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We demonstrated that, in contrast to classical opioid receptors, ACKR3 would not result in classical G protein signaling and is not modulated through the classical prescription or analgesic opioids, like morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists like naloxone. As an alternative, we proven that LIH383, an ACKR3-sele