Ridogrel
(Synonyms: 利多格雷,R 68070) 目录号 : GC64765
Ridogrel (R 68070) 是一种口服活性的血栓素 A2 合成酶 (combined thromboxane A2 synthetase) 抑制剂和血栓素 A2/前列腺素内过氧化物受体 (thromboxane A2/prostaglandin endoperoxide receptor) 阻滞剂。Ridogrel 是一种有效的抗血小板剂，具有抗炎活性。
Cas No.:110140-89-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
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- SDS (Safety Data Sheet)
- Datasheet
Ridogrel (R 68070) is an orally active combined thromboxane A2 synthetase inhibitor and thromboxane A2/prostaglandin endoperoxide receptor blocker. Ridogrel is potent antiplatelet agent. Anti-inflammatory activities[1][2][3].
In rats, R 68 070 (1.25 mg/kg orally, -2 h) singly prolongs tail bleeding times as much as a combination of TXA2 synthetase inhibition (dazoxiben 10 mg/kg) and TXA2/prostaglandin endoperoxide receptor blockade (BM 13177 40 mg/kg). In dogs, the compound reduces coronary thrombosis induced by electrical damage (1.25 mg/kg i.v.) and prevents the evolution of occlusion/reperfusion-induced arrhythmias into ventricular fibrillation (2.5 mg/kg i.v.)[2.
[1]. De Clerck F, et al. R 68 070: thromboxane A2 synthetase inhibition and thromboxane A2/prostaglandin endoperoxide receptor blockade combined in one molecule--II. Pharmacological effects in vivo and ex vivo. Thromb Haemost. 1989;61(1):43-49.
[2]. Di Perri T, et al. Ridogrel, una nuova molecula antiaggregante piastrinica a doppio meccanismo d'azione. Profilo farmacologico e clinico [Ridogrel, a new platelet antiaggregant molecule with a double mechanism of action. A pharmacological and clinical profile]. Recenti Prog Med. 1991;82(10):533-540.
[3]. Carty E, et al. Ridogrel, a dual thromboxane synthase inhibitor and receptor antagonist: anti-inflammatory profile in inflammatory bowel disease. Aliment Pharmacol Ther. 2000;14(6):807-817.
| Cas No. | 110140-89-1 | SDF | Download SDF |
| 别名 | 利多格雷,R 68070 | ||
| 分子式 | C18H17F3N2O3 | 分子量 | 366.33 |
| 溶解度 | 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 | 2.7298 mL | 13.6489 mL | 27.2978 mL |
| 5 mM | 0.546 mL | 2.7298 mL | 5.4596 mL |
| 10 mM | 0.273 mL | 1.3649 mL | 2.7298 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 | ||||||||||
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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。
Ridogrel, a dual thromboxane synthase inhibitor and receptor antagonist: anti-inflammatory profile in inflammatory bowel disease
Aliment Pharmacol Ther 2000 Jun;14(6):807-17.PMID:10848666DOI:10.1046/j.1365-2036.2000.00779.x.
Background: Thromboxanes, prostaglandins, reactive oxygen metabolites and pro-inflammatory cytokines are produced in excess in inflammatory bowel disease. Preliminary reports suggest that Ridogrel, a thromboxane synthesis inhibitor and receptor blocker, may have therapeutic benefits in ulcerative colitis. Aims: To investigate the anti-inflammatory profile of Ridogrel. Methods: The effects of Ridogrel on the production of eicosanoids, reactive oxygen metabolites and cytokines by cultured inflamed colorectal mucosal biopsies were made using ELISA and chemiluminescence, reactive oxygen metabolite generation in a cell-free system, and platelet activation using flow cytometry. The effects of oral Ridogrel on mucosal release of eicosanoids in two patients with active ulcerative colitis were assessed using rectal dialysis. Results: Ridogrel significantly reduced the release of thromboxane B2, but not prostaglandin E2 or tumour necrosis factor-alpha, from biopsies (P < 0.01 for 10 microM Ridogrel). Ridogrel showed no direct antioxidant activity but significantly reduced reactive oxygen metabolite production from cultured biopsies (P < 0.01 for 10 microM Ridogrel). Platelet activation in vitro was inhibited by Ridogrel (P /= 10 microM Ridogrel). Mean rectal mucosal thromboxane B2 release was reduced to 86% of pre-treatment levels in two patients treated with oral Ridogrel. Conclusions: Its inhibition of mucosal production of thromboxane B2, reactive oxygen metabolites, and of platelet activation, suggests that Ridogrel could have a therapeutic role in inflammatory bowel disease.
Ridogrel enemas in distal ulcerative colitis
Eur J Gastroenterol Hepatol 2001 Apr;13(4):397-400.PMID:11338069DOI:10.1097/00042737-200104000-00016.
Objective: To evaluate the effect of Ridogrel enemas (Janssen Research Foundation, Beerse, Belgium) on disease activity and mucosal inflammatory mediators in patients with active left-sided ulcerative colitis. Design and methods: Eleven patients with active left-sided ulcerative colitis were evaluated in an open non-placebo-controlled pilot study. All patients were treated with Ridogrel enemas (300 mg/40 ml once daily) over four weeks. A disease activity score based on clinical, endoscopic and histological criteria was obtained before and after treatment with Ridogrel. The concentrations of thromboxane B2 (TxB2), prostaglandin E2 (PGE2), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) were measured in mucosal biopsies before and after treatment. Results: One patient discontinued treatment because of progression of disease, the other ten patients tolerated the Ridogrel enemas well. Mucosal TxB2 concentration decreased significantly in all patients. The mucosal concentrations of the other inflammatory mediators (PGE2, IL-6 and TNF-alpha) were unaltered. The disease score decreased in five patients. However, clinical improvement was not always associated with a decrease in endoscopic and/or histological scores. Conclusions: This pilot study shows that Ridogrel enemas selectively reduce mucosal TxB2 concentration.
Ridogrel improves maternal/fetal homeostasis in an ovine model of pregnancy-induced hypertension
Prostaglandins 1994 Mar;47(3):247-63.PMID:8016393DOI:10.1016/0090-6980(94)90064-7.
The effects of Ridogrel (a thromboxane synthetase inhibitor/endoperoxide receptor antagonist) were assessed in an ovine model of pregnancy-induced hypertension. Maternal serum prostacyclin and thromboxane levels were quanitiated using RIA, and maternal and neonatal coagulation status was assessed. Pregnancy and neonatal outcome were recorded. Ridogrel, (E)-5-[[[3-pyridinyl)[3-(trifluoromethyl)phenyl]methylen]amin++ +] oxy]pentanoic acid, was administered in one bolus dose at 0.1 or 1.0 mg/kg IV, three hours following the onset of a 27 hour magnesium sulfate infusion given hypertensive ewes to prevent maternal seizures. At both doses, Ridogrel improved neonatal outcome (0% neonatal mortality in each Ridogrel group versus 67% neonatal mortality in the magnesium sulfate group), and Ridogrel at 0.1 mg/kg IV normalized birth weights. Abnormalities of maternal platelet function (abnormal or no response to collagen), occurring during the ovine syndrome, resolved following Ridogrel treatment. Ridogrel's effects on maternal and neonatal coagulation were more dramatic at the 0.1 mg/kg IV dose. Ridogrel appeared to be beneficial in this model of pregnancy-induced hypertension.
Efficacy and safety of oral Ridogrel in the treatment of ulcerative colitis: two multicentre, randomized, double-blind studies
Aliment Pharmacol Ther 2002 Jan;16(1):87-99.PMID:11856082DOI:10.1046/j.1365-2036.2002.01121.x.
Background: Ridogrel at low doses inhibits thromboxane synthase. Oral Ridogrel, from 5 mg once daily to 150 mg twice daily, improves the endoscopic appearance of colonic mucosa and clinical manifestations in mild to moderate ulcerative colitis. Aim: One US trial and one international trial were conducted to determine the effect of Ridogrel on mild to severe active ulcerative colitis. Methods: Two 12-week, double-blind, randomized, parallel-group trials were conducted. A US trial compared 0.5 mg, 2.5 mg and 5 mg of Ridogrel once daily with placebo. An international trial compared 0.5 mg of Ridogrel once daily with 2.5 mg and 5.0 mg of Ridogrel once daily and 800 mg of mesalazine (known as mesalamine in the USA) three times daily. The primary efficacy outcome measure was the rate of complete remission. Results: In the US trial, complete remission was achieved in 20.8% of patients in the 0.5 mg Ridogrel group, 17.9% in the 2.5 mg Ridogrel group, 20.6% in the 5.0 mg Ridogrel group and 13.6% in the placebo group. In the international trial, 14.4% of patients in the 0.5 mg Ridogrel group, 19.6% in the 2.5 mg Ridogrel group, 19.4% in the 5.0 mg Ridogrel group and 16.4% in the mesalazine group experienced complete remission. In the international trial, rates of complete remission at the end-point were greater in the 2.5 mg and 5.0 mg Ridogrel groups than in the 0.5 mg Ridogrel group, but the differences were not statistically significant. In the US trial, rates of complete remission at the end-point were greater in the 2.5 mg and 5.0 mg Ridogrel groups than in the placebo group, but the differences were not statistically significant. Approximately 30% of the patients in each group discontinued treatment before the 12-week end-point owing to a lack of therapeutic response. All doses of Ridogrel were well tolerated and comparable with placebo or mesalazine in terms of safety. Conclusions: No significant differences in the primary efficacy outcome measure were found between either the 2.5 mg or the 5.0 mg dose of Ridogrel and placebo in the US trial and between either the 2.5 mg or the 5.0 mg dose of Ridogrel and the 0.5 mg dose of Ridogrel, a surrogate dose for placebo, in the international trial. There was no clear indication in either trial of an effective dose of Ridogrel in the treatment of ulcerative colitis.
The in vitro effect of Ridogrel on platelet function in normocholesterolaemic and familial hypercholesterolaemic type IIa subjects
Thromb Res 1997 Dec 1;88(5):399-407.PMID:9556227DOI:10.1016/s0049-3848(97)00271-5.
Platelets from familial hypercholesterolaemia type IIa patients are hyperreactive and produce increased amounts of thromboxane A2. These modifications of platelet function may play an important role in the occurrence of premature atherosclerosis. One approach to the prevention of the thromboembolic complications of atherosclerosis is the use of antiplatelet agents which depress platelet function. Ridogrel, a combined thromboxane synthase inhibitor and thromboxane A2/prostaglandin endoperoxide receptor blocker inhibits platelet aggregation. This study was designed to investigate the in vitro effect of Ridogrel on platelet function in normocholesterolaemic and familial hypercholesterolaemia type IIa subjects. In citrated platelet rich plasma Ridogrel significantly inhibited platelet aggregation and thromboxane A2 production in response to collagen, ADP and arachidonic acid stimulation. In washed platelets Ridogrel significantly decreased aggregation and serotonin release. Ridogrel significantly increased cAMP levels in response to thrombin stimulation. In conclusion, Ridogrel at low concentrations significantly inhibited the in vitro function of platelets in a dose dependant manner in both normocholesterolaemic subjects and familial hypercholesterolaemia IIa subjects.