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prazosin (Alpress LP / Minipress XL / prazosin, Alza)

✓ Approved

Johnson & Johnson Services, Inc. · ADRA1D · Small Molecule

What is prazosin?

prazosin is a small molecule developed by Johnson & Johnson Services, Inc.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesAlpress LP, Minipress XL, prazosin, Alza
CompanyJohnson & Johnson Services, Inc.
Drug ClassSmall Molecule
Molecular TargetADRA1D, ADRA1B, ADRA1A, ADRA2A, ADRA2B, ADRA2C
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Johnson & Johnson Services, Inc.

Mechanism of Action

Molecular Targets

prazosin acts on 6 molecular targets:

ADRA1Dadrenoceptor alpha 1D (ADRA1R, ADRA1)
ADRA1Badrenoceptor alpha 1B (ADRA1, ALPHA1BAR)
ADRA1Aadrenoceptor alpha 1A (ALPHA1AAR, ADRA1C)
ADRA2Aadrenoceptor alpha 2A (ADRAR, ADRA2R)
ADRA2Badrenoceptor alpha 2B (ALPHA2BAR, FAME2)
ADRA2Cadrenoceptor alpha 2C (ADRA2L2, ADRARL2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

prazosin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedCNS neuroscience & therapeutics2026-11-08

Pan-Adrenergic Inhibition Alleviates Post-Hemorrhagic Hydrocephalus by Attenuating Neutrophil Extracellular Traps-Mediated Glymphatic Dysfunction.

Yang Yijian Y, Zhou Yanjie Y, Ouyang Qian Q, Nuerlanbieke Hanati H et al.

Post-hemorrhagic hydrocephalus (PHH) is a devastating complication. This study aims to elucidate how the acute post-hemorrhagic adrenergic storm drives neutrophil extracellular traps (NETs) formation, blocks the glymphatic system (GS), and causes an imbalance in intracranial fluid homeostasis, leading to PHH. It is necessary to explore whether pan-adrenergic inhibition as non-surgical intervention strategies can rescue this neuro-immune dysregulation. Single-cell RNA sequencing (scRNA-seq) was used to draw the immune infiltration map. Utilizing a rat PHH model, ventricular volumes and glymphatic fluid dynamics were assessed via MRI and fluorescent tracer tracking. Multiple behavioral analyses were used to observe the neurological dysfunction. The structural integrity of the GS was assessed using IF staining and TEM. The formation of NETs was detected using ELISA, WB, and IF. In vitro, flow cytometry and molecular assays were used to explore the changes in molecular pathways in epinephrine-stimulated primary neutrophils, and NETs were used to treat astrocytes to study the interaction between them. A pharmacological intervention using pan-adrenergic inhibitor cocktail PPA (prazosin, propranolol, atipamezole), NETs agonist, NETs inhibitor, and AKT activator was conducted to explore the mechanism. scRNA-seq identified a pathogenic neutrophil subset presented as a transcriptional phenotype consistent with NETs, which dominated hemorrhagic stroke. Structurally, adrenergic storm-driven NETs extrusion occluded perivascular spaces and stripped aquaporin-4 (AQP4) polarization at astrocytic endfeet, precipitating glymphatic stasis and severe ventricular dilation. Molecular analysis revealed that epinephrine might promote the formation of NETs by activating the PI3K/AKT/mTOR cascade. PPA blocked this pathological axis, inhibited NETs, polarized AQP4 distribution, restored the fluid dynamics of the GS, and relieved cognitive deficits after intraventricular hemorrhage and alleviated hydrocephalus. After PHH, targeted pan-adrenergic inhibition can block the adrenergic storm and inhibit NET formation, protect the clearance function and structural integrity of the GS, stabilize the intracranial fluid homeostasis, and alleviate hydrocephalus in the acute phase. The molecular mechanism may involve the PI3K/AKT/mTOR cascade. This mechanism provides a potential therapeutic strategy for neuro-immune-based drug protection.

PMID 42995676
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PubMedBehavioral sciences (Basel, Switzerland)2026-10-27

Trauma, Hyperarousal, and Sleep: Neurobehavioral Pathways in Affective Disorders.

Marano Giuseppe G, Acanfora Mariateresa M, Conci Luca L, Traversi Gianandrea G et al.

Sleep disturbances are common across affective disorders and may coexist with traumatic stress and persistent hyperarousal. This narrative review examines how trauma-related hyperarousal and sleep dysfunction are associated with major depressive disorder (MDD) and bipolar disorder (BD), while distinguishing observed associations from proposed mechanisms. A targeted search of PubMed, Scopus, and Google Scholar identified clinical, neurobiological, and translational literature on trauma, hyperarousal, insomnia, nightmares, circadian disruption, MDD, and BD. The evidence supports a multidimensional view of hyperarousal involving partly overlapping autonomic, cognitive-attentional, affective, and behavioral domains; however, it does not establish hyperarousal as a unitary mechanism or justify equating trauma-related vigilance with manic activation. Sleep disturbance may function as a symptom, vulnerability factor, or prodromal change, but no single sleep measure is currently a validated individual-level prognostic marker. Clinically, trauma history, sleep phenotype, affective state, comorbidity, medication effects, and current safety should be assessed jointly. Cognitive behavioral therapy for insomnia and established trauma-focused treatments have the strongest clinical basis within their indicated populations, whereas imagery rehearsal therapy, prazosin, chronobiological strategies, and candidate biomarkers require diagnosis-specific and evidence-graded interpretation. Longitudinal studies integrating objective sleep measures and explicit temporal modeling are needed before proposed pathways or precision approaches can be considered clinically validated.

PMID 42938483
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PubMedAmerican journal of physiology. Regulatory, integrative and comparative physiology2026-10-26

Autonomic dysregulation and high arterial blood pressure in male Crtc1-deficient mice.

Morhenn Karoline K, Morellini Fabio F, Seniuk Anika A, Vitzthum Helga H et al.

Epidemiological evidence links cardiovascular disease, sympathetic nervous system overactivity, obesity, and depression. Whether this association is causal and what mechanisms may be involved remains unknown. Mice deficient in the cAMP response element-binding protein-regulated transcription coactivator 1 (CRTC1) show depression-related behavior and a metabolic profile resembling the metabolic syndrome. This study aimed to characterize arterial blood pressure regulation in these mice to determine whether global CRTC1 deficiency is also associated with arterial hypertension, another key characteristic of the metabolic syndrome. Telemetric measurements in unrestrained male mice revealed high blood pressure in Crtc1-deficient animals before the onset of obesity or hypertrophy of arterioles, accompanied by decreased heart rate variability, increased systolic blood pressure variability, enhanced environmental stress sensitivity and increased urinary catecholamine excretion. Pharmacological α1-adrenoceptor blockade with prazosin induced greater blood pressure reductions in Crtc1-deficient mice and eliminated genotype-dependent pressure differences, whereas the β1-adrenoceptor antagonist metoprolol showed no genotype-specific effect. Regulation of renal sodium transport proteins, activity of the renin-angiotensin-aldosterone system, and cardiac systolic function were unchanged between genotypes. Crtc1-deficient animals also exhibited impaired glucose tolerance and a depression-related phenotype associated with reduced locomotion, increased agmatinase, and decreased cerebral brain-derived neurotrophic factor (Bdnf) and c-fos expression. These findings indicate that CRTC1 deficiency leads to high blood pressure, likely driven by excessive peripheral α1-adrenoceptor-mediated vasoconstriction caused by autonomic dysregulation. The co-occurrence of increased blood pressure, metabolic dysregulation, and the depressive-like phenotype in male Crtc1-deficient mice suggests a regulatory role of CRTC1 in the complex central network of signaling pathways involved in the frequent comorbidity of metabolic syndrome and depression.NEW & NOTEWORTHY Male Crtc1-deficient mice develop autonomic dysfunction and high arterial blood pressure, likely driven by enhanced α1-adrenergic vasoconstriction and independent of obesity or increased arteriolar wall thickness. The co-occurrence of elevated sympathetic activity, early cardiac remodeling, impaired glucose tolerance, and depression-related behavior suggests an involvement of CRTC1-dependent signaling in the coordination of autonomic, metabolic, and affective phenotypes.

PMID 42932902
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PubMedBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas2026-10-15

Alpha1-adrenoceptor antagonists block the positive chronotropic effect of 6-nitrodopamine in the isolated rat right atrium.

Alves B L BL, Niederauer A J S AJS, Britto-Júnior J J, Sobanski J F JF et al.

6-Nitrodopamine (6-ND) released from isolated rat atria produces potent positive chronotropic actions. Direct negative chronotropic responses to some selective α1-adrenoceptor (AR) antagonists like prazosin have been reported. Since α1-AR antagonists inhibit 6-ND-induced smooth muscle contractions, we have hypothesized that negative chronotropism induced by α1-AR antagonists reflects 6-ND blockade. This study investigated whether selective α1-AR antagonists affect 6-ND-induced positive chronotropism in isolated rat atria. Alfuzosin at 10 nM did not affect the atrial rate, but at 100 nM, it significantly reduced the atrial rate. This effect was not observed in L-NAME (100 mM)-treated preparations or in atria from rats chronically treated with L-NAME. Alfuzosin (100 nM) significantly reduced the 6-ND-induced positive chronotropism without affecting the chronotropic responses to noradrenaline, adrenaline, or dopamine. Similar results were obtained with doxazosin (1-10 nM), tamsulosin (10-100 nM), and prazosin (1-10 nM). Isoprenaline induced concentration-dependent increases in atrial rate, which were not significantly affected by any of these α1-AR antagonists. The results demonstrated that α1-AR antagonists reduced atrial basal rate only at concentrations affecting the positive chronotropic effect of 6-ND, and this reduction was not observed when NO synthesis was blocked, indicating that the negative chronotropic effect may involve 6-ND receptor blockade.

PMID 42879640
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PubMedPaediatric drugs2026-10-15

Pharmacological Interventions for Acute Stress Disorder and for the Prevention and Treatment of Post-traumatic Stress Disorder in Children and Adolescents: A Narrative Review.

Tesnières Charles C, Kerbage Hala H, Bui Eric E, Rolling Julie J

Traumatic events are common during childhood and adolescence and may lead to acute stress disorder (ASD) or post-traumatic stress disorder (PTSD), both associated with developmental, cognitive and functional impairment. Although trauma-focused psychotherapies are recommended as first-line treatments, pharmacological interventions are frequently used in clinical practice despite limited evidence in paediatric populations. To review the evidence on pharmacological interventions for the prevention and treatment of paediatric ASD and PTSD, we reviewed the literature published up to December 2025. Eligible studies included participants aged younger than 18 years and evaluated pharmacological interventions targeting ASD, PTSD prevention or PTSD treatment. After screening and a full-text review, 75 publications were included. Given the methodological heterogeneity, findings were synthesised narratively. Evidence for pharmacological interventions in paediatric trauma-related disorders remains limited and heterogeneous. For PTSD prevention, only limited data support sertraline and, in the context of ASD, imipramine. Limited data also suggest that opioids used for pain management after trauma may reduce subsequent PTSD risk. Early opioid (morphine) exposure for pain management was also associated with lower subsequent severity symptoms in observational paediatric burn studies. Evidence for PTSD treatment is weaker. Anticonvulsants (sodium valproate, carbamazepine, oxcarbazepine, lamotrigine), antipsychotics (clozapine, quetiapine, aripiprazole), glutamatergics (D-cycloserine, ketamine, ifenprodil), propranolol and cannabidiol do not appear to provide sufficient benefit for routine use. Alpha-adrenergic agents (prazosin, clonidine, guanfacine) have shown preliminary signals of benefit, particularly for hyperarousal and trauma-related sleep disturbances. However, these findings are based on non-randomised and uncontrolled studies. Antidepressants (sertraline, citalopram) show mixed results; among them, citalopram was associated with symptomatic improvement in one small open-label study and one case series. These findings should be considered preliminary and hypothesis generating. No pharmacological treatment has sufficient evidence to warrant routine recommendation for paediatric PTSD and ASD. Pharmacotherapy should therefore be considered only as an adjunct to trauma-focused psychotherapy in selected clinical situations. Further randomised controlled trials are needed.

PMID 42879122
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PubMedACS omega2026-10-09

Synthesis and Biological Evaluation of Prazosin-Derived Antitrypanosomal Agents Putatively Targeting FAZ1.

Salem Fatma M FM, Martin William R WR, Zhao Xiaotong X, Roeper Tyler E TE et al.

Current therapeutic interventions for Human African Trypanosomiasis (HAT) are severely limited by emerging drug resistance and profound systemic toxicity, necessitating the urgent development of novel chemotypes. Building upon our previous identification of the alpha-adrenoceptor antagonist Prazosin as a scaffold with off-target activity against Trypanosoma brucei brucei (T. b. brucei), we have targeted the Flagellum Attachment Zone 1 (FAZ1) filament. As a parasite-specific protein, FAZ1 presents an ideal target for achieving high selectivity and minimizing host toxicity. In this study, we designed and synthesized a series of Prazosin derivatives and characterized their Structure-Activity Relationship (SAR) through biological evaluation against T. b. brucei and mammalian cell lines (HEK293 and RAW264.7). Several derivatives exhibited potent antitrypanosomal activity with IC50 values below 50 nM and a selectivity index exceeding 500-fold relative to mammalian cells. Crucially, these candidates demonstrated negligible affinity for alpha-adrenoceptors at their effective antiparasitic concentrations. Molecular docking simulations, utilizing AlphaFold-generated FAZ1 structures, suggest that these candidates interact specifically with the FAZ1 N-terminal domain. Furthermore, in vivo studies indicated that the lead derivatives extended the lifespan of T. b. brucei-infected mice without the marked toxicity observed with the parent compound, Prazosin. These findings identify prazosin-derived compounds as promising antitrypanosomal agents and suggest FAZ1 as a potential target for future mechanistic validation, warranting further optimization as safer, more effective alternatives for the treatment of HAT.

PMID 42852209
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