Naltrexone is an opioid receptor antagonist used primarily in the management of alcohol dependence and opioid dependence.
IC50 Value:
Target: Opioid Receptor
Naltrexone is competitive antagonist for μ, κ, δ, and σ-opioid receptors, Naltrexone has greater oral efficacy and longer duration of action than naloxone. Naltrexone treatment caused a doubling in the density of [3H]DAMGO binding sites in both whole brain membranes and the 7315c cell membranes. Naltrexone treatment may have slightly diminished the affinity of mu opioid receptors for [3H]DAMGO (by 1.5- to 2-fold), but the precision of the assay was inadequate to determine whether this difference was significant. Naltrexone treatment also had no effect on the potency or efficacy of guanosine 5'-O-(3-thiotriphosphate) in diminishing [3H]DAMGO binding to either whole brain or 7315c cell membranes.  Naltrexone which has no SP receptor antagonistic action, not only indirectly acts on SP-ergic neurons but also causes a change in the apparent affinity of NK-1 receptor (as reflected by changes in IC50 values) in the striatum. Cellular inositol-1,4,5-trisphosphate [Ins(1,4,5)P3], quantified by a highly sensitive and selective radioreceptor mass assay, was increased in the striatum by 28% relative to control levels.

ADL-5859  ADL5859 is a δ-opioid receptor agonist with Ki of 0.8 nM, selectivity against opioid receptor κ, μ, and weak inhibitory activity at the hERG channel.

IC50 value: 0.8 nM(Ki)
Target: δ-opioid receptor
ADL-5859 (ADL5859) is an δ-opioid receptor agonist (Ki=0.84 nM, EC50=20 nM). ADL-5859 (ADL5859)  is an agonist agent that selectively stimulates the δ-opioid receptor with potential application in a wide range of inflammatory, neuropathic and acute pain conditions. In addition, Delta agonists are thought to modulate other biological processes that may manifest themselves in disease states or conditions such as overactive bladder and depression.ADL-5859  (ADL5859)  is useful for inflammatory, neuropathic and acute pain conditions.