Cytarabine Research Paper

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Cytarabine (arabinofuranosyl cytidine or ara-C) is a chemotherapeutic antimetabolic agent, used to treat cancers of white blood cells like acute myeloid leukemia and non-Hodgkin lymphoma. Its chemical name is 1β-arabinofuranosylcytosine. It kills cancer cells by interfering with synthesis of DNA, when the cell is in S-phase of the cell cycle. It is also called cytosine arabinoside implying that it combines arabinose sugar with cytosine base. Usually, cytosine pairs with deoxyribose to form deoxycytidine (a DNA component). Cytarabine is an analogue of deoxcytidine and gets incorporated into DNA. By this mechanism, it kills cancer cells.
Cells have an uptake transporter called human equilibrative nucleoside transporter (hENT1), which is important for uptake of ara-C into the cell. Inside the cell, ara-C rapidly gets activated by many phosphorylation steps to form ara-CTP (cytosine arabinoside triphosphate). When this ara-CTP is incorporated into DNA/RNA, it inhibits DNA and RNA synthesis and triggers cell death. Thus DNA replication for mitosis is affected and the cells
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It is rapidly deaminated by cytidine deaminase to biologically inactive uracil arabinoside (Ara-U), and is eliminated in urine. Thus the drug is administered through continuous intravenous injection. Plama protein binding of the drug is 13% and it is metabolized in the liver. Some effective formulations and cytarabine derivatives that are not easily deaminated and with better pharmacokinetic patterns, are used. The drug is encapsulated into pharmacologically acceptable carriers to protect it from rapid degradation and elimination, eg: encapsulation of cytarabine into multivesicular liposomes for intrathecal treatment of lymphomatous meningitis, minimizes its conversion into Ara-U, as stated by Japanese researcher Akinobu Hamada et al, in

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