We demonstrated that, in distinction to classical opioid receptors, ACKR3 does not cause classical G protein signaling and is not modulated via the classical prescription or analgesic opioids, like morphine, fentanyl, or buprenorphine, or by nonselective opioid antagonists for instance naloxone. Alternatively, we recognized that LIH383, an ACKR3-selective subnanomolar https://camillam147mlh9.blog-eye.com/profile