Evaluation of N-[(11)C]methyl-AMD3465 as a PET tracer for imaging of CXCR4 receptor expression in a C6 glioma tumor model

Mol Pharm. 2014 Nov 3;11(11):3810-7. doi: 10.1021/mp500398r. Epub 2014 Aug 18.

Abstract

The chemokine receptor CXCR4 and its ligand CXCL12 play an important role in tumor progression and metastasis. CXCR4 receptors are expressed by many cancer types and provide a potential target for treatment. Noninvasive detection of CXCR4 may aid diagnosis and improve therapy selection. It has been demonstrated in preclinical studies that positron emission tomography (PET) with a radiolabeled small molecule could enable noninvasive monitoring of CXCR4 expression. Here, we prepared N-[(11)C]methyl-AMD3465 as a new PET tracer for CXCR4. N-[(11)C]Methyl-AMD3465 was readily prepared by N-methylation with [(11)C]CH3OTf. The tracer was obtained in a 60 ± 2% yield (decay corrected), the purity of the tracer was >99%, and specific activity was 47 ± 14 GBq/μmol. Tracer stability was tested in vitro using liver microsomes and rat plasma; excellent stability was observed. The tracer was evaluated in rat C6 glioma and human PC-3 cell lines. In vitro cellular uptake of N-[(11)C]methyl-AMD3465 was receptor mediated. The effect of transition metal ions (Cu(2+), Ni(2+), and Zn(2+)) on cellular binding was examined in C6 cells, and the presence of these ions increased the cellular binding of the tracer 9-, 7-, and 3-fold, respectively. Ex vivo biodistribution and PET imaging of N-[(11)C]methyl-AMD3465 were performed in rats with C6 tumor xenografts. Both PET and biodistribution studies demonstrated specific accumulation of the tracer in the tumor (SUV 0.6 ± 0.2) and other CXCR4 expressing organs, such as lymph node (1.5 ± 0.2), liver (8.9 ± 1.0), bone marrow (1.0 ± 0.3), and spleen (1.0 ± 0.1). Tumor uptake was significantly reduced (66%, p < 0.01) after pretreatment with Plerixafor (AMD3100). Biodistribution data indicates a tumor-to-muscle ratio of 7.85 and tumor-to-plasma ratio of 1.14, at 60 min after tracer injection. Our data demonstrated that N-[(11)C]methyl-AMD3465 is capable of detecting physiologic CXCR4 expression in tumors and other CXCR4 expressing tissues. These results warrant further evaluation of N-[(11)C]methyl-AMD3465 as a potential PET tracer for CXCR4 receptor imaging.

Keywords: AMD3465; PET; cancer and metastasis; chemokine receptor 4; radiotracer; tumor imaging.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzylamines
  • Brain Neoplasms / diagnostic imaging*
  • Carbon Radioisotopes / pharmacokinetics*
  • Cell Line, Tumor
  • Cyclams
  • Gene Expression Regulation
  • Glioma / diagnostic imaging*
  • Heterocyclic Compounds / pharmacokinetics
  • Humans
  • Ions
  • Ligands
  • Male
  • Microsomes, Liver / metabolism
  • Neoplasm Metastasis
  • Neoplasm Transplantation
  • Positron-Emission Tomography
  • Pyridines / chemistry
  • Pyridines / pharmacokinetics*
  • Rats
  • Rats, Wistar
  • Receptors, CXCR4 / metabolism*

Substances

  • Benzylamines
  • CXCR4 protein, human
  • CXCR4 protein, mouse
  • Carbon Radioisotopes
  • Cyclams
  • Heterocyclic Compounds
  • Ions
  • Ligands
  • N-(1,4,8,11- tetraazacyclotetradecanyl-1,4-phenylenebis(methylene))-2-(aminomethyl)- pyridine
  • Pyridines
  • Receptors, CXCR4
  • plerixafor