Bunazosin
(Synonyms: 布那唑嗪) 目录号 : GC64450
Bunazosin 是一种有效的选择性 α1-肾上腺素受体 (α1-adrenoceptor) 拮抗剂。Bunazosin 可用于抗高血压和降眼压研究。
Cas No.:80755-51-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Bunazosin is a potent and selective α1-adrenoceptor antagonist. Bunazosin can be used for antihypertensive and ocular hypotensive research[1].
[1]. Hideaki Hara , et al. Bunazosin, a selective alpha1-adrenoceptor antagonist, as an anti-glaucoma drug: effects on ocular circulation and retinal neuronal damage. Cardiovasc Drug Rev. Spring 2005;23(1):43-56.
| Cas No. | 80755-51-7 | SDF | Download SDF |
| 别名 | 布那唑嗪 | ||
| 分子式 | C19H27N5O3 | 分子量 | 373.45 |
| 溶解度 | 储存条件 | Store at -20°C | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.6777 mL | 13.3887 mL | 26.7773 mL |
| 5 mM | 0.5355 mL | 2.6777 mL | 5.3555 mL |
| 10 mM | 0.2678 mL | 1.3389 mL | 2.6777 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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2.
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Bunazosin, a selective alpha1-adrenoceptor antagonist, as an anti-glaucoma drug: effects on ocular circulation and retinal neuronal damage
Cardiovasc Drug Rev 2005 Spring;23(1):43-56.PMID:15867947DOI:10.1111/j.1527-3466.2005.tb00156.x.
Bunazosin hydrochloride is a potent and selective alpha1-adrenoceptor antagonist that has been clinically used both as a systemic antihypertensive as well as an ocular hypotensive drug. In a number of studies, we have examined some effects of Bunazosin hydrochloride that might indicate its potential as an anti-glaucoma drug. In normal rabbit eyes, topically instilled Bunazosin hydrochloride reached the posterior retina by local penetration at concentrations sufficient to attenuate the phenylephrine- or endothelin-1 (ET-1)-induced constriction of retinal arteries. Furthermore, Bunazosin hydrochloride improved the impairment of optic nerve head (ONH) blood flow, the prolongation of visual-evoked potentials (VEP) implicit time, the enlargement of the optic disk cup, and the decrease in the number of retinal ganglion cell layer cells induced by repeated injections of ET-1 in rabbits. Topically instilled Bunazosin hydrochloride improved the reductions in ONH capillary blood flow and VEP amplitude induced in rabbit eyes by nitric oxide synthase inhibition. In rat primary retinal cultures, Bunazosin hydrochloride reduced glutamate-induced neuronal cell death, presumably through a Na+ channel blocking effect. In healthy humans, topically instilled Bunazosin hydrochloride reportedly increases blood velocity in the ONH, retina and choroid, without significantly altering either blood pressure or heart rate. These results indicate that Bunazosin hydrochloride exerts both an improvement effect within the ocular circulation and a direct neuroprotective effect. Hence, Bunazosin hydrochloride may be useful as a therapeutic drug against ischemic retinal diseases (such as glaucoma and retinal vascular occlusive diseases) that are associated with disturbances of the ocular circulation.
Pharmacokinetic and pharmacodynamic properties and therapeutic use of Bunazosin in hypertension. A review
Arzneimittelforschung 1995 Nov;45(11):1166-71.PMID:8929232doi
Bunazosin (CAS 52712-76-2), a quinazoline derivative, selectively blocks alpha1-receptors. In addition to its potent antihypertensive property, beneficial effects on lipid metabolism, glucose metabolism, vascular smooth muscle cell proliferation, it can be used in the presence of concomitant diseases, such as obstructive bronchitis, chronic renal insufficiency, peripheral arterial occlusive disease, and diabetes mellitus. In its extended-release formulation (Bunazosin retard), it is generally a well-tolerated alpha1-blocker when compared to other agents in its class. Pharmacokinetic studies in normotensive volunteers showed that plasma peak concentration (Cmax) of Bunazosin retard and bioavailability were approximately 50% and 81%, respectively, of the values of the standard non-retarded formulation. Bunazosin is metabolized mainly in the liver, and urine excretion accounts for only 10% of unchanged Bunazosin. Following oral administration of 6 mg Bunazosin retard to healthy volunteers, Cmax was 15 ng/ml, time to reach peak level (tmax) was 4 h and elimination half life was about 12 h. Bunazosin retard has Cmax and area underthe concentration curve (AUC) to be linearly related to the dose between 3 and 18 mg (r = 0.8). As expected, patients with impaired hepatic functions have shown an increase in AUC, Cmax, and elimination half live values. The hemodynamic effects of Bunazosin are due to arterial vasodilation, reduced peripheral vascular resistance and cardiac afterload with moderate increase increase of cardiac output. Bunazosin was shown to decrease the systolic and diastolic blood pressure without a reflex tachycardia. In addition to its hypotensive effects Bunazosin significantly increased the effective renal blood flow (by 34%) and creatinine clearance (by 37%) in patients with essential hypertension. In patients with impaired renal function Bunazosin exhibits better increase in the effective renal plasma flow and glomerular filtration rate when compared to other alpha1-blockers (e.g. prazosin). Results of double-blind, randomized trials in 343 hypertensive patients showed Bunazosin to be a equipotent hypertensive agent without multiple titration as usually necessary for other alpha-blockers. Diastolic blood pressure was normalized (< or equal 90 mmHg) or reduced by at least 10 mm Hg in 47% and 46% of patients, respectively. Results of two one-year long term studies in more than 600 ¿young¿ and ¿elderly¿ hypertensive patients gave no hint for tachyphylaxia. Bunazosin proved to be superior to prazosin in terms of orthostatic tolerance, as tested with the Schellong test. In conclusion due to its antihypertensive properties, beneficial effects on vascular smooth muscle cells, glucose metabolism , and lipid profile, and the less likelihood of orthostatic hypotension following treatment, Bunazosin reard can be considered a useful antihypertensive agent.
Bunazosin reduces intraocular pressure in rabbits by increasing uveoscleral outflow
J Ocul Pharmacol Ther 1998 Jun;14(3):217-28.PMID:9671429DOI:10.1089/jop.1998.14.217.
The mechanism of the ocular hypotensive effect of Bunazosin hydrochloride (an alpha1-adrenergic antagonist) and the possible intermediary role of prostaglandins were studied in New Zealand albino rabbits. Aqueous flow, outflow facility and uveoscleral outflow were determined by fluorophotometry, and intraocular pressure (IOP) was measured by pneumatonometry on the fourth day of twice daily topical treatment with 0.1% Bunazosin. Uveoscleral outflow was measured with a tracer infusion technique at 1 to 2 hours after one dose of 0.1% Bunazosin. Total outflow facility was measured by a two-level constant-pressure infusion method before and at one hour after one dose of 0.1% Bunazosin. The effect of topically applied cyclooxygenase inhibitors, including 0.25% indomethacin and 0.03% flurbiprofen, on the IOP reduction after Bunazosin was evaluated. At 3 hours after the seventh consecutive dose given twice-daily, Bunazosin significantly (P<0.001) reduced IOP to 13.4+/-0.8 mm Hg (mean +/- SEM) from a baseline of 19.6+/-1.1 mm Hg. Indomethacin significantly inhibited the IOP reduction after one dose of Bunazosin, whereas flurbiprofen did not (repeated measures ANOVA). Bunazosin significantly increased uveoscleral outflow (P<0.05) and total outflow facility (P<0.02), but not fluorophotometric outflow facility or aqueous flow. It is concluded that, in rabbits, 0.1% Bunazosin reduces IOP predominantly by increasing uveoscleral outflow. The role of prostaglandins in this effect is equivocal.
Properties of [3H]Bunazosin binding in rat kidney
Clin Ther 1988;10(5):559-67.PMID:2908804doi
Properties of alpha 1-adrenoceptor binding in the renal cortex of rats were studied with [3H]Bunazosin as the radiolabeled ligand. Both temperature and incubation time influenced Bunazosin receptor binding. Subcellular distribution of [3H]-bunazosin binding revealed that the membrane fraction (30,000 x g pellet) had the largest proportion of total binding sites. Pretreatment of membrane preparation at 56 degrees C for 30 minutes greatly decreased the specific binding of [3H]-bunazosin, though there was no significant effect of the pretreatment at 24 degrees C and 37 degrees C for 30 minutes. Among various cations, some divalent ions such as Cu++ and Zn++ greatly decreased Bunazosin binding, whereas monovalent ions had no effect on specific binding. Results of Scatchard analysis suggested that the rat renal cortex membrane has single binding sites with an apparent dissociation constant of 0.38 +/- 0.06 nmol/L, though the rat medulla membrane has no potent binding activity with Bunazosin. The displacement study revealed that various adrenergic agents inhibit [3H]Bunazosin binding in dose-dependent fashion; the rank order of potencies was Bunazosin prazosin > phentolamine >> dl-norepinephrine > clonidine, yohimbine >> pindolol, propranolol. These findings reveal that Bunazosin has specific receptor binding in the rat renal cortex, indicating that alpha 1-adrenoceptors exist in the rat renal cortex.
Efficacy of Bunazosin hydrochloride 0.01% as adjunctive therapy of latanoprost or timolol
J Glaucoma 2004 Feb;13(1):73-80.PMID:14704548DOI:10.1097/00061198-200402000-00014.
Purpose: To evaluate the ocular hypotensive response of Bunazosin hydrochloride 0.01% administered as adjunctive therapy in patients with glaucoma who were already receiving latanoprost 0.005% or timolol 0.5%. Methods: Patients with primary open angle glaucoma who had received latanoprost (n = 60) or timolol (n = 60) for 6 months or longer were enrolled and prospectively randomized to receive additional administration of Bunazosin or placebo. One hundred twenty eyes of 120 patients were thus divided into 4 subgroups of 30 patients each. Bunazosin was administered twice daily, and timolol or latanoprost was administered per label. The patients were followed up for 3 months. Responders were defined as having a reduction in intraocular pressure of greater than 2 mm Hg from baseline. Results: Mean baseline intraocular pressure was 22.3 +/- 3.0 mm Hg in the Bunazosin subgroup and 22.3 +/- 3.1 mm Hg in the placebo subgroup of the latanoprost arm, and 22.5 +/- 3.5 mm Hg in the Bunazosin subgroup and 22.3 +/- 3.0 mm Hg in the placebo subgroup of the timolol arm. In the Bunazosin subgroups of both arms, intraocular pressure was significantly reduced compared with baseline measurements (P < 0.05) with mean intraocular pressure measurement reductions of 2.1 +/- 2.4 mm Hg and 2.8 +/- 2.1 mm Hg in the latanoprost arm and 2.6 +/- 2.1 mm Hg and 2.8 +/- 2.1 mm Hg in the timolol arm at 6 and 12 weeks after the start of the follow-up, respectively. In the latanoprost group, Bunazosin provided a further reduction of intraocular pressure (7.7%) at 12 weeks from that initially obtained at 2 weeks (P = 0.0377). In the placebo subgroups of the latanoprost and timolol arms, no significant change was found between at baseline and at any visit after the start of the follow-up. In the latanoprost and timolol arms, there was a significant difference in intraocular pressure and its change between the Bunazosin subgroup and placebo subgroup at any visit after 4 weeks from the start of the follow-up (P < 0.01). Conclusion: Bunazosin hydrochloride 0.01% may provide an additional intraocular pressure reduction in patients already receiving latanoprost or timolol. Since adding Bunazosin to eyes treated with latanoprost caused a relatively small hypotensive response at 2 weeks and provided a further reduction from 2 weeks to 12 weeks, longer than 4 weeks may be required to evaluate a clinically meaningful response to treatment. Further investigation on more cases and longer follow-up are needed.