrug, capecitabine is selectively activated by tumor cells to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells. FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand.


Chemical Structure

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Capecitabine
CAS# 154361-50-9

Theoretical Analysis

MedKoo Cat#: 100120
Name: Capecitabine
CAS#: 154361-50-9
Chemical Formula: C15H22FN3O6
Exact Mass: 359.14926
Molecular Weight: 359.35
Elemental Analysis: C, 50.14; H, 6.17; F, 5.29; N, 11.69; O, 26.71

Price and Availability

Size Price Availability Quantity
5.0g USD 150.0 Same day
20.0g USD 450.0 Same day
50.0g USD 950.0 Same day
100.0g USD 1650.0 Same day
200.0g USD 2650.0 2 Weeks
500.0g USD 3650.0 2 Weeks
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Synonym: Ro 091978000; Ro-091978000; Ro091978000; Capecitabine; Abbreviation: CAPE. US brand name: Xeloda.

IUPAC/Chemical Name: pentyl (1-((2R,3R,4S,5R)-3,4-dihydroxy-5-methyltetrahydrofuran-2-yl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl)carbamate

InChi Key: GAGWJHPBXLXJQN-UORFTKCHSA-N

InChi Code: 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

SMILES Code: O=C(OCCCCC)NC(C(F)=CN1[C@@H]2O[C@H](C)[C@@H](O)[C@H]2O)=NC1=O

Appearance: Solid powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility: Soluble in DMSO, not in water

Shelf Life: >2 years if stored properly

Drug Formulation: This drug may be formulated in DMSO

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001

Preparing Stock Solutions

The following data is based on the product molecular weight 359.35 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL

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1: Stanciu M, Aubut N, Gagné E, Thibeault MM. Capecitabine-induced inflammation of actinic keratosis: case report and literature review. J Cutan Med Surg. 2012 Sep-Oct;16(5):298-9. Review. PubMed PMID: 22971302.

2: Fernández-Martos C, Nogué M, Cejas P, Moreno-García V, Machancoses AH, Feliu J. The role of capecitabine in locally advanced rectal cancer treatment: an update. Drugs. 2012 May 28;72(8):1057-73. doi: 10.2165/11633870-000000000-00000. Review. PubMed PMID: 22621694.

3: O'Shaughnessy JA, Kaufmann M, Siedentopf F, Dalivoust P, Debled M, Robert NJ, Harbeck N. Capecitabine monotherapy: review of studies in first-line HER-2-negative metastatic breast cancer. Oncologist. 2012;17(4):476-84. doi: 10.1634/theoncologist.2011-0281. Epub 2012 Mar 14. Review. PubMed PMID: 22418569; PubMed Central PMCID: PMC3336834.

4: Miles D, Zielinski C, Martin M, Vrdoljak E, Robert N. Combining capecitabine and bevacizumab in metastatic breast cancer: a comprehensive review. Eur J Cancer. 2012 Mar;48(4):482-91. doi: 10.1016/j.ejca.2011.12.007. Epub 2012 Jan 16. Review. PubMed PMID: 22257791.

5: Lau PC, Zheng SF, Ng WT, Yu SC. Inoperable pancreatic adenocarcinoma rendered complete remission by high-intensity focused ultrasound concurrent with gemcitabine-capecitabine chemotherapy: case report and topic review. J Dig Dis. 2012 Jan;13(1):60-4. doi: 10.1111/j.1751-2980.2011.00546.x. Review. PubMed PMID: 22188918.

6: Tunio MA, Hashmi A, Shoaib M. Capecitabine induced cardiotoxicity: a case report and review of literature. Pak J Pharm Sci. 2012 Jan;25(1):277-81. Review. PubMed PMID: 22186341.

7: Hoesly FJ, Baker SG, Gunawardane ND, Cotliar JA. Capecitabine-induced hand-foot syndrome complicated by pseudomonal superinfection resulting in bacterial sepsis and death: case report and review of the literature. Arch Dermatol. 2011 Dec;147(12):1418-23. doi: 10.1001/archdermatol.2011.320. Review. PubMed PMID: 22184763.

8: Bang YJ. Capecitabine in gastric cancer. Expert Rev Anticancer Ther. 2011 Dec;11(12):1791-806. doi: 10.1586/era.11.172. Review. PubMed PMID: 22117147.

9: Croom KF, Dhillon S. Bevacizumab: a review of its use in combination with paclitaxel or capecitabine as first-line therapy for HER2-negative metastatic breast cancer. Drugs. 2011 Nov 12;71(16):2213-29. doi: 10.2165/11207720-000000000-00000. Review. PubMed PMID: 22035518.

10: Kounis NG, Tsigkas GG, Almpanis G, Mazarakis A. Kounis syndrome is likely culprit of coronary vasospasm induced by capecitabine. J Oncol Pharm Pract. 2012 Jun;18(2):316-8. doi: 10.1177/1078155211423118. Epub 2011 Oct 21. Review. PubMed PMID: 22020660.

11: Ma Y, Tang L, Wang HX, Xu YC, Ma Y, Zhang FC. Capecitabine for the treatment for advanced gastric cancer: efficacy, safety and ethnicity. J Clin Pharm Ther. 2012 Jun;37(3):266-75. doi: 10.1111/j.1365-2710.2011.01289.x. Epub 2011 Sep 26. Review. PubMed PMID: 21950464.

12: Chan AK, Choo BA, Glaholm J. Pulmonary toxicity with oxaliplatin and capecitabine/5-Fluorouracil chemotherapy: a case report and review of the literature. Onkologie. 2011;34(8-9):443-6. doi: 10.1159/000331133. Epub 2011 Aug 19. Review. PubMed PMID: 21934344.

13: Leonard R, Hennessy BT, Blum JL, O'Shaughnessy J. Dose-adjusting capecitabine minimizes adverse effects while maintaining efficacy: a retrospective review of capecitabine for metastatic breast cancer. Clin Breast Cancer. 2011 Dec;11(6):349-56. doi: 10.1016/j.clbc.2011.06.005. Review. PubMed PMID: 21856245.

14: Yoh T, Yamamichi K, Oishi M, Iwaki R, Motohiro T. [A case of effective neoadjuvant chemoradiotherapy with capecitabine for locally advanced sigmoid colon cancer]. Gan To Kagaku Ryoho. 2011 Jun;38(6):1021-4. Review. Japanese. PubMed PMID: 21677500.

15: Petrelli F, Cabiddu M, Barni S. 5-Fluorouracil or capecitabine in the treatment of advanced colorectal cancer: a pooled-analysis of randomized trials. Med Oncol. 2012 Jun;29(2):1020-9. doi: 10.1007/s12032-011-9958-0. Epub 2011 Apr 24. Review. PubMed PMID: 21516482.

16: Cosar-Alas R, Alas A, Ozen A, Denizli B, Saynak M, Uzunoglu S, Aydogdu N, Karagol H, Uzal C, Kocak Z. Capecitabine-related intracranial hypotension syndrome mimicking dural metastasis in a breast cancer patient: case report and review of the literature. J Cancer Res Ther. 2010 Oct-Dec;6(4):557-9. doi: 10.4103/0973-1482.77070. Review. PubMed PMID: 21358101.

17: Li M, Jiang M, Yan X, Wang F, Luo F. Metastatic pancreatic cancer response to treatment with cetuximab and gemcitabine plus capecitabine: a case report and review of the literature. Tumori. 2010 Sep-Oct;96(5):764-7. Review. PubMed PMID: 21302625.

18: Zhang SZ. [Advances in research on capecitabine as adjuvant treatment for colon cancer after radical resection]. Zhonghua Zhong Liu Za Zhi. 2010 Nov;32(11):801-3. Review. Chinese. PubMed PMID: 21223682.

19: Saif MW. Capecitabine and hand-foot syndrome. Expert Opin Drug Saf. 2011 Mar;10(2):159-69. doi: 10.1517/14740338.2011.546342. Epub 2010 Dec 22. Review. PubMed PMID: 21174613.

20: Silvestris N, Maiello E, De Vita F, Cinieri S, Santini D, Russo A, Tommasi S, Azzariti A, Numico G, Pisconti S, Petriella D, Lorusso V, Millaku A, Colucci G. Update on capecitabine alone and in combination regimens in colorectal cancer patients. Cancer Treat Rev. 2010 Nov;36 Suppl 3:S46-55. doi: 10.1016/S0305-7372(10)70020-7. Review. PubMed PMID: 21129610.
   



Additional Information

XELODA (capecitabine) is a fluoropyrimidine carbamate with antineoplastic activity. It is an orally administered systemic prodrug of 5'-deoxy-5-fluorouridine (5'-DFUR) which is converted to 5-fluorouracil. The chemical name for capecitabine is 5'-deoxy-5-fluoro-N-[(pentyloxy) carbonyl]-cytidine and has a molecular weight of 359.35.
 
Capecitabine is a white to off-white crystalline powder with an aqueous solubility of 26 mg/mL at 20°C. XELODA is supplied as biconvex, oblong film-coated tablets for oral administration. Each light peach-colored tablet contains 150 mg capecitabine and each peach-colored tablet contains 500 mg capecitabine. The inactive ingredients in XELODA include: anhydrous lactose, croscarmellose sodium, hydroxypropyl methylcellulose, microcrystalline cellulose, magnesium stearate and purified water. The peach or light peach film coating contains hydroxypropyl methylcellulose, talc, titanium dioxide, and synthetic yellow and red iron oxides.
 
Capecitabine is FDA-approved for: * Adjuvant in colorectal cancer Stage III Dukes' C - used as first-line monotherapy. * Metastatic colorectal cancer - used as first-line monotherapy, if appropriate. * Metastatic breast cancer - used in combination with docetaxel, after failure of anthracycline-based treatment. Also as monotherapy, if the patient has failed paclitaxel-based treatment, and if anthracycline-based treatment has either failed or cannot be continued for other reasons (i.e., the patient has already received the maximum lifetime dose of an anthracycline). In the UK, capecitabine is approved by the National Institute for Health and Clinical Excellence (NICE) for colon and colorectal cancer, and locally advanced or metastatic breast cancer.[1] On March 29,2007, the European Commission approved Capecitabine, in combination with platinum-based therapy (with or without epirubicin), for the first-line treatment of advanced stomach cancer.
 
CLINICAL PHARMACOLOGY
XELODA is relatively non-cytotoxic in vitro. This drug is enzymatically converted to 5-fluorouracil (5-FU) in vivo. Capecitabine is readily absorbed from the gastrointestinal tract. In the liver, a 60 kDa carboxylesterase hydrolyzes much of the compound to 5'-deoxy-5-fluorocytidine (5'-DFCR). Cytidine deaminase, an enzyme found in most tissues, including tumors, subsequently converts 5'-DFCR to 5'-deoxy-5-fluorouridine (5'-DFUR). The enzyme, thymidine phosphorylase (dThdPase), then hydrolyzes 5'-DFUR to the active drug 5-FU. Many tissues throughout the body express thymidine phosphorylase. Some human carcinomas express this enzyme in higher concentrations than surrounding normal tissues.
XELODA is relatively non-cytotoxic in vitro. This drug is enzymatically converted to 5-fluorouracil (5-FU) in vivo. Capecitabine is readily absorbed from the gastrointestinal tract. In the liver, a 60 kDa carboxylesterase hydrolyzes much of the compound to 5'-deoxy-5-fluorocytidine (5'-DFCR). Cytidine deaminase, an enzyme found in most tissues, including tumors, subsequently converts 5'-DFCR to 5'-deoxy-5-fluorouridine (5'-DFUR). The enzyme, thymidine phosphorylase (dThdPase), then hydrolyzes 5'-DFUR to the active drug 5-FU. Many tissues throughout the body express thymidine phosphorylase. Some human carcinomas express this enzyme in higher concentrations than surrounding normal tissues.
Mechanism of Action
Mechanism of Action
Both normal and tumor cells metabolize 5-FU to 5-fluoro-2'-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). These metabolites cause cell injury by two different mechanisms. First, FdUMP and the folate cofactor, N5-10-methylenetetrahydrofolate, bind to thymidylate synthase (TS) to form a covalently bound ternary complex. This binding inhibits the formation of thymidylate from 2'-deoxyuridylate. Thymidylate is the necessary precursor of thymidine triphosphate, which is essential for the synthesis of DNA, so that a deficiency of this compound can inhibit cell division. Second, nuclear transcriptional enzymes can mistakenly incorporate FUTP in place of uridine triphosphate (UTP) during the synthesis of RNA. This metabolic error can interfere with RNA processing and protein synthesis.
Both normal and tumor cells metabolize 5-FU to 5-fluoro-2'-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). These metabolites cause cell injury by two different mechanisms. First, FdUMP and the folate cofactor, N5-10-methylenetetrahydrofolate, bind to thymidylate synthase (TS) to form a covalently bound ternary complex. This binding inhibits the formation of thymidylate from 2'-deoxyuridylate. Thymidylate is the necessary precursor of thymidine triphosphate, which is essential for the synthesis of DNA, so that a deficiency of this compound can inhibit cell division. Second, nuclear transcriptional enzymes can mistakenly incorporate FUTP in place of uridine triphosphate (UTP) during the synthesis of RNA. This metabolic error can interfere with RNA processing and protein synthesis.