Clonidine

Alpha-2 adrenergic agonist, ADHD medicine, Antihypertensive, Opioid withdrawal medicine

Clonidine

Kapvay (ER, ADHD), Catapres (IR, antihypertensive), Catapres-TTS (transdermal patch), Duraclon (epidural injection)

Experience

👥 No personal reports yet

⚕ No clinical reports yet

Log in to add your own experience.

Problems

No problems yet. Be the first to suggest one.

+ Add a problem

Titration strategies

No titration strategies yet. Be the first to suggest one.

+ Add a titration strategy

Effects

No effects listed yet. Be the first to suggest one.

+ Add an effect

Relevant anecdote

No anecdotes yet. Share a relevant one.

+ Add an anecdote

Relevant Literature

No literature entries yet.

Log in to submit relevant literature.

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

Bioavailability

~75-85% (oral); ~60% (transdermal at steady state)

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

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.