Biological Activity

Bioactivity / Mechanism

Prazosin hydrochloride competed for α1-adrenoceptor binding in isolated rat arterial segments, with reported pKi values of 9.4±0.1 in tail artery and 9.9±0.1 in thoracic aorta (mean±s.e.m.; five experiments). These measurements describe native tissue binding rather than isolated receptor-subtype selectivity. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target	Activity	Value
alpha-adrenergic receptor

In Vitro Studies

In CHO-K1 cells expressing human α1A-adrenoceptors, 300 nM prazosin shifted noradrenaline- and A61603-induced ERK1/2 responses rightward. Its weaker inhibition of oxymetazoline and lack of inhibition of 5-HT responses highlight the contribution of endogenous receptor signalling to this assay. [2]

Prazosin competes for α1-adrenoceptor binding in isolated rat arteries

Biochemical assay · Endothelium-denuded tail artery and thoracic aorta segments from male Wistar rats (10–12 weeks; approximately 320 g). [1]

Unlabelled prazosin competed with [3H]-prazosin in both arterial preparations. These are mixed native receptor populations, not individual cloned-subtype affinity measurements.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Inhibition of specific [3H]-prazosin binding in tail artery segments	pKi 9.4±0.1 (mean±s.e.m.; five experiments)	[1]
Inhibition of specific [3H]-prazosin binding in thoracic aorta segments	pKi 9.9±0.1 (mean±s.e.m.; five experiments)	[1]

Literature-Reported Treatment Conditions

Treatment concentration: Increasing concentrations of unlabelled prazosin; tracer 500 pM in tail artery and 100 pM in aorta.
Exposure duration: 10 h at 4°C
Method: Tissue-segment radioligand competition; nonspecific binding defined with 30 μM phentolamine.
Vehicle: Prazosin stock in ethanol; diluted in binding buffer.
Reported limits: Prazosin concentration series and final ethanol fraction are not specified in the adopted table/methods. Values are affinity estimates, not treatment doses or IC50 values.

Methods and source locations

Compound reported in the paper: Prazosin hydrochloride; Compound label in the paper: Prazosin

Evidence for the reported hydrochloride material and model; no validation of Adooq lots or salt conversion.

Table 2 (Prazosin row and footnote); Methods: Tissue segment-binding experiments, Data analysis, Drugs; Results: binding competition and membrane comparison

Inhibition of specific [3H]-prazosin binding in tail artery segments: Competition binding; 500 pM [3H]-prazosin; duplicate determinations at each competing-ligand concentration. — Table 2 (Prazosin row and footnote); Methods: Tissue segment-binding experiments, Data analysis, Drugs; Results: binding competition and membrane comparison

Inhibition of specific [3H]-prazosin binding in thoracic aorta segments: Competition binding; 100 pM [3H]-prazosin; duplicate determinations at each competing-ligand concentration. — Table 2 (Prazosin row and footnote); Methods: Tissue segment-binding experiments, Data analysis, Drugs; Results: binding competition and membrane comparison

Agonist-dependent antagonism of ERK1/2 phosphorylation

Cell-based study · CHO-K1 cells stably expressing human α1A-adrenoceptors. [2]

At 300 nM, prazosin shifted noradrenaline and A61603 response curves rightward but was much less effective against oxymetazoline and ineffective against 5-HT. Antagonist comparisons implicate endogenous 5-HT1B signalling as a confounder in this recombinant model.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
ERK1/2 phosphorylation in response to increasing agonist concentrations	Concentration-response shift Approximately 10-fold rightward shift for noradrenaline and A61603 (author description); much weaker antagonism of oxymetazoline. n=7, 8 and 10 independent experiments, respectively; plotted mean±SEM.	[2]
ERK1/2 response to 5-HT and oxymetazoline	Antagonist specificity control Prazosin ineffective against 5-HT (n=6); combined prazosin/SB216641 shifted oxymetazoline potency approximately ninefold (author description; n=6). Curves plotted mean±SEM.	[2]

Literature-Reported Treatment Conditions

Treatment concentration: Prazosin 300 nM; SB216641 300 nM in comparator/combination conditions.
Exposure duration: 30 min antagonist preincubation, then 5 min agonist stimulation.
Method: AlphaScreen SureFire ERK1/2 phosphorylation assay; serum-starved cells.
Co-treatment: Prazosin alone or with SB216641; noradrenaline, A61603, oxymetazoline or 5-HT concentration-response challenges.
Reported limits: Final prazosin solvent/vehicle is not specified in the read Materials and ERK assay sections. The 300 nM value is an experimental concentration, not an IC50.

Methods and source locations

Compound reported in the paper: Prazosin hydrochloride; Compound label in the paper: Prazosin

Evidence for the reported hydrochloride material and model; no validation of Adooq lots or salt conversion.

Figures 2A–C, 4A–B, 5C–D and captions; Results: Characterization of ERK1/2 phosphorylation; Methods: AlphaScreen ERK1/2 signalling assays, Materials, Data analysis

ERK1/2 phosphorylation in response to increasing agonist concentrations: AlphaScreen SureFire assay; agonist-only curves as controls. — Figure 2A–C and caption; accompanying Results

ERK1/2 response to 5-HT and oxymetazoline: Compare prazosin alone, SB216641 alone, combined antagonists, and agonist-only controls; no exact curve-derived affinity assigned. — Figure 4A–B; Figure 5C–D and captions; accompanying Results

In Vivo Studies

In male Long-Evans rats, prazosin (1 or 2 mg/kg, i.p.) reduced hyperlocomotion and avoidance errors associated with 0.20 mg/kg MK-801. It did not rescue maximum avoidance time; the error reduction therefore does not establish improved cognition. [3]

Limited behavioural modulation in MK-801-treated rats

Animal study · Adult male Long-Evans rats in the active allothetic place avoidance task. [3]

Prazosin effects depended on the endpoint and MK-801 dose; prazosin alone did not significantly alter the measured behaviour. Fewer errors may reflect altered locomotion rather than improved cognition.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Final-session locomotion, errors and maximum time avoided	Behavioural outcomes Reduced locomotion/errors with 0.20 mg/kg MK-801; no significant rescue of maximum time avoided. For maximum time avoided, prazosin main effect F(2,63)=0.23; P>0.05.	[3]

Conditions shared by the study groups

Route: Intraperitoneal
Frequency: Before each daily session
Treatment course: Four daily 20-min sessions; fourth session analysed.
Vehicle: Prazosin dissolved in distilled water; MK-801 dissolved in saline.

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
Prazosin × MK-801 factorial design Prazosin 0, 1 or 2 mg/kg crossed with MK-801 0, 0.15 or 0.20 mg/kg.	Saline controls for both injections; prazosin-alone and MK-801-alone groups included.	Both prazosin doses reduced hyperlocomotion and errors with 0.20 mg/kg MK-801; errors remained above control. Maximum time avoided was not rescued.	[3]

Prazosin × MK-801 factorial design: Model: 72 adult male Long-Evans rats; 3–5 months; 300–400 g; n=8/group.; Reported limits: Saline control was not solvent-matched to the distilled-water prazosin formulation. Randomization/blinding not stated in the read manuscript methods.

Methods and source locations

Compound reported in the paper: Prazosin hydrochloride; Compound label in the paper: Prazosin

Evidence for the reported hydrochloride material and model; no validation of Adooq lots or salt conversion.

Revised prepress PDF: Methods pp2–4; Results pp4–5; Discussion pp5–7; Figure 2A–C/caption p11

Final-session locomotion, errors and maximum time avoided: Two-way ANOVA and Newman–Keuls post hoc test; plotted means±S.E.M.; n=8/group. — Revised prepress PDF: Methods pp2–4; Results pp4–5; Discussion pp5–7; Figure 2A–C/caption p11

Prazosin × MK-801 factorial design · Revised prepress PDF: Methods pp2–4; Results pp4–5; Discussion pp5–7; Figure 2A–C/caption p11

Specifications

Manufacturer	Adooq Bioscience
Actions	Antagonist
CAS Number	19237-84-4
Formula	C₁₉H₂₁N₅O₄.HCl
Molecular Weight	419.87
SMILES	COC1=C(C=C2C(=C1)C(=NC(=N2)N3CCN(CC3)C(=O)C4=CC=CO4)N)OC.Cl

Storage & Solubility

In Vitro Solubility

Reported Solubility

Solvent	Reported Solubility
DMSO	Warmed: 4 mg/mL (9.52 mM)
Water	Insoluble
Ethanol	Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] Takashi Tanaka, Li Zhang, Fumiko Suzuki, et al. Alpha-1 adrenoceptors: evaluation of receptor subtype-binding kinetics in intact arterial tissues and comparison with membrane binding British Journal of Pharmacology (2004). PMID: 14718262 DOI: 10.1038/sj.bjp.0705627 Source material
[2] Edilson Dantas da Silva Junior, Masaaki Sato, Jon Merlin, et al. Factors influencing biased agonism in recombinant cells expressing the human α1A-adrenoceptor British Journal of Pharmacology (2017). PMID: 28444738 DOI: 10.1111/bph.13837 Source material
[3] Ales Stuchlik, Tomas Petrasek, Karel Vales. Effect of alpha1-adrenergic antagonist prazosin on behavioral alterations induced by MK-801 in a spatial memory task in Long-Evans rats Physiological Research (2009). PMID: 19093715 DOI: 10.33549/physiolres.931636 Source material

Publications

1 publication citing this product

Reiko Watanabe, .et al. , J Med Chem, 2021, Mar 11;64(5):2725-2738 PMID: 33619967

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Prazosin HCl

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Biological Activity

Bioactivity / Mechanism

Target & Activity

In Vitro Studies

Prazosin competes for α1-adrenoceptor binding in isolated rat arteries

Literature-Reported Treatment Conditions

Agonist-dependent antagonism of ERK1/2 phosphorylation

Literature-Reported Treatment Conditions

In Vivo Studies

Limited behavioural modulation in MK-801-treated rats

Conditions shared by the study groups

Specifications

Storage & Solubility

In Vitro Solubility

Reported Solubility

Preparing Stock Solutions

Storage

Research References

Publications

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