We shown that, in distinction to classical opioid receptors, ACKR3 would not trigger classical G protein signaling and isn't modulated with the classical prescription or analgesic opioids, like morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists for example naloxone. Rather, we proven that LIH383, an ACKR3-selective subnanomolar competitor https://camillam580tqj1.wikibriefing.com/user