Apraclonidine (hydrochloride)
(Synonyms: 盐酸安普乐定,ALO 2145) 目录号 : GC42830
A α2-AR agonist
Cas No.:73218-79-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Apraclonidine is an α2-adrenergic receptor (α2-AR) agonist and structural analog of clonidine . It binds to α2-ARs in calf cortex, rat kidney, and rat spleen with IC50 values of 0.9, 4.3, and 4.2 nM, respectively. Apraclonidine also binds to α2-ARs in rat cerebral cortex, pig submandibular gland and lung tissue, and in dog kidney membrane (Kds = 0.87, 5.28, 1.30, and 5.25 nM, respectively). It inhibits noradrenaline-stimulated contraction in guinea pig ileum and rabbit vas deferens (EC50s = 7.59 and 6.76 nM, respectively). Opthalmic formulations containing apraclonidine have been used to treat elevated intraocular pressure.
| Cas No. | 73218-79-8 | SDF | |
| 别名 | 盐酸安普乐定,ALO 2145 | ||
| Canonical SMILES | ClC1=C(NC2=NCCN2)C(Cl)=CC(N)=C1.Cl | ||
| 分子式 | C9H10Cl2N4•HCl | 分子量 | 281.6 |
| 溶解度 | DMSO: Slightly Soluble,Methanol: Slightly Soluble | 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 | 3.5511 mL | 17.7557 mL | 35.5114 mL |
| 5 mM | 0.7102 mL | 3.5511 mL | 7.1023 mL |
| 10 mM | 0.3551 mL | 1.7756 mL | 3.5511 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。
Botulinum toxin-induced blepharoptosis: Anatomy, etiology, prevention, and therapeutic options
J Cosmet Dermatol 2021 Oct;20(10):3133-3146.PMID:34378298DOI:10.1111/jocd.14361.
Background: Botulinum toxin A (BoNT-A) has grown tremendously in aesthetic dermatology since 2002 when the United States Food and Drug Administration (FDA) first approved its use for treating moderate-to-severe glabellar lines. Blepharoptosis, due to local spread of toxin, is a reported side effect of BoNT-A which, although rare, more frequently occurs among inexperienced practitioners. Objectives: The purpose of this review is to highlight the causes and management of eyelid ptosis secondary to BoNT-A administration including new anatomic pathways for BoNT-A spread from the brow area to the levator palpebrae superioris muscle. Methods: A literature search was conducted using electronic databases (PubMed, Science Direct, MEDLINE, Embase, CINAHL, EBSCO) regarding eyelid anatomy and the underlying pathogenesis, presentation, prevention, and treatment of eyelid ptosis secondary to BoNT-A. Anatomic dissection has been performed to assess the role of neurovascular pedicles and supraorbital foramen anatomic variations. Results: Blepharoptosis occurs due to weakness of the levator palpebrae superioris muscle. Mean onset is 3-14 days after injection and eventually self-resolves after the paralytic effect of BoNT-A wanes. Administration of medications, such as oxymetazoline hydrochloride or Apraclonidine hydrochloride eye drops, anticholinesterase agents, or transdermal BoNT-A injections to the pre-tarsal orbicularis, can at least partially reverse eyelid ptosis. Anatomic study shows that a supraorbital foramen may be present in some patients and constitutes a shortcut from the brow area directly into the orbital roof, following the supraorbital neurovascular pedicle. Conclusion: Providers should understand the anatomy and be aware of the causes and treatment for blepharoptosis when injecting BoNT-A for the reduction of facial wrinkles. Thorough anatomic knowledge of the supraorbital area and orbital roof is paramount to preventing incorrect injection into "danger zones," which increase the risk of eyelid ptosis.
Apraclonidine and my pupil
Clin Auton Res 2011 Oct;21(5):347-51.PMID:21384091DOI:10.1007/s10286-011-0118-6.
Purpose: Used in the diagnosis of Horner's syndrome, Apraclonidine 1% dilatates the involved eye due to denervation supersensitivity. Recent literature suggests that in healthy volunteers, Apraclonidine provokes a mild miotic effect. Since the comparison of both the pathologic and the non-pathologic eye is important, we wanted to further investigate the effect of Apraclonidine on the healthy eye. By measuring the effect on the pupil intermittently over a few hours, we tried to determine the best moment for evaluation after instillation with Apraclonidine. Therefore, the effect of Apraclonidine on pupillary parameters was investigated in 14 healthy volunteers. Methods: Infrared pupillography was used to measure the scotopic pupil diameter and the dynamic pupil responses to light. The first measurements were performed prior to instillation of Apraclonidine. Measurements were retaken 30, 60, 90, 120, 180, 240, 300 and 360 min after random instillation of one eye with one drop of 1% Apraclonidine. Results: The anisocoria after dark adaptation and at minimum pupil diameter differed significantly for the measurements obtained 30 and 60 min after instillation with Apraclonidine. The eye with Apraclonidine drops showed relative miosis and an increased amplitude of constriction to light. No significant influence was found on the latency, the constriction velocity and redilation velocity. Conclusions: Instillation of Apraclonidine 1% in healthy subjects causes relative miosis, which is most pronounced after 30-60 min. The amplitude of constriction to light also differs significantly. The relative miotic effect of Apraclonidine could be explained by the α-2 receptor agonistic effect which is more pronounced than the α-1 agonistic effect in healthy subjects. In patients with Horner's syndrome, the α-1 agonistic effect will dominate because of the supersensitivity of the α-1 receptors, resulting in relative mydriasis. These findings stress the necessity to instill the unaffected eye in diagnosing a suspected Horner's pupil.
Apraclonidine in the treatment of ptosis
J Neurol Sci 2017 May 15;376:129-132.PMID:28431598DOI:10.1016/j.jns.2017.03.025.
Transient ptosis is a known complication of botulinum toxin (BoNT) injection due to inadvertent migration of toxin into the levator palpebrae superioris muscle. Currently there is no treatment available for BoNT induced ptosis. Apraclonidine hydrochloride is a topical ophthalmic solution with selective alpha-2 and weak alpha-1 receptor agonist activity that has the ability to elevate the eye lid. Apraclonidine has been used as a diagnostic test in Horner's syndrome. We evaluated the effects Apraclonidine in a cohort of BoNT induced ptosis and a patient with Horner syndrome. Each patient was administered 2 drops of Apraclonidine 0.5% solution to the eye with the ptosis and was re-examined 20-30min later. All 6 patients showed improvement in ptosis. There was also improvement in ptosis in a patient with Horner's syndrome. Apraclonidine is not only useful as a diagnostic test in Horner's syndrome, but may be an effective and safe treatment for BoNT-induced ptosis.
Apraclonidine hydrochloride: an evaluation of plasma concentrations, and a comparison of its intraocular pressure lowering and cardiovascular effects to timolol maleate
Trans Am Ophthalmol Soc 1990;88:149-59; discussion 159-62.PMID:1982747doi
We performed a prospective, placebo-controlled, cross-over study in 20 young healthy female volunteers. We evaluated both the cardiovascular and IOP effects of both timolol maleate and Apraclonidine hydrochloride. In addition, we evaluated the plasma levels of various Apraclonidine concentrations. We utilized 0.5% timolol and both the 0.25% and 0.50% concentrations of Apraclonidine. Both timolol and Apraclonidine lowered IOP comparably. Timolol lowered the resting pulse rate and blunted exercise-induced tachycardia. Apraclonidine did not affect blood pressure or heart rate any differently than placebo. We detected plasma levels of Apraclonidine in many individuals for up to 8 hours. These serum levels were variable and did not appear to relate to the quantity of IOP lowering.
Topical Apraclonidine hydrochloride in eyes with poorly controlled glaucoma. The Apraclonidine Maximum Tolerated Medical Therapy Study Group
Trans Am Ophthalmol Soc 1995;93:421-38; discussion 439-41.PMID:8719690doi
Object: We determined whether the addition of topical Apraclonidine hydrochloride to eyes receiving maximal medical therapy, with inadequate intraocular pressure (IOP) control, and scheduled to undergo surgery, could adequately lower IOP, postponing the need for surgical intervention. Design: A prospective 90 day, multi-centered, placebo-controlled, doublemasked parallel study. Patients: We enrolled 174 glaucoma patients with inadequate IOP control on maximally tolerated medical therapy. All were candidates for either laser trabeculoplasty or invasive surgical intervention. We enrolled only one eye per patient. Interventions: We continued to administer maximum-tolerated medical therapy for glaucoma. Patients took the study medication every eight hours. Study medications were either Apraclonidine hydrochloride 0.5% or placebo (Apraclonidine's vehicle). Major outcome measures: We evaluated IOP, IOP change from baseline, and the number of eyes requiring surgery after the addition of study medication. Results: Sixty one percent of patients treated with Apraclonidine maintained adequate IOP control throughout the study, avoiding additional surgery compared to 33.9% patients treated with placebo (P < .001). Apraclonidine treatment resulted in significantly more patients achieving either an additional > or = 20% reduction in IOP from baseline (resulting in an IOP < or = 20 mm Hg) (P < 0.05). The most common ocular complications were conjunctival hyperemia (12.6%), itching and foreign body sensation (6.8%), and tearing (4.5%). The most frequent non-ocular adverse events related to Apraclonidine were dry mouth (4.5%) and unusual taste perception (2.2%). Conclusions: Apraclonidine appears safe and efficacious. It significantly lowered IOP when used in combination with a patient's maximum tolerated medical therapy. This delayed or prevented further glaucoma surgery for at least 90 days in approximately 60% of treated patients.