[{"from": "human", "value": "Could you give me a brief overview of this molecule? [C][N][C][C][C@][C@@H1][C][=Branch1][C][=O][C][C][C@][Ring1][#Branch1][Branch2][Ring1][Branch2][C@H1][Ring1][O][C][C][=C][Ring1][O][C][=Branch1][#Branch2][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][O][C][O][Ring1][P][O]"}, {"from": "gpt", "value": "The molecule is only found in individuals that have used or taken this drug. It is a semisynthetic derivative of codeine that acts as a narcotic analgesic more potent and addicting than codeine. Oxycodone acts as a weak agonist at mu, kappa, and delta opioid receptors within the central nervous system (CNS). Oxycodone primarily affects mu-type opioid receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. Opioids such as oxycodone also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. Opioids close N-type voltage-operated calcium channels (kappa-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (mu and delta receptor agonist). This results in hyperpolarization and reduced neuronal excitability."}]