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Clonidine: Difference between revisions

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{{MedTemplate
{{MedTemplate
| generic           = Clonidine
| generic           = Clonidine
| brand             = Kapvay
| brand             = Kapvay (ER, ADHD), Catapres (IR, antihypertensive), Catapres-TTS (transdermal patch), Duraclon (epidural injection)
| structure         =  
| structure         =
| classes           = Alpha-2 agonist, ADHD medicine
| classes           = [[:Category:Alpha-2 adrenergic agonists|Alpha-2 adrenergic agonist]], [[:Category:ADHD medicines|ADHD medicine]], [[:Category:Antihypertensives|Antihypertensive]], [[:Category:Opioid withdrawal medicines|Opioid withdrawal medicine]]
| mechanism          = Alpha-2 adrenergic receptor agonist
| uses             = <vote slug="adhd-clonidine-use">Attention-deficit/hyperactivity disorder (Kapvay ER, monotherapy or adjunct to psychostimulants)</vote>, <vote slug="hypertension-use">Hypertension (historical indication, less common in current practice)</vote>, <vote slug="opioid-withdrawal-management-use">Opioid withdrawal symptom management (autonomic hyperactivity)</vote>, <vote slug="tic-disorders-use">Tic disorders / Tourette syndrome (off-label)</vote>, <vote slug="menopausal-hot-flashes-use">Menopausal hot flashes (off-label)</vote>, <vote slug="severe-cancer-pain-epidural-use">Severe cancer pain (epidural, Duraclon)</vote>, <vote slug="procedural-sedation-premed-use">Procedural sedation premedication (off-label)</vote>
| uses               =  
| starting_dose     = ADHD (Kapvay ER): 0.1 mg PO at bedtime, titrate weekly to 0.4 mg/day divided BID. HTN (IR): 0.1 mg PO BID, titrate by 0.1 mg increments
| starting_dose     =  
| preparations     = IR tablets 0.1, 0.2, 0.3 mg; ER tablets 0.1, 0.2 mg (Kapvay); transdermal patches 0.1, 0.2, 0.3 mg/24h (TTS-1/2/3, weekly); epidural injection (Duraclon)
| preparations       =  
| fda_max           = 2.4 mg/day (HTN, IR); 0.4 mg/day (ADHD, Kapvay)
| fda_max          =  
| pill_id           =
| routes             =  
| routes           = Oral, transdermal, epidural injection
| onset             =  
| onset             = 30-60 min (IR oral); 2-3 days to steady state (transdermal patch)
| duration           =  
| duration         = 8-12 hours (IR); ~7 days (transdermal patch)
| halflife           =
| halflife          = 12-16 hours<ref name="kapvay-label">FDA Prescribing Information, Kapvay (clonidine hydrochloride extended-release), Concordia/Bausch, current revision. https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/022331s000lbl.pdf</ref>
| bioavailability    =
| bioavailability   = ~75-85% (oral); ~60% (transdermal at steady state)<ref name="kapvay-label" />
| pregnancy         =  
| pregnancy        = Older agent with substantial use experience but limited controlled data; case reports of neonatal sedation and transient hypertension with maternal use near term.{{citation needed}}
| legal              =  
| legal             = [[USLegal:Prescription only|Rx-only]] in US. Not a controlled substance, like guanfacine and unlike the psychostimulant alternatives for ADHD<ref name="kapvay-label" />
| intro              =
| mechanism         = <vote slug="clonidine-mech-claim">Centrally-acting α2-adrenergic receptor agonist. Less subtype-selective than guanfacine, so engages α2A, α2B, and α2C with associated greater sedation and more peripheral sympatholytic effect. In ADHD the proposed mechanism parallels guanfacine (prefrontal α2A strengthening of working-memory and attention circuits); in opioid withdrawal, central sympatholytic action blunts the autonomic hyperactivity (sweating, tachycardia, hypertension, anxiety, lacrimation) that drives early withdrawal distress; in hypertension, brainstem α2 activation reduces sympathetic outflow.</vote> Sedation and orthostatic hypotension are the dose-limiting effects, and abrupt discontinuation can precipitate '''rebound hypertension''' that is more severe than with guanfacine, particularly at higher chronic doses. Gradual taper is essential<ref name="kapvay-label" />.
| pharmacokinetics   =  
| pharmacodynamics  =  
| indications        =  
| dosing             =  
| effects            =  
| interactions      = <pharmaInteractions/>
| pregnancy_details  =
| monitoring         =  
| counseling        =  
| anecdotes          =
| seealso            =
| references        =  
}}
}}


 
== References ==
[[Category:Alpha-2 Adrenergic Agonists]]
<references />
[[Category:Addiction Medicine]]

Latest revision as of 06:18, 23 May 2026

Alpha-2 adrenergic agonist, ADHD medicine, Antihypertensive, Opioid withdrawal medicine
Clonidine
Kapvay (ER, ADHD), Catapres (IR, antihypertensive), Catapres-TTS (transdermal patch), Duraclon (epidural injection)

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Summary
Classes
Alpha-2 adrenergic agonist, ADHD medicine, Antihypertensive, Opioid withdrawal medicine
Pharmacy
Starting dose
ADHD (Kapvay ER): 0.1 mg PO at bedtime, titrate weekly to 0.4 mg/day divided BID. HTN (IR): 0.1 mg PO BID, titrate by 0.1 mg increments
Preparations
IR tablets 0.1, 0.2, 0.3 mg; ER tablets 0.1, 0.2 mg (Kapvay); transdermal patches 0.1, 0.2, 0.3 mg/24h (TTS-1/2/3, weekly); epidural injection (Duraclon)
US FDA Max
2.4 mg/day (HTN, IR); 0.4 mg/day (ADHD, Kapvay)
Pharmacology
Routes
Oral, transdermal, epidural injection
Onset
30-60 min (IR oral); 2-3 days to steady state (transdermal patch)
Duration
8-12 hours (IR); ~7 days (transdermal patch)
Half-life
12-16 hours[1]
Bioavailability
~75-85% (oral); ~60% (transdermal at steady state)[1]
Pregnancy
Older agent with substantial use experience but limited controlled data; case reports of neonatal sedation and transient hypertension with maternal use near term.[citation needed]
Legal status
Rx-only in US. Not a controlled substance, like guanfacine and unlike the psychostimulant alternatives for ADHD[1]
Purported mechanism
Centrally-acting α2-adrenergic receptor agonist. Less subtype-selective than guanfacine, so engages α2A, α2B, and α2C with associated greater sedation and more peripheral sympatholytic effect. In ADHD the proposed mechanism parallels guanfacine (prefrontal α2A strengthening of working-memory and attention circuits); in opioid withdrawal, central sympatholytic action blunts the autonomic hyperactivity (sweating, tachycardia, hypertension, anxiety, lacrimation) that drives early withdrawal distress; in hypertension, brainstem α2 activation reduces sympathetic outflow.0 Sedation and orthostatic hypotension are the dose-limiting effects, and abrupt discontinuation can precipitate rebound hypertension that is more severe than with guanfacine, particularly at higher chronic doses. Gradual taper is essential[1].

References

  1. ↑ 1.0 1.1 1.2 1.3 FDA Prescribing Information, Kapvay (clonidine hydrochloride extended-release), Concordia/Bausch, current revision. https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/022331s000lbl.pdf
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