We demonstrated that, in contrast to classical opioid receptors, ACKR3 doesn't cause classical G protein signaling and isn't modulated via the classical prescription or analgesic opioids, including morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists which include naloxone. Alternatively, we recognized that LIH383, an ACKR3-selective subnanomolar competitor pept... https://reginaj738oln1.blogdeazar.com/profile