α adrenergic receptor
α1-adrenergic receptor (Ki = 0.36 nM for α1A, 0.44 nM for α1B, 0.61 nM for α1D subtypes) [5]
- α1-adrenergic receptor (IC50 = 1.2 nM for α1A, 1.5 nM for α1B, 2.1 nM for α1D subtypes) [2]
- α1B-adrenergic receptor (Ki = 0.8 nM) [4]

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]

---

Incubation of vascular smooth muscle cells with Prazosin HCl (10 nM) inhibited phenylephrine-induced Ca²⁺ influx by 78%, suppressing cell contraction via α1-adrenergic receptor blockade [1]
- Treatment of cardiomyocytes with Prazosin HCl (1-100 nM) dose-dependently reduced α1-adrenergic receptor-mediated cAMP accumulation, with maximum inhibition (65%) at 100 nM [1]
- Prazosin HCl (0.1-10 nM) competitively displaced [³H]prazosin binding to α1-adrenergic receptors in rat brain membrane preparations, with high selectivity over α2 and β-adrenergic receptors [5]
- In human recombinant α1-adrenergic receptor-expressing cells, Prazosin HCl (0.01-100 nM) blocked norepinephrine-induced inositol phosphate production, with IC50 values consistent across α1A, α1B, and α1D subtypes [2]

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].

---

Oral administration of Prazosin HCl (1 mg/kg) to spontaneously hypertensive rats (SHRs) reduced systolic blood pressure by 35 mmHg within 2 hours, maintaining hypotensive effect for 6 hours [1]
- Intraperitoneal injection of Prazosin HCl (0.5 mg/kg) in mice inhibited stress-induced increases in locomotor activity by 40%, mediated via central α1-adrenergic receptor antagonism [3]
- In normotensive rats, Prazosin HCl (0.3 mg/kg, iv) decreased peripheral vascular resistance by 28%, without significant effect on heart rate [5]
- Chronic administration of Prazosin HCl (0.2 mg/kg/day, po) to SHRs for 4 weeks normalized blood pressure and reduced left ventricular hypertrophy by 22% [1]

Membrane preparations were isolated from rat tissues (brain, vascular smooth muscle) and incubated with [³H]prazosin (0.5 nM) in the presence or absence of Prazosin HCl (0.01-1000 nM). After incubation at 25°C for 60 minutes, unbound ligand was removed by rapid filtration, and bound radioactivity was measured by liquid scintillation counting. Binding affinity (Ki) was calculated using Scatchard analysis [5]
- Recombinant α1-adrenergic receptor-expressing cells were lysed, and membrane fractions were mixed with Prazosin HCl (0.001-100 nM) and [³H]norepinephrine (1 nM). The mixture was incubated at 37°C for 30 minutes, followed by centrifugation to pellet membranes. Bound radioactivity was quantified, and IC50 values were determined by nonlinear regression [2]

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]

---

Vascular smooth muscle cells were seeded in 24-well plates and cultured to confluence. Cells were pretreated with Prazosin HCl (0.1-100 nM) for 30 minutes, then stimulated with phenylephrine (1 μM). Intracellular Ca²⁺ concentration was measured using a fluorescent Ca²⁺ indicator, and cell contraction was assessed by phase-contrast microscopy [1]
- Cardiomyocytes were isolated from adult rats and plated in culture dishes. After 24 hours of culture, cells were treated with Prazosin HCl (1-100 nM) and norepinephrine (1 μM). cAMP levels were determined by enzyme-linked immunosorbent assay (ELISA) following 15 minutes of incubation [1]

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).

---

Spontaneously hypertensive rats (male, 12 weeks old) were randomly divided into control and treatment groups. Prazosin HCl was dissolved in 0.9% saline and administered orally at 1 mg/kg once daily for 4 weeks. Blood pressure was measured weekly using tail-cuff plethysmography, and heart weight/body weight ratio was calculated at the end of the study [1]
- Male C57BL/6 mice (8 weeks old) received intraperitoneal injections of Prazosin HCl (0.5 mg/kg) or vehicle 30 minutes before exposure to restraint stress. Locomotor activity was monitored for 60 minutes using an open-field test apparatus [3]
- Normotensive Wistar rats (male, 10 weeks old) were anesthetized, and Prazosin HCl (0.3 mg/kg) was administered via intravenous injection. Peripheral vascular resistance and heart rate were measured using a carotid artery catheter connected to a pressure transducer [5]

Absorption, Distribution and Excretion
The absorption rate and plasma concentration of prazosin vary between and within individuals. The absolute oral bioavailability of prazosin also varies among individuals, but has been reported to average approximately 60% (range: 43-82%). One study indicated that the presence of food may delay drug absorption in some patients, but does not affect the extent of absorption. Following oral administration of prazosin hydrochloride, peak plasma drug concentrations are reached in most fasting patients within 2-3 hours. Plasma concentrations of prazosin are generally not correlated with therapeutic efficacy. One manufacturer reported plasma drug concentrations ranging from 0.01 to 0.075 μg/ml after a single 5 mg dose. Blood pressure begins to decrease within 2 hours after oral administration; the maximum decrease occurs between 2 and 4 hours. The antihypertensive effect of prazosin lasts less than 24 hours. Animal studies show that prazosin is widely distributed throughout the body. In dogs, after intravenous injection, the highest drug concentrations were found in the lungs, coronary arteries, aorta, paw arteries, and heart; the lowest concentrations were found in the brain. During prazosin treatment, approximately 97% of the drug in plasma is bound to proteins. It is currently unknown whether the drug can cross the placenta. A small amount of prazosin is secreted into breast milk. Approximately 6-10% of the dose is excreted in the urine, with the remainder excreted in the feces via bile. The drug (prazosin hydrochloride) is tightly bound to plasma proteins (primarily α1-acid glycoproteins), with only 5% of the drug circulating freely in the bloodstream; certain diseases (such as inflammation) can affect the concentration of this protein, thus altering the proportion of free drug. Prazosin is extensively metabolized in the liver, with almost no unexcreted drug via the kidneys. Animal studies have shown that prazosin hydrochloride is extensively metabolized in the liver, primarily through demethylation and conjugation, and is excreted as the original drug (5-11%) and metabolites. Four metabolites have been shown to possess 10-25% of the antihypertensive activity of prazosin, which may contribute to the drug's antihypertensive effect.
6-O-demethyl and 7-O-demethyl analogs of the novel antihypertensive drug prazosin [2-[4-(2-furanoyl)-piperazin-1-yl]-4-amino-6,7-dimethoxyquinazoline hydrochloride] have been definitively synthesized via a 10-step reaction sequence, starting with isovanillin and vanillin, respectively. The 6-O-demethyl derivative was found to be identical to the major prazosin metabolite formed in dogs and mice, while the 7-O-demethyl derivative was identical to another less abundant but important metabolite. Two minor metabolites of prazosin, 2-(1-piperazinyl)-4-amino-6,7-dimethoxyquinazoline and 2,4-diamino-6,7-dimethoxyquinazoline, were also described. All four metabolites showed weaker antihypertensive effects than prazosin in dogs, but since they constitute a large portion of the administered dose, they may contribute to the antihypertensive effect of prazosin.

---

Biological half-life
Elimination half-life is about 3 hours.
It has been reported that the plasma half-life after oral administration of prazosin is 2-4 hours.

---

After oral administration of prazosin hydrochloride (1 mg/kg) to rats, the peak plasma concentration (Cmax) reached 8.2 ng/mL in 1 hour, and the oral bioavailability was 68%[5].
- The elimination half-life (t1/2) of prazosin hydrochloride in rats was 2.3 hours, and 72% of the administered dose was excreted in urine within 24 hours (45% as the original drug and 27% as metabolites). (Metabolites)[5]
- In humans, prazosin hydrochloride is rapidly absorbed from the gastrointestinal tract. After a single oral administration of 2 mg, the peak plasma concentration (Cmax) was 5.4 ng/mL, and the half-life (t1/2) was 2.5-3 hours[2]

Hepatotoxicity
Prazosin is associated with a low incidence of elevated serum transaminase levels, which, in controlled trials, were not higher than in the placebo group. These elevations are transient and do not require dose adjustment. No clinically significant acute liver injury caused by prazosin has been reported in the literature, but the sponsor has received reports of cholestatic hepatitis. Among alpha-adrenergic receptor antagonists, alfuzosin is the most commonly associated with liver injury, while other alpha-blockers have only been associated with liver injury in isolated cases with insufficient evidence. Therefore, acute symptomatic liver injury caused by prazosin is very rare, and severe hepatotoxicity, even if it occurs, is extremely rare. Probability score: E (Rare cause of suspected but unproven clinically significant liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation Due to limited information on the use of prazosin during lactation, alternative medications may be preferred, especially in breastfeeding newborns or preterm infants.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
No published information found on lactating women as of the revision date. Prazosin does not affect serum prolactin concentrations in patients with hypertension. Prolactin levels in established lactating mothers may not affect their ability to breastfeed.

---

Protein binding It binds highly to proteins, with binding rates up to 97% to albumin and α1-acid glycoprotein. Prazosin is considered to bind primarily (approximately 80-90%) to albumin.

---

Male oral TDLo 1714 ug/kg Behavior: Coma; Lungs, pleura or respiration: Dyspnea, Human Toxicology, 4(53), 1985 [PMID:3988304]
Human TDLo oral 285 ug/kg Vascular: Decreased blood pressure not described in the autonomic part, JAMA, 238(157), 1977 [PMID:577290]
Female TDLo oral 13 mg/kg/6W-I Brain and meninges: Encephalitis; Behavior: Somnolence (overall activity inhibition); Behavior: Toxic psychosis, BMJ, 293(1347), 1986
Female TDLo oral 10 ug/kg Behavior: Coma; Vascular: Decreased blood pressure not described in the autonomic part; Skin and appendages (skin): Sweating; Other, Drug Information and Clinical Pharmacy, 21(723), 1987 [PMID:3652934]
Rat LD50 Oral administration of 1950 mg/kg Gastrointestinal tract: alteration of salivary gland structure or function; Gastrointestinal tract: nausea or vomiting; Kidneys, ureters and bladder: other changes, The Pharmacy. Pharmacology and Metrology, 17(39), 1979
Prazosin hydrochloride, oral administration of up to 10 mg/kg/day in rats for 3 months did not cause significant changes in liver and kidney function [5]
- Prazosin hydrochloride has a plasma protein binding rate of 95% in human plasma and 92% in rat plasma [2]
- Intravenous administration of prazosin hydrochloride to mice at doses up to 5 mg/kg did not show acute toxicity [3]

[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.

Prazosin hydrochloride is a synthetic piperazine derivative with antihypertensive and antiadrenergic properties. As a selective α1-adrenergic receptor antagonist, prazosin hydrochloride reduces peripheral resistance and relaxes vascular smooth muscle through a mechanism not fully understood. It is used to treat heart failure, hypertension, pheochromocytoma, Raynaud's syndrome, benign prostatic hyperplasia, and urinary retention. (NCI04)
A selective α1-adrenergic receptor antagonist used to treat heart failure, hypertension, pheochromocytoma, Raynaud's disease, benign prostatic hyperplasia, and urinary retention.
See also: Prazosin (with active moiety); Polythiazides; Prazosin hydrochloride (component).
Mechanism of Action

Animal studies have shown that the antihypertensive effect of prazosin is not mediated through the central nervous system. Prazosin does not interfere with nerve impulse transmission in sympathetic ganglia, nor does it cause adrenergic neuronal blockade.
The exact mechanism of prazosin's antihypertensive effect is unclear. Prazosin reduces total peripheral resistance and was initially thought to have a direct vasodilatory effect on vascular smooth muscle. Animal studies have shown that the vasodilatory effect of prazosin is also related to the blockade of postsynaptic α-adrenergic receptors. Canine forelimb experiments indicated that the peripheral vasodilatory effect of prazosin is primarily limited to resistance vessels (arterioles). Unlike traditional α-receptor blockers, the hypotensive effect of prazosin is usually not accompanied by reflex tachycardia. Prazosin…is a very potent and selective α1-adrenergic antagonist. …Interestingly, it is also a relatively potent inhibitor of cyclic nucleotide phosphodiesterase… Blocking central α1-adrenergic receptors is considered one of the possible factors contributing to the atypical antipsychotic effects of clozapine. Therefore, in this study, we investigated the effects of simultaneous blocking of α1-adrenergic receptors and dopamine D2 receptors on conditioned avoidance responses (as an indicator of antipsychotic-like activity) and the induction of rigidity in rats (as a test for the risk of extrapyramidal side effects). Studies have found that pre-administration of the α1-adrenergic receptor antagonist prazosin (0.2 mg/kg, subcutaneous injection) enhances the inhibitory effect of the dopamine D2 receptor antagonist rivulipride (0.05–0.20 mg/kg, subcutaneous injection) on conditioned avoidance responses. This effect is most pronounced at the threshold dose of rivulipride (0.05 mg/kg). At these doses, neither prazosin nor rivulipride, alone or in combination, induces rigidity. Furthermore, pre-administration of prazosin (0.2 mg/kg, subcutaneous injection) does not alter the rigidity induced by higher doses of rivulipride (1.0 mg/kg, subcutaneous injection). Some studies suggest that additional α1-adrenergic receptor blockade may improve the efficacy of antipsychotic drugs, thereby improving the therapeutic window for Parkinson's disease, in cases of low dopamine D2 receptor occupancy. [4]

---

This study investigated the potential inhibitory effects of the α1-adrenergic receptor antagonist prazosin (1-(4-amino-6,7-dimethoxy-2-quinazolinyl)-4-(2-furanylcarbonyl)piperazine) on the motility activity of the nucleus accumbens and the concentrations of extracellular dopamine and its metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), as well as the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA), induced by the psychostimuli-induced noncompetitive NMDA receptor antagonist MK-801 ((+)-5-methyl-10,11-dihydroxy-5H-dibenzo-(a,d)cycloheptene-5,10-imine), as well as these changes were assessed by microdialysis in freely moving rats. Subcutaneous injection of MK-801 (0.1 and 0.3 mg/kg) significantly increased horizontal motility activity in a dose-dependent manner, but had no effect on orthostatic behavior. Prazosin alone (1 mg/kg, subcutaneous injection) only slightly reduced horizontal motor activity during the initial 10-minute measurement period, but persistently reduced upright behavior. However, prazosin pretreatment effectively inhibited motor stimulation induced by MK-801 (0.1 and 0.3 mg/kg) throughout the observation period (40 minutes). Both doses of MK-801 significantly increased extracellular dopamine levels in the nucleus accumbens, with increases up to approximately 90%. Furthermore, MK-801 dose-dependently increased the concentration of dopamine metabolites in the nucleus accumbens, but 5-hydroxyindoleacetic acid (5-HIAA) only showed a significant increase at high doses of MK-801. Prazosin alone had no effect on levels of dopamine, DOPAC, HVA, or 5-HIAA. However, prazosin pretreatment effectively blocked the MK-801-induced increase in dialysate dopamine concentrations. Therefore, the potent and selective α1-adrenergic receptor antagonist prazosin was found to specifically inhibit MK-801-induced dopamine release in the nucleus accumbens, rather than basal dopamine release, while effectively blocking MK-801-induced motor excitation with negligible effects on basal motor activity. This suggests that α1-adrenergic receptor antagonism may exert its effects by reducing the sensitivity of the mesolimbic dopamine system to drug or environmental stimuli. Since most antipsychotic drugs possess dopamine D2 receptor and α1-adrenergic receptor antagonistic properties, they can alleviate psychosis not only by blocking postsynaptic dopamine receptors but also by acting on the presynaptic mesolimbic dopamine system through their α1-adrenergic receptor antagonism. This latter effect may help reduce induced dopamine overactivity, such as in stress responses. [5] Prazosin hydrochloride is a selective α1-adrenergic receptor antagonist used clinically to treat hypertension and benign prostatic hyperplasia. [1] Prazosin hydrochloride’s effects on the central nervous system include inhibiting stress-induced noradrenergic activation, which may contribute to its use in treating nightmares associated with post-traumatic stress disorder (PTSD). [3] Prazosin hydrochloride exerts its hypotensive effect by blocking α1-adrenergic receptors in vascular smooth muscle, resulting in vasodilation and reduced peripheral resistance. [1]

C19H22CLN5O4

419.86

419.136

C, 54.35; H, 5.28; Cl, 8.44; N, 16.68; O, 15.24

19237-84-4

Prazosin; 19216-56-9; Prazosin-d8; 1006717-55-0

68546

White to off-white crystalline powder

638.4ºC at 760 mmHg

277 - 280 °C

339.9ºC

3.4E-16mmHg at 25°C

2.519

2

8

4

29

544

0

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]

WFXFYZULCQKPIP-UHFFFAOYSA-N

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

[4-(4-amino-6,7-dimethoxyquinazolin-2-yl)piperazin-1-yl]-(furan-2-yl)methanone;hydrochloride

2934.99.9001

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.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

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.

---

View More

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.)