Pharmacodynamic endpoints as clinical trial objectives to answer important questions in oncology drug development

Semin Oncol. 2016 Aug;43(4):514-25. doi: 10.1053/j.seminoncol.2016.07.002. Epub 2016 Jul 26.

Abstract

Analyzing the molecular interplay between malignancies and therapeutic agents is rarely a straightforward process, but we hope that this special issue of Seminars has highlighted the clinical value of such endeavors as well as the relevant theoretical and practical considerations. Here, we conclude with both an overview of the various high-value applications of clinical pharmacodynamics (PD) in developmental therapeutics and an outline of the framework for incorporating PD analyses into the design of clinical trials. Given the increasingly recognized importance of determining and administering the biologically effective dose (BED) and schedule of targeted agents, we explain how clinical PD biomarkers specific to the agent mechanism of action (MOA) can be used for the development of pharmacodynamics-guided biologically effective dosage regimens (PD-BEDR) to maximize the efficacy and minimize the toxicity of targeted therapies. In addition, we discuss how MOA-based PD biomarker analyses can be used both as patient selection diagnostic tools and for designing novel drug combinations targeting the specific mutational signature of a given malignancy. We also describe the role of PD analyses in clinical trials, including for MOA confirmation and dosage regimen optimization during phase 0 trials as well as for correlating molecular changes with clinical efficacy when establishing proof-of-concept in phase I/II trials. Finally, we outline the critical technological developments that are needed to enhance the quality and quantity of future clinical PD data collection, broaden the types of molecular questions that can be answered in the clinic, and, ultimately, improve patient outcomes.

Keywords: Cancer drug development; Pharmacodynamics; Proof-of-mechanism trials.

Publication types

  • Review
  • Research Support, N.I.H., Extramural

MeSH terms

  • Antineoplastic Agents / pharmacokinetics*
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Biomarkers, Pharmacological / metabolism*
  • Clinical Trials as Topic
  • Drug Administration Schedule
  • Drug Design
  • Drug Discovery / methods*
  • Humans
  • Molecular Targeted Therapy / methods*
  • Neoplasms / drug therapy*
  • Pancreatic Neoplasms / drug therapy
  • Pancreatic Neoplasms / metabolism
  • Poly (ADP-Ribose) Polymerase-1 / antagonists & inhibitors
  • Poly (ADP-Ribose) Polymerase-1 / metabolism
  • Poly(ADP-ribose) Polymerase Inhibitors / pharmacokinetics
  • Poly(ADP-ribose) Polymerase Inhibitors / pharmacology
  • Poly(ADP-ribose) Polymerases / metabolism
  • Proto-Oncogene Proteins c-met / antagonists & inhibitors
  • Proto-Oncogene Proteins c-met / metabolism

Substances

  • Antineoplastic Agents
  • Biomarkers, Pharmacological
  • Poly(ADP-ribose) Polymerase Inhibitors
  • PARP1 protein, human
  • PARP2 protein, human
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerases
  • Proto-Oncogene Proteins c-met