• Corpus ID: 86088471

Enhancementof the AntitumorActivityof Arabinofuranosyladenineby 2'-Deoxycoformycin1

@inproceedings{Lepage1976EnhancementofTA,
  title={Enhancementof the AntitumorActivityof Arabinofuranosyladenineby 2'-Deoxycoformycin1},
  author={Gerald A. Lepage and L S Worth and A. P. Kimball},
  year={1976}
}
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13 Citations
Highly Influential Citations
1
Background Citations
5

13 Citations

Physiologic model for the pharmacokinetics of 2′deoxycoformycin in normal and leukemic mice

  • F. KingR. Dedrick
  • Biology, Medicine
    Journal of Pharmacokinetics and Biopharmaceutics
  • 2005
A flow-limited physiologic mathematical model has been developed to describe the time course of 2′deoxycoformycin concentrations in the plasma and tissues of mice following iv and ip doses and has been used to predict pharmacokinetic behaviour of2′dCF in both normal and leukemic mice.

Lymphoblasts-d-Arabinofuranosyl-2-fluoroadenine in Human Leukemic β-d-Arabinofuranosyladenine and 9-β Differences in Metabolism and Cytotoxicity between 9-Updated Version

  • 2006

9-β-D-Arabinofuranosyl-2-fluoroadenine 5′-monophosphate pharmacokinetics in plasma and tumor cells of patients with relapsed leukemia and lymphoma

F-ara-ATP concentrations were three times higher in bone marrow cells from patients with lymphomatous bone marrow involvement than from those without evidence of marrow disease and DNA-synthetic capacity of leukemic cells was inversely related to the associated F-ara.

Adenosine deaminase inhibitors: Their role in chemotherapy and immunosuppression

  • R. Glazer
  • Biology, Medicine
    Cancer Chemotherapy and Pharmacology
  • 2004
The use of ADA inhibitors has helped enormously in understanding the mechanism of action of adenosine metabolites and analogs whose catabolism was heretofore neglected with respect to their specificities of action.

Clinical pharmacology of arabinofuranosyladenine in combination with deoxycoformycin

Five courses of arabinofuranosyladenine (ara-A) and deoxycoformycin (DCF) to two patients and the effects of DCF on the pharmacokinetics of ara-A were administered and abrupt declines in peripheral blast counts were observed in each patient.

In vivo toxicity to lymphoid tissue by 2′-Deoxycoformycin

No toxicity to tissues other than the lymphoid system was observed, which is consistent with the hypothesis that 2′-deoxycoformycin offers a new and selective approach to the treatment of lymphoid malignancies.

Presynaptic inhibitory actions of 2-substituted adenosine derivatives on neurotransmission in rat vas deferens: Effects of inhibitors of adenosine uptake and deamination

  • M. MullerD. Paton
  • Biology, Chemistry
    Naunyn-Schmiedeberg's Archives of Pharmacology
  • 2004
Results indicate that 2-substituted adenosine derivatives, likeadenosine, produce inhibition of transmission by acting on a presynaptic site which can be blocked by theophylline.

2,6-Diaminopurinedeoxyriboside as a prodrug of deoxyguanosine in L1210 cells.

DAPdR exerts its toxicity on L1210 cells as a prodrug of deoxyguanosine as a result of concentration-dependent decrease in DNA synthesis and ribonucleotide reductase activity.

Metabolism and therapeutic efficacy of 9-beta-D-arabinofuranosyl-2-fluoroadenine against murine leukemia P388.

Results suggest that the equal toxicity of the two regimens of F-ara-A may be attributed to the similar extent of inhibition of host-tissue DNA synthesis evoked by each, which was responsible for its superior therapeutic activity.

The biochemical and clinical consequences of 2'-deoxycoformycin in refractory lymphoproliferative malignancy.

Patients with chronic lymphocytic leukemia receiving weekly low doses of the drug demonstrated minimal toxicity and some efficacy, and the chemotherapeutic potential o 2'-deoxycoformycin, as either a single agent or in combination with Ara-A, merits further exploration.

8 References

Inhibition of Mammalian DNA Polymerase by the 5′-Triphosphate of 1-β-d-Arabinofuranosylcytosine and the 5′-Triphosphate of 9-β-d-Arabinofuranosyladenine

Studies indicate that the inhibition of mammalian DNA polymerase by the 5′-triphosphate of 9-β-d-arabinofuranosylcytosine (ara-ATP) is also competitive with the corresponding deoxytriphosphates.

A novel adenosine and ara‐a deaminase inhibitor, (R)‐3‐(2‐deoxy‐β‐D‐erythro‐pentofuranosyl)‐3,6,7,8‐tetrahydroimidazo[4,5 ‐d] [1,3]diazepin‐8‐ol

Experimental evaluation of potential anticancer agents. XXI. Scheduling of arabinosylcytosine to take advantage of its S-phase specificity against leukemia cells.

9-BETA-D-ARABINOFURANOSYLADENINE AS AN INHIBITOR OF METABOLISM IN NORMAL AND NEOPLASTIC CELLS.

Treatment of L1210 ascites tumors in vivo with combinations of 9-β-D-arabinosyladenine and 6-methyladenine nucleosides repressed cell growth by approximately 30%. This repression was measured by th...

Rational development of a soluble prodrug of a cytotoxic nucleoside: preparation and properties of arabinosyladenine 5'-formate.

The 5'-O-formate ester of arabinosyladenine was synthesized and shown to be suitable as a water-soluble prodrug, being at least 60 times more soluble than the parent cytotoxic nucleoside. This…

Arabinosyl cytosine: a useful agent in the treatment of acute leukemia in adults.

The recommended schedule of treatment for ara-C based on data is, therefore, daily infusions of 100 or 50 mg./m.2 in one hour for approximately 3 to 6 weeks followed by maintenance therapy of once weekly subcutaneous injection of 30 mg./ m.2 of aRA-C.

9-β-d-Arabinofuranosyladenine 5′-Phosphate Metabolism and Excretion in Humans

Indications are that this derivative provides important advantages (solubility and sustained blood levels) over ara-A.

Scheduling of arabinosylcytosine and 6-thioguanine therapy.

Mice treated simultaneously with 1-β-d-arabinofuranosylcytosine (ara-C) and 6-thioguanine (6-TG) were protected from the lethal effects of 6-TG, and DNA synthesis in mouse bone marrow and L1210 cells treated in vivo with ara-C was depressed to less than 1% of control and did not begin to recover until almost 16 hr.