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We shown that, in distinction to classical opioid receptors, ACKR3 isn't going to induce classical G protein signaling and isn't modulated from the classical prescription or analgesic opioids, which include morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists for example naloxone. In its place, we proven that LIH383, an ACKR3