It is 25-50 times more potent than morphine; about 0.4 mg buprenorphine is equianalgesic with 10 mg morphine given intramuscularly .
Because buprenorphine is a partial μ-opioid receptors agonist, it may cause symptoms of abstinence in patients who have been receiving receptor agonists for several weeks.
Buprenorphine is relatively well absorbed by most route; it comes in many forms including SL tablets, ampules for SC, IM and IV injection, and transdermal patches.
Sublingual: moderate to severe pain 200-400 mcg 6-8 hrly.
IV: perioperative analgesia 300-450 mcg via slow inj.
IV/IM: moderate to severe pain 300-600 mcg 6-8 hrly.
Adverse drug reactions: cardiovascular and other side effects (e.g, sedation, nausea, vomiting dizziness, sweating and headache) appear to be similar to those of morphine-like opioids.
Buprenorphine is a synthetic opioid with analgesic and sedative activities. It binds to and activates the mu-opioid receptors in the central nervous system (CNS), thereby mimicking the effects of the endogenous opiates. Binding to opioid receptors stimulates exchange of GTP for GDP, inhibits adenylate cyclase, and decreases intracellular cAMP. This inhibits the release of various nociceptive neurotransmitters, such as substance P, gamma-aminobutyric acid (GABA), dopamine, acetylcholine, noradrenaline, vasopressin, and somatostatin. In addition, buprenorphine closes N-type voltage-gated calcium channels and opens calcium-dependent inwardly rectifying potassium channels, resulting in hyperpolarization, reduced neuronal excitability, analgesia and sedation.
Buprenorphine is a partial agonist at the mu-opioid receptor and an antagonist at the kappa-opioid receptor in the CNS.