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We demonstrated that, in contrast to classical opioid receptors, ACKR3 would not set off classical G protein signaling and isn't modulated by the classical prescription or analgesic opioids, including morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists like naloxone. As a substitute, we recognized that LIH383, an ACKR3-selec