We demonstrated that, in distinction to classical opioid receptors, ACKR3 would not set off classical G protein signaling and is not modulated by the classical prescription or analgesic opioids, including morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists which include naloxone. Rather, we founded that LIH383, an ACKR3-selective https://jeanm126jif7.sharebyblog.com/profile