Phase I trial of a selective c-MET inhibitor ARQ 197 incorporating proof of mechanism pharmacodynamic studies

J Clin Oncol. 2011 Apr 1;29(10):1271-9. doi: 10.1200/JCO.2010.31.0367. Epub 2011 Mar 7.

Abstract

Purpose: The hepatocyte growth factor/c-MET axis is implicated in tumor cell proliferation, survival, and angiogenesis. ARQ 197 is an oral, selective, non-adenosine triphosphate competitive c-MET inhibitor. A phase I trial of ARQ 197 was conducted to assess safety, tolerability, and target inhibition, including intratumoral c-MET signaling, apoptosis, and angiogenesis.

Patients and methods: Patients with solid tumors amenable to pharmacokinetic and pharmacodynamic studies using serial biopsies, dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), and circulating endothelial cell (CEC) and circulating tumor cell (CTC) enumeration were enrolled.

Results: Fifty-one patients received ARQ 197 at 100 to 400 mg twice per day. ARQ 197 was well tolerated, with the most common toxicities being grade 1 to 2 fatigue, nausea, and vomiting. Dose-limiting toxicities included grade 3 fatigue (200 mg twice per day; n = 1); grade 3 mucositis, palmar-plantar erythrodysesthesia, and hypokalemia (400 mg twice per day; n = 1); and grade 3 to 4 febrile neutropenia (400 mg twice per day, n = 2; 360 mg twice per day, n = 1). The recommended phase II dose was 360 mg twice per day. ARQ 197 systemic exposure was dose dependent and supported twice per day oral dosing. ARQ 197 decreased phosphorylated c-MET, total c-MET, and phosphorylated focal adhesion kinase and increased terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling (TUNEL) staining in tumor biopsies (n = 15). CECs decreased in 25 (58.1%) of 43 patients, but no significant changes in DCE-MRI parameters were observed after ARQ 197 treatment. Of 15 patients with detectable CTCs, eight (53.3%) had ≥ 30% decline in CTCs after treatment. Stable disease, as defined by Response Evaluation Criteria in Solid Tumors (RECIST), ≥ 4 months was observed in 14 patients, with minor regressions in gastric and Merkel cell cancers.

Conclusion: ARQ 197 safely inhibited intratumoral c-MET signaling. Further clinical evaluation focusing on combination approaches, including an erlotinib combination in non-small-cell lung cancer, is ongoing.

Trial registration: ClinicalTrials.gov NCT00612209.

Publication types

  • Clinical Trial, Phase I
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Angiogenesis Inhibitors / adverse effects
  • Angiogenesis Inhibitors / pharmacokinetics
  • Angiogenesis Inhibitors / therapeutic use*
  • Apoptosis / drug effects
  • Aryl Hydrocarbon Hydroxylases / genetics
  • Aryl Hydrocarbon Hydroxylases / metabolism
  • Biopsy
  • Cytochrome P-450 CYP2C19
  • Endothelial Cells / drug effects
  • Endothelial Cells / pathology
  • England
  • Female
  • Focal Adhesion Kinase 1 / metabolism
  • Humans
  • In Situ Nick-End Labeling
  • Magnetic Resonance Imaging
  • Male
  • Maximum Tolerated Dose
  • Middle Aged
  • Neoplasms / blood supply
  • Neoplasms / drug therapy*
  • Neoplasms / enzymology
  • Neoplasms / pathology
  • Neoplastic Cells, Circulating / drug effects
  • Neoplastic Cells, Circulating / pathology
  • Neovascularization, Pathologic / prevention & control
  • Phosphorylation
  • Polymorphism, Single Nucleotide
  • Protein Kinase Inhibitors / adverse effects
  • Protein Kinase Inhibitors / pharmacokinetics
  • Protein Kinase Inhibitors / therapeutic use*
  • Proto-Oncogene Proteins c-met / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-met / metabolism
  • Pyrrolidinones / adverse effects
  • Pyrrolidinones / pharmacokinetics
  • Pyrrolidinones / therapeutic use*
  • Quinolines / adverse effects
  • Quinolines / pharmacokinetics
  • Quinolines / therapeutic use*
  • Receptors, Growth Factor / antagonists & inhibitors*
  • Receptors, Growth Factor / metabolism
  • Signal Transduction / drug effects*
  • Treatment Outcome
  • Young Adult

Substances

  • ARQ 197
  • Angiogenesis Inhibitors
  • Protein Kinase Inhibitors
  • Pyrrolidinones
  • Quinolines
  • Receptors, Growth Factor
  • Aryl Hydrocarbon Hydroxylases
  • CYP2C19 protein, human
  • Cytochrome P-450 CYP2C19
  • MET protein, human
  • Proto-Oncogene Proteins c-met
  • Focal Adhesion Kinase 1
  • PTK2 protein, human

Associated data

  • ClinicalTrials.gov/NCT00612209