LAUSR

Extended-release naltrexone (XR-NTX) has several properties that make it an important addition to the pharmacopoeia for addictive disorders. It has no abuse potential, is administeredmonthly and, creating no physiological dependence, has nowithdrawal syndrome on discontinuation. As a result, XR-NTX has generated great interest for the treatment of alcohol and opioid use disorders in settings where agonist therapies have been less accepted, such as “abstinence-oriented” treatment programs, drug court and community reentry after incarceration. However, the empirical evidence supporting its many theoretical uses is in its infancy. This Special Issue called for original research reports, reviews and commentaries addressing the effectiveness, implementation and realworld use of XR-NTX in multiple settings. Naltrexone is a mu opioid receptor antagonist that extinguishes substance-using behavior by blocking the euphoric effect of opioids. Although the newly formed National Institute on Drug Abuse (NIDA) in the early 1970’s promoted oral naltrexone as a promising treatment for heroin addiction, a number of issues kept it from widespread use as pharmacotherapy for opioid use disorder (OUD). First, naltrexone precipitates withdrawal in the presence of opioids; hence, the standard recommendation is that OUDpatientsmaintain 5 to 10days of complete abstinence before initiation, a major challenge in the face of the agonizing, negative-reinforcing effects of the opioid withdrawal syndrome. Naltrexone has no agonist effect to reinforce medication-taking and nowithdrawal syndromewhen it is discontinued. Thus, daily adherence to oral naltrexone has been poor among persons with OUD. Programs designed to improve adherence to oral naltrexone through financial incentives or supervised administration increase adherence, though those interventions are labor-intensive and may be difficult to implement in real-world settings (Carroll et al., 2001; Carroll, Sinha, Nich, Babuscio, & Rounsaville, 2002; Dunn et al., 2013; Grabowski et al., 1979; Nunes, Rothenberg, Sullivan, Carpenter, & Kleber, 2006; Preston et al., 1999; Rawson, Glazer, Callahan, & Liberman, 1979; Rothenberg et al., 2002). Despite FDA-approval as a treatment for heroin addiction in 1984, poor adherence effectively blocked oral naltrexone’s acceptance as an OUD treatment for all but the most motivated patients (Adi et al., 2007; Minozzi et al., 2011). Early in its development, oral naltrexone was also found to attenuate the intoxicating and reinforcing effects of alcohol. Much research has subsequently found that oral naltrexone decreases craving, drinking days, rates of relapse, and increases abstinence among persons with alcohol use disorder (AUD) (Johnson, 2008; Pettinatiet al., 2010; Aboujaoude & Salame, 2016). Other studies, including a major trial among Veterans, found that oral naltrexone did not decrease drinking, with poor adherence again being the major limitation to its effectiveness (Johnson,