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@ARTICLE{Matusch:52934,
      author       = {Matusch, A. and Meyer, P. T. and Bier, D. and Holschbach,
                      M. H. and Woitalla, D. and Elmenhorst, D. and Winz, O. H.
                      and Zilles, K. and Bauer, A.},
      title        = {{M}etabolism of the {A}1 adenosine receptor {PET} ligand
                      [18{F}]{CPFPX} by {CYP}1{A}2: implications for
                      bolus/infusion {PET} studies},
      journal      = {Nuclear medicine and biology},
      volume       = {33},
      issn         = {1872-9614},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {PreJuSER-52934},
      pages        = {891 - 898},
      year         = {2006},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {The A1 adenosine receptor positron emission tomography
                      (PET) ligand
                      8-cyclopentyl-3-(3-[18F]fluoropropyl)-1-propylxanthine
                      ([18F]CPFPX, ) undergoes a fast hepatic metabolism. An
                      optimal design of PET quantitation approaches (e.g.,
                      bolus/infusion studies) necessitates the knowledge of
                      factors that influence this metabolism. Metabolites of were
                      separated by radio thin-layer chromatography. Metabolism in
                      vivo, in pooled human liver microsomes and in recombinant
                      human cytochrome isoenzyme preparations was studied. Dynamic
                      PET studies using were performed on three controls and two
                      patients, one treated with the antidepressant and inhibitor
                      of cytochrome CYP1A2 fluvoxamine, the other suffering from
                      liver cirrhosis. CPFPX is metabolized by cytochrome CYP1A2
                      with high selectivity [KM=1.1 microM $(95\%$ confidence
                      interval, or CI, 0.6-2.0 microM) and Vmax=243 pmol min(-1)
                      mg(-1) $(95\%$ CI, 112-373 pmol min(-1) mg(-1))
                      corresponding to 2.4 pmol min(-1) pmol(-1) cytochrome
                      P-450]. This metabolism can competitively be inhibited by
                      fluvoxamine with KI=68 nM $(95\%$ CI, 34-138 nM). At least
                      eight compounds found in human plasma and in the CYP1A2 in
                      vitro preparations have an identical migration pattern and
                      account together for $>90\%$ and $>80\%$ of the respective
                      metabolite yield. Metabolism was considerably delayed in the
                      two patients. In conclusion, is metabolized by cytochrome
                      CYP1A2. Its metabolism is therefore subdued to
                      disease-related or xenobiotic-induced changes of CYP1A2
                      activity. The identification of the metabolic pathway of 1
                      allows to optimize image quantification in A1 adenosine
                      receptor PET studies.},
      keywords     = {Animals / Cytochrome P-450 CYP1A2: metabolism / Cytochromes
                      / Infusions, Parenteral / Male / Metabolic Clearance Rate /
                      Positron-Emission Tomography: methods / Rats / Rats, Inbred
                      F344 / Receptor, Adenosine A1: metabolism / Xanthines:
                      administration $\&$ dosage / Xanthines: diagnostic use /
                      Xanthines: pharmacokinetics /
                      8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine (NLM
                      Chemicals) / Cytochromes (NLM Chemicals) / Receptor,
                      Adenosine A1 (NLM Chemicals) / Xanthines (NLM Chemicals) /
                      cytochrome P-448 (NLM Chemicals) / Cytochrome P-450 CYP1A2
                      (NLM Chemicals) / J (WoSType)},
      cin          = {IME / INC / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)VDB54 / I:(DE-Juel1)VDB53 /
                      $I:(DE-82)080010_20140620$},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Radiology, Nuclear Medicine $\&$ Medical Imaging},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:17045169},
      UT           = {WOS:000241530100009},
      doi          = {10.1016/j.nucmedbio.2006.07.006},
      url          = {https://juser.fz-juelich.de/record/52934},
}