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New strategies to maximize therapeutic opportunities for NAMPT inhibitors in oncology

Anne Roulston1, Gordon C Shore1

  • 1Laboratory for Therapeutic Development, Rosalind and Morris Goodman Cancer Research Centre, and Dept. Biochemistry, McGill University , Montreal, QC, Canada.

Molecular & Cellular Oncology
|June 17, 2016
PubMed

Insights

Nicotinamide phosphoribosyltransferase (NAMPT) inhibitors are promising anticancer agents targeting NAD(+) metabolism. New strategies and biomarkers offer opportunities to improve their clinical efficacy and therapeutic window.

Area of Science:

  • Biochemistry
  • Oncology
  • Pharmacology

Background:

  • Nicotinamide phosphoribosyltransferase (NAMPT) is essential for NAD(+) biosynthesis in mammalian cells.
  • NAMPT inhibitors are multifunctional anticancer agents targeting cellular NAD(+) metabolism.
  • Cancer cells exhibit increased metabolic demands for NAD(+), making them susceptible to NAMPT inhibition.

Purpose of the Study:

  • To review recent discoveries in NAD(+) and NAMPT inhibitor biology.
  • To explore strategies for optimizing the clinical outcomes of NAMPT inhibitors.
  • To discuss new opportunities for widening the therapeutic window of these agents.

Main Methods:

  • Review of recent scientific literature on NAMPT inhibitor biology and clinical studies.
  • Analysis of NAD(+) metabolism pathways and their role in cancer.
  • Examination of alternative rescue pathways and potential biomarkers for patient selection.

Main Results:

  • Initial clinical studies faced challenges with dose-limiting toxicities.
  • New understanding of alternative NAD(+) salvage pathways and biomarkers offers improved patient selection.
  • Drug combination strategies show potential for enhanced therapeutic effects.

Conclusions:

  • NAMPT inhibitors hold significant promise as anticancer agents.
  • Optimizing patient selection and employing combination therapies can improve clinical efficacy.
  • Further research into NAMPT inhibitor biology is crucial for maximizing their therapeutic potential.
Keywords:
DNA damageNAMPTNAPRT1PARPniacin

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