is an analogue of γ-aminobutyric acid (GABA), but there is no conclusive evidence that actions on GABA systems are involved in the production of its clinical effects.

blocks interneuronal activity in descending reticular formation and spinal cord, resulting in muscle relaxation

relieves skeletal muscle spasm of local origin without interfering with muscle function. It is ineffective in muscle spasm due to CNS disease

Evidence suggests that the net effect of ______ is a reduction in tonic motor activity, influencing both gamma (𝛾) and alpha (α) motor systems.

Inhibition of the COX-2 enzyme isoform is thought to be responsible for the anti-inflammatory effects of NSAIDs.

 is an agonist of α2-adrenergic receptors, which decreases spasticity by increasing presynaptic inhibition; however, it does not have antihypertensive properties.

is a centrally acting muscle relaxant. The drug is an imidazole derivative, structurally unrelated to other muscle relaxants.

The mechanism of action of _______ in humans has not been established but may be due to general CNS depression. It has no direct action on the contractile mechanism of striated muscle, the motor end plate, or the nerve fiber.

Nonselective inhibitor of cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2).

Nonselective inhibitor of cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2), and reversibly alters platelet function and prolongs bleeding time.

Nonselective inhibitor of COX-1 and COX-2 which results in decreased formation of prostaglandin precursors; has antipyretic, analgesic, and anti-inflammatory properties; reversibly alters platelet function and prolongs bleeding time.

 binds with high affinity to serotonin (5-HT) subtypes 1B, 1D, and 1F receptors. It has no significant affinity or pharmacologic activity at adrenergic α1, α2, or β; dopaminergic D1 or D2; muscarinic; or opioid receptors.

receptor agonists are believed to be effective in migraine either through vasoconstriction (via activation of 5-HT1 receptors located on intracranial blood vessels) or through activation of 5-HT1 receptors on sensory nerve endings in the trigeminal system resulting in the inhibition of proinflammatory neuropeptide release.

is 3-methylmorphine, a phenanthrene opioid with very low affinity for opioid receptors. Its analgesic activity appears to result from conversion to morphine.

is a phenylpiperidine opioid agonist with predominant effects on the mu opioid receptor and is about 50-100 times more potent as an analgesic than morphine

is an opioid analgesic and antitussive with unknown mechanism of action, but it is thought to be related to the presence of opiate receptors in the CNS.

Binds to opiate receptors in CNS, causing inhibition of ascending pain pathways, altering perception to pain, and produces generalized CNS depression

is a phenylethylamine opioid agonist qualitatively similar to morphine but with a chemical structure unrelated to the alkaloid-type structures of the opium derivatives.

Analgesic activity of (R)-______ is 8-50 times that of (S)-_____, and (R)-_______ has a tenfold higher affinity for opioid receptors.

is a μ-opioid receptor partial agonist and a κ-opioid receptor antagonist.

is a μ-opioid receptor antagonist that causes opioid withdrawal when injected parenterally and is included in the formulation to reduce the risk of abuse

is a mu agonist and a weak inhibitor of serotonin and norepinephrine reuptake. Mu receptors are responsible for analgesia, respiratory depression, miosis, decreased GI motility, and euphoria. In the CNS, it promotes analgesia and respiratory depression by decreasing brain stem respiratory centers' response to carbon dioxide tension and electrical stimulation.

is a pure mu agonist. Mu receptors are responsible for analgesia, respiratory depression, miosis, decreased GI motility, and euphoria. In the CNS, it promotes analgesia and respiratory depression by decreasing brain stem respiratory centers' response to carbon dioxide tension and electrical stimulation. It also decreases gastric, biliary, and pancreatic secretion, induces peripheral vasodilation, and promotes opioid-induced hypotension due to histamine release.