We demonstrated that, in distinction to classical opioid receptors, ACKR3 does not induce classical G protein signaling and is not modulated via the classical prescription or analgesic opioids, including morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists for example naloxone. Instead, we established that LIH383, an ACKR3-selective subnanomolar https://paula962znl9.bloggazzo.com/profile