Fentanyl, sufentanil, morphine, hydromorphone, remifentanil, ketorolac, acetaminophen
Synthetic phenylpiperidine opioid agonist (μ)
μ-opioid receptor agonist. ~100× potency of morphine.
Ultra-short-acting μ-opioid agonist
μ-opioid agonist. Ester linkage hydrolyzed by nonspecific tissue + plasma esterases — no organ-dependent clearance.
Phenanthrene μ-opioid agonist (prototype opioid, potency reference = 1)
μ-opioid receptor agonist. Active metabolite morphine-6-glucuronide (M6G) is analgesic and renally cleared — accumulates in renal failure → prolonged sedation/respiratory depression. Causes histamine release.
Semisynthetic μ-opioid agonist (hydrogenated ketone of morphine)
μ-opioid agonist ~5–7× more potent than morphine. No clinically significant active metabolites → safer than morphine in renal failure. Less histamine release.
Synthetic phenylpiperidine μ-opioid agonist
Most potent opioid in common clinical use — ~1000× morphine, ~10× fentanyl. High lipid solubility.
Synthetic short-acting μ-opioid agonist
μ-opioid agonist ~1/5–1/10 the potency of fentanyl but FASTEST onset of the family — low pKa means a high non-ionized fraction at physiologic pH.
Synthetic phenylpiperidine μ-opioid agonist (with κ and anticholinergic activity)
μ-opioid agonist ~1/10 morphine, plus κ-agonism (anti-shivering). Active metabolite normeperidine is renally cleared, proconvulsant, and neurotoxic.
Synthetic μ-opioid agonist + NMDA antagonist + monoamine reuptake inhibitor
μ-opioid agonist with NMDA-receptor antagonism (blunts tolerance + opioid-induced hyperalgesia) and monoamine reuptake inhibition. Very long, variable half-life.
Mixed opioid — κ-agonist / μ-antagonist
κ-receptor agonist + μ-receptor antagonist. Ceiling on respiratory depression. Reverses μ-mediated pruritus/respiratory depression while preserving some analgesia.
Partial μ-agonist / κ-antagonist
High-affinity PARTIAL μ-agonist — binds tightly and is hard to displace with naloxone or other opioids. Ceiling on respiratory depression; blunts the effect of full agonists.
Semisynthetic oral μ-opioid agonist
μ-opioid agonist, ~1.5× the potency of oral morphine. Oral bioavailability far higher than morphine.
Semisynthetic oral μ-opioid agonist
μ-opioid agonist, roughly equipotent to oral morphine; partly a prodrug converted to hydromorphone via CYP2D6.
Weak μ-opioid agonist + serotonin/norepinephrine reuptake inhibitor
Weak μ-agonist plus SNRI. Active metabolite (M1, O-desmethyltramadol) via CYP2D6 is the stronger μ-agonist.
Non-selective NSAID (COX-1/COX-2 inhibitor)
Inhibits cyclooxygenase → ↓ prostaglandin synthesis → anti-inflammatory + analgesic + antipyretic.
Para-aminophenol analgesic / antipyretic
Central COX inhibition + endocannabinoid + descending serotonergic modulation. Minimal peripheral COX → no NSAID-like GI/renal/platelet effects.
Selective Nav1.8 sodium-channel blocker — non-opioid analgesic
Selectively inhibits the peripheral Nav1.8 voltage-gated sodium channel on pain-sensing neurons → blocks nociceptive signaling WITHOUT CNS/opioid activity (no euphoria, no dependence).
Gabapentinoid (α2δ voltage-gated calcium channel modulator)
Binds the α2δ subunit of presynaptic voltage-gated Ca²⁺ channels → ↓ excitatory neurotransmitter release. Anticonvulsant + neuropathic analgesic (despite the name, no GABA activity).
IV non-steroidal anti-inflammatory (non-selective COX inhibitor)
Reversibly inhibits COX-1/COX-2 → ↓ prostaglandins → analgesia, antipyresis, anti-inflammation. Opioid-sparing multimodal component.