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Medicines (732)
Medicines
> mechanism:
Potent 5-HT2A agonist
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None
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5-HT2A agonist
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GABAA positive allosteric modulator
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Monoamine releasing agent
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CB1/CB2 agonist
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Potent mu-opioid receptor agonist
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Sodium channel blocker
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Dopamine/norepinephrine reuptake inhibitor
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GABAA potentiator; NMDA antagonist
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Phenothiazine D2 antagonist
· Potent 5-HT2A agonist ·
5-HT1B/1D agonist
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LSD analogue; 5-HT2A agonist
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Mu-opioid receptor agonist
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Muscarinic receptor antagonist
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Prodrug of LSD; 5-HT2A agonist
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Selective norepinephrine reuptake inhibitor
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GABAA positive allosteric modulator (non-benzodiazepine)
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GABAA potentiator and direct activator
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Irreversible non-selective MAO inhibitor
Other values:
1-acetyl-LSD; prodrug of LSD
5-HT1A agonist, 5-HT2A antagonist, with weaker activity at D4 and other receptors. Net effect involves enhanced prefrontal dopaminergic/noradrenergic tone with decreased serotonergic inhibition of sexual desire.
5-HT1B/1D agonist; alpha-adrenergic agonist
5-HT1B/1D agonist; long half-life
5-HT1F receptor agonist
5-HT2A agonist; 5-HT3 antagonist
5-HT2A agonist; D2 partial agonist
5-HT2A agonist; MAO inhibitor
5-HT2A agonist; long duration
5-HT2A agonist; milder than other 2C-x
5-HT2A agonist; minor psilocybin mushroom alkaloid
5-HT2A agonist; primarily auditory effects
5-HT2A agonist; sigma-1 agonist
5-HT2A partial agonist
5-HT2A partial agonist; sigma-1 agonist
5-HT2C agonist; 5-HT2A antagonist; serotonin releasing agent
5-MeO-DMT is a potent 5-HT1A agonist (greater than 5-HT2A). Distinct from N,N-DMT in producing a more unitive, less visual, often ego-dissolving experience.
5HT1a
ACTH analogue; BDNF upregulator
AMPA modulator; catecholaminergic
AMPA receptor antagonist
AMPA receptor modulator
AMPA receptor positive allosteric modulator
AMPA/NMDA modulator; NGF/BDNF upregulation
Acetylcholinesterase and butyrylcholinesterase inhibitor
Acetylcholinesterase inhibitor; nicotinic ACh receptor modulator
Active alkaloid is cytisine, a nicotinic acetylcholine receptor agonist. NOT a classical 5-HT2A psychedelic.
Active metabolite of DXM; NMDA antagonist
Active metabolite of tramadol; mu-opioid agonist
Active oils are myristicin, elemicin, and safrole, phenethylamine precursors that may be aminated in vivo to MMDA, TMA, and MDA respectively (Shulgin's 'essential amphetamines' hypothesis).
Active principle is thujone, a GABA-A antagonist (the opposite of most CNS depressants). Also present in cooking sage (''Salvia officinalis''), tansy, and ''Thuja'' cedars.
Adenosine receptor antagonist
Adenosine receptor antagonist; dopaminergic
Adenosine receptor antagonist; phosphodiesterase inhibitor
Agonist at the metabotropic GABAB receptor and the endogenous γ-hydroxybutyrate (GHB) receptor. Produces deep sleep with increased slow-wave architecture, suppression of REM intrusion, and cataplexy reduction.
Agonist of the [[GLP-1 receptor]]; exendin-4 derivative from Gila monster venom.
Aldehyde dehydrogenase inhibitor
Alpha-2 adrenergic receptor agonist
Alpha-adrenergic agonist; monoamine releaser
Alpha-methylated amphetamine analogue; norepinephrine releasing agent
Anticholinergic; NMDA antagonist
Apomorphine and nuciferine; dopaminergic activity
Biphasic activity at CB1: neutral antagonist at low doses, partial agonist at high doses; partial agonist at CB2.
Buprenorphine: high-affinity partial agonist at the μ-opioid receptor with ceiling effect on respiratory depression. Naloxone: abuse-deterrent, inactive SL but precipitates withdrawal if injected.
Butyrophenone D2 antagonist
CB1 partial agonist
CB1 partial agonist (lower potency than delta-9)
CB1/CB2 agonist (higher potency than THC)
CB1/CB2 partial agonist
CGRP receptor antagonist
CNS mechanism incompletely understood
Caffeine (1.5–2%) + theobromine + kolanin (a glycoside).
Caffeine (highest of the ''Ilex'' genus) plus saponins that produce ritual vomiting at high doses.
Caffeine (sometimes called 'mateine' historically, though chemically identical), theobromine, theophylline, plus polyphenols.
Caffeine + theophylline + L-theanine. L-theanine (an amino acid unique to tea) modulates glutamate and produces an 'alpha-wave' calming overlay on caffeine's stimulation, hence tea's reputation as a 'cleaner' stimulant than coffee.
Caffeine is a non-selective adenosine A1/A2A receptor antagonist; also weak PDE inhibition. Beans contain theobromine (3,7-DMX) and theophylline (1,3-DMX) in smaller amounts.
Cardioselective β1-adrenergic antagonist. Selectivity is dose-dependent and partially lost at higher doses.
Cathinone analogue; monoamine reuptake inhibitor
Central and peripheral COMT inhibitor
Cleaves SNAP-25 protein in presynaptic motor and autonomic nerve terminals, blocking acetylcholine release; in chronic migraine, hypothesized to inhibit peripheral sensitization of trigeminovascular nociceptors
Competitive antagonist at OX1R and OX2R. Faster receptor association/dissociation kinetics than suvorexant (~16 sec dissociation vs ~57 sec) hypothesized to support sleep onset, with sufficient duration for maintenance.
Competitive antagonist at OX1R and OX2R. First-in-class DORA. Receptor dissociation slower than lemborexant or daridorexant.
Competitive mu/kappa/delta opioid receptor antagonist
Contains LSA
Contains atropine, scopolamine, hyoscyamine
Contains bufotenin and DMT
Contains harmine, harmaline, tetrahydroharmine
Contains ibogaine; kappa-opioid agonist
Contains mescaline
Contains muscimol and ibotenic acid
Contains psilocybin and psilocin
Contains salvinorin A
Contains the β-carboline alkaloids harmine, harmaline, and tetrahydroharmine, reversible monoamine oxidase inhibitors (RIMAs) that allow oral DMT to reach the brain.
Contains varying amounts of DMT, 5-MeO-DMT, bufotenine, and gramine depending on strain and growing conditions.
D1/D2/D3 receptor agonist
D2 agonist; D1 partial agonist
D2 receptor agonist
D2 receptor antagonist; also H1, alpha-1, muscarinic antagonist
D2/5-HT2A antagonist
D2/5-HT2A antagonist; 5-HT7 antagonist
D2/5-HT2A antagonist; SRI and NRI
D2/5-HT2A antagonist; active metabolite of risperidone
DMT + MAOI (harmine/harmaline); 5-HT2A agonist
DMT-containing plant used in psychedelic preparations
Dibenzoxazepine D2/5-HT2 antagonist
Dihydroindolone D2 antagonist
Diphenhydramine salt; H1 antagonist
Diphenylbutylpiperidine D2 antagonist
Donepezil: reversible AChE inhibitor, increases synaptic acetylcholine. Memantine: uncompetitive low-affinity NMDA receptor antagonist, dampens pathological glutamate overactivation while preserving normal synaptic signaling. Targets two distinct mechanisms in Alzheimer's.
Dopamine D2 and serotonin 5-HT2A receptor antagonist'"`UNIQ--ref-0000008D-QINU`"' '"`UNIQ--vote-0000008E-QINU`"'
Dopamine and norepinephrine reuptake inhibitor
Dopamine and serotonin reuptake inhibitor; actoprotector
Dopamine precursor
Dopamine precursor + DOPA decarboxylase inhibitor
Dopamine reuptake inhibitor; mechanism incompletely understood
Dopamine reuptake inhibitor; tropane analogue
Dual agonist of the [[GIP receptor]] and [[GLP-1 receptor]] ("twincretin").
Endogenous androgen binding to androgen receptors; mediates male secondary sex characteristics, anabolism, libido, erythropoiesis, and CNS effects on mood/energy/aggression. Aromatized peripherally to estradiol; reduced to DHT.
Extremely potent 5-HT2A agonist; vasoconstrictor
Extremely potent 5-HT2A agonist; very long duration
Extremely potent GABAA positive allosteric modulator
Extremely potent mu-opioid receptor agonist
Fluorinated phenibut; GABAB agonist
Full CB1/CB2 agonist
GABA enhancer; sodium channel blocker; histone deacetylase inhibitor
GABA reuptake inhibitor (GAT-1 blocker)
GABA-A positive allosteric modulator'"`UNIQ--ref-00000067-QINU`"' '"`UNIQ--vote-00000068-QINU`"'
GABAA agonist
GABAA modulator; glycine receptor agonist
GABAA modulator; meprobamate prodrug
GABAA positive allosteric modulator; lactate dehydrogenase inhibitor
GABAA positive allosteric modulator; low sedation
GABAA positive allosteric modulator; prodrug of desmethyldiazepam
GABAA positive allosteric modulator; very long half-life
GABAA potentiator
GABAA potentiator; glycine receptor agonist
GABAA potentiator; possible glycine/NMDA modulation
GABAA potentiator; ultra-short-acting
GABAB agonist; GHB receptor agonist
GABAB agonist; alpha-2-delta calcium channel ligand
Glutamate receptor agonist
Glutamate receptor antagonist; GABA modulator
H1 antagonist; muscarinic antagonist
H1 receptor antagonist
High-affinity D2 receptor antagonist
High-affinity choline uptake enhancer
Highest natural caffeine content of any plant (2–7% by dry weight, ~2–4× coffee). Caffeine is bound to tannins, producing a slower release than pure coffee caffeine.
Highly potent mu-opioid receptor agonist
Highly β1-selective adrenergic antagonist. Greater selectivity than metoprolol or atenolol.
Human IgG1 monoclonal antibody targeting aggregated forms of amyloid-β (Aβ), soluble oligomers and insoluble fibrils. Reduces Aβ plaque burden on PET imaging via Fc-mediated microglial clearance. Whether plaque reduction translates to clinical benefit is the core controversy.
Humanized IgG1 monoclonal antibody binding CGRP peptide; IV infusion enables fastest onset of any CGRP mAb
Humanized IgG2 monoclonal antibody binding both isoforms of CGRP peptide
Humanized IgG2 monoclonal antibody binding the CGRP receptor (not the peptide); blocks CGRP-mediated vasodilation and nociceptive signaling
Humanized IgG4 monoclonal antibody binding CGRP peptide; prevents CGRP from activating its receptor
Indirect sympathomimetic; norepinephrine releaser
Irreversible GABA-T inhibitor
Irreversible selective MAO-B inhibitor
Kappa agonist; mu antagonist
Kappa agonist; mu partial agonist
Kappa agonist; mu partial agonist/antagonist
Kappa-opioid agonist; NMDA antagonist; SERT/DAT/NET inhibitor
Kappa-opioid receptor agonist
Kavalactones; GABAA modulator; sigma receptor activity
Local anti-inflammatory; TRPA1 antagonist at therapeutic doses
Long-acting agonist of the [[GLP-1 receptor]].
Long-acting agonist of the [[GLP-1 receptor]]; Fc-fusion construct.
Lysergic acid 2,4-dimethylazetidide; 5-HT2A agonist
Lysergic acid hydroxyethylamide; 5-HT2A agonist
MAO inhibitor; monoamine releasing agent
MAO inhibitor; serotonin releasing agent
MAO-B inhibitor; sodium channel blocker; glutamate release inhibitor
Mechanism incompletely understood
Melatonin receptor agonist
Melatonin receptor agonist; 5-HT2C antagonist
Methaqualone analogue; GABAA potentiator
Mitragynine/7-hydroxymitragynine; mu-opioid partial agonist
Monoamine releasing agent, TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport
Monoamine releasing agent; 5-HT2A agonist
Monoamine releasing agent; 5-HT2A agonist; MAO inhibitor
Monoamine releasing agent; active ingredient in khat
Monoamine releasing agent; serotonergic at higher doses
Monoamine reuptake inhibitor; sodium channel blocker
Mu-opioid agonist; modulates glutamate AMPA receptors
Mu-opioid agonist; norepinephrine reuptake inhibitor
Mu-opioid receptor agonist; NMDA antagonist
Mu-opioid receptor agonist; fentanyl analogue
Mu-opioid receptor agonist; prodrug (metabolized to morphine)
Mu-opioid receptor agonist; sodium channel blocker
Mu/delta antagonist; kappa partial agonist
Mu/kappa/delta agonist; NMDA antagonist
Multi-receptor antagonist (D2, 5-HT2A, H1, alpha)
Multi-receptor antagonist; low D2 affinity
Multiple mechanisms; GPR55 antagonist; TRPV1 agonist
Muscarinic receptor antagonist; dopamine reuptake inhibitor
N-methyl analogue of 2-AI
NMDA antagonist
NMDA antagonist; GABAA modulator
NMDA antagonist; GABAA potentiator
NMDA antagonist; SERT inhibitor; sigma-1 agonist
NMDA antagonist; dopamine releasing agent
NMDA antagonist; endogenous opioid releaser
NMDA antagonist; fluorinated ketamine analogue
NMDA antagonist; kappa-opioid agonist
NMDA antagonist; ketamine analogue
NMDA antagonist; more stimulating than PCP
NMDA antagonist; opioid agonist
NMDA antagonist; potent opioid agonist
NMDA antagonist; sigma receptor agonist
NMDA antagonist; sigma receptor agonist; dopaminergic
NMDA antagonist; sigma-1 agonist; serotonin reuptake inhibitor
NMDA-receptor antagonism
Nicotinic acetylcholine receptor agonist
Non-selective competitive antagonist at β1 and β2 adrenergic receptors. Lipophilic; significant blood–brain barrier penetration, accounting for its CNS effects.
Non-selective dopamine receptor agonist
Norepinephrine and dopamine releasing agent
Norepinephrine releaser
Norepinephrine/dopamine releasing agent
Norepinephrine/dopamine reuptake inhibitor
Norepinephrine–dopamine reuptake inhibition (DAT, NET)
Norepinephrine–dopamine reuptake inhibition (DAT, NET), d-threo enantiomer of methylphenidate
Norepinephrine–dopamine reuptake inhibitor
Once-daily COMT inhibitor
Once-daily agonist of the [[GLP-1 receptor]].
Opioid receptor partial agonist/antagonist; toxic alkaloid
Partial CB1/CB2 agonist
Partial MAOI; anticholinergic effects
Partial agonist at D2 and 5HT1A. Antagonist at 5HT2A, α1A, α1B, α2C. More potent 5HT2A antagonism, 5HT1A partial agonism, and α1 antagonism (relative to D2 partial agonism) than aripiprazole, proposed to reduce akathisia and enhance affective/cognitive effects.
Partial mu-opioid agonist; kappa antagonist
Partial mu-opioid receptor agonist; alpha-2 agonist
Partial nicotinic ACh receptor agonist
Peripheral COMT inhibitor
Phosphodiesterase inhibitor; calcium channel blocker
Positive allosteric modulator of the GABA<sub>A</sub> receptor at the benzodiazepine binding site; increases frequency of Cl<sup>−</sup> channel opening, producing anxiolytic, sedative, hypnotic, anticonvulsant, and skeletal-muscle relaxant effects.
Potent 5-HT2A agonist; no oral activity
Potent 5-HT2A agonist; sigma-1 agonist
Potent 5-HT2A agonist; very long duration
Potent dopamine and norepinephrine reuptake inhibitor
Potent dopamine/norepinephrine reuptake inhibitor
Potent serotonin reuptake inhibitor; also NRI
Primary alkaloid is (S)-(-)-cathinone, a phenylpropanolamine close kin to amphetamine. Releases dopamine and norepinephrine. Also contains cathine (=norpseudoephedrine) and norephedrine.
Primary alkaloid is arecoline, a muscarinic agonist (M1, M2, M3, M4) and partial agonist at nicotinic receptors. Produces alertness, salivation, sweating, mild euphoria.
Primary alkaloid is cocaine, a tropane that blocks reuptake of dopamine and norepinephrine (and serotonin). At low oral doses from leaf chewing, the slow release favors NE-mediated alertness over DA-mediated euphoria.
Primary alkaloid is theobromine (3,7-dimethylxanthine), with minor caffeine. Also contains phenethylamine, anandamide (an endogenous cannabinoid), tryptophan (serotonin precursor), and flavanols. The combined effect is mild stimulation + mood elevation.
Prodrug of 4-HO-DET; 5-HT2A agonist
Prodrug of 4-HO-DiPT; 5-HT2A agonist
Prodrug of 4-HO-MET; 5-HT2A agonist
Prodrug of 4-HO-MiPT; 5-HT2A agonist
Prodrug of GHB
Prodrug of amphetamine + theophylline
Prodrug of modafinil
Prodrug of morphine; mu-opioid receptor agonist
Prodrug of phenytoin; sodium channel blocker
Prodrug of psilocin; 5-HT2A agonist
Prodrug to [[Psilocin|psilocin]] (4-hydroxy-N,N-dimethyltryptamine), a partial agonist at the [[Receptor:5-HT2A|5-HT2A]] serotonin receptor; the action that defines the classical-psychedelic mechanism
Prodrug; converted to [[Morphine|morphine]] by [[Enzyme:CYP2D6|CYP2D6]] for analgesic action.
R-enantiomer of modafinil; mechanism incompletely understood
Reversible MAO-A inhibitor; NMDA antagonist; beta-carboline
Reversible MAO-A inhibitor; beta-carboline
Reversible inhibitor of MAO-A
Root bark contains ~1% N,N-dimethyltryptamine (DMT) and related tryptamines. Oral activity requires MAOI co-administration.
SV2A ligand (higher affinity than levetiracetam)
Selective GABAA agonist (extrasynaptic delta subunit)
Selective M1 muscarinic antagonist
Selective NET inhibitor (no significant DAT activity, distinguishes from amphetamine/methylphenidate). Also: 5HT1A receptor partial agonism, 5HT2B and 5HT7 receptor antagonism. The serotonergic actions may underlie better tolerability and possibly different efficacy spectrum than atomoxetine.
Selective alpha-1 adrenergic receptor antagonist. Lowers peripheral vascular resistance via vasodilation; in the CNS, blunts noradrenergic hyperarousal thought to drive trauma-related nightmares.
Selective alpha-2A adrenergic receptor agonist
Selective dopamine and norepinephrine reuptake inhibitor (DAT and NET inhibition). Unlike amphetamine, does not significantly release monoamines, pure reuptake inhibition.
Selective inhibitor of PDE5 with a substantially longer half-life than other PDE5 inhibitors, allowing once-daily continuous dosing.
Selective inhibitor of PDE5. Slightly higher PDE5/PDE6 selectivity vs sildenafil (less visual side effect) but more PDE1 cross-activity (occasional QT effects at high doses).
Selective inhibitor of phosphodiesterase type 5 (PDE5), preventing cGMP breakdown in vascular smooth muscle. In the corpus cavernosum, potentiates the NO/cGMP cascade triggered by sexual stimulation.
Selective inhibitor of phosphodiesterase type 5 (PDE5); increases cGMP in cavernous smooth muscle, producing erection in response to sexual stimulation.
Selective inverse agonist at 5HT2A receptors with weaker activity at 5HT2C. Has no significant dopamine D2 affinity, unique among approved antipsychotics. Inverse agonism (rather than antagonism) reduces constitutive 5HT2A receptor activity below baseline.
Selective mu-opioid receptor agonist
Semi-synthetic; CB1 agonist
Serotonin and norepinephrine reuptake inhibitor
Serotonin precursor; 5-hydroxytryptophan
Serotonin releaser; sigma-1 agonist
Serotonin releasing agent
Serotonin releasing agent; 5-HT2A agonist
Serotonin releasing agent; monoamine reuptake inhibitor
Serotonin reuptake inhibitor and 5-HT2A antagonist
Serotonin/dopamine/norepinephrine releasing agent; 5-HT2A agonist
Serotonin/norepinephrine/dopamine releasing agent
Serotonin–norepinephrine reuptake inhibition (balanced)
Serotonin–norepinephrine reuptake inhibitor
Slow-inactivation sodium channel enhancer; CRMP-2 ligand
Small-molecule CGRP receptor antagonist; intranasal formulation
Sodium channel blocker; GABAA positive allosteric modulator
Sodium channel modulator
Sodium/T-type calcium channel blocker; carbonic anhydrase inhibitor
Source of DMT-class tryptamines
Source of [[DMT]], bufotenine, and 5-MeO-DMT
Source of [[DMT|N,N-dimethyltryptamine]]
Synthetic T4 (thyroxine); peripherally deiodinated to T3 (triiodothyronine), the active hormone. '"`UNIQ--vote-00000031-QINU`"' Narrow therapeutic index; brand-to-generic switches can shift TSH and require re-titration'"`UNIQ--ref-00000032-QINU`"'.
Synthetic THC; CB1/CB2 agonist
Synthetic cannabinoid; CB1/CB2 agonist
Synthetic neuroactive steroid (an analog of allopregnanolone), bioavailable orally unlike brexanolone. Positive allosteric modulator at GABA-A receptors including extrasynaptic δ-containing subtypes.
T-type calcium channel blocker
TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport, net release of dopamine and norepinephrine
TBD
THC + CBD; CB1/CB2 agonist
The d-enantiomer is a highly β1-selective antagonist; the l-enantiomer triggers endothelial nitric-oxide–mediated vasodilation. Unique among beta blockers for this NO mechanism.
Thioxanthene D2 antagonist
Trace amine-associated receptor 1 (TAAR1) agonist; monoamine releaser
TrkB/BDNF'"`UNIQ--ref-00000040-QINU`"' '"`UNIQ--vote-00000041-QINU`"'
TrkB/BDNF'"`UNIQ--ref-00000084-QINU`"' '"`UNIQ--vote-00000085-QINU`"'
Tropane alkaloids: hyoscyamine (dominant; the racemic form is atropine), scopolamine. Competitive muscarinic antagonism.
Tropane alkaloids: hyoscyamine, scopolamine, atropine, apoatropine.
Tropane alkaloids: hyoscyamine, scopolamine, in higher seed concentrations than belladonna or datura.
Tropane alkaloids: scopolamine (dominant), hyoscyamine, atropine. Competitive antagonism at muscarinic acetylcholine receptors.
Ultra-short-acting mu-opioid agonist
Very potent 5-HT2A agonist; long duration
Weak CB1 partial agonist; weak CB2 partial agonist; multiple secondary targets.
Weak SRI; primarily H1/D2/alpha antagonist
Weak partial agonist at CB1 and CB2; alpha-2 adrenergic agonist; 5-HT1A antagonist; multiple TRP channel effects.
Weak serotonin reuptake inhibitor; beta-carboline
'"`UNIQ--vote-00000013-QINU`"' Anticholinergic burden (dry mouth, blurred vision, urinary retention, cognitive effects) is the principal adverse-event concern and the basis for Beers-list cautions in elderly patients'"`UNIQ--ref-00000014-QINU`"'.
'"`UNIQ--vote-00000013-QINU`"' Does not stimulate insulin secretion; minimal hypoglycemia risk as monotherapy. Cleared renally unchanged; dose-adjust by eGFR'"`UNIQ--ref-00000014-QINU`"'. Rare lactic acidosis primarily in renal failure or acute illness.
'"`UNIQ--vote-00000013-QINU`"' Once converted, dextroamphetamine acts by displacing dopamine and norepinephrine from presynaptic vesicles via VMAT-2 and reversing DAT and NET transport, the shared mechanism of all amphetamine-class agents'"`UNIQ--ref-00000014-QINU`"'.
'"`UNIQ--vote-00000013-QINU`"' Strong CYP3A4 induction via the phenobarbital metabolite produces many interactions (reduces oral contraceptives, warfarin, many psychotropics). Essential-tremor efficacy is the unique pharmacological selling point'"`UNIQ--ref-00000014-QINU`"'.
'"`UNIQ--vote-00000015-QINU`"' CYP2D6 metabolism produces stereoselective clearance; CYP2D6 poor metabolizers have higher plasma exposure and may need lower doses'"`UNIQ--ref-00000016-QINU`"'.
'"`UNIQ--vote-00000015-QINU`"' Pediatric ingestion (capsule chewed or punctured) releases the free local anesthetic and causes seizures, cardiac arrhythmia, and death'"`UNIQ--ref-00000016-QINU`"'.
'"`UNIQ--vote-00000015-QINU`"' The favorable pregnancy safety profile and the dual mechanism support its first-line role in pregnancy-associated hypertension and in hypertensive emergencies where rapid, controllable BP reduction is needed'"`UNIQ--ref-00000016-QINU`"'.
'"`UNIQ--vote-00000016-QINU`"' Bicarbonate is not benign: high-volume use produces hypernatremia, metabolic alkalosis, hypokalemia, and (in arrest) paradoxical intracellular acidosis'"`UNIQ--ref-00000017-QINU`"'.
'"`UNIQ--vote-00000017-QINU`"' '''Priapism''' is a recognized rare adverse effect via α1 antagonism in penile vasculature and is the marquee counseling point for male patients'"`UNIQ--ref-00000018-QINU`"'.
'"`UNIQ--vote-00000017-QINU`"' Anticholinergic and sedating, with the standard first-generation antihistamine Beers-list concerns in elderly patients'"`UNIQ--ref-00000018-QINU`"'.
'"`UNIQ--vote-00000019-QINU`"' Once-daily dosing is a clinical advantage over short-half-life NSAIDs'"`UNIQ--ref-0000001A-QINU`"'.
'"`UNIQ--vote-00000019-QINU`"' Sedation and hypotension are the dose-limiting effects; gradual titration and bedtime or split dosing mitigate both. Abrupt discontinuation can precipitate rebound hypertension, particularly with long-standing use'"`UNIQ--ref-0000001A-QINU`"'.
'"`UNIQ--vote-00000019-QINU`"' Therapeutic plasma-level monitoring is standard practice for TCAs given the narrow therapeutic index and the established plasma-level-efficacy correlation. CYP2D6 substrate; CPIC PGx guidance applies for dose individualization'"`UNIQ--ref-0000001A-QINU`"'.
'"`UNIQ--vote-0000001D-QINU`"' '''QT prolongation''' risk at high doses prompted the FDA's 2015 caution against use in patients with prolonged QT or with concurrent QT-prolonging medicines'"`UNIQ--ref-0000001E-QINU`"'.
'"`UNIQ--vote-0000001D-QINU`"' CYP2C19 + CYP3A4 metabolism, with CPIC PGx guidance: poor CYP2C19 metabolizers have ~3-fold higher exposure and benefit from a lower starting dose; ultrarapid metabolizers may have inadequate response'"`UNIQ--ref-0000001E-QINU`"'.
'"`UNIQ--vote-0000001D-QINU`"' Major Beers-list concern in elderly patients for cognitive and fall risks. CYP2D6 substrate. At massive overdose, also produces sodium channel blockade with cardiac toxicity'"`UNIQ--ref-0000001E-QINU`"'. '"`UNIQ--effect-0000001F-QINU`"'
'"`UNIQ--vote-00000032-QINU`"' Brand-to-brand and lot-to-lot variability in T3:T4 ratio is greater than with synthetic levothyroxine, which is why endocrine guidelines prefer the synthetic'"`UNIQ--ref-00000033-QINU`"'.
'"`UNIQ--vote-00000037-QINU`"' Hypertonic 3% is the standard urgent treatment of severely symptomatic hyponatremia'"`UNIQ--ref-00000038-QINU`"'.
'"`UNIQ--vote-0000004E-QINU`"' The EPA+DHA mix is biochemically and clinically distinct from icosapent ethyl'"`UNIQ--ref-0000004F-QINU`"'.
'"`UNIQ--vote-00000053-QINU`"' Also raises bradykinin, contributing to vasodilation and the characteristic dry cough. Renally cleared, unmetabolized; dose-adjust by eGFR'"`UNIQ--ref-00000054-QINU`"'.
'"`UNIQ--vote-00000054-QINU`"' The clinical efficacy endpoint is adequate visualization at colonoscopy, scored by the Boston Bowel Preparation Scale'"`UNIQ--ref-00000055-QINU`"'.
'"`UNIQ--vote-00000073-QINU`"' The long half-life gives smooth, once-daily BP control with low rebound. CYP3A4 substrate; pedal edema is the characteristic, dose-related, non-fluid-overload side effect'"`UNIQ--ref-00000074-QINU`"'.
'"`UNIQ--vote-00000086-QINU`"' Calcium content is a relative contraindication for co-administration with citrated blood products through the same line'"`UNIQ--ref-00000087-QINU`"'.
'"`UNIQ--vote-00000093-QINU`"' At higher doses β2 selectivity is lost, producing β1 effects (tachycardia, tremor) and hypokalemia from intracellular potassium shift'"`UNIQ--ref-00000094-QINU`"'.
'"`UNIQ--vote-000000B6-QINU`"' Active metabolite EXP3174 is ~10-40-fold more potent than the parent and accounts for most of the antihypertensive effect; CYP2C9 polymorphism affects conversion'"`UNIQ--ref-000000B7-QINU`"'.
'"`UNIQ--vote-000000D8-QINU`"' Recovery of acid output requires synthesis of new pump enzyme. CYP2C19 substrate; PGx genotype substantially affects exposure and efficacy'"`UNIQ--ref-000000D9-QINU`"'.
'"`UNIQ--vote-000000F7-QINU`"' Minimal CYP3A4 dependence (CYP2C9 minor) reduces drug-drug interactions; transport in and out of hepatocytes is largely via OATP1B1, making SLCO1B1 PGx genotype the most clinically actionable marker for statin-associated myopathy'"`UNIQ--ref-000000F8-QINU`"'.
'"`UNIQ--vote-00000117-QINU`"' Compared with omeprazole, pantoprazole has a more linear pharmacokinetic profile and is metabolized predominantly via CYP2C19 with CYP3A4 contribution; less CYP2C19-driven drug interaction with clopidogrel than omeprazole'"`UNIQ--ref-00000118-QINU`"'.
'"`UNIQ--vote-00000138-QINU`"' Decreases urinary calcium (used in stone prevention); raises serum uric acid, glucose, and lipids modestly; non-anion-gap hypokalemic metabolic alkalosis is the characteristic electrolyte pattern'"`UNIQ--ref-00000139-QINU`"'.
'"`UNIQ--vote-00000199-QINU`"' Extends ampicillin's spectrum with better oral bioavailability. Susceptible to β-lactamases; clavulanate co-administration restores activity against many resistant organisms'"`UNIQ--ref-0000019A-QINU`"'.
'"`UNIQ--vote-000001F6-QINU`"' CYP3A4 (primary) and P-glycoprotein substrate; strong dual inhibitors or inducers materially shift exposure. Reversal: andexanet alfa for life-threatening bleeding; 4F-PCC commonly used off-label when andexanet unavailable'"`UNIQ--ref-000001F7-QINU`"'.
'"`UNIQ--vote-00000237-QINU`"' Binds the same insulin receptor as endogenous insulin with comparable mitogenic-to-metabolic ratio; provides basal hepatic glucose suppression and peripheral glucose uptake without prandial peaks'"`UNIQ--ref-00000238-QINU`"'.
'"`UNIQ--vote-00000255-QINU`"' Less potent and shorter-acting than PPIs but with faster on-effect; suitable for on-demand acid suppression. Largely renally cleared; dose-adjust in renal impairment to avoid CNS effects (confusion in elderly)'"`UNIQ--ref-00000256-QINU`"'.
'"`UNIQ--vote-000002D7-QINU`"' Hypoglycemia is the central risk, especially in elderly and renally impaired patients (glipizide has shorter half-life than glyburide, which is one reason it is preferred in older adults). CYP2C9 substrate; weight gain typical.
'"`UNIQ--vote-0000032A-QINU`"' D3 (cholecalciferol) is more potent at raising serum 25(OH)D per dose; D2 remains widely prescribed in the US Rx 50,000 IU formulation'"`UNIQ--ref-0000032B-QINU`"'.
'"`UNIQ--vote-00000391-QINU`"' Minimal CYP metabolism; mostly renally cleared unchanged. Cetirizine is the active racemate; levocetirizine is the active R-enantiomer marketed separately'"`UNIQ--ref-00000392-QINU`"'.
'"`UNIQ--vote-000003D1-QINU`"' SLCO1B1 polymorphism affects exposure but is most clinically actionable for simvastatin'"`UNIQ--ref-000003D2-QINU`"'.
'"`UNIQ--vote-0000042C-QINU`"' D3 is more potent than D2 at raising and sustaining serum 25(OH)D per dose, and is the more common OTC formulation; D2 remains the dominant Rx 50,000 IU formulation in the US for historical reasons.
'"`UNIQ--vote-000004A9-QINU`"' Modest HDL rise; LDL effects mixed. Renally cleared; combination with statin carries elevated myopathy risk (greater for gemfibrozil than fenofibrate, but caution still warranted)'"`UNIQ--ref-000004AA-QINU`"'.
'"`UNIQ--vote-000004C8-QINU`"' Largely hepatically cleared (~80% biliary); no active metabolite. Sacubitril-valsartan (Entresto) combines an ARB with neprilysin inhibition for HFrEF and was a notable advance over the ARB-alone trial (PARADIGM-HF, 2014)'"`UNIQ--ref-000004C9-QINU`"'.
'"`UNIQ--vote-0000050D-QINU`"' CYP3A4 (primary) and P-glycoprotein substrate; strong dual inhibitors or inducers materially shift exposure. Reversal: andexanet alfa for life-threatening bleeding; 4F-PCC commonly used off-label when andexanet unavailable'"`UNIQ--ref-0000050E-QINU`"'.
'"`UNIQ--vote-00000584-QINU`"' Binds the same insulin receptor as endogenous insulin with comparable mitogenic-to-metabolic ratio. Ultra-rapid formulations (Lyumjev) add treprostinil and citrate to accelerate absorption further'"`UNIQ--ref-00000585-QINU`"'.
'"`UNIQ--vote-000005D0-QINU`"' Selectivity comes from the viral-kinase-only initial phosphorylation step, which is why uninfected cells generate minimal active drug'"`UNIQ--ref-000005D1-QINU`"'. Dose-adjust by renal function; rare crystalline nephropathy with rapid IV acyclovir.
'"`UNIQ--vote-0000061E-QINU`"' Less reliably anticholinergic than first-generation H1s; minimal antiemetic effect. Desloratadine (Clarinex) is the active enantiomer-of-metabolite version marketed as a Rx alternative.
'"`UNIQ--vote-0000063C-QINU`"' Avoid in HFrEF (negative inotropy). CYP3A4 substrate AND moderate inhibitor — interacts substantially with statins (especially simvastatin), tacrolimus, cyclosporine, and many other CYP3A4 substrates'"`UNIQ--ref-0000063D-QINU`"'.
'"`UNIQ--vote-000006BE-QINU`"' Drug-holiday concept (3-5 years on, 1-2 years off) emerged from FLEX and long-term safety data balancing fracture protection against atypical femoral fracture and osteonecrosis of the jaw signals'"`UNIQ--ref-000006BF-QINU`"'.
'"`UNIQ--vote-00000762-QINU`"' Largely renally cleared, hence the eGFR-tiered dosing. Rare but well-documented signals: acute pancreatitis (uncertain causal contribution), severe joint pain, and bullous pemphigoid (class effect, especially in older Asian patients)'"`UNIQ--ref-00000763-QINU`"'.
'"`UNIQ--vote-0000083E-QINU`"' CYP2C9 substrate; no clinically active metabolites. The IDNT trial established renoprotection in diabetic nephropathy independent of BP lowering, contributing to the ARB class indication in T2DM with proteinuria'"`UNIQ--ref-0000083F-QINU`"'.
'"`UNIQ--vote-00000860-QINU`"' Activates the glucocorticoid receptor to broadly remodel inflammatory, immune, and metabolic transcription. Unlike prednisone, it does not require hepatic activation, making it the preferred oral choice in severe hepatic dysfunction'"`UNIQ--ref-00000861-QINU`"'.
'"`UNIQ--vote-000008BE-QINU`"' Preferred over prednisone in advanced hepatic dysfunction where hepatic 11β-HSD1 activation is impaired. Liquid formulations are the workhorse pediatric oral corticosteroid for asthma and croup'"`UNIQ--ref-000008BF-QINU`"'.
'"`UNIQ--vote-000008E1-QINU`"' Like omeprazole, it is an acid-activated prodrug that covalently and irreversibly binds the H+/K+ ATPase. CYP2C19 PGx remains clinically relevant for both'"`UNIQ--ref-000008E2-QINU`"'.
'"`UNIQ--vote-00000950-QINU`"' Mostly renally cleared unchanged; dose-reduce in renal impairment. Like cetirizine, retains slightly more sedation than fexofenadine in some users'"`UNIQ--ref-00000951-QINU`"'.
'"`UNIQ--vote-00000975-QINU`"' Hyperammonemic encephalopathy (consider in any unexplained CNS depression), thrombocytopenia, and polycystic ovary syndrome are characteristic chronic-use adverse effects beyond hepatic and pancreatic risks'"`UNIQ--ref-00000976-QINU`"'.
'"`UNIQ--vote-000009FD-QINU`"' Active against gram-positive cocci including MRSA; the unique target underlies the absence of cross-resistance with other antibiotic classes. High-level resistance (plasmid-mediated mupA) is rising and limits prolonged or repeated use'"`UNIQ--ref-000009FE-QINU`"'.
'"`UNIQ--vote-00000A1D-QINU`"' Like other ACE inhibitors, it raises bradykinin (driving the dry cough and rare angioedema). Renally cleared; dose-adjust in renal impairment'"`UNIQ--ref-00000A1E-QINU`"'.
'"`UNIQ--vote-00000AEA-QINU`"' The 24-hour half-life supports once-daily dosing with consistent overnight BP control. Largely hepatically cleared (~98% biliary); no significant renal clearance dependence'"`UNIQ--ref-00000AEB-QINU`"'.
'"`UNIQ--vote-00000B40-QINU`"' The TRANSFORM-HF trial (2023) found no all-cause mortality difference between torsemide and furosemide in heart failure, although torsemide remains pharmacologically preferred where furosemide oral absorption is unreliable'"`UNIQ--ref-00000B41-QINU`"'.
'"`UNIQ--vote-00000CC9-QINU`"' Mostly excreted unchanged in feces and urine; P-glycoprotein substrate (the basis of the fruit-juice interaction).
'"`UNIQ--vote-00000D11-QINU`"' Same mechanistic family as amphotericin B but with prohibitive systemic toxicity at therapeutic doses, hence restriction to topical and luminal-gut indications. No clinically meaningful resistance after decades of use'"`UNIQ--ref-00000D12-QINU`"'.
'"`UNIQ--vote-00000D7A-QINU`"' Substantial QT-interval prolongation — the most QT-prolonging fluoroquinolone — limits use in patients on other QT-prolonging agents or with electrolyte abnormalities'"`UNIQ--ref-00000D7B-QINU`"'.
'"`UNIQ--vote-00000DFA-QINU`"' CYP3A4 substrate; QT-interval prolongation has been reported at higher doses. Like other antimuscarinics, contributes to cumulative anticholinergic burden in older adults'"`UNIQ--ref-00000DFB-QINU`"'.
'"`UNIQ--vote-00000E4A-QINU`"' The narrow safe-bolus window for IV use (sharp risk of arrhythmia, hypertensive emergency, intracerebral hemorrhage) is why anaphylaxis dosing is '''IM, not IV''', outside critical care'"`UNIQ--ref-00000E4B-QINU`"'.
'"`UNIQ--vote-00000ECD-QINU`"' Agranulocytosis is the most-feared adverse effect (~0.3%, usually first 90 days of treatment; warn patients to seek urgent CBC for fever or severe sore throat). Hepatotoxicity is class-recognized but more often associated with PTU'"`UNIQ--ref-00000ECE-QINU`"'.
'"`UNIQ--vote-00001014-QINU`"' Activates the glucocorticoid receptor to broadly remodel inflammatory, immune, and metabolic transcription. The dipropionate, valerate, and augmented dipropionate ester forms determine topical potency (high to super-high)'"`UNIQ--ref-00001015-QINU`"'.
'"`UNIQ--vote-0000104D-QINU`"' Adequate hydration is at least as important as the drug in producing the expectorant effect clinically. Used in combination with dextromethorphan, decongestants, or antihistamines in many proprietary OTC cold preparations.
'"`UNIQ--vote-00001067-QINU`"' Chronic use is associated with cathartic colon (colonic dilation, loss of haustration), hypokalemia, and laxative dependence; reserved for short-term use or bowel prep with breaks between courses'"`UNIQ--ref-00001068-QINU`"'.
'"`UNIQ--vote-000010F8-QINU`"' Pre-treatment screening for latent TB (PPD or IGRA) and chronic hepatitis B is standard. Anti-drug antibody formation is a recognized cause of secondary loss of response'"`UNIQ--ref-000010F9-QINU`"'.
'"`UNIQ--vote-0000111B-QINU`"' Intraoperative floppy iris syndrome is a recognized class effect. Recently emerging evidence (observational) suggests possible Parkinson's disease risk reduction via PGK1 binding — investigational and not a clinical indication'"`UNIQ--ref-0000111C-QINU`"'.
'"`UNIQ--vote-0000113A-QINU`"' Concomitant β-blocker or CCB is required when used for AF to prevent 1:1 atrial flutter conduction (flecainide can slow atrial rate to a level where AV conduction allows dangerous ventricular rates). CYP2D6 substrate'"`UNIQ--ref-0000113B-QINU`"'.
'"`UNIQ--vote-00001197-QINU`"' Extracellular cGMP separately activates submucosal sensory afferents in a way that reduces visceral pain perception, distinguishing linaclotide from purely osmotic laxatives in IBS-C. Diarrhea is the dose-limiting effect'"`UNIQ--ref-00001198-QINU`"'.
'"`UNIQ--vote-000011D5-QINU`"' Minimal systemic absorption and the dual mechanism underlie its first-line role in seasonal allergic conjunctivitis. Comfort drops without preservatives are available for sensitive patients'"`UNIQ--ref-000011D6-QINU`"'.
'"`UNIQ--vote-000011F4-QINU`"' Like all NSAIDs, raises CV thrombotic risk modestly (FDA 2014/2015 advisory) and produces GI, renal, hypertensive, and platelet-inhibitory effects characteristic of the class'"`UNIQ--ref-000011F5-QINU`"'.
'"`UNIQ--vote-00001233-QINU`"' Onychomycosis cure rates with nail lacquer are modest (mycologic cure ~30-50%, complete cure ~5-12% at 48 weeks); oral terbinafine remains substantially more effective when systemic therapy is acceptable'"`UNIQ--ref-00001234-QINU`"'.
'"`UNIQ--vote-0000124C-QINU`"' The 400 mg/d dose for migraine prophylaxis is supported by randomized trials (Schoenen 1998) and remains a low-risk evidence-based supplement option. Characteristic bright-yellow urine fluorescence with high-dose oral supplementation.
'"`UNIQ--vote-00001269-QINU`"' Renal, GI, hypertensive, and CV effects parallel the class profile; modest COX-2 preference may underlie some literature suggesting slightly better GI tolerability than non-selective NSAIDs, though clinically the difference is small'"`UNIQ--ref-0000126A-QINU`"'.
'"`UNIQ--vote-00001284-QINU`"' Systemic oral ketotifen (available outside US) has historical use for asthma adjunct therapy via the same dual mechanism, but oral use produces sedation and weight gain — the topical ophthalmic application largely avoids both'"`UNIQ--ref-00001285-QINU`"'.
'"`UNIQ--vote-00001302-QINU`"' Renally cleared; accumulation in advanced CKD can produce neuromuscular and cardiac depression. Hypomagnesemia frequently co-exists with hypokalemia and is often the reason refractory potassium loss does not correct until magnesium is repleted.
'"`UNIQ--vote-0000132D-QINU`"' Electrolyte-balanced bowel-prep formulations are designed to be iso-osmotic with plasma so the volume passes through without net fluid or electrolyte shifts, the basis of their safety for whole-bowel evacuation.
'"`UNIQ--vote-00001356-QINU`"' Binds the same insulin receptor as endogenous insulin with comparable mitogenic-to-metabolic ratio'"`UNIQ--ref-00001357-QINU`"'.
'"`UNIQ--vote-000013B1-QINU`"' Topical application minimizes systemic antihistaminic burden; the characteristic bitter taste with nasal use (drainage to oropharynx) is the main tolerability issue'"`UNIQ--ref-000013B2-QINU`"'.
'"`UNIQ--vote-000013EE-QINU`"' Higher-dose Aygestin (5 mg) achieves more reliable ovulation suppression and is used for endometriosis and DUB. POP requires strict daily timing because the 24-hour cervical-mucus effect window is narrower than COC'"`UNIQ--ref-000013EF-QINU`"'.
'"`UNIQ--vote-000014BC-QINU`"' Topical ophthalmic and otic formulations remain widely used in ENT and ophthalmology. Subject to all fluoroquinolone-class restrictions (tendinitis/rupture, peripheral neuropathy, QT prolongation)'"`UNIQ--ref-000014BD-QINU`"'.
'"`UNIQ--vote-000014DD-QINU`"' The combination is the most-prescribed opioid analgesic in the US for moderate-to-severe acute pain. CPIC PGx guidance addresses CYP2D6-driven exposure variation'"`UNIQ--ref-000014DE-QINU`"'.
'"`UNIQ--vote-000014F7-QINU`"' Falling out of favor for acute pain due to aspirin's GI bleeding and antiplatelet effects compared with acetaminophen-opioid combinations; still used in selected indications'"`UNIQ--ref-000014F8-QINU`"'.
'"`UNIQ--vote-00001513-QINU`"' The combination with acetaminophen provides additive non-opioid analgesia and lowers required codeine dose. CYP2D6 PGx is one of the most clinically actionable in current pharmacology; CPIC supports genotype-guided opioid selection'"`UNIQ--ref-00001514-QINU`"'.
'"`UNIQ--vote-00001549-QINU`"' Metabolic effects (weight gain, dyslipidemia, glucose dysregulation) dominate the long-term tolerability profile; routine metabolic monitoring is standard'"`UNIQ--ref-0000154A-QINU`"'.
'"`UNIQ--vote-00001580-QINU`"' First FDA-approved treatment for PBA. The 10 mg quinidine daily dose is far below antiarrhythmic levels but sufficient to nearly fully inhibit CYP2D6, the basis of the combination's pharmacokinetic rationale'"`UNIQ--ref-00001581-QINU`"'.
'"`UNIQ--vote-000015CE-QINU`"' The dual-mechanism design exploits the inflammatory component of migraine that triptan monotherapy does not fully address. Risk of serotonin syndrome with SSRIs/SNRIs is theoretical but generally not seen clinically at triptan doses'"`UNIQ--ref-000015CF-QINU`"'.
µ-opioid agonism
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uses:
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(There are no values for this filter)
preparations:
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None
· 24 hours ·
4-6 hours
·
12 hours
·
6-8 hours
·
Daily dosing
·
8-12 hours
·
12-24 hours
·
Hours
· Hours per application ·
24 hours (HS dosing)
·
24 hours (once-daily dosing)
·
24 h
·
N/A
·
N/A (replacement)
·
Variable
·
~7-8 hours
·
3-5 hours
·
4-6 hours (IR); 24 hours (ER)
·
6-12 hours
Other values:
'''Antiplatelet effect lasts the platelet's lifetime (~7-10 days)''' due to irreversible COX-1 acetylation; analgesic 4-6 hours
10-12 hours (smoother profile than immediate-release amphetamine salts)
12 hours (BID dosing required)
12 hours (IR); 24 hours (ER)
12 hours (Macrobid)
12 hours (oral BID); 24 hours (Timoptic-XE)
12-24 hours (IR BID); 24 hours (ER once-daily)
12-24 hours (IR); 24 hours (Amrix ER)
12-24 hours (long for an antihistamine)
12-24 hours per dose
12–24 h (oral); decanoate IM 3–4 weeks
12–24 h or longer
14-day course; effect persists after discontinuation in trials
2 weeks per dose
2-4 hours; headache recurrence rate ~20-30% within 24 hours
2-4 weeks per dose
2-5 days after stopping (factor II resynthesis-limited)
24 hours (0.7% formulation); 8-12 hours (lower-strength)
24 hours (XR); 12 hours (IR)
24 hours (evening dosing aligns with overnight HMG-CoA reductase peak)
24 hours (long receptor dissociation half-life from M3)
24 hours (most ER formulations)
24 hours (often divided BID at higher doses)
24 hours (once-daily dosing supported by long elimination)
24 hours (once-daily dosing supported by long half-life)
24 hours (once-daily or split BID dosing)
24 hours (oral); 2-4 weeks (LAI formulations)
24 hours (oral); 2-4 weeks (LAI)
24 hours (oral); 4-8 weeks (LAI)
24 hours; tissue effects persist weeks
24+ hours (irreversible enzyme binding)
24-48 hours per dose
24-72 hours
24-72 hours per dose (irreversible enzyme binding)
24-72 hours per dose (irreversible enzyme binding; effect outlasts plasma exposure)
24–36 h (driven by buprenorphine)
2–4 h
3-4 hours
3-5 hours (IR); 8-24 hours (ER); 12-24 hours (epidural / intrathecal)
3-6 hours per dose
3-8 hours
3-month dosing interval
30-90 minutes (infiltration without epinephrine); 90-200 minutes (with epinephrine); 12 hours (patch)
3–4 h
3–5 h (subjective)
4 hours
4 hours (IR); 12 hours (ER)
4-12 hours
4-6 hours (IR); 12 hours (ER)
4-6 hours (IR); 12-24 hours (ER)
4-6 hours (oral, TID-QID dosing)
4-6 hours; headache recurrence is common
4-8 h
4-8 hours
4-8 hours typical; longer at high doses; residual cognitive and perceptual effects up to 48 hours
48-72 hours per dose (much longer than hydrochlorothiazide)
4–5 h
4–6 h
4–6 hours
5-15 minutes
5-7 days (platelet lifespan; irreversible receptor binding)
6 h (immediate-release); ~11 h (extended-release)
6 hours per dose
6-12 hours (long-acting among benzodiazepines)
6-12 hours systemic
6-24 hours (parent); much longer when accounting for the long-lived active metabolites
6-8 h (immediate-release); 24 h (extended-release)
6-8 hours (IR oral); 12-24 hours (ER)
6-8 hours (IR); 24 hours (ER)
6-8 hours (IR); 8 hours (CR via biphasic release)
6–10 h subjective; full pharmacologic effect considerably longer.
6–12 h (IR); 24 h (ER)
6–12 h (tartrate); 24 h (succinate)
6–8 h
8 hours per dose
8 hours per oral dose
8-12 hours (IR); ~7 days (transdermal patch)
8-12 hours (TID dosing needed)
8-12 hours (oral); 4-6 hours (IV)
8-12 hours (the long-duration feature relative to ibuprofen)
8–12 hours
>42 hours per dose (effectively flat once at steady state)
About 20 minutes
Acute effect ~24 hours; cumulative effect builds with repeated dosing
BID at higher doses (IR); once-daily (CR)
BID dosing (IR); once-daily (XR)
BID dosing for IR; once-daily for XR
BID-QID dosing (IR); BID for ER formulations
BID-TID dosing
BID-TID dosing for IR; once-daily for CR
Biologic 12-36 hours (intermediate-acting)
Biologic 12-36 hours (intermediate-acting); Depo-Medrol depot weeks
Biologic 36-54 hours (long-acting)
Biologic 36-72 hours (long-acting)
Biologic half-life ~12-36 hours (intermediate-acting); plasma half-life shorter
Biologic ~8-12 hours (short-acting)
Chronic daily dosing
Continuous daily dosing
Daily dosing; active metabolites with very long half-lives (up to 1-3 weeks)
Daily morning dosing
Depot IM 13 weeks (designed); often persists longer
Dosing-frequency dependent
Hours (nasal); ~24 h (gel/patch); 1–2 weeks (cypionate/enanthate IM); ~10 weeks (undecanoate IM)
Hours per application (topical); 24 hours (oral)
Hours per dose
Hours per dose (much shorter biologic effect than ergocalciferol/cholecalciferol because it is the already-active form, not the storage form)
Hours per topical application
Hours to days per application
IM benzathine: 3-4 weeks of detectable levels
IR 3–5 h; LA/SR 6–8 h; Concerta 10–12 h; Daytrana ~9 h wear time
IR 4-8 hours; ER 24 hours
IR 4–6 h; XR 10–12 h; Mydayis 14–16 h
IR 4–6 h; XR 8–12 h
IR: 4-8 hours; ER: 24 hours
IR: 6-10 hours; ER: 24 hours
IR: 6-8 hours; ER: 24 hours
IV: 1-4 hours; PO: 3-8 hours
IV: hours, dependent on ongoing acid load; oral antacid: ~30 minutes
IV: ~2 hours; PO: 6-8 hours
Intra-articular 3-6 months (depot effect of acetonide microcrystals)
Long
Long; fat-soluble storage in adipose
Long; fat-soluble, stored in adipose
Mononitrate ER: 12-24 hours; dinitrate IR: 4-6 hours
Monthly dosing
Monthly or quarterly dosing
Once-weekly dosing in rheumatology
Ongoing dosing
Oral: 8-12 hours; vaginal: 24+ hours; IM: days
Persistent activity 6+ hours (residual binding to skin and oral surfaces)
Roughly 20-25% of an IV bolus remains intravascular at 1 hour
Roughly 20-30% remains intravascular at 1 hour
Route- and formulation-dependent
SL: 30 minutes; patch: 12-14 hours; IV continuous
SR ~12 hours; XL 24 hours
Single infusion course
Steady-state at 4-6 weeks
Sustained with twice-daily dosing
TID dosing (IR); once-daily (ER)
TID dosing (IR); once-daily (XL)
TID dosing for IR; once-daily for ER formulations
Tissue half-life supports once-daily and post-treatment effect
Treatment can be discontinued upon achieving amyloid clearance
Up to 36 h ("the weekend pill")
Variable; biologically active metabolite carries effect beyond plasma half-life
Variable; depends on ongoing losses
Very long
Weeks (fat-soluble)
Weeks (long half-life)
Weeks after discontinuation (extremely long half-life)
Weeks; bone retention years
Withdrawn
~10 hours (Byetta)'"`UNIQ--ref-000000EB-QINU`"' · ~7 days steady-state (Bydureon, after ~6–7 weeks of weekly dosing to reach steady state)'"`UNIQ--ref-000000EC-QINU`"'
~12 hours (IR); 24 hours (CR)
~12 hours (IR); 24 hours (ER)
~12 weeks
~12-14 hours
~12-24 hours
~12-24 hours (dose-dependent; BID dosing often needed at higher doses)
~15 min
~24 h (daily dosing)'"`UNIQ--ref-00000189-QINU`"'
~24 hours (ER formulation supports once-daily dosing)
~24 hours per dose (peakless profile by design)
~24 hours per dose (strict timing required for POP — within 3-hour window each day)
~3 h per dose (twice-nightly schedule required)
~4 h
~48 h sustained pain freedom in responders
~48 hours of headache freedom
~6-8 hours (IR); 24 hours (Oleptro ER)
~7 days (weekly SC dosing)'"`UNIQ--ref-00000251-QINU`"' · ~24 h (oral)'"`UNIQ--ref-00000252-QINU`"'
~7 days (weekly dosing)'"`UNIQ--ref-00000058-QINU`"'
~7 days (weekly dosing)'"`UNIQ--ref-00000302-QINU`"'
~8 hours (TID dosing)
~8 hours per dose
~9 hours
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