We demonstrated that, in distinction to classical opioid receptors, ACKR3 would not trigger classical G protein signaling and is not modulated by the classical prescription or analgesic opioids, such as morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists such as naloxone. Alternatively, we recognized that LIH383, an ACKR3-selective https://sandray371djn1.eqnextwiki.com/user