Iopanoic acid
(Synonyms: 碘番酸) 目录号 : GC32404
Iopanoic acid (Acidum iopanoicum, Iodopanoic acid) is an iodine-containing radiocontrast medium used in cholecystography.
Cas No.:96-83-3
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
Cell experiment: | Rat pituitary fragments are superfused by Medium-199. After a 90 min equilibration period, the superfusion is continued for 135 min with or without inclusion into the superfusion medium of 3,5,3'-triiodothyronin (T3) 10-7 M, triiodothyroacetic acid (TRIAC) (stock solution 10-4 M in 20% methanol, final concentrations 10-8 to 10-6 M), Iopanoic acid (stock solution 10-3 M in 0.2 M NaOH, final concentrations 10-7 to 10-5 M), or potassium iodide 10-7 to 10-4 M. The superfusion is followed by a 6-min pulse of thyrotropin-releasing-hormone (TRH)[2]. |
Animal experiment: | Wistar rats initially weighing 180 to 200 g are used. The administration of Iopanoic acid (IOP) is started at day 18 of gestation. Pregnant rats are injected subcutaneously with 10 mg of Iopanoic acid every 12 h, from day 18 of gestation to 12 h before they are killed on the morning of day 20 or 22 of gestation. Control animals receive the vehicle solution with identical timing. Iopanoic acid effectiveness in decreasing interscapular brown adipose tissue (IBAT) nuclear 3,5,3'-triiodothyronin (T3) is assessed by Iopanoic acid (IOP) administration to adult male rats (220 to 250 g body weight) following the same dose and time schedule as in pregnant dams during two days. Caesarean sections are performed at 18 (only untreated animals), 20 and 22 days of gestation. Fetuses are killed by decapitation, and IBAT, brain, and liver are removed. Tissue samples are immediately frozen in liquid nitrogen with the exception of brown fat from several 22 day-old fetuses, which is directly homogenized in 0.25 M sucrose for mitochondria isolation[1]. |
References: [1]. Tuca A, et al. Inhibition of iodothyronine 5'-deiodinase by iopanoic acid does not block nuclear T3 accumulation during rat fetal development. Pediatr Res. 1994 Jan;35(1):91-5. | |
Iopanoic acid (Acidum iopanoicum, Iodopanoic acid) is an iodine-containing radiocontrast medium used in cholecystography.
| Cas No. | 96-83-3 | SDF | |
| 别名 | 碘番酸 | ||
| Canonical SMILES | O=C(O)C(CC)CC1=C(I)C=C(I)C(N)=C1I | ||
| 分子式 | C11H12I3NO2 | 分子量 | 570.93 |
| 溶解度 | DMSO : 113.3 mg/mL (198.45 mM) | 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 | 1.7515 mL | 8.7576 mL | 17.5153 mL |
| 5 mM | 0.3503 mL | 1.7515 mL | 3.5031 mL |
| 10 mM | 0.1752 mL | 0.8758 mL | 1.7515 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。
Iopanoic acid as an adjunct to carbimazole in the management of hyperthyroidism
Natl Med J India 1992 May-Jun;5(3):108-11.PMID:1304283doi
Background: The thiourea drugs take a few weeks to control the symptoms of hyperthyroidism whilst iodine containing radiographic contrast agents (Iopanoic acid and sodium ipodate) have a more rapid effect. There is no report on the use of Iopanoic acid administered in conjunction with carbimazole, so we evaluated the efficacy of this combination in the early medical management of patients with hyperthyroidism. Methods: Thirty hyperthyroid patients diagnosed by clinical and biochemical criteria were randomized into two treatment groups. Group A (n = 16) received Iopanoic acid (500 mg orally twice a day for the first 3 weeks) and carbimazole (30 mg orally in three divided doses) while group B (n = 14) received carbimazole alone. Clinical examination and estimation of serum total T3, total T4 and TSH were done by radioimmunoassay at the start of therapy, weekly for 4 weeks and then at 6, 8 and 12 weeks. Results: In the initial 3 weeks, Iopanoic acid induced a significantly greater fall in mean serum total T3 levels (Z = 2.298, p < 0.02) and a slower fall in mean serum total T4 (Z = 2.396, p < 0.05) in group A patients compared to those in group B. This was accompanied by earlier clinical improvement in group A patients. The mean serum total T3 and T4 values rose to higher levels in group A at 4 weeks, one week after discontinuation of Iopanoic acid. At the end of 12 weeks, however, there was no significant difference in the mean serum total T3 and T4 levels between the two groups (p > 0.05). Biochemical euthyroidism (i.e. total T3 < 3 nmol/L and total T4 < 170 nmol/L) was achieved later in group A patients than in group B (10.4 +/- 5.0 weeks v. 3.6 +/- 1.2 weeks, p < 0.0001). Conclusions: Iopanoic acid given together with carbimazole induces rapid clinical improvement in hyperthyroid patients than carbimazole alone. However, the delayed achievement of euthyroidism may preclude its routine use in the management of patients with hyperthyroidism except in those with thyrotoxic emergencies.
Inhibitory effect of Iopanoic acid on the thyrotropin-stimulated release of cyclic adenosine 3',5'-monophosphate and of 3,5,3'-triiodothyronine from perifused rat thyroids
Endocrinology 1985 Nov;117(5):1813-7.PMID:2412801DOI:10.1210/endo-117-5-1813.
Using a perifusion system, we studied the effect of Iopanoic acid, an iodinated contrast agent used in oral cholecystography, on the release of cAMP, T3, T4, and rT3 from perifused rat thyroid pieces. A 0.1 mg/ml Iopanoic acid solution significantly inhibited the TSH-stimulated release of cAMP (without Iopanoic acid, 8175 +/- 373; with Iopanoic acid, 5169 +/- 355 fmol/mg thyroid X 3 h, mean +/- SE) and T3 (without Iopanoic acid, 971 +/- 32; with Iopanoic acid, 659 +/- 32 pg/mg thyroid X 3 h) in the presence of 3-isobutyl-1-methylxanthine. T4 and rT3 releases were not significantly affected. Inhibition of TSH-stimulated T3 release by Iopanoic acid was also observed at a concentration of 0.01 mg/ml. Propylthiouracil completely abolished the inhibitory effect of Iopanoic acid on TSH-stimulated cAMP release but not on TSH-stimulated T3 release. TSH-stimulated cAMP release was augmented by iodide at a concentration of 1 X 10(-3) M in the presence of 3-isobutyl-1-methylxanthine but suppressed by iodide at a concentration of 1 X 10(-5) M. TSH-stimulated T3 release was suppressed slightly at both concentrations of iodide. These results suggest that Iopanoic acid may have an inhibitory effect on the TSH-stimulated cAMP and T3 release from perifused rat thyroids. This effect can probably be attributed to the iodide contained in the agent and to the inhibited intrathyroidal conversion of T4 to T3.
Iopanoic acid in the management of neonatal Graves' disease
J Perinatol 2004 Feb;24(2):105-8.PMID:14762455DOI:10.1038/sj.jp.7211046.
Objective: Traditionally, neonatal thyrotoxicosis has been managed with antithyroid drugs and/or iodine as well as sedatives, propranol and digitalis when necessary. The purpose of this study was to evaluate the management of neonatal thyrotoxicosis using the radio-contrast agent Iopanoic acid. Methods: We managed five cases of neonatal thyrotoxicosis. All infants were treated initially with propranolol (1.7 mg/kg/day) and Iopanoic acid 250 to 500 mg every third or fourth day. Results: In all cases, clinical signs improved and T(3) and T(4) levels decreased dramatically within 24 to 72 hours. No toxic side effects were noted. Conclusion: Neonatal thyrotoxicosis can be managed successfully using Iopanoic acid. Iopanoic acid is essentially free of side effects and need only be administered every 3 to 4 days. When administered until (transplacental) maternal TSI has been metabolized by the neonate, Iopanoic acid maintains euthyroid status with no risk of hypothyroidism. With conventional therapy, propylthiouracil (PTU) must be administered three times a day. PTU also carries a significant risk of toxic side effects and a week or more of therapy is required to correct the hyperthyroid state and may induce hypothyroidism.
Efficacy of Iopanoic acid for treatment of spontaneous hyperthyroidism in cats
J Feline Med Surg 2011 Jun;13(6):441-7.PMID:21515081DOI:10.1016/j.jfms.2011.02.003.
Iopanoic acid is an iodine containing oral cholecystographic agent that has been used to treat hyperthyroidism in humans and has recently been evaluated in an experimental model of feline hyperthyroidism. The aim of this study was to evaluate the efficacy of Iopanoic acid in cats with spontaneous hyperthyroidism. Eleven cats were included in the study. Eight were treated initially with 50mg orally q 12h and three were treated with 100mg orally q 12h. Prior to treatment (baseline) and at 2, 4, and 12 weeks of treatment, owner questionnaires, physical exams, complete blood count, biochemistry analyses, and T(3) and T(4) concentrations were evaluated. The mean serum T(3) concentration decreased with treatment at all time periods compared to baseline. Mean T(4) concentrations were increased at weeks 4 and 12 compared to baseline. Five cats had a partial response during the initial 4 weeks of therapy, but the effects were transient and no significant improvements in clinical signs or physical exam findings were noted at any time period. Results suggest that Iopanoic acid may be beneficial for acute management of thyrotoxicosis in some cats, but is not suitable for long-term management.
Iopanoic acid-induced decrease of circulating T3 causes a significant increase in GH responsiveness to GH releasing hormone in thyrotoxic patients
Clin Endocrinol (Oxf) 1999 Oct;51(4):461-7.PMID:10583313DOI:10.1046/j.1365-2265.1999.00822.x.
Objective: Thyroid hormones participate in GH synthesis and secretion, and an impaired GH response to many pharmacological stimuli, including GH releasing hormone (GHRH), has been found in thyrotoxicosis. Although the mechanisms involved in this process have not been fully elucidated, there is evidence that thyroid hormones could act at both hypothalamic and pituitary levels. There are no data in the literature about the effect of an acute reduction of circulating T3 levels on GH secretion in hyperthyroidism. The GH responsiveness to GHRH was therefore evaluated in a group of hyperthyroid patients during short-term treatment with Iopanoic acid. Iopanoic acid is a compound that induces a rapid decrease in serum T3 levels, mainly by inhibition of peripheral conversion of T4 to T3. To the authors' knowledge, there is no evidence of a direct effect of Iopanoic acid on GH secretion. Design: Hyperthyroid patients were submitted to a GHRH test (100 microg, i.v.) before (day 0), and on days 4, 7 and 15 after oral treatment with Iopanoic acid (3 g every 3 days) and propylthiouracil (200 mg every 8 h). A group of normal control subjects was also submitted to a single GHRH test (100 microg, i.v.). Patients: Nine patients with thyrotoxicosis (eight women, one man), with a mean age of 34 years, were studied. All patients had high serum levels of total T3 and total T4, and suppressed TSH levels. None of them had taken any medication for at least 3 months before the study. The patients were compared with a group of nine control subjects (five women, four men) with a mean age of 31 years. Measurements: GH and TSH were measured by immunofluorometric assays. Total T3, total T4 and IGF-I were determined by radioimmunoassay. Albumin levels were measured by a colorimetric method. Results: Iopanoic acid induced a rapid and maintained decrease in serum T3 concentrations, with a significant reduction on days 4, 7 and 15 compared with pre-treatment values. In hyperthyroidism, peak GH levels (mean +/- SE mU/l) after GHRH were significantly higher on day 15 (24.4 +/- 3.8) than those observed on days 0 (14.2 +/- 1.6), 4 (15.2 +/- 3.0) and 7 (19.6 +/- 5.0). There was a 79% increase in this response on day 15 compared with the pre-treatment period. Hyperthyroid patients had a blunted GH response to GHRH on days 0, 4 and 7 in comparison with control subjects. However, on day 15, no differences were observed between the area under the curve (mean +/- SE mU/l.120 min) in thyrotoxic patients (1770 +/- 306) and in the control group (3300 +/- 816). IGF-I and albumin levels did not change during Iopanoic acid administration. Conclusions: The results show that an acute reduction in serum T3 levels elicits an increase in GH responsiveness to GHRH in hyperthyroidism. Although the mechanisms involved in this process are still unknown, it is possible that T3 influences GH responsiveness to GHRH via hypothalamic somatostatin release. Alternatively, T3 could have a direct effect at the pituitary somatotroph, modulating GHRH intracellular pathways.