Buprenorphine is used for opioid use disorder. Its 'ceiling effect' for respiratory depression (but not analgesia) is explained by its receptor profile:
- A Buprenorphine is a partial agonist at mu opioid receptors, so maximal receptor activation is limited regardless of dose; it also has kappa antagonist properties ✓
- B Buprenorphine is a full agonist at mu receptors with slow receptor dissociation preventing overdose
- C Buprenorphine is rapidly metabolised to norbuprenorphine which is an antagonist at mu receptors
- D Buprenorphine blocks delta opioid receptors, compensating for mu-mediated respiratory depression
Correct answer: A. Buprenorphine is a partial agonist at mu opioid receptors, so maximal receptor activation is limited regardless of dose; it also has kappa antagonist properties
Explanation
Buprenorphine is a high-affinity partial agonist at mu opioid receptors; as a partial agonist, it has intrinsic efficacy below 100%, so increasing the dose does not produce full receptor activation — this creates a ceiling effect for respiratory depression. It also acts as an antagonist at kappa receptors (reducing dysphoria) and as a partial agonist at ORL-1 (nociceptin) receptors. Its high receptor affinity and slow dissociation kinetics prevent full agonists from displacing it easily, making reversal with naloxone require higher doses.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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