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Clonidine

From Pharmacopedia
(Redirected from Kapvay)
Clonidine
Kapvay (ER, ADHD), Catapres (IR, antihypertensive), Catapres-TTS (transdermal patch), Duraclon (epidural injection)

Experience

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Titration strategies

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Summary
Common uses
Attention-deficit/hyperactivity disorder (Kapvay ER, monotherapy or adjunct to psychostimulants)0, Hypertension (historical indication, less common in current practice)0, Opioid withdrawal symptom management (autonomic hyperactivity)0, Tic disorders / Tourette syndrome (off-label)0, Menopausal hot flashes (off-label)0, Severe cancer pain (epidural, Duraclon)0, Procedural sedation premedication (off-label)0
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