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Disclaimer:  This information is not meant as direct medical advice. Readers should always review options with their local medical team. This is the sole opinion of Dr. Meakin based on literature review at the time of the blog and may change as new evidence evolves.

Low Dose Naltrexone and Cancer

Questions from the Clinic:

What is naltrexone? Does low-dose naltrexone have anti-cancer properties? If so, in which cancers is it most effective? How does it compare with existing standards of care?

Figure 1: Naltrexone (C20H23NO4) has many purported uses beyond the treatment of alcohol and opioid use disorders at low doses, but its value in cancer is currently contested.

I. Introduction

Naltrexone is a semi-synthetic opioid antagonist approved by the U.S. Food and Drug Administration (FDA) in 1984 for the treatment of patients with alcoholism or opioid use disorders. Since receiving initial regulatory approval, naltrexone has gained traction in off-label settings at doses ten times less than those administered in patients with substance abuse disorders.(1) Clinical evidence, ranging from case reports to randomized controlled trials, indicates that low-dose naltrexone (LDN) has therapeutic value in Crohn’s disease, fibromyalgia, and other disease states featuring chronic inflammation or immune dysregulation.(2,3) That said, considerable controversy still surrounds the quality of evidence supporting the use of LDN among patients with cancer.(4) Clarifying the utility of LDN in cancer is paramount, as a well-tolerated, affordable, and relatively easy to administer drug would be a welcome addition to evolving oncology treatment arsenal. Many chemotherapies, while effective, have severe treatment-related adverse events that can prompt treatment discontinuation; others can lose efficacy over time and leave patients seeking viable alternatives.(5,6)

II. Mechanism of Action

Naltrexone’s properties appear dependent upon the concentration present inside the body.(4) At the standard dose of 50 mg, naltrexone functions as expected as a competitive antagonist of µ-opioid receptors expressed by cells in the central nervous system. Certain substances, like alcohol, promote the endogenous relea