Prazosin
Alpha-1 Adrenergic Antagonist
Prazosin
Minipress
Prazosin is best known in psychiatry as an off-label treatment for PTSD nightmares, it suppresses noradrenergic hyperactivity at night and reduces both nightmare frequency and severity in many patients. Originally an antihypertensive; now more often prescribed in mental health than cardiology. First-dose orthostatic hypotension is well-known, start at 1 mg HS and titrate slowly.
Blood pressure (especially orthostatic) during titration.
First-dose effect: marked orthostatic hypotension within 30–90 min. Take initial dose at bedtime. Rise slowly from supine. Effect on nightmares emerges in 1–3 weeks; titrate by 1–2 mg every few nights as needed.
Clonidine, Guanfacine
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Pharmacokinetics
Absorption
~60% oral bioavailability.Distribution
Plasma protein binding ~97%.Metabolism
Extensive hepatic metabolism.Elimination
Primarily fecal as metabolites.Interactions
Pharmacogenomic + mechanism interactions
Pharmacokinetic mechanismSubstrate / metabolism relationships from primary literature
FDA Drug Interactions Table: transporter substrate (ABCG2).
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Clinical relevance: does this interaction matter in practice?trivialcritical
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Inferred from pharmacokinetic dataMaterialised by the inference engine; provenance shown per row
Novobiocin inhibits ABCG2 (inhibitor, intensity 70); Prazosin is a substrate of ABCG2 (intensity 70). Derived: Prazosin exposure raised.
Inferred via Enzyme:ABCG2 (exposure raised)
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Clinical relevance: does this interaction matter in practice?trivialcritical
Confidence in this inference: is the inferred magnitude sound?overstatedsound
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See also
References
Summary
Classes
Alpha-1 Adrenergic Antagonist
Common uses
PTSD nightmares0, Hypertension0, BPH0
Pharmacy
Starting dose
1 mg at bedtime (PTSD nightmares); 1 mg BID–TID (HTN)
Preparations
1, 2, 5 mg caps
US FDA Max
40 mg/d
Pharmacology
Routes
Oral
Onset
30–90 min
Duration
6–8 h
Half-life
2–3 h
Bioavailability
~60%
Pregnancy
Category C
Legal status
Rx-only in US
Purported mechanism
Selective alpha-1 adrenergic receptor antagonist. Lowers peripheral vascular resistance via vasodilation; in the CNS, blunts noradrenergic hyperarousal thought to drive trauma-related nightmares.