We demonstrated that, in contrast to classical opioid receptors, ACKR3 does not induce classical G protein signaling and is not modulated from the classical prescription or analgesic opioids, for instance morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists including naloxone. Rather, we set up that LIH383, an ACKR3-selective https://keiths728mdt4.thenerdsblog.com/profile