Dopexamine hydrochloride (FPL60278AR)
(Synonyms: 盐酸多培沙明,FPL60278AR) 目录号 : GC32627
Dopexamine hydrochloride (FPL60278AR) 是一种 β2 肾上腺素能受体激动剂。
Cas No.:86484-91-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Dopexamine hydrochloride is a β2 adrenergic receptor agonist.
Dopexamine is a dopamine analogue with agonist activity at β2 and dopaminergic receptors. Dopexamine can attenuate the systemic inflammatory response, reduce tissue leukocyte infiltration, and protect against organ injury at doses that do not alter global hemodynamics or regional microvascular flow[1]. Dopexamine is a dopamine analog that stimulates β-adrenergic and dopamine 1 and 2 receptors, conferring some vasodilatory effects. Dopexamine reduces the systemic inflammatory response to endotoxin, including cytokine release, endothelial adhesion molecules, and oxidative stress, without substantially changing systemic hemodynamics, either blood pressure or stroke volume[2].
[1]. Bangash MN, et al. Dopexamine can attenuate the inflammatory response and protect against organ injury in the absence of significant effects on hemodynamics or regional microvascular flow. Crit Care. 2013 Mar 28;17(2):R57. [2]. Hollenberg SM. Dopexamine: immunomodulatory, hemodynamic, or both? Crit Care. 2013 May 13;17(3):143.
| Cas No. | 86484-91-5 | SDF | |
| 别名 | 盐酸多培沙明,FPL60278AR | ||
| Canonical SMILES | [H]Cl.[H]Cl.OC1=CC=C(CCNCCCCCCNCCC2=CC=CC=C2)C=C1O | ||
| 分子式 | C22H34Cl2N2O2 | 分子量 | 429.42 |
| 溶解度 | DMSO : 100 mg/mL (232.87 mM; Need ultrasonic) | 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 | 2.3287 mL | 11.6436 mL | 23.2872 mL |
| 5 mM | 0.4657 mL | 2.3287 mL | 4.6574 mL |
| 10 mM | 0.2329 mL | 1.1644 mL | 2.3287 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Dopexamine hydrochloride. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in acute cardiac insufficiency
Drugs 1990 Feb;39(2):308-30.PMID:1970288DOI:10.2165/00003495-199039020-00009.
Dopexamine hydrochloride is a novel synthetic catecholamine, structurally related to dopamine, with marked intrinsic agonist activity at beta 2-adrenoceptors, lesser agonist activity at dopamine DA1- and DA2-receptors and beta 1-adrenoceptors, and an inhibitory action on the neuronal catecholamine uptake mechanism. The drug is administered by intravenous infusion, and is characterized by a rapid onset and short duration of action. Short term haemodynamic studies in volunteers and patients with severe chronic heart failure have indicated that Dopexamine hydrochloride reduces afterload through pronounced arterial vasodilatation, increases renal perfusion by selective renal vasodilation and evokes mild cardiac stimulation through direct and indirect positive inotropism. Preliminary small-scale noncomparative studies indicate that Dopexamine hydrochloride displays beneficial haemodynamic effects in patients with acute heart failure and those requiring haemodynamic support following cardiac surgery, and that these effects are substantially maintained during longer term administration (less than or equal to 24 hours). Dopexamine hydrochloride appears to be generally well tolerated. Nausea and vomiting are the most frequently reported adverse effects, and respond to dosage reduction. Occasional reports of chest pain/angina pectoris precipitated by tachycardia indicates the need for caution in the use of Dopexamine hydrochloride in patients with ischaemic heart disease. Thus, Dopexamine hydrochloride may prove to be a useful alternative to dopamine and dobutamine in the treatment of acute heart failure and the postoperative management of low cardiac output states, although controlled studies are required to establish its efficacy and tolerability with respect to that of established therapies.
Dopexamine hydrochloride in the human heart: receptor binding and effects on cAMP generation
Eur Heart J 1992 Dec;13(12):1709-17.PMID:1363232DOI:10.1093/oxfordjournals.eurheartj.a060128.
Dopexamine hydrochloride is a synthetic catecholamine proposed for the short-term treatment of heart failure and postoperative low cardiac output. The pharmacological profile and anatomical localization of dopexamine binding were investigated in sections of right and left ventricle using [3H]-dopexamine and ligand techniques associated with light microscope autoradiography. Its effects on the 3-5-cyclic adenosine monophosphate (cAMP) generating system in membrane particles of the human right or left ventricle were also studied. [3H]-Dopexamine was specifically bound to sections of human right or left ventricle. The binding was time-, temperature- and concentration-dependent and was dissociable. The apparent equilibrium constant of dissociation was 3.5 nM. A decreased [3H]-dopexamine binding capacity from the base to the apex and ventricles was noticeable. The pharmacological profile of [3H]-dopexamine binding to sections of right or left ventricle was consistent with the labelling of both beta 2-adrenoceptors and dopamine DA-2 receptors. The most potent displacer of [3H]-dopexamine was the beta 2-adrenoceptor antagonist ICI 118,551 followed by dopamine, noradrenaline and domperidone. The beta 1-adrenoceptor antagonist metoprolol or the dopamine DA-1 receptor antagonist SCH 23390 were ineffective as displacers of [3H]-dopexamine binding. Light microscope autoradiography revealed the localization of [3H]-dopexamine binding sites within the wall of the human right and left ventricle. The density of silver grains was slightly higher in the right than in the left ventricle and showed a uniform transmural distribution across the ventricular wall.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of Dopexamine hydrochloride on sympathetic neuroeffector transmission in rabbit isolated pulmonary artery
Pharmacol Toxicol 1996 Mar;78(3):161-6.PMID:8882349DOI:10.1111/j.1600-0773.1996.tb00198.x.
The effects of Dopexamine hydrochloride on sympathetic neuroeffector transmission were studied in rabbit isolated pulmonary artery. Short-term exposure of dopexamine (10(-8) x 10(-7) M) and cocaine (10(-6)-3 x 10(-5) M), but not desipramine (3 x 10(-9)-3 x 10(-7) M), to the artery enhanced the contractions evoked by electrical-field stimulation. Corticosterone (4 x 10(-5) M), corticosterone (4 x 10(-5) M) plus cocaine (3 x 10(-8) M), but not cocaine (3 x 10(-5) M), attenuated the enhancement seen with dopexamine. High concentrations of dopexamine (10(-5)-3 x 10(-5) M), cocaine (10(-4) M), and desipramine (10(-6)-10(-5) M) decreased the stimulation-evoked contractions. Dopexamine (10(-7)-3 x 10(-5) M), but neither cocaine nor desipramine, caused an increase in resting tension that waned with time. Corticosterone (4 x 10(-5) M), but not cocaine (3 x 10(-5) M), attenuated the increase in resting tension. Propranolol (10(-6) M) did not alter the enhancing and inhibitory effects of dopexamine. A single concentration (10(-7) and 10(-6) M) of either dopexamine or desipramine caused a time-dependent biphasic response as regards the repetitive stimulation-evoked contractions of pulmonary artery: initial enhancement followed by inhibition. The inhibitory effect of dopexamine (10(-6) M) and desipramine (3 x 10(-6) M) seen after prolonged exposure was almost irreversible and partially reversible, respectively, by washing the preparations with drug-free salt solution. Cocaine caused a monophasic steady-state response: either enhancement (10(-5) M) or inhibition (2 x 10(-4) M). In both cases, the onset was rapid. The reduction caused by cocaine (2 x 10(-4) M) and by prazosin (10(-9) M) was fully reversed. Dopexamine (10(-5) M) antagonized competitively the contractions evoked by noradrenaline (3 x 10(-9)-10(-4) M). It is concluded that (1) the dopexamine-induced enhancement of neurogenic contractions is not due to either inhibition of neuronal and extraneuronal uptake of noradrenaline or an agonist action on prejunctional beta 2-adrenoceptors; (2) that the dopexamine-induced inhibition of stimulation-evoked contraction is due to an inhibition of postjunctional alpha 1-adrenoceptors; and (3) that the dopexamine-induced increase in resting tension is due to its metabolite methyldopexamine.
An introduction to the pharmacologic properties of Dopacard (Dopexamine hydrochloride)
Am J Cardiol 1988 Aug 11;62(5):9C-17C.PMID:2900602DOI:10.1016/s0002-9149(88)80061-4.
Dopexamine hydrochloride (Dopacard) has been developed as a peripherally acting dopamine receptor agonist with afterload reducing properties for use in the acute management of low cardiac output states. Dopexamine hydrochloride is one-third as potent as dopamine in stimulating DA1 receptors but 60 times as potent as a beta 2-adrenoceptor agonist. Unlike dopamine, it is a weak beta 1-adrenoceptor agonist and does not stimulate vascular alpha adrenoceptors. Its stimulant properties at vascular DA1 receptors and at vascular beta 2 adrenoceptors endow it with the ability to improve renal blood flow and to increase cardiac output secondary to afterload reduction. In addition, mild positive inotropic activity arises from stimulation of cardiac beta 2 adrenoceptors, potentiation of endogenous norepinephrine due to uptake-1 blockade, and activation of the baroreceptor reflex. Other features of Dopexamine hydrochloride that should enhance its clinical use are lack of arrhythmogenicity and rapid responsiveness to alterations in infusion rate.
Inhibition of 3H-noradrenaline accumulation by Dopexamine hydrochloride in the isolated aorta of the rabbit
Naunyn Schmiedebergs Arch Pharmacol 1989 Sep;340(3):270-3.PMID:2572974DOI:10.1007/BF00168509.
The aim of the present work was to study the ability of Dopexamine hydrochloride to interfere with the neuronal and extraneuronal uptake mechanisms by investigating the effect of Dopexamine hydrochloride on 3H-noradrenaline accumulation by rabbit isolated aorta. Dopexamine hydrochloride (3 x 10(-9) - 10(-5) mol/l) reduced the accumulation of tritium by aorta incubated with 3H-noradrenaline (10(-8) mol/l). The effect of dopexamine was compared to cocaine, dopamine, dobutamine, ADTN [(+/-)-2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene], ouabain and isoprenaline. Dopexamine hydrochloride (3 x 10(-9)-10(-7) mol/l) caused the same degree of inhibition irrespective of whether corticosterone (4 x 10(-5) mol/l) was present or not. The order of inhibitory potency was: desipramine greater than Dopexamine hydrochloride greater than dopamine greater than ADTN greater than or equal to cocaine greater than dobutamine greater than ouabain greater than isoprenaline. In the presence of desipramine (10(-6) mol/l), corticosterone (10(-6)-10(-4) mol/l), but not Dopexamine hydrochloride (10(-6) - 10(-4) mol/l), reduced the 3H-accumulation. It is concluded that Dopexamine hydrochloride is a potent inhibitor of uptake-1 in rabbit isolated aorta. Dopexamine hydrochloride has no affinity for the uptake-2 mechanism in this tissue.