We demonstrated that, in distinction to classical opioid receptors, ACKR3 won't induce 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 for example naloxone. Alternatively, we proven that LIH383, an ACKR3-selective subnanomolar competitor https://mayah721phc5.activablog.com/profile