Capecitabine - CAS 154361-50-9

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Category
APIs
Product Name
Capecitabine
Catalog Number
154361-50-9
CAS Number
154361-50-9
Molecular Weight
359.35
Molecular Formula
C15H22FN3O6
Quality Standard
USP
COA
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MSDS
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Structure
CAS 154361-50-9 Capecitabine
Specification
Purity
>99%
Appearance
White crystalline powder
Related Products
Reference Reading
1. Nanostructured self-assembly materials from neat and aqueous solutions of C18 lipid pro-drug analogues of Capecitabine—a chemotherapy agent. Focus on nanoparticulate cubosomesTM of the oleyl analogue
Xiaojuan Gong, Minoo J. Moghaddam, Calum J. Drummond*. Soft Matter, 2011, 7, 5764–5776
Female BALB/c mice were obtained from the Animal Resource Centre (Canning Vale, WA, Australia) at 6–8 weeks of age and observed for at least 1 week prior to beginning experiments.Mice were injected with 5 ×104 4T1 cells per 10 ml PBS into the 2nd mammary fat pad on the right hand side to initiate tumour development. Daily treatment was started 6 days post-inoculation when tumours were palpable in the majority of mice. Throughout the course of the experiment, approximately 5% of animals did not form tumours. Mice were divided into seven groups of six and administered, via orogastric gavage, the following daily treatments for 21 days (calculations are based on a 20 g mouse): 0.5 mmol 5-FCOle, 0.25 mmol 5-FCOle, 0.1 mmol 5-FCOle, 0.5 mmol Capecitabine, 0.25 mmol Capecitabine, 0.1 mmol Capecitabine, or a 1.5 mg ml-1 solution of F127 in water. The length and breadth of the tumors were measured on days 1, 4, 7, 14, and 21 of drug administration. Mice were euthanized on day 22 of drug administration. Blood was collected via cardiac puncture, followed by removal of the tumour, liver, spleen and kidney for histological analysis. Lungs were injected with indium ink prior to removal to allow for examination and quantification of lung metastases in each animal.
2. Evaluation of the aquatic toxic effect varied during the degradation of capecitabine under the environmental abiotic and biotic processes
Ruixin Guo, Fengzhu Zheng and Jianqiu Chen*. RSC Adv.,2015, 5, 76772–76778
Because of many advanced methods for the detection of anticancer drugs, many anticancer agents now have been detected in aquatic systems; for example, 5-fluorouracil (5-FU), ifosfamide, and cyclophosphamide, and several new compounds, such as imatinib mesylate (IM), and temozolomide, and capecitabine (CAP). CAP is a new oral anticancer drug, playing its role by converting to the active compound 5-FU in vivo. 5-FU and its pro-drug CAP are pyrimidine analogues characterized as antimetabolites. This class of drugs inhibits DNA polymerase and induces cell cycle arrest and apoptosis. Because of a better clinical curative effect and higher security, CAP is popular with cancer patients and has been detected as a new compound in environmental samples, thus expanding the list of anticancer drugs measured in the environment. Based on therapeutical function and on the biological mode of action, certain groups of anticancer drugs are suspected to cause damage to key organisms in ecosystems. Thus, the environmental risk assessment for CAP in Europe has been considered and experienced.
3. A UV-sensitive hydrogel based combinatory drug delivery chip (UV gel-Drug Chip) for cancer cocktail drug screening
Ying-Ting Chen, Venkanagouda S. Goudar, Fan-Gang Tseng*. RSC Adv.,2016, 6, 44425–44434
Conventional drug delivery techniques are time consuming, painful and can cause side effects. As such, there is a need for alternative, high throughput, cost effective and user friendly laboratory drug screening methods for highly efficient drug testing. Current trends in point-of-care, automatized and precise drug assay platforms are superior to conventional techniques. Because they can achieve higher accuracy with lower drug dosages. Microfluidic based platforms have emerged as an efficient chip based assay for cell line tests. With their in-built advantages of low reagent consumption, precise control and high throughput scalability will provide robust analytical tools to investigate complex biological processes at the cellular level. Depending on cancer type and location of cancer, anticancer drugs will have specific targeting sites. For example, 5-fluorouracil and capecitabine drugs are anti- metabolites, irinotecan is a plant alkaloid and acts as a topo-isomerase inhibitor, folinic acid is a chemo-protectant, which causes folic acid deficiency in cancer cells, which leads to cell death, oxaliplatin is alkylating agent used for inhibiting cell cycles, bevacizumub is a genetically modified drug for regulating angiogenesis by inhibiting vascular endothelial factor and cetuximub is a protein based drug, which targets endothelial growth factor receptor proteins.
4. Preparation of a ZnO nanoparticles/multiwalled carbon nanotubes/carbon paste electrode as a sensitive tool for capecitabine determination in real samples
Tayyebeh Madrakian,* Hojjat Ghasemi, Esmaeel Haghshenas and Abbas Afkhami. RSC Adv.,2016, 6, 33851–33856
Capecitabine (Cap), chemically 50-deoxy-5-fluoro-N4-pentyloxycarbonyl-cytidine (Scheme 1) is the pro-drug for the anti-metabolite 5-fluorouracil (5-FU). It is a novel oral tumor- activated and tumor-elective fluoropyrimidine carbamate and an oral chemotherapeutic agent used in the treatment of breast, esophageal and larynx, gastrointestinal and genitourinary tract cancers. As a prodrug, Cap is converted into the active agent 5-fluorouracil (5-FU) through a three-step enzymatic process after oral drug administration. First, hydrolysis by carboxylesterases leads to the formation of 5’-deoxy-5-fluorocytidine (DFCR). Second, cytidine deaminase catalyzes the conversion of DFCR to 5’-deoxy-5-fluorouridine (DFUR). Finally, further catabolism by thymidine phosphorylase produces 5-FU.
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