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Seite 1 von 79 Ergebnisse
Effective combination therapy of metastatic murine solid tumors with edatrexate and the vinca alkaloids, vinblastine, navelbine and vindesine.
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Studies are described in which a new folate analogue, edatrexate (EDX), in combination with the vinca alkaloids, vinblastine (VBL), navelbine (NVB) or vindesine (DVA) was evaluated against E0771 mammary adenocarcinoma, T241 fibrosarcoma and the Lewis lung tumor. Each of the four agents when given
Dyspnea following vinblastine or vindesine administration in patients receiving mitomycin plus vinca alkaloid combination therapy.
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Pulmonary toxicity is not commonly associated with the vinca alkaloids vinblastine and vindesine. Three patients receiving the combination of mitomycin plus vindesine or vinblastine developed acute dyspnea 1-5 hours following vinca alkaloid administration. Two of the three patients continued to
Pharmacology, clinical efficacy and adverse effects of vindesine sulfate, a new vinca alkaloid.
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Vindesine is a new vinca alkaloid antineoplastic agent derived from vinblastine. However, its antineoplastic spectrum more closely resembles that of vincristine. Clinical studies indicate activity against acute leukemia, lung cancer, carcinoma of the breast, squamous cell carcinoma of the esophagus
Correlation of the clinical neurotoxicity of the vinca alkaloids vincristine, vinblastine, and vindesine with their effects on cultured rat midbrain cells.
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Clinical experience with three vinca alkaloids currently in use as antineoplastic agents has shown a difference in the degree of peripheral neurotoxicity manifested by these compounds: vincristine greater than vindesine greater than vinblastine. This phenomenon may reflect differences in
Vindesine: a new vinca alkaloid.
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Vindesine (VDS) is an analogue of the vinca alkaloids. Its spectrum of antitumoral activity is similar to that of vincristine (VCR), but with milder experimental neurotoxicity, and it inhibits the polymerization of tubulin. Its terminal half-life is 24 h and its plasma clearance is intermediate
Proceedings of the 7th Lilly Vinca Alkaloid Symposium on Vindesine Washington, D.C., 6-7 October 1979.
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[Vindesine, a new cytostatic agent from the vinca alkaloids].
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Vinca Alkaloid Toxicity
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Vinca alkaloids, which belong to a class of cell cycle phase M specific anti-tubulin agents, are one of the first plant alkaloids to be developed for use as anti-cancer agents in humans. This class of drugs derived from Vinca rosea (Catharanthus roseus) consists of first-generation
Molecular docking and pharmacogenomics of vinca alkaloids and their monomeric precursors, vindoline and catharanthine.
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Vinblastine and vincristine are dimeric indole alkaloids derived from Catharanthus roseus (formerly: Vinca rosea). Their monomeric precursor molecules are vindoline and catharanthine. While vinblastine and vincristine are well-known mitotic spindle poisons, not much is known about vindoline and
[Cisplatin and vinca alkaloid combination chemotherapy of advanced non-small-cell lung cancer in the aged].
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Fifteen patients aged over 65 years of age with advanced non-small-cl lung cancer (mean age = 70.7, stage IIIb: IV = 4:11) were treated with combination chemotherapy consisting of Cisplatin (50 or 80 mg/m2) and a vinca-alkaloid (Vindesine 3 mg/m2 or Etoposide 80 mg/m2). The effectiveness and side
Human pharmacokinetics of a new Vinca alkaloid S 12363 with use of a monoclonal antibody-based radio- or enzyme immunoassay.
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S 12363 is a new Vinca alkaloid derivative, characterized by the grafting of an alpha-aminophosphonate, onto the Vinca nucleus, facilitating drug penetration and increasing intracellular drug retention. As a high cytotoxic activity had been demonstrated in in vitro and in vivo models recommended by
Uptake of Vinca alkaloids into mammalian nerve and its subcellular components.
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Three Vinca alkaloids, vinblastine (VLB), vincristine (VCR), and vindesine (VDS), were recently found to affect axoplasmic transport to different degrees, with VCR the most potent. The uptake of these three species by desheathed cat sciatic nerves in vitro was determined by using tritium-labeled
Differential involvement of glutathione S-transferase mu 1 and multidrug resistance protein 1 in melanoma acquired resistance to vinca alkaloids.
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On account of its extreme intrinsic resistance to apoptosis and of its strong ability to become chemoresistant after a primary response to drugs, malignant melanoma (MM) is still a therapeutic challenge. We previously showed that glutathione S-transferase mu 1 (GSTM1) acts in synergy with multidrug
The use of a fluorescent methotrexate probe to monitor the effects of three vinca alkaloids on a mixed population of parental L1210 and gene-amplified methotrexate-resistant cells by flow cytometry.
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Cells resistant to methotrexate (L1210/R7A) and possessing an increased level of dihydrofolate reductase due to gene amplification can be detected by the technique of flow cytofluorimetry using a new fluorescent derivative of methotrexate (F-MTX) based on a putrescine linker. Comparative studies of
Vinca alkaloids inhibit conversion of arachidonic acid to thromboxane by human platelet microsomes: comparison with other microtubule-active drugs.
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The Vinca alkaloid vinblastine causes dose-dependent inhibition of malondialdehyde formation and aggregation in activated human platelets as a result of inhibition of arachidonic acid metabolism via the thromboxane pathway (Brammer, J.P., Kerecsen, L. and Maguire, M.H. (1982) Eur. J. Pharmacol. 81,
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