Reaction of mer-trichloro (diethylenetriamine)platmum(IV) chloride, (mer-[Pt(dien)Cl3]Cl), with purine nucleosides and nucleotides results in formation of platinum(II) as well as platinum(IV) complexes

Roat, Rosette M.

doi:10.1016/0162-0134(93)80030-d

Cited by 54 publications

(14 citation statements)

References 26 publications

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“…It was shown that platinum(IV) complexes can directly bind to DNA without any reducing agents and that the rate of the reaction is much lower than that for cisplatin [27]. Cisplatin can bind to DNA quantitatively within 48 h at 37°C in 0.01 M NaClO 4 , while only about 10% of oxoplatin bound to DNA after 12 days under identical conditions [28].…”

Section: Discussionmentioning

confidence: 99%

DNA damage and repair in human lymphocytes exposed to three anticancer platinum drugs

Błasiak

Kowalik

Małecka‐Panas

et al. 2000

Teratog. Carcinog. Mutagen.

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Section: Discussionmentioning

confidence: 99%

DNA damage and repair in human lymphocytes exposed to three anticancer platinum drugs

Błasiak

Kowalik

Małecka‐Panas

et al. 2000

Teratog. Carcinog. Mutagen.

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“…Extracellular or intracellular reduction to the divalent oxidation state has generally been considered a prerequisite for reactivity towards DNA. This assumption has been somewhat challenged, since direct reaction of platinum(IV) species with 5'-GMP (Roat and Reedijk 1993;Talman et al 1997;Galanski and Keppler 2000) and DNA (Brabec et al 1986;Novµkovµ et al 1995) has been observed in cell-free model experiments. However, reactions of platinum(IV) species with 5'-GMP or DNA have been noted to proceed generally much slower than those of platinum(II) analogues.…”

Section: Oral Platinum Drugsmentioning

confidence: 99%

Tumour-inhibiting platinum complexes—state of the art and future perspectives

Jakupec

Galanski

Keppler

2003

Reviews of Physiology, Biochemistry and Pharmacology

383

349

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Thirty years after the onset of the first clinical studies with cisplatin, the development of antineoplastic platinum drugs continues to be a productive field of research. This article reviews the current preclinical and clinical status, including a discussion of the molecular basis for the activity of the parent drug cisplatin and platinum drugs of the second and third generation, in particular their interaction with DNA. Further emphasis is laid on the development of third generation platinum drugs with activity in cisplatin-resistant tumours, particularly on chelates containing 1,2-diaminocyclohexane (DACH) and on the promising and more recently evolving field of non-classic ( trans- and multinuclear) platinum complexes. The development of oral platinum drugs and drug targeting strategies using liposomes, polymers or low-molecular-weight carriers in order to improve the therapeutic index of platinum chemotherapy are also covered.

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“…It is generally believed that platinum(IV) compounds need to be reduced in order to bind to the DNA, however, Novakova and others demonstrated that platinum(IV) complexes can bind to DNA directly without previous reduction, even though more slowly and to a lesser extent than cisplatin [21–24, 31–34]. Cisplatin-DNA adducts lead to a conformational change of the DNA double-helix allowing protein binding of molecules containing high mobility group domains impairing DNA replication and transcription [35–38].…”

Section: Discussionmentioning

confidence: 99%

In Vitro Evaluation of Oxoplatin: An Oral Platinum(IV) Anticancer Agent

et al. 2009

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Platinum(IV) compounds like oxoplatin (cis, cis, trans-diammine-dichlorido-dihydroxido-platinum(IV))show increased stability and therefore can be applied orally. In a panel of 38 human cancer cell lines this drug induced S-phase arrest and cell death with IC 50 values 2.5-fold higher than cisplatin. Oxoplatin may be converted to cisplatin by intracellular reducing agents, however, exposure to 0.1 M HCl mimicking gastric acid yielded cis-diammine-tetrachlorido-platinum(IV) exhibiting twofold increased activity. Similar results were obtained for another platinum(IV) compound, JM 149 (ammine-dichlorido-(cyclohexylamine)-dihydroxido-platinum(IV)), but not for its parent drug JM 216/satraplatin. Genome-wide expression profiling of H526 small cell lung cancer cells treated with these platinum species revealed clear differences in the expression pattern of affected genes between oxoplatin and cisplatin. In conclusion, oxoplatin constitutes a potent oral agent that is either reduced or converted to distinct active compounds, for example, by gastric acid or acidic areas prevailing in solid tumors, in dependence of the respective pharmaceutical formulation.

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Reaction of mer-trichloro (diethylenetriamine)platmum(IV) chloride, (mer-[Pt(dien)Cl3]Cl), with purine nucleosides and nucleotides results in formation of platinum(II) as well as platinum(IV) complexes

Cited by 54 publications

References 26 publications

DNA damage and repair in human lymphocytes exposed to three anticancer platinum drugs

DNA damage and repair in human lymphocytes exposed to three anticancer platinum drugs

Tumour-inhibiting platinum complexes—state of the art and future perspectives

In Vitro Evaluation of Oxoplatin: An Oral Platinum(IV) Anticancer Agent

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