We shown that, in distinction to classical opioid receptors, ACKR3 doesn't cause classical G protein signaling and isn't modulated by the classical prescription or analgesic opioids, which include morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists including naloxone. Alternatively, we founded that LIH383, an ACKR3-selective subnanomolar competitor peptide, https://actorq678hrd3.thekatyblog.com/profile