A triphosphate nucleotide analog which is the biologically active form of CYTARABINE. It inhibits nuclear DNA synthesis.
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
Guanosine 5'-(tetrahydrogen triphosphate). A guanine nucleotide containing three phosphate groups esterified to the sugar moiety.

All-trans-retinoic acid increases cytosine arabinoside cytotoxicity in HL-60 human leukemia cells in spite of decreased cellular ara-CTP accumulation. (1/66)

BACKGROUND: Accumulation of the cytosine arabinoside (ara-C) metabolite ara-C-triphosphate (ara-CTP) in leukemic blast cells is considered to be the main determinant of ara-C cytotoxicity in vitro and in vivo. Retinoids such as all-trans-retinoic acid (ATRA) have been shown to increase the sensitivity of acute myelogenous leukemic (AML) blast cells to ara-C. To investigate the mechanism of this sensitisation, the hypothesis was tested that ATRA augments cellular ara-CTP levels in human-derived myelogenous leukemia HL-60 cells. MATERIALS AND METHODS: The effect of ATRA and 13-cis-retinoic acid on ara-CTP accumulation and ara-C-induced apoptosis was studied. Ara-CTP levels were measured by high-performance liquid chromatography (HPLC), cytotoxicity by the tetrazolium (MTT) assay, and apoptosis by occurrence of DNA fragmentation (gel electrophoresis), cell shrinkage and DNA loss (flow cytometry). RESULTS: Pretreatment of HL-60 cells with ATRA (0.01-1 microM) caused a significant decrease in intracellular ara-CTP levels; e.g., incubation for 72 hours with ATRA 1 microM prior to one hour ara-C 10 microM reduced ara-CTP levels to 41% +/- 4% of control. Similar results were obtained after preincubation with 13-cis-retinoic acid. In spite of decreased ara-CTP levels, the cytotoxicity of the combination was supraadditive and ATRA augmented ara-C-induced apoptosis. CONCLUSION: At therapeutically relevant concentrations ATRA increased ara-C cytotoxicity and ara-C induced apoptosis but this augmentation is not the corollary of elevated ara-CTP levels. The feasibility of ara-C treatment optimisation via strategies other than those involving elevation of ara-CTP levels should be investigated further.  (+info)

Interim comparison of a continuous infusion versus a short daily infusion of cytarabine given in combination with cladribine for pediatric acute myeloid leukemia. (2/66)

PURPOSE: To identify the optimal schedule for infusion of cytarabine (ara-C) given with cladribine (2-CdA) to pediatric patients with acute myeloid leukemia (AML), and to compare the effects of the two schedules on the pharmacokinetics of ara-C triphosphate (ara-CTP) in leukemic cells. PATIENTS AND METHODS: Forty-nine pediatric patients with newly diagnosed primary AML received a 5-day course of ara-C 500 mg/m(2)/d and 2-CdA 9 mg/m(2)/d. They were randomly assigned to receive ara-C as either a 2-hour daily infusion (arm A) or a continuous infusion (arm B). Cellular pharmacokinetics were studied on days 1 and 2. All patients then received two courses of remission induction chemotherapy with daunorubicin, ara-C, and etoposide (DAV). RESULTS: Thirty-two percent of patients (seven of 22) in arm A and 63% (17 of 27) in arm B entered complete remission (P =.045) after ara-C and 2-CdA therapy. Coadministration of 2-CdA increased the intracellular concentration of ara-CTP in 20 of 36 patients, although we found no statistically significant difference between the treatment arms in this effect (P =.63). The incidence of toxicity did not differ significantly between the two treatment arms (P =.53). After two courses of DAV, the rate of complete remission was 91% in arm A and 96% in arm B (P =.58). CONCLUSION: Intracellular accumulation of ara-CTP is increased when 2-CdA is given with ara-C, but no schedule-dependent differences in this effect were seen. The combination of 2-CdA and ara-C seems to be effective therapy for pediatric AML.  (+info)

Differential mRNA expression of Ara-C-metabolizing enzymes explains Ara-C sensitivity in MLL gene-rearranged infant acute lymphoblastic leukemia. (3/66)

Infant acute lymphoblastic leukemia (ALL) is characterized by a high incidence of mixed lineage leukemia (MLL) gene rearrangements, a poor outcome, and resistance to chemotherapeutic drugs. One exception is cytosine arabinoside (Ara-C), to which infant ALL cells are highly sensitive. To investigate the mechanism underlying Ara-C sensitivity in infants with ALL, mRNA levels of Ara-C-metabolizing enzymes were measured in infants (n = 18) and older children (noninfants) with ALL (n = 24). In the present study, infant ALL cells were 3.3-fold more sensitive to Ara-C (P =.007) and accumulated 2.3-fold more Ara-CTP (P =.011) upon exposure to Ara-C, compared with older children with ALL. Real-time quantitative reverse trancriptase-polymerase chain reaction (RT-PCR) (TaqMan) revealed that infants express 2-fold less of the Ara-C phosphorylating enzyme deoxycytidine kinase (dCK) mRNA (P =.026) but 2.5-fold more mRNA of the equilibrative nucleoside transporter 1 (hENT1), responsible for Ara-C membrane transport (P =.001). The mRNA expression of pyrimidine nucleotidase I (PN-I), cytidine deaminase (CDA), and deoxycytidylate deaminase (dCMPD) did not differ significantly between both groups. hENT1 mRNA expression inversely correlated with in vitro resistance to Ara-C (r(s) = -0.58, P =.006). The same differences concerning dCK and hENT1 mRNA expression were observed between MLL gene-rearranged (n = 14) and germ line MLL cases (n = 25). An oligonucleotide microarray screen (Affymetrix) comparing patients with MLL gene-rearranged ALL with those with nonrearranged ALL also showed a 1.9-fold lower dCK (P =.001) and a 2.7-fold higher hENT1 (P =.046) mRNA expression in patients with MLL gene-rearranged ALL. We conclude that an elevated expression of hENT1, which transports Ara-C across the cell membrane, contributes to Ara-C sensitivity in MLL gene-rearranged infant ALL.  (+info)

The antimetabolite ara-CTP blocks long-term memory of conditioned taste aversion. (4/66)

We examined the hypothesis that processes related to DNA recombination and repair are involved in learning and memory. Rats received intracerebroventricular (i.c.v.) infusions of the antimetabolite 1-beta-D-arabinofuranosylcytosine triphosphate (ara-CTP) or its precursor cytosine arabinoside (ara-C) 30 min prior to conditioned taste aversion (CTA) training. Both ara-CTP and ara-C caused significant impairments in long-term memory (LTM) of CTA. Control experiments indicate that the effect of ara-CTP on CTA memory is related to interference with learning. Furthermore, as it was previously demonstrated for the protein synthesis inhibitor anisomycin, ara-CTP had no effect on CTA memory when it was injected 1 h after training. Importantly, although both ara-CTP and anisomycin significantly blocked LTM in the task, short-term memory (STM) measured 1 h after training was not affected by either of the drugs. Finally, ara-CTP had no effect on in vitro transcription, but it did effectively block nonhomologous DNA end joining (NHEJ) activity of brain protein extracts. We suggest that DNA ligase-mediated DNA recombination and repair processes are necessary for the expression of LTM in the brain.  (+info)

The value of fludarabine in addition to ARA-C and G-CSF in the treatment of patients with high-risk myelodysplastic syndromes and AML in elderly patients. (5/66)

Fludarabine in addition to cytosine-arabinoside (ARA-C) increases the accumulation of ARA-C-5'-triphosphate (ARA-CTP), which is responsible for the cytotoxic effect in leukemic blasts. In a randomized phase 3 trial, patients with high-risk myelodysplastic syndrome (MDS) (n = 91) or elderly patients with acute myeloid leukemia (AML) (n = 43) were randomized to receive 2 induction courses consisting of ARA-C (2 g/m2 days 1 through 5) and granulocyte colony-stimulating factor (G-CSF) (filgrastim, 5 microg/kg) during and after chemotherapy with or without fludarabine (25 mg/m2, days 1 through 5) (FLAG versus AG). Consolidation consisted of daunorubicin (45 mg/m2, days 1 through 3) and ARA-C (200 mg/m2, days 1 through 7). Complete remission (CR) rate following AG was 65% versus 71% with FLAG (P =.49). Overall survival (OS) at 24 months was 24% for AG treatment and 39% for FLAG (P =.32). Event-free survival (EFS) at 2 years was 10% and 19% (P =.31) for the AG and FLAG treatments, respectively. Platelet and granulocyte recovery times after the second cycle were prolonged in the FLAG treatment group. Grades 3 to 4 neurotoxicities were more often reported in the FLAG arm (14% versus 3%, P =.03), whereas no significant differences in other toxicities were observed. In a cohort of patients, the in vivo accumulation of ARA-CTP in leukemic cells was determined. Although ARA-CTP accumulation in leukemic cells after FLAG was enhanced, clinical outcome in terms of CR rate, OS, EFS, and disease-free survival (DFS) was not significantly improved by combining fludarabine with ARA-C.  (+info)

Human immunodeficiency virus type 1 induces 1-beta-D-arabinofuranosylcytosine resistance in human H9 cell line. (6/66)

We have found that chronically HIV-1(IIIB)-infected H9 cells showed 21-fold resistance to 1-beta-D-arabinofuranosylcytosine (ARA-C) compared with uninfected H9 cells. In the infected H9 cells, a 37% increase of dCTP pool and a 34% increase of dATP were observed, and no alteration of dTTP and dGTP was observed, compared with the uninfected H9 cells. A marked decrease of ARA-CTP generation was observed in the infected H9 cells after 3-h incubation with 0.1-10 microM ARA-C. The level of deoxycytidine kinase activity with ARA-C as substrate was similar in both the infected and the uninfected cells; however, a 37-fold increase of cytidine deaminase activity was observed in the infected H9 cells. These results indicate that the induction of cytidine deaminase activity by HIV-1(IIIB) infection conferred ARA-C resistance to H9 cells. This conclusion was supported by the observation that a marked reversal of ARA-C resistance in the infected H9 cells occurred after treatment with the inhibitor of cytidine deaminase, 3,4,5,6-tetrahydrouridine. The understanding of these cellular alterations in drug sensitivity may facilitate the development of effective therapeutic strategies against HIV-1-infected cells.  (+info)

GATA1, cytidine deaminase, and the high cure rate of Down syndrome children with acute megakaryocytic leukemia. (7/66)

Down syndrome children with acute megakaryocytic leukemia (AMkL) have higher cure rates than non-Down syndrome acute myeloid leukemia (AML) patients treated with cytosine arabinoside (ara-C). Megakaryoblasts from Down syndrome AML patients are more sensitive in vitro to ara-C than cells from non-Down syndrome AML patients. Somatic mutations in the GATA1 transcription factor have been detected exclusively and almost uniformly in Down syndrome AMkL patients, suggesting a potential linkage to the chemotherapy sensitivity of Down syndrome megakaryoblasts. Stable transfection of wild-type GATA1 cDNA into the Down syndrome AMkL cell line CMK resulted in decreased (8- to 17-fold) ara-C sensitivity and a threefold-lower generation of the active ara-C metabolite ara-CTP compared with that for mock-transfected CMK cells. High intracellular levels of uridine arabinoside (ara-U) (an inactive ara-C catabolite generated by cytidine deaminase) and cytidine deaminase transcripts were detected in GATA1-transfected CMK sublines, whereas no ara-U was detected in mock-transfected cells. Cytidine deaminase transcripts were a median 5.1-fold (P = .002) lower in Down syndrome megakaryoblasts (n = 16) than in blast cells from non-Down syndrome patients (n = 56). These results suggest that GATA1 transcriptionally upregulates cytidine deaminase and that the presence or absence of GATA1 mutations in AML blasts likely confers differences in ara-C sensitivities due to effects on cytidine deaminase gene expression, which, in turn, contributes to the high cure rate of Down syndrome AMkL patients.  (+info)

An inhibitor of DNA recombination blocks memory consolidation, but not reconsolidation, in context fear conditioning. (8/66)

Genomic recombination requires cutting, processing, and rejoining of DNA by endonucleases, polymerases, and ligases, among other factors. We have proposed that DNA recombination mechanisms may contribute to long-term memory (LTM) formation in the brain. Our previous studies with the nucleoside analog 1-beta-D-arabinofuranosylcytosine triphosphate (ara-CTP), a known inhibitor of DNA ligases and polymerases, showed that this agent blocked consolidation of conditioned taste aversion without interfering with short-term memory (STM). However, because polymerases and ligases are also essential for DNA replication, it remained unclear whether the effects of this drug on consolidation were attributable to interference with DNA recombination or neurogenesis. Here we show, using C57BL/6 mice, that ara-CTP specifically blocks consolidation but not STM of context fear conditioning, a task previously shown not to require neurogenesis. The effects of a single systemic dose of cytosine arabinoside (ara-C) on LTM were evident as early as 6 h after training. In addition, although ara-C impaired LTM, it did not impair general locomotor activity nor induce brain neurotoxicity. Importantly, hippocampal, but not insular cortex, infusions of ara-C also blocked consolidation of context fear conditioning. Separate studies revealed that context fear conditioning training significantly induced nonhomologous DNA end joining activity indicative of DNA ligase-dependent recombination in hippocampal, but not cortex, protein extracts. Finally, unlike inhibition of protein synthesis, systemic ara-C did not block reconsolidation of context fear conditioning. Our results support the idea that DNA recombination is a process specific to consolidation that is not involved in the postreactivation editing of memories.  (+info)

Arabinofuranosylcytosine triphosphate (Ara-C triphosphate) is a nucleotide analog that is formed from the conversion of arabinofuranosylcytosine (Ara-C) by deoxycytidine kinase in cells. It is an active metabolite of Ara-C, which is a chemotherapeutic drug used to treat various types of cancer, including leukemia and lymphoma.

Ara-C triphosphate works by getting incorporated into DNA during replication, causing the DNA synthesis process to stop, which leads to cell death. It has a higher affinity for DNA polymerase than normal nucleotides, allowing it to be preferentially incorporated into the DNA, leading to its anticancer effects.

Cytarabine is a chemotherapeutic agent used in the treatment of various types of cancer, including leukemias and lymphomas. Its chemical name is cytosine arabinoside, and it works by interfering with the DNA synthesis of cancer cells, which ultimately leads to their death.

Cytarabine is often used in combination with other chemotherapy drugs and may be administered through various routes, such as intravenous (IV) or subcutaneous injection, or orally. The specific dosage and duration of treatment will depend on the type and stage of cancer being treated, as well as the patient's overall health status.

Like all chemotherapy drugs, cytarabine can cause a range of side effects, including nausea, vomiting, diarrhea, hair loss, and an increased risk of infection. It may also cause more serious side effects, such as damage to the liver, kidneys, or nervous system, and it is important for patients to be closely monitored during treatment to minimize these risks.

It's important to note that medical treatments should only be administered under the supervision of a qualified healthcare professional, and this information should not be used as a substitute for medical advice.

Adenosine Triphosphate (ATP) is a high-energy molecule that stores and transports energy within cells. It is the main source of energy for most cellular processes, including muscle contraction, nerve impulse transmission, and protein synthesis. ATP is composed of a base (adenine), a sugar (ribose), and three phosphate groups. The bonds between these phosphate groups contain a significant amount of energy, which can be released when the bond between the second and third phosphate group is broken, resulting in the formation of adenosine diphosphate (ADP) and inorganic phosphate. This process is known as hydrolysis and can be catalyzed by various enzymes to drive a wide range of cellular functions. ATP can also be regenerated from ADP through various metabolic pathways, such as oxidative phosphorylation or substrate-level phosphorylation, allowing for the continuous supply of energy to cells.

Guanosine triphosphate (GTP) is a nucleotide that plays a crucial role in various cellular processes, such as protein synthesis, signal transduction, and regulation of enzymatic activities. It serves as an energy currency, similar to adenosine triphosphate (ATP), and undergoes hydrolysis to guanosine diphosphate (GDP) or guanosine monophosphate (GMP) to release energy required for these processes. GTP is also a precursor for the synthesis of other essential molecules, including RNA and certain signaling proteins. Additionally, it acts as a molecular switch in many intracellular signaling pathways by binding and activating specific GTPase proteins.

... is a nucleotide that inhibits the synthesis of DNA by acting as an antimetabolic agent ...
Cytidine triphosphate Arabinofuranosylcytosine triphosphate This set index page lists chemical structure articles associated ...
... arabinofuranosylcytosine triphosphate MeSH D13.695.740.246.115 - cyclic cmp MeSH D13.695.740.246.150 - cytidine diphosphate ... arabinofuranosylcytosine triphosphate MeSH D13.695.065.900 - vidarabine phosphate MeSH D13.695.201.100 - deoxyadenine ... uridine triphosphate MeSH D13.695.900.380 - guanosine 5'-o-(3-thiotriphosphate) The list continues at List of MeSH codes (D20 ... ethenoadenosine triphosphate MeSH D13.695.667.138.382 - coenzyme a MeSH D13.695.667.138.382.300 - acyl coenzyme a MeSH D13.695. ...
... -5´-triphosphate is a substrate for SAMHD1. Furthermore, SAMHD1 has been shown to limit the efficacy of cytarabine ... It is an antimetabolic agent with the chemical name of 1β-arabinofuranosylcytosine. Certain sponges, where similar compounds ... Its mode of action is due to its rapid conversion into cytosine arabinoside triphosphate, which damages DNA when the cell cycle ... When used as an antiviral, cytarabine-5´-triphosphate functions by inhibiting viral DNA synthesis. Cytarabine is able to ...
Arabinofuranosylcytosine triphosphate is a nucleotide that inhibits the synthesis of DNA by acting as an antimetabolic agent ...
... triphosphate, Cytosine arabinoside 5-triphosphate, 1-beta-D-Arabinofuranosylcytosine triphosphate, Cytosine, 1-beta-D- ... Arabinofuranosylcytosine triphosphate (5 suppliers). IUPAC Name: [[(2R,3S,4S,5R)-5-(4-amino-2-oxopyrimidin-1-yl)-3,4- ... beta-D-Arabinofuranosyl 5-triphosphate, D-Arabinose, 5-(tetrahydrogen triphosphate), D-Arabinose,5-(tetrahydrogen triphosphate ... Synonyms: Arabinose 5-triphosphate, AG-G-94955, AC1L2QDI, D-Arabinose 5-triphosphate, Ara-5-P(3), CTK5D9574, ...
Arabinofuranosylcytosine Triphosphate 39% * 2-deoxycytidine 5-triphosphate 34% * DNA-Directed DNA Polymerase 25% ...
Studies in mouse L-cells on the incorporation of 1-beta-D-arabinofuranosylcytosine into DNA and on inhibition of DNA polymerase ... by 1-beta-D-arabinofuranosylcytosine 5-triphosphate. Academic Article * Studies of the renal action of melatonin: evidence ...
Arabinofuranosylcytosine Triphosphate. *Cyclic CMP. *Cytidine Diphosphate. *Cytidine Monophosphate. *Cytidine Triphosphate. * ...
clofarabine, cytarabine, leukemia, acute, arabinofuranosylcytosine triphosphate, c-reactive protein, cyclic amp receptor ... Quantitation of 1-β-D-arabinofuranosylcytosine 5′-triphosphate in the leukemic cells from bone marrow and peripheral blood of ... Cellular pharmacology of ara-CTP and clofarabine triphosphate suggested that clofarabine triphosphate accumulation resulted in ... Triphosphates were separated on an anion-exchange Partisil-10 SAX column (Waters, Milford, MA) using HPLC as described in ...
In addition there is incorporation of 5 -fluorouridine triphosphate into RNA. 3. RESISTANCE: Multiple mechanisms including ... CYTARABINE (Cytosine arabinoside, ara-C) 1. CHEMICAL NATURE: 1 -beta-arabinofuranosylcytosine (analog of the pyrimidine ... nucleoside, cytosine, with substitution of arabinose for ribose) 2. MECHANISM OF ACTION: The triphosphate metabolite inhibits ...
Synthesis of guanylyl-(3→5)-uridylyl-(3→5)-arabinofuranosyluracil and guanylyl-(3→5)-uridylyl-(3→5)-arabinofuranosylcytosine ... The synthesis of 6-azauridine-5 triphosphate. 1963, Vol. 28, Issue 1, pp. 241-244 [Abstract] ... One-step synthesis of 1-β-D-arabinofuranosylcytosine. 1977, Vol. 42, Issue 5, pp. 1588-1594 [Abstract] ... Synthesis of 1-β-D-arabinofuranosylcytosine. 1974, Vol. 39, Issue 11, pp. 3100-3108 [Abstract] ...
Protein activation and expression were analysed by western blotting, deoxyribonucleoside triphosphate levels by HPLC, ... Determination of deoxyribonucleoside triphosphates. The extraction of cellular dNTPs was performed according to a method ... synergistic antitumor activity with arabinofuranosylcytosine. Int J Oncol 31 (5): 1261-1266 ... Protein activation and expression were analysed by western blotting, deoxyribonucleoside triphosphate levels by HPLC, ...
The combination index revealed antagonism between forodesine and ara-G. The intracellular production of ara-G triphosphate was ... Safety assessment of 4-thio-beta-D-arabinofuranosylcytosine in the beagle dog suggests a drug-induced centrally mediated ... The intracellular concentration of the triphosphate metabolite of cytarabine was reduced to 1/10, and that of clofarabine was ... Plasma clofarabine levels generated clofarabine triphosphate accumulation, which resulted in an increase in ara-CTP in the ...
4-thio-beta-D-arabinofuranosylcytosine + UTP <=> UDP + 4-thio-beta-D-arabinofuranosylcytosine_5-phosphate 2.7.1.74 ... dATP + UTP <=> dAMP + uridine_3-diphosphate_5-triphosphate 2.7.6.4 nucleotide diphosphokinase - ... UTP + cytosine_arabinoside <=> UDP + 1-beta-D-arabinofuranosylcytosine_5-phosphate 2.7.1.74 deoxycytidine kinase - ... 3.6.1.15 nucleoside-triphosphate phosphatase 3.6.1.28 thiamine-triphosphatase 3.6.1.39 thymidine-triphosphatase 3.6.1.45 UDP- ...
Whitman S.P., Civoli F., Daniel L.W. Protein kinase С beta2 activation by 1-beta-D-arabinofuranosylcytosine is antagonistic to ... Reynolds E.C., Harris A.W., Finch L.R. Deoxyribonucleoside triphosphate pools and differential thymidine sensitivities of ... Fram R, Kufe D. DNA strand breaks caused by inhibitors of DNA synthesis: l-(5-D-arabinofuranosylcytosine and aphidicolin // ... Wang S., Wang Z., Grant S. Bryostatin 1 and UCN-01 potentiate 1-beta-D-arabinofuranosylcytosine-induced apoptosis in human ...
5-ethynyl-1-beta-d-arabinofuranosylcytosine (eac) was prepared from 1-(2,3,5-tri-o-acetyl-beta-d-arabinofuranosyl)cytosine by ... characterization of a herpes simplex virus type 2 deoxyuridine triphosphate nucleotidohydrolase and mapping of a gene ... 1) the accumulation of guanosine analog-triphosphates in infected cells, which is .... 1987. 2823702. ... the herpes simplex virus type 2 (hsv-2)-induced deoxyuridine triphosphate nucleotidohydrolase (dutpase) was purified ...
2 -Deoxy-2 -fluoroadenosine 5 -Triphosphate. 10 µmol. 134. 141. 104-02. 2 -Deoxy-2 -fluorocytidine 5 -Triphosphate. 10 µmol. ... 1-(2-Deoxy-2-fluoro- -D-arabinofuranosyl)cytosine hydrochloride (2 -FANA-C). 1 g. 779. 820. ... 2 -Deoxy-2 -fluoroguanosine 5 -Triphosphate. 10 µmol. 134. 141. 104-04. 2 -Deoxy-2 -fluorouridine 5 -Triphosphate. 10 µmol. 134 ... Modified Purine Nucleoside 5-Triphosphates. 107-01. 2-Deoxy-2,2-difluoroadenosine 5 -triphosphate, tetra-lithium salt. 10 ...
Correlation between Leukemic Cell Retention of 1-β-d-Arabinofuranosylcytosine 5′-Triphosphate and Response to Therapy1 Youcef M ... A correction has been published: Correlation between Leukemic Cell Retention of 1-β-d-Arabinofuranosylcytosine 5′-Triphosphate ... Correlation between Leukemic Cell Retention of 1-β-d-Arabinofuranosylcytosine 5′-Triphosphate and Response to Therapy ... d-arabinofuranosylcytosine triphosphate (ara-CTP) in vitro by leukemic myeloblasts and the response of patients to treatment ...
5. Long intracellular retention of 4-thio-arabinofuranosylcytosine 5-triphosphate as a critical factor for the anti-solid ... Degradation of 1-beta-D-arabinofuranosylcytosine 5-triphosphate in human leukemic myeloblasts and lymphoblasts.. Jamieson GP; ... 1-beta-D-arabinofuranosylcytosine nucleotide inhibition of sialic acid metabolism in WI-38 cells.. Myers-Robfogel MW; Spataro ... 2. Delivery of high levels of anti-proliferative nucleoside triphosphates to CYP3A-expressing cells as a potential treatment ...
Saturation of 1-beta-D-arabinofuranosylcytosine 5-triphosphate accumulation in leukemia cells during high-dose 1-beta-D- ... A pilot study of high-dose 1-beta-D-arabinofuranosylcytosine for acute leukemia and refractory lymphoma: clinical response and ... Pharmacology studies of 1-beta-D-arabinofuranosylcytosine in pediatric patients with leukemia and lymphoma after a ... arabinofuranosylcytosine therapy. Plunkett W, Liliemark JO, Adams TM, Nowak B, Estey E, Kantarjian H, Keating MJ. Plunkett W, ...
After cellular uptake, it is phosphorylated into its active triphosphate form (Ara-CTP), which primarily exerts its cytotoxic ... Arabinofuranosylcytosine Triphosphate / therapeutic use Actions. * Search in PubMed * Search in MeSH * Add to Search ... 1-Beta-arabinofuranosylcytosine in therapy of leukemia: preclinical and clinical overview. Rustum YM, Raymakers RA. Rustum YM, ... After cellular uptake, it is phosphorylated into its active triphosphate form (Ara-CTP), which primarily exerts its cytotoxic ...
Arabinofuranosylcytosine Triphosphate Preferred Concept UI. M0001640. Registry Number. 13191-15-6. Scope Note. A triphosphate ... Arabinosylcytosine Triphosphate Cytarabine Triphosphate Cytosine Arabinoside Triphosphate Pharm Action. Nucleic Acid Synthesis ... Arabinofuranosylcytosine Triphosphate Preferred Term Term UI T003292. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1979). ... Arabinofuranosylcytosine Triphosphate. Tree Number(s). D03.383.742.686.246.050. D13.695.065.200. D13.695.740.246.050. Unique ID ...
Arabinofuranosylcytosine Triphosphate Preferred Concept UI. M0001640. Registry Number. 13191-15-6. Scope Note. A triphosphate ... Arabinosylcytosine Triphosphate Cytarabine Triphosphate Cytosine Arabinoside Triphosphate Pharm Action. Nucleic Acid Synthesis ... Arabinofuranosylcytosine Triphosphate Preferred Term Term UI T003292. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1979). ... Arabinofuranosylcytosine Triphosphate. Tree Number(s). D03.383.742.686.246.050. D13.695.065.200. D13.695.740.246.050. Unique ID ...
Aquaporin 6 N0000169764 Aquaporins N0000170147 Arabidopsis Proteins N0000170788 Arabinofuranosylcytosine Triphosphate ... N0000170773 Cytidine Monophosphate N0000170774 Cytidine Monophosphate N-Acetylneuraminic Acid N0000170775 Cytidine Triphosphate ... N0000170836 Inosine Monophosphate N0000170833 Inosine Nucleotides N0000170644 Inosine Pranobex N0000170834 Inosine Triphosphate ... N0000168226 Uridine Kinase N0000170786 Uridine Monophosphate N0000168361 Uridine Phosphorylase N0000170787 Uridine Triphosphate ...
D3.383.742.686.50 Arabinofuranosylcytosine Triphosphate D3.383.742.686.246.50 Arabinofuranosyluracil D3.383.742.680.852.150 ... D3.438.759.590.616.450 Inosine Triphosphate D3.438.759.646.616.800 Insulin D6.472.610.575 D6.472.699.587.740.625 D6.472.699.350 ... D3.383.742.686.850.877 Uridine Triphosphate D3.383.742.686.850.950 Urinary Calculi C12.777.809 C12.777.967.500 C13.351.968.967. ... D3.438.759.646.138.180.80 Adenosine Triphosphate D3.438.759.646.138.236 Adenosine-5-(N-ethylcarboxamide) D3.438.759.590.138.25 ...
Arabinofuranosylcytosine Triphosphate [D03.383.742.686.246.050] Arabinofuranosylcytosine Triphosphate * Cyclic CMP [D03.383. ...
Cytarabine is chemically 1-β-D-Arabinofuranosylcytosine. The structural formula is:. Cytarabine is an odorless, white to off- ... Cytarabine is metabolized by deoxycytidine kinase and other nucleotide kinases to the nucleotide triphosphate, an effective ...
Synthesis of guanylyl-(3→5)-uridylyl-(3→5)-arabinofuranosyluracil and guanylyl-(3→5)-uridylyl-(3→5)-arabinofuranosylcytosine ... The synthesis of 6-azauridine-5 triphosphate. 1963, Vol. 28, Issue 1, pp. 241-244 [Abstract] ... C. Arabinofuranosyluracil and arabinofuranosylcytosine phosphates. 1967, Vol. 32, Issue 11, pp. 3958-3965 [Abstract] ...
It was found that cores contained an enzymatic activity which rapidly converted the added nucleoside triphosphates to ... arabinofuranosylcytosine, A(l) RNA accumulated in WT-infected cells for 9 h and then decreased in concentration to 6% of the 9- ... infected at 40.5 degrees C in the presence of 1-beta-d-arabinofuranosylcytosine by: (i) ts125 and WT; (ii) two other ts early ...
Synthesis of conjugates of 1-(carboxymethyl)cytosine and 1-(5-O-carboxymethyl-β-D-arabinofuranosyl)cytosine with proteins. 1979 ... Preparation of 5-O-phosphonylmethyl analogues of nucleoside-5-phosphates, 5-diphosphates and 5-triphosphates. 1982, Vol. 47 ...
effects of x-irradiation on dna precursor metabolism and deoxyribonucleoside triphosphate pools in chinese hamster cells.. 1974 ... studies on 1-beta-d-arabinofuranosyl-cytosine (ara-c) resistant mutants of chinese hamster fibroblasts. ii. high resistance to ... nuclear and cytoplasmic pools of deoxyribonucleoside triphosphates in chinese hamster ovary cells.. 1974. 4472692. ...
Methods: We used a multiplexed [two end points in one screen; MMP and adenosine triphosphate (ATP) content] quantitative high ... Bryostatin 1 and UCN-01 potentiate 1-β-d-arabinofuranosylcytosine-induced apoptosis in human myeloid leukemia cells through ... 1999). Most of the cell energy is generated as adenosine triphosphate (ATP) within the mitochondria through two complementary ...
Cytarabine is metabolized intracellularly into its active triphosphate form (cytosine arabinoside triphosphate). This ...
  • Arabinofuranosylcytosine triphosphate is a nucleotide that inhibits the synthesis of DNA by acting as an antimetabolic agent against deoxycytidine (a component of DNA). (wikipedia.org)
  • Arabinofuranosylcytosine triphosphate is a nucleotide that inhibits the synthesis of DNA by acting as an antimetabolic agent against deoxycytidine (a component of DNA). (wikipedia.org)
  • 14. 1-beta-D-arabinofuranosylcytosine nucleotide inhibition of sialic acid metabolism in WI-38 cells. (nih.gov)
  • A triphosphate nucleotide analog which is the biologically active form of CYTARABINE . (nih.gov)
  • Cytarabine is metabolized intracellularly into its active triphosphate form (cytosine arabinoside triphosphate). (pharmacycode.com)
  • The relationship between the phosphorylation of 1-β- d -arabinofuranosylcytosine (ara-C) and intracellular retention of 1-β- d -arabinofuranosylcytosine triphosphate (ara-CTP) in vitro by leukemic myeloblasts and the response of patients to treatment with ara-C and anthracycline was studied. (aacrjournals.org)
  • 17. Degradation of 1-beta-D-arabinofuranosylcytosine 5'-triphosphate in human leukemic myeloblasts and lymphoblasts. (nih.gov)
  • 5. Long intracellular retention of 4'-thio-arabinofuranosylcytosine 5'-triphosphate as a critical factor for the anti-solid tumor activity of 4'-thio-arabinofuranosylcytosine. (nih.gov)
  • Cytarabine is chemically 1-β-D-Arabinofuranosylcytosine. (nih.gov)
  • 18. Transport and metabolism of 1-beta-D-arabinofuranosylcytosine in human ovarian adenocarcinoma cells. (nih.gov)
  • effects of x-irradiation on dna precursor metabolism and deoxyribonucleoside triphosphate pools in chinese hamster cells. (liverpool.ac.uk)
  • nuclear and cytoplasmic pools of deoxyribonucleoside triphosphates in chinese hamster ovary cells. (liverpool.ac.uk)
  • 9. Clinical pharmacology of 1-beta-D-arabinofuranosylcytosine-5'-stearylphosphate, an orally administered long-acting derivative of low-dose 1-beta-D-arabinofuranosylcytosine. (nih.gov)
  • A pilot study of high-dose 1-beta-D-arabinofuranosylcytosine for acute leukemia and refractory lymphoma: clinical response and pharmacology. (nih.gov)
  • 2. Delivery of high levels of anti-proliferative nucleoside triphosphates to CYP3A-expressing cells as a potential treatment for hepatocellular carcinoma. (nih.gov)
  • Saturation of 1-beta-D-arabinofuranosylcytosine 5'-triphosphate accumulation in leukemia cells during high-dose 1-beta-D-arabinofuranosylcytosine therapy. (nih.gov)
  • MMP and adenosine triphosphate (ATP) content] quantitative high throughput screening (qHTS) approach combined with informatics tools to screen the Tox21 library of 10,000 compounds (~ 8,300 unique chemicals) at 15 concentrations each in triplicate to identify chemicals and structural features that are associated with changes in MMP in HepG2 cells. (nih.gov)