α2/α1 receptor

由于盐酸阿帕氯定 (ALO 2145) 的负面全身影响较小，且对角膜和血脑屏障的渗透较少，因此更常局部用于治疗青光眼 [2]。

阿普乐定（1.15%，单次输注）可抑制 98% PGE2 诱导的房水耀斑增加 [3]。 Aproclonidine Hydrochloride (ALO 2145) 对人类青光眼和眼压升高的动物模型有效。阿普乐定的降低眼压作用通常归因于房水合成减少和眼动脉前分支血管收缩[2]。

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单次滴注1.15%Aproclonidine、两次滴注1.25%肾上腺素、两次输注0.1%地匹韦林和两次滴入0.04%地匹韦仑滴眼液分别抑制了PGE（2）诱导的房水闪光升高的98%、96%、87%、73%和47%。0.5%的噻吗洛尔、0.25%的尼普利洛尔、1%的多唑胺和2%的匹罗卡品滴眼液对PGE（2）诱导的发作的增加没有影响。 结论：Aproclonidine、肾上腺素和地匹韦林滴眼液可抑制PGE（2）诱导的色素兔房水闪光的升高[3]。

Animal/Disease Models: Male rabbit [3].
Doses: 1.15%
Route of Administration: Apraclonidine (1.15%, single infusion)
Experimental Results: Inhibited PGE2-induced increase in aqueous humor flare in pigmented rabbits.

Absorption, Distribution and Excretion
Topical use of apraclonidine ophthalmic solution leads to systemic absorption. Studies of apraclonidine (0.5% ophthalmic solution) dosed one drop three times a day in both eyes for 10 days in normal volunteers yielded mean peak and trough concentrations of 0.9 ng/mL and 0.5 ng/mL, respectively.

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Biological Half-Life
8 hours

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the use of apraclonidine during breastfeeding. To substantially diminish the amount of drug that reaches the breastmilk after using eye drops, place pressure over the tear duct by the corner of the eye for 1 minute or more, then remove the excess solution with an absorbent tissue. One manufacturer recommends avoiding breastfeeding on the one day on which it is used for argon laser trabeculoplasty, argon laser iridotomy or posterior capsulotomy.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
98.7%

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rat LD50 oral 38 mg/kg Medicamentos de Actualidad., 24(557), 1988
rat LD50 intravenous 9 mg/kg Medicamentos de Actualidad., 24(557), 1988
mouse LD50 oral 3 mg/kg Medicamentos de Actualidad., 24(557), 1988
mouse LD50 intravenous 6 mg/kg Medicamentos de Actualidad., 24(557), 1988

[1]. Apraclonidine in the treatment of ptosis. J Neurol Sci. 2017;376:129‐132.

[2]. Aqueous humor dynamics in anesthetized rats infused with intracameral apraclonidine. Pharmacology. 1999;58(4):220‐226.

[3]. Effects of topical antiglaucoma eye drops on prostaglandin E(2)-induced aqueous flare elevation in pigmented rabbits. Invest Ophthalmol Vis Sci. 2002 Apr;43(4):1142-5.

Apraclonidine hydrochloride is the hydrochloride salt of apraclonidine. It has a role as an alpha-adrenergic agonist and an antiglaucoma drug. It contains an apraclonidine.
Apraclonidine Hydrochloride is the hydrochloride salt form of apraclonidine, a clonidine derivative with selective alpha-2-adrenergic agonistic property. When administered directly to eyes, apraclonidine hydrochloride enhances aqueous humor outflow and decreases aqueous production by vasoconstriction. It is used mostly in ophthalmic preparations for decreasing intraocular pressure.
See also: Apraclonidine (has active moiety).

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Apraclonidine is an imidazoline that is 2-amino 4,5-dihydro-1H-imidazoline in which one of the exocyclic amino hydrogens has been replaced by a 4-amino-2,6-dichlorophenyl group. It has a role as an alpha-adrenergic agonist, an antiglaucoma drug, an ophthalmology drug, a beta-adrenergic agonist and a diagnostic agent. It is a member of imidazolines, a dichlorobenzene and a member of guanidines. It is a conjugate base of an apraclonidine(1+).
Apraclonidine, also known as iopidine, is a sympathomimetic used in glaucoma therapy. It is an alpha2-adrenergic agonist.
Apraclonidine is an alpha-Adrenergic Agonist. The mechanism of action of apraclonidine is as an Adrenergic alpha-Agonist.
Apraclonidine is a clonidine derivative with selective alpha-2-adrenergic agonistic activity. Upon ocular administration, apraclonidine enhances aqueous humor uveoscleral outflow and decreases aqueous production by vasoconstriction. This may decrease intraocular pressure (IOP).
See also: Apraclonidine Hydrochloride (has salt form).

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Drug Indication
For prevention or reduction of intraoperative and postoperative increases in intraocular pressure (IOP) before and after ocular laser surgery when used prophylactically. Also used as a short-term adjunctive therapy in patients with open-angle glaucoma who are on maximally tolerated medical therapy requiring additional IOP reduction.
FDA Label

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Mechanism of Action
Apraclonidine is a relatively selective alpha2 adrenergic receptor agonist that stimulates alpha1 receptors to a lesser extent. It has a peak ocular hypotensive effect occurring at two hours post-dosing. The exact mechanism of action is unknown, but fluorophotometric studies in animals and humans suggest that Apraclonidine has a dual mechanism of action by reducing aqueous humor production through the constriction of afferent ciliary process vessels, and increasing uveoscleral outflow.

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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.[1]

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We studied the acute effects of the ocular hypotensive drug, apraclonidine (AP), on intraocular pressure (IOP) and aqueous humor dynamics of anesthetized rats during infusion-induced ocular hypertension. Two infusions were made into the anterior chamber of the eye: one was constant at a rate of 0.05 microl/min, the other was cyclic, at a rate of 0.25 microl/min, with the pump on for 4 min, then off for 4 min. Data were processed by complex demodulation and analysis of a second-order transfer function. This permitted separate calculations of resistive components (Ao), i.e., trabecular meshwork and uveoscleral outflows, and residual pressure (RP) estimating nonresistive components, i.e., aqueous synthesis and episcleral venous pressure. A balanced salt solution (BSS) and AP (0. 0005%) were tested. AP markedly delayed the within-group rise in IOP: 20 min for BSS vs. 60 min for AP (p < 0.001). IOP of AP rats was less than control for 100 min (p < 0.05). The infusions raised Ao in both groups (p < 0.05). AP initially had a transient inhibitory effect (p < 0.05). Infusions raised RP in both groups. AP had a strong inhibitory effect for the first 8 cycles (p < 0.05). These data document that the acute effects of AP in this in vivo rat model of ocular hypertension were to delay increases in IOP, mainly by reducing nonresistive components of aqueous humor dynamics. Transient inhibition of resistive mechanisms also occurred. [2]

C9H11CL3N4

281.5694

280.005

C, 38.39; H, 3.94; Cl, 37.77; N, 19.90

73218-79-8

Apraclonidine;66711-21-5; 73218-79-8 (HCl); 73217-88-6

51763

Off-white to light yellow solid powder

1.63 g/cm3

395.5ºC at 760 mmHg

>230ºC

193ºC

3.167

62.44

4

2

2

16

247

0

OTQYGBJVDRBCHC-UHFFFAOYSA-N

InChI=1S/C9H10Cl2N4.ClH/c10-6-3-5(12)4-7(11)8(6)

2,6-dichloro-N1-(4,5-dihydro-1H-imidazol-2-yl)benzene-1,4-diamine hydrochloride

4-Aminoclonidine; Apraclonidina; APRACLONIDINE HYDROCHLORIDE; 73218-79-8; Apraclonidine HCl; p-Aminoclonidine hydrochloride; 2,6-dichloro-N1-(4,5-dihydro-1H-imidazol-2-yl)benzene-1,4-diamine hydrochloride; Iopidine; NC 14 hydrochloride; ALO-2145; Iopidine; P-aminoclonidine; Apraclonidinum

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

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

DMSO : ~125 mg/mL (~443.94 mM)
H2O : ≥ 12.5 mg/mL (~44.39 mM)

配方 1 中的溶解度: ≥ 2.08 mg/mL (7.39 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 20.8 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.08 mg/mL (7.39 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
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7、 以上所有助溶剂都可在 Invivochem.cn网站购买。