Ketobemidone is a powerful opioid analgesic with some NMDA-antagonist properties. Ketobemidone is an agonist of mu, kappa, and delta opioid receptors. Mu-binding sites are discretely distributed in the brain, spinal cord, and other tissues. It exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Ketobemidone also depresses the respiratory centers, depresses the cough reflex, and constricts the pupils. Ketobemidone binds very strongly to mu opioid receptors and acts as a competitive agonist. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators 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 GABA is inhibited. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. Carfentanil acts at A delta and C pain fibres in the dorsal horn of the spinal cord. By decreasing neurotransmitter action there is less pain transmittance into the spinal cord. This leads to less pain perception.

Ketobemidone Opioid Agonist Pathway References