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Prazosin HCl

Alias: cp-12299-1; Prazosin Hydrochloride; Prazosin HCl; Prazosin hydrochloride; 19237-84-4; Prazosin HCl; Minipress; Vasoflex; Furazosin hydrochloride; Peripress; Minipress Xl; Furazosin hydrochloride; cp12299-1; cp 12299-1; Minipress; Peripress; Prazosin
Cat No.:V1137 Purity: ≥98%
Prazosin HCl (Furazosin, cp12299-1; cp-12299-1; Minipress, Peripress), the hydrochloride salt of prazosin, is a potent and competitive alpha-1 adrenoceptor antagonist with antihypertensive effects.
Prazosin HCl
Prazosin HCl Chemical Structure CAS No.: 19237-84-4
Product category: Adrenergic Receptor
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Prazosin HCl:

  • Prazosin
  • Prazosin-d8 (prazosin-d8)
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Top Publications Citing lnvivochem Products
Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Prazosin HCl (Furazosin, cp12299-1; cp-12299-1; Minipress, Peripress), the hydrochloride salt of prazosin, is a potent and competitive alpha-1 adrenoceptor antagonist with antihypertensive effects. It has been used to treat heart failure, hypertension, pheochromocytoma, Raynaud disease, prostratic hypertrophy, high blood pressure, or benign prostatic hyperplasia (BPH). It has also been used to treat urinary retention. Only in the presence of eNOS does prazosin cause a notable rise in VEGF concentration in endothelial cells and angiogenesis. Prazosin attaches itself to the α1-adrenergic receptors found on the smooth muscle cells encircling all major blood vessels.

Biological Activity I Assay Protocols (From Reference)
Targets
α adrenergic receptor
ln Vitro
In vitro activity: Prazosin only causes angiogenesis and a marked rise in VEGF concentration in endothelial cells when eNOS is present. All larger blood vessels' smooth muscle cells have α1-adrenergic receptors, which are bound by prazosin.[1] Prazosin (0.1 nM) does not considerably lessen the vasomotor effect of exogenous noradrenaline, but it does block the increases in perfusion pressure brought on by electrical stimulation of the perimesenteric nerves.[2]
ln Vivo
Prazosin (0.05-0.20 mg/kg s.c.), a dopamine D2 receptor antagonist, increases the suppression of the conditioned avoidance response when prazosin (0.2 mg kg(-1) s.c.) is administered in rats.[4] In rats that are free to move, the administration of 1 mg/kg of prazosin s.c. consistently lowers rearing but only marginally decreases horizontal activity during the first 10-minute study period. In rats that are free to roam around, prazosin successfully inhibits the locomotor stimulation brought on by either dosage of MK-801.[5]
The increase of wall shear stress in capillaries by oral administration of the alpha1-adrenergic receptor antagonist prazosin induces angiogenesis in skeletal muscles. Because endothelial nitric oxide synthase (eNOS) is upregulated in response to elevated wall shear stress, we investigated the relevance of eNOS for prazosin-induced angiogenesis in skeletal muscles. Prazosin and/or the NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) were given to C57BL/6 wild-type mice and eNOS-knockout mice for 14 days. The capillary-to-fiber (C/F) ratio and capillary density (CD; no. of capillaries/mm2) were determined in frozen sections from extensor digitorum longus (EDL) muscles of these mice. Immunoblotting was performed to quantify eNOS expression in endothelial cells isolated from skeletal muscles, whereas VEGF (after precipitation with heparin-agarose) and neuronal NOS (nNOS) concentrations were determined in EDL solubilizates. In EDL muscles of C57BL/6 mice treated for 14 days, the C/F ratio was 28% higher after prazosin administration and 11% higher after prazosin and L-NAME feeding, whereas the CD increased by 21 and 13%, respectively. The C/F ratio was highest after day 4 of prazosin treatment and decreased gradually to almost constant values after day 8. Prazosin administration led to elevation of eNOS expression. VEGF levels were lowest at day 4, whereas nNOS values decreased after day 8. In EDL muscles of eNOS-knockout mice, no significant changes in C/F ratio, CD, or VEGF and nNOS expression were observed in response to prazosin administration. Our data suggest that the presence of eNOS is essential for prazosin-induced angiogenesis in skeletal muscle, albeit other signaling molecules might partially compensate for or contribute to this angiogenic activity. Furthermore, subsequent remodeling of the capillary system accompanied by sequential downregulation of VEGF and nNOS in skeletal muscle fibers characterizes shear stress-dependent angiogenesis. [1]
Prazosin (0.5-2.0 mg/kg) blocked yohimbine-induced reinstatement of food and alcohol seeking, as well as footshock-induced reinstatement of alcohol seeking. Guanfacine attenuated yohimbine-induced reinstatement of alcohol seeking at the highest dose (0.5 mg/kg), but its effect on yohimbine-induced reinstatement of food seeking was not significant. Neither prazosin nor guanfacine affected high-rate food-reinforced responding. Conclusions: Results demonstrate an important role of postsynaptic alpha-1 adrenoceptors in stress-induced reinstatement of alcohol and food seeking[3].
Cell Assay
Background: Prazosin, a non-selective α1-adrenoceptor and a selective α2B-adrenoceptor antagonist, is reported to possess anti-cancer activity in some types of cancer. The aim of this study was to investigate the effect of prazosin on acute myeloid leukemia (AML) and the underlying relevant mechanisms.
Methods: AML cell lines U937 and HL60 were treated with different concentration of prazosin (5, 10 and 15 μM), CCK8 and flow cytometry assays were performed to examine the effects of prazosin on cell viability, cell cycle distribution and apoptosis. Western blot assay was used to detect the expression of related proteins.
Results: We observed that prazosin inhibited cell viability of U937 and HL60 cells and induced the rate of apoptosis in a dose-dependent manner, as well as induced cell cycle arrest at G1 phase. The activation of PI3K/Akt/mTOR signaling pathway was significantly suppressed by prazosin via reducing the phosphorylation of Akt and mTOR. Moreover, by RNA-seq analysis, we found that the expression of tensin 1 (TNS1) was down-regulated by prazosin, and down-regulation of TNS1 could inhibit cell viability of U937 and HL60 cells, as well as induced cell apoptosis. The PI3K/Akt/mTOR signaling pathway was also suppressed by depletion of TNS1. Furthermore, up-regulation of TNS1 could reverse the effects of prazosin on viability and apoptosis in U937 and HL-60 cells, as well as the PI3K/Akt/mTOR signaling pathway.
Conclusion: These results highlight an anti-cancer activity of prazosin on AML by inhibiting the PI3K/Akt/mTOR pathway and targeting TNS1. [Biomed Pharmacother. 2020 Apr:124:109731]
Animal Protocol
In exp. 1, we trained rats to self-administer alcohol (12% w/v, 1 h/day), and after extinction of alcohol-reinforced lever pressing, we tested prazosin's (0.5, 1.0, and 2.0 mg/kg, i.p.) or guanfacine's (0.125, 0.25, and 0.5 mg/kg, i.p.) effect on yohimbine (1.25 mg/kg, i.p.)-induced reinstatement; we also examined prazosin's effect on intermittent-footshock-stress-induced reinstatement. In exp. 2, we trained food-restricted rats to self-administer 45 mg food pellets and first examined prazosin's or guanfacine's effects on food-reinforced responding, and then, after extinction of lever presses, on yohimbine-induced reinstatement. [3]
Animals and experimental procedures. [1]
In accordance with approvals obtained from the university and state authorities for animal welfare, this study was performed on C57BL/6 wild-type mice and eNOS-knockout mice, which were bred in our animal care facility under standard conditions. The eNOS-knockout strain was originally purchased from Jackson Laboratories. For the experiments, 195 healthy mice weighing 25–30 g (3–5 mo old) were used. The mice were anesthetized with ketamine and killed by heart excision.
To dissolve prazosin, tap water was adjusted with HCl to pH 5.8 and heated to 60°C before addition of 50 mg/l ground prazosin powder. This concentration has been shown to induce angiogenesis in rats. The inhibitor Nω-nitro-l-arginine methyl ester (l-NAME), which is specific for all NOS forms, was obtained from Sigma and freshly prepared in a concentration of 1 mg/ml dissolved in tap water as previously described to be applied daily. Because a mouse drinks ∼3 ml of water/day, 150 μg of prazosin and/or 3 mg of l-NAME, respectively, were required each day.
For determination of angiogenesis and its relation to NO availability, mice from each of the two mouse strains were assigned to four groups consisting of at least five animals each. For 14 days, one group was treated with prazosin dissolved in drinking water, whereas the control group received water without prazosin. A third group of mice was treated with a combination of prazosin and l-NAME, and a forth group was fed with l-NAME alone.
The time course of prazosin-induced angiogenesis was investigated in groups of C57BL/6 mice and eNOS-knockout mice (3 animals/group) treated with prazosin for 3, 4, 8, or 14 days compared with control animals that received tap water alone (0 days).
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
There is intraindividual and interindividual variation in the rate of absorption and plasma concentrations of prazosin. The absolute oral bioavailability of prazosin is also variable but is reported to average about 60% (range: 43-82%). Results of one study indicate that the presence of food may delay absorption of the drug in some patients, but does not affect the extent of absorption.
Following oral administration of prazosin hydrochloride, plasma concentrations of the drug reach a peak in 2-3 hrs in most fasting patients. Plasma concentrations of prazosin generally do not correlate with therapeutic effect. One manufacturer reports that plasma concentrations of the drug after a single 5 mg dose range from 0.01-0.075 ug/ml. Blood pressure begins to decrease within 2 hr after an oral dose; the maximum decrease occurs in 2-4 hr. The hypotensive effect of prazosin lasts less than 24 hr.
Animal studies indicate that prazosin is widely distributed in body tissues. After iv administration in dogs, highest concentrations of the drug are found in the lungs, coronary arteries, aorta, paw arteries and heart; the lowest concentrations are in the brain. During prazosin therapy, approximately 97% of the drug in plasma is bound to proteins. It is not known whether the drug crosses the placenta. Prazosin is distributed into milk in small amounts.
Approximately 6-10% of a dose is excreted in urine and the remainder in feces via bile.
The drug /prazosin hydrochloride/ is tightly bound to plasma proteins (primarily alpha1-acid glycoprotein), and only 5% of the drug is free in the circulation; diseases that modify the concentration of this protein (e.g., inflammatory processes) may change the free fraction. Prazosin is extensively metabolized in the liver, and little unchanged drug is excreted by the kidneys.
Metabolism / Metabolites
Animal studies show that prazosin hydrochloride is metabolized extensively in the liver, principally by demethylation and conjugation, and excreted as unchanged drug (5-11%) and metabolites. Four of the metabolites have been shown to possess 10-25% of the hypotensive activity of prazosin and they may contribute to the antihypertensive effect of the drug.
The 6-O-demethyl and 7-O-demethyl analogues of the new antihypertensive drug prazosin [2-[4-(2-furoyl)-piperazin-1-yl]-4-amino-6,7-dimethoxyquinazoline hydrochloride] have been unequivocally synthesized via separate 10-step reaction sequences starting from isovanillin and vanillin, respectively. The 6-O-demethyl derivative was found to be identical with the major prazosin metabolite formed in dog and rat, while the 7-O-demethyl derivative was identical with another, less prevalent but significant metabolite. Two minor metabolites of prazosin, 2-(1-piperazinyl)-4-amino-6,7-dimethoxyquinazoline and 2,4-diamino-6,7-dimethoxyquinazoline, are also described. All 4 metabolites are less potent blood pressure lowering agents in dogs than prazosin but may contribute to its antihypertensive effect, since they account for a major portion of the administered dose.
Biological Half-Life
Elimination half-life approx 3 hr.
The plasma half-life of prazosin after oral administration has been reported to be 2-4 hr.
Toxicity/Toxicokinetics
Hepatotoxicity
Prazosin has been associated with a low rate of serum aminotransferase elevations that in controlled trials was no higher than with placebo therapy. These elevations were transient and did not require dose modification. No instances of clinically apparent acute liver injury due to prazosin have been published in the literature, but reports of cholestatic hepatitis have been received by the sponsor. Among the alpha adrenergic receptor antagonists, the most frequently implicated agent in causing liver injury has been alfuzosin with only single, and not well documented cases linked to other alpha blockers. Thus, acute symptomatic liver injury due to prazosin is quite rare, and severe hepatotoxicity must be exceeding rare, if it occurs at all.
Likelihood score: E* (unproven but suspected rare cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because little is available on the use of prazosin during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information in nursing mothers was not found as of the revision date. Prazosin does not affect serum prolactin concentration in patients with hypertension. The prolactin level in a mother with established lactation may not affect her ability to breastfeed.
Protein Binding
Highly bound to proteins with 97% binding to albumin and alpha 1-acid glycoprotein. Prazosin is thought to be mostly (about 80-90%) bound to albumin.
man TDLo oral 1714 ug/kg BEHAVIORAL: COMA; LUNGS, THORAX, OR RESPIRATION: DYSPNEA Human Toxicology., 4(53), 1985 [PMID:3988304]
human TDLo oral 285 ug/kg VASCULAR: BP LOWERING NOT CHARACTERIZED IN AUTONOMIC SECTION JAMA, Journal of the American Medical Association., 238(157), 1977 [PMID:577290]
women TDLo oral 13 mg/kg/6W-I BRAIN AND COVERINGS: ENCEPHALITIS; BEHAVIORAL: SOMNOLENCE (GENERAL DEPRESSED ACTIVITY); BEHAVIORAL: TOXIC PSYCHOSIS British Medical Journal., 293(1347), 1986
women TDLo oral 10 ug/kg BEHAVIORAL: COMA; VASCULAR: BP LOWERING NOT CHARACTERIZED IN AUTONOMIC SECTION; SKIN AND APPENDAGES (SKIN): SWEATING: OTHER Drug Intelligence and Clinical Pharmacy., 21(723), 1987 [PMID:3652934]
rat LD50 oral 1950 mg/kg GASTROINTESTINAL: CHANGES IN STRUCTURE OR FUNCTION OF SALIVARY GLANDS; GASTROINTESTINAL: NAUSEA OR VOMITING; KIDNEY, URETER, AND BLADDER: OTHER CHANGES Oyo Yakuri. Pharmacometrics., 17(39), 1979
References

[1]. Am J Physiol Heart Circ Physiol . 2004 Nov;287(5):H2300-8.

[2]. J Pharmacol Exp Ther . 1997 Aug;282(2):691-8.

[3]. Psychopharmacology (Berl) . 2011 Nov;218(1):89-99.

[4]. J Neural Transm (Vienna) . 2000;107(10):1229-38.

[5]. Eur J Pharmacol . 1996 Aug 1;309(1):1-11.

Additional Infomation
Prazosin Hydrochloride is a synthetic piperazine derivative with hypotensive antiadrenergic properties, Prazosin Hydrochloride reduces peripheral resistance and relaxes vascular smooth muscles as a selective adrenergic alpha-1 antagonist by a mechanism not completely known. It is used in the treatment of heart failure, hypertension, pheochromocytoma, Raynaud's syndrome, prostatic hypertrophy, and urinary retention. (NCI04)
A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.
See also: Prazosin (has active moiety); Polythiazide; prazosin hydrochloride (component of).
Mechanism of Action
Animal studies indicate that prazosin does not have its antihypertensive effect in the CNS. Prazosin does not interfere with nerve impulse transmission across sympathetic ganglia nor does it cause adrenergic neuronal blockade.
The exact mechanism of the hypotensive action of prazosin is unknown. Prazosin causes a decrease in total peripheral resistance and was originally thought to have a direct relaxant action on vascular smooth muscle. Animal studies have suggested that the vasodilator effect of prazosin is also related to blockade of postsynaptic alpha-adrenoceptors. The results of dog forelimb experiments demonstrate that that the peripheral vasodilator effect of prazosin is confined mainly to the level of the resistance vessels (arterioles). Unlike conventional alpha- blockers, the antihypertensive action of prazosin is usually not accompanied by reflex tachycardia.
Prazosin ... is a very potent and selective alpha 1-adrenergic antagonist. ... Interestingly, the drug also is a relatively potent inhibitor of cyclic nucleotide phosphodiesterases...
Blockade of central alpha1-adrenoceptors has been implicated as a possible factor contributing to the atypical antipsychotic profile of clozapine. Thus, in the present study we examined the effects of concomitant alpha1-adrenoceptor and dopamine D2 receptor blockade on conditioned avoidance response performance, as an index of antipsychotic-like activity, and on the induction of catalepsy, as a test for extrapyramidal side effect liability, in rats. It was found that pretreatment with the alpha1-adrenoceptor antagonist prazosin (0.2mg kg(-1) s.c.) caused an enhancement of a suppression of conditioned avoidance response in the presence of the dopamine D2 receptor antagonist raclopride (0.05-0.20 mg kg(-1) s.c.). The effect was most prominent at a subthreshold dose of raclopride (0.05 mg kg(-1)). At these doses, prazosin or raclopride by themselves, or in combination, did not produce catalepsy. In addition, pretreatment with prazosin (0.2mgkg(-1) s.c.) did not alter the catalepsy produced by a higher dose of raclopride (1.0 mg kg(-1) s.c.). It is suggested that, in the presence of low dopamine D2 receptor occupancy, additional alpha1-adrenoceptor blockade might improve antipsychotic efficacy, and thereby improve the therapeutic window with regard to parkinsonism. [4]
This study examined the putative inhibitory effect of the alpha 1-adrenoceptor antagonist prazosin (1-(4-amino-6,7-dimethoxy-2-quinazolinyl)-4-(2-furanylcarbonyl)pip erazine) on changes evoked by the psychotomimetic, non-competitive NMDA receptor antagonist, MK-801((+)-5-methyl-10,11-dihydroxy-5H-dibenzo-(a,d)cyclohepten-5, 10-imine), in locomotor activity and extracellular concentrations of dopamine and its metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the nucleus accumbens as assessed by microdialysis in freely moving rats. MK-801 (0.1 and 0.3 mg/kg, s.c.) induced a significant, dose-dependent increase in horizontal locomotor activity but did not affect rearing. Prazosin administration alone (1 mg/kg, s.c.) only slightly reduced horizontal activity during an initial 10 min measurement period, although it consistently reduced rearing. However, pretreatment with prazosin effectively suppressed the locomotor stimulation caused by either dose of MK-801 throughout the whole observation period, i.e. 40 min. Both doses of MK-801 significantly increased extracellular levels of dopamine in the nucleus accumbens up to approximately 90%. In addition, MK-801 dose dependently increased dopamine metabolite concentrations in the nucleus accumbens, but 5-HIAA was significantly increased only by the high dose of MK-801. When given alone, prazosin did not affect either dopamine, DOPAC, HVA or 5-HIAA levels. However, prazosin pretreatment effectively blocked MK-801-evoked increases in dialysate dopamine concentrations. Consequently, the potent and selective alpha 1-adrenoceptor antagonist prazosin was found to specifically suppress MK-801-evoked, but not basal dopamine release in the nucleus accumbens, while effectively blocking MK-801-evoked locomotor stimulation with only negligible effects on basal locomotor activity. Thus, alpha 1-adrenoceptor antagonism may act by reducing the sensitivity of the mesolimbic dopamine system to pharmacological or environmental challenge. Since most antipsychotic drugs exhibit both dopamine D2 receptor and alpha 1-adrenoceptor antagonistic properties, they may alleviate psychosis not only through blockade of postsynaptic dopamine receptors, but also presynaptically on the mesolimbic dopamine system, through their alpha 1-adrenoceptor antagonistic action. This latter action may contribute to reduce evoked dopamine hyperactivity, e.g. in response to stress.[5]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C19H22CLN5O4
Molecular Weight
419.86
Exact Mass
419.136
Elemental Analysis
C, 54.35; H, 5.28; Cl, 8.44; N, 16.68; O, 15.24
CAS #
19237-84-4
Related CAS #
Prazosin; 19216-56-9; Prazosin-d8; 1006717-55-0
PubChem CID
68546
Appearance
White to off-white crystalline powder
Boiling Point
638.4ºC at 760 mmHg
Melting Point
277 - 280 °C
Flash Point
339.9ºC
Vapour Pressure
3.4E-16mmHg at 25°C
LogP
2.519
Hydrogen Bond Donor Count
2
Hydrogen Bond Acceptor Count
8
Rotatable Bond Count
4
Heavy Atom Count
29
Complexity
544
Defined Atom Stereocenter Count
0
SMILES
Cl[H].O=C(C1=C([H])C([H])=C([H])O1)N1C([H])([H])C([H])([H])N(C2N=C(C3=C([H])C(=C(C([H])=C3N=2)OC([H])([H])[H])OC([H])([H])[H])N([H])[H])C([H])([H])C1([H])[H]
InChi Key
WFXFYZULCQKPIP-UHFFFAOYSA-N
InChi Code
InChI=1S/C19H21N5O4.ClH/c1-26-15-10-12-13(11-16(15)27-2)21-19(22-17(12)20)24-7-5-23(6-8-24)18(25)14-4-3-9-28-14;/h3-4,9-11H,5-8H2,1-2H3,(H2,20,21,22);1H
Chemical Name
[4-(4-amino-6,7-dimethoxyquinazolin-2-yl)piperazin-1-yl]-(furan-2-yl)methanone;hydrochloride
Synonyms
cp-12299-1; Prazosin Hydrochloride; Prazosin HCl; Prazosin hydrochloride; 19237-84-4; Prazosin HCl; Minipress; Vasoflex; Furazosin hydrochloride; Peripress; Minipress Xl; Furazosin hydrochloride; cp12299-1; cp 12299-1; Minipress; Peripress; Prazosin
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 4~14.3 mg/mL (9.5~34.0 mM)
Water: ~<1 mg/mL
Ethanol: ~<1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 1.43 mg/mL (3.41 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 14.3 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 1.43 mg/mL (3.41 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 14.3 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 1.43 mg/mL (3.41 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 14.3 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.3817 mL 11.9087 mL 23.8175 mL
5 mM 0.4763 mL 2.3817 mL 4.7635 mL
10 mM 0.2382 mL 1.1909 mL 2.3817 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT02965027 Active
Recruiting
Drug: Prazosin
Drug: Placebos
Post-Traumatic Headache Seattle Institute for Biomedical
and Clinical Research
November 29, 2016 Phase 4
NCT04793685 Recruiting Drug: Prazosin
Behavioral: 12-Step Facilitation
with Relapse Prevention and
Contingency Management
Alcohol Withdrawal Yale University July 1, 2021 Phase 1
Phase 2
NCT03539614 Recruiting Drug: Prazosin
Drug: Placebo
Posttraumatic Stress Disorder VA Office of Research andCDevelopment June 4, 2018 Phase 3
NCT04721353 Recruiting Drug: Prazosin Hydrochloride Cannabis Dependence
Cannabis Use Disorder
VA Puget Sound Health Care
System
November 9, 2020 Phase 4
NCT06147622 Not yet recruiting Drug: KT110
Drug: Prazosin + cyproheptadine
Alcohol Use Disorder Kinnov Therapeutics February 2024 Phase 1
Biological Data
  • Effect of prazosin or guanfacine on yohimbine-induced reinstatement and effect of prazosin on intermittent footshock-induced reinstatement. Psychopharmacology (Berl) . 2011 Nov;218(1):89-99.
  • Effect of prazosin or guanfacine on food-reinforced responding. Psychopharmacology (Berl) . 2011 Nov;218(1):89-99.
  • Upregulation of eNOS in skeletal muscles of C57BL/6 mice in response to prazosin. Am J Physiol Heart Circ Physiol . 2004 Nov;287(5):H2300-8.
  • Quantification of VEGF in EDL muscle homogenates of C57BL/6 mice and eNOS-knockout mice during 14 days of prazosin administration. Am J Physiol Heart Circ Physiol . 2004 Nov;287(5):H2300-8.
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