Iganidipine
(Synonyms: 伊加地平) 目录号 : GC32537
Iganidipine是一种钙离子通道拮抗剂。
Cas No.:119687-33-1
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
Animal experiment: | Monkeys[1] Five adult cynomolgus monkeys (age, 5-8 years; weight, 3-5 kg; sex, 5 males) are used. All examinations are performed with the monkeys sitting in a modified monkey chair. On the first experimental day, after general anesthesia is induced by Ketamine hydrochloride at a dose of 8 to 10 mg/kg intramuscularly, pupil dilation is induced with one drop of Tropicamide in both eyes. The NBONH, IOP, blood pressure, pulse rate, SaO2, and body temperature are measured at 9AM. Starting on the 2nd experimental day, Iganidipine (0.03% or 0.1%, 30 mL) is administered in one randomly chosen eye and vehicle solution into the other eye twice daily at 8AM and 8PM for 7 days. At 9AM on the 8th experimental day, the same measurements are repeated after general anesthesia and bilateral pupil dilation. After a 4-week interval, a second series of experiments is performed using a different Iganidipine concentration according to the same time schedule. |
References: [1]. Ishii K, et al. Iganidipine, a new water-soluble Ca2+ antagonist: ocular and periocular penetration after instillation. Invest Ophthalmol Vis Sci. 2003 Mar;44(3):1169-77. | |
Iganidipine is a Ca2+ antagonist.
Iganidipine (0.03% solution) significantly increases optic nerve head (ONH) tissue blood velocity (NBONH) by 8 to 10% in treated eyes after a single administration (p<0.05) or by 18 to 35% after 7-, 14-, or 21-day twicedaily administration in rabbits (p<0.05). In monkeys, 0.03% and 0.1% Iganidipine significantly increases NBONH in treated eyes by 20 and 41% after 7-day (p<0.05) twice-daily administration, respectively[1].
[1]. Ishii K, et al. Iganidipine, a new water-soluble Ca2+ antagonist: ocular and periocular penetration after instillation. Invest Ophthalmol Vis Sci. 2003 Mar;44(3):1169-77.
| Cas No. | 119687-33-1 | SDF | |
| 别名 | 伊加地平 | ||
| Canonical SMILES | O=C(C1=C(C)NC(C)=C(C(OC)=O)C1C2=CC=CC([N+]([O-])=O)=C2)OCC(C)(C)CN3CCN(CC=C)CC3 | ||
| 分子式 | C28H38N4O6 | 分子量 | 526.62 |
| 溶解度 | Soluble in DMSO | 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 | 1.8989 mL | 9.4945 mL | 18.989 mL |
| 5 mM | 0.3798 mL | 1.8989 mL | 3.7978 mL |
| 10 mM | 0.1899 mL | 0.9495 mL | 1.8989 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。
Iganidipine, a new water-soluble Ca2+ antagonist: ocular and periocular penetration after instillation
Invest Ophthalmol Vis Sci 2003 Mar;44(3):1169-77.PMID:12601046DOI:10.1167/iovs.02-0482.
Purpose: To evaluate the potential of topical Iganidipine ophthalmic solution to exert Ca(2+)-antagonistic activity in the posterior parts of the eye without inducing systemic effects, ocular and periocular penetration of topically instilled Iganidipine was studied in pigmented rabbits. Method: First, (14)C-iganidipine solution (0.03%, 30 microL) was instilled into one eye, and vehicle into the other eye to determine the intraocular penetration of Iganidipine and to measure the radioactivity of ocular tissues 0.25, 0.5, 1, 2, 4, and 12 hours after a single instillation (n = 3, respectively). Second, Iganidipine (0.03%) or betaxolol (0.5%) was unilaterally instilled twice daily for 20 days to study the effects on intravitreously injected various doses of endothelin (ET)-1-induced retinal artery constriction to evaluate whether a pharmacologically active level of the drug penetrated to the posterior retina and to estimate the drug level in the posterior retina (n = 6, respectively). Third, Iganidipine (0, 10, or 30 microg/kg: n = 6, 3, and 6, respectively) was intravenously injected to study the effects on intravitreously injected ET-1-induced retinal artery constriction to evaluate Iganidipine levels in the posterior retina. Fourth, periocular penetration of Iganidipine was studied by means of whole-head autoradiography after a single instillation of (14)C-iganidipine (0.09%, 30 microL; n = 5). Results: Penetration of topically applied Iganidipine to the cornea or aqueous humor was high and estimated to be at least 10 times higher than that reported for timolol or carteolol. Concentrations in the iris-ciliary body or retina-choroid were much higher than in the plasma, both in the treated and control eyes, suggesting that Iganidipine binds to uveal pigments. Twice-daily 20-day instillation of Iganidipine (0.03%), but not of betaxolol (0.5%), significantly suppressed constriction of the retinal arteries induced by intravitreous injection of ET-1 at a dose of 2.5 or 0.5 ng in the ipsilateral eye. Intravenous injection of Iganidipine at a dose of 30 microg/kg (giving a free plasma concentration of approximately 10(-8) M), but not at a dose of 10 microg/kg, significantly suppressed intravitreous ET-1-induced (0.5 ng) constriction of the retinal artery to a similar degree as twice-daily 20-day instillation of 0.03% Iganidipine. After a single instillation of 0.09% Iganidipine, the equivalent concentration of Iganidipine in the ipsilateral retrobulbar periocular space estimated from autoradiography was approximately 3.9 x 10(-8) M between 15 minutes and 1 hour after instillation, consistently higher than in the untreated contralateral eyes by approximately 3.0 x 10(-8) M (P = 0.043). Conclusions: In rabbits, topically instilled Iganidipine, a Ca(2+) antagonist, in a 0.03% solution reaches the ipsilateral posterior retina or retrobulbar periocular space by local penetration at concentrations sufficient to act as a Ca(2+) antagonist.
Preventive effect of Iganidipine on renal and cerebral injuries in salt-induced hypertension
Am J Hypertens 1997 Aug;10(8):869-78.PMID:9270081DOI:10.1016/s0895-7061(97)00094-0.
Iganidipine, a new water-soluble calcium antagonist, was administered at a nonhypotensive dose (NHD) of 0.3 mg/kg/day, a moderate-hypotensive dose (MHD) of 1.0 mg/kg/day, and a sustained-hypotensive dose (SHD) of 3.0 mg/kg/day to Dahl salt-sensitive (Dahl-S) rats fed a high-salt diet for 8 weeks. The effects on survival, and on renal and cerebral injuries, were then examined. Iganidipine completely prevented hypertensive death at the SHD and tended to increase the survival at the NHD and MHD. Iganidipine reduced glomerulosclerosis and renal arterial and tubular injuries in a dose-dependent manner. Iganidipine at the SHD, but not NHD or MHD, improved plasma creatinine, serum urea nitrogen, and glomerular filtration rate. Iganidipine at all doses examined increased the urinary prostaglandin (PG) I2 and PGE2, but not PGF2alpha or thromboxane B2, and decreased plasma angiotensin II (AII) level and renin activity. The renal glomerular, tubular, and arterial injuries were significantly correlated with blood pressure (r = 0.56 to 0.80) and plasma AII level (r = 0.50 to 0.71) but not with urinary prostanoids. Iganidipine also reduced the incidence of cerebral infarction. The infarction area was slightly and significantly correlated with urinary PGI2 (r = 0.42) and PGE2 (r = 0.41) but not with blood pressure or plasma AII. In conclusion, Iganidipine prevented renal and cerebral injuries in Dahl-S rats. In addition to the reduced blood pressure, the reduction of plasma AII and the increase of vasodilatory prostanoids may also partially contribute to the renal and cerebral protective effects of Iganidipine.
Effect of topically applied Iganidipine dihydrochloride, a novel calcium antagonist, on optic nerve head circulation in rabbits
Jpn J Ophthalmol 2001 Jan-Feb;45(1):76-83.PMID:11163049DOI:10.1016/s0021-5155(00)00302-6.
Purpose: To study the effect of topically applied Iganidipine dihydrochloride (Iganidipine), a novel water-soluble calcium channel blocker, on blood flow in the optic nerve head (ONH), intraocular pressure, and systemic blood pressure in rabbits. Methods: After 0.1% Iganidipine (20 microL) was instilled into normal eyes, the change in ONH blood flow was measured using a hydrogen gas clearance flowmeter. Iganidipine (0.0001% to 0.1%) was instilled into eyes with impaired ocular circulation before or after the intravitreal injection of endothelin-1, and the change in ONH blood flow was measured. Changes in intraocular pressure and blood pressure after instillation of 0.1% Iganidipine were measured. In all experiments, physiological saline was instilled into the contralateral eye as a control. Results: Iganidipine significantly increased the ONH blood flow in normal eyes with the maximum increment of 31.7% at 45 minutes after instillation. Preinstillation of 0.01% and 0.1% Iganidipine significantly inhibited the decrease in ONH blood flow in the eyes with impaired circulation. Moreover, ONH blood flow recovered with postinstillation of 0.1% Iganidipine. These effects were persistent. Instillation of 0.1% Iganidipine did not change either the intraocular pressure or the blood pressure. Conclusion: The instillation of Iganidipine persistently increased and maintained the ONH blood flow in rabbit eyes with normal and impaired ocular circulation.
Topical administration of Iganidipine, a new water-soluble Ca2+ antagonist, increases ipsilateral optic nerve head circulation in rabbits and cynomolgus monkeys
Curr Eye Res 2004 Jul;29(1):67-73.PMID:15370369DOI:10.1080/02713680490513236.
Purpose: To evaluate the effects of topically administered Iganidipine hydrochloride, a novel water-soluble Ca2+- channel blocker, on optic nerve head (ONH) circulation in Dutch rabbits and cynomolgus monkeys. Methods: ONH tissue blood velocity (NBONH) was determined using the laser speckle method. In rabbits, NBONH was measured for 90 minutes before and after a single Iganidipine administration, or before and after twice-daily ad- ministrations for 21 days (0.03%). In monkeys, NBONH was measured before and after twice-daily administrations of Iganidipine for 7 days (0.03 or 0.1%). Results: Iganidipine (0.03% solution) significantly increased NBONH by 8 to 10% in treated eyes after a single administration (p < 0.05) or by 18 to 35% after 7-, 14-, or 21-day twice-daily administration in rabbits (p < 0.05). In monkeys, 0.03% and 0.1% Iganidipine significantly increased NBONH in treated eyes by 20 and 41% after 7-day (p < 0.05) twice-daily administration, respectively. Conclusion: Topical Iganidipine significantly increased ONH blood velocity in treated eyes.
Effect of Topically Applied Iganidipine Dihydrochloride, a Novel Ca(2+) Antagonist, on Optic Nerve Head Circulation in Rabbits
Jpn J Ophthalmol 2001 Jan;45(1):114.PMID:11341901DOI:10.1016/s0021-5155(00)00326-9.
Purpose: We studied the effect of topically applied Iganidipine dihydrochloride, a novel water-soluble calcium channel blocker on the blood flow of optic nerve head (ONH), intraocular pressure, and blood pressure in rabbits.Methods: (1) 0.1% Iganidipine (20 &mgr;l) was instilled into a normal eye. The change in blood flow in the ONH was measured using a hydrogen gas clearance flowmeter. (2) Iganidipine (0.0001%-0.1%) was instilled into a circulation-disordered eye before or after the intravitreal injection of endothelin-1, and change in the blood flow in the ONH was measured. (3) Changes in intraocular pressure and blood pressure after instillation of 0.1% Iganidipine were measured. In all experiments, physiological saline was instilled in each contralateral eye as a control.Results: (1) Instillation of Iganidipine significantly increased the blood flow in the ONH by 40% at 45 minutes after instillation. (2) Pre-instillation of 0.01 and 0.1% Iganidipine almost completely inhibited the decrease of blood flow in the ONH in the circulation-disordered model. The decrease of blood flow in the ONH was corrected with post-instillation of 0.1% Iganidipine. These effects were continuous. (3) Instillation of 0.1% Iganidipine did not change either intraocular pressure or blood pressure.Conclusion: It was shown that instillation of Iganidipine continuously increased and maintained the blood flow in the ONH in normal and circulation-disordered rabbit eye models.