We demonstrated that, in distinction to classical opioid receptors, ACKR3 does not induce classical G protein signaling and isn't modulated via the classical prescription or analgesic opioids, which include morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists including naloxone. Instead, we established that LIH383, an ACKR3-selective subnanomolar competitor https://shirinu849phy6.yourkwikimage.com/user