Rats' tail bleeding time was prolonged by R 68 070 alone (1.25 mg/kg orally, -2 hours), which was in line with TXA2 synthase inhibition (darzoxiben 10 mg/kg) and TXA2/prostaglandin. The combination of superoxide receptor blocker (BM 13177 40 mg) also had a similar effect. /Kilogram. In dogs, the chemical inhibits electrical injury-induced coronary thrombosis (1.25 mg/kg iv) and prevents occlusion/reperfusion-induced arrhythmias from evolving into ventricular fibrillation (2.5 mg/kg iv) [2.

Absorption, Distribution and Excretion
Rapidly absorbed after oral administration (30-60 minutes)

Toxicity Summary
Lidogre inhibits thromboxane A2 synthase and blocks the thromboxane A2/prostaglandin intracellular peroxidase receptor. Thrombosome synthase produces thromboxane in platelets. Thrombosome is a vasoconstrictor that promotes platelet aggregation. Therefore, by inhibiting thromboxane production and promoting its production, thrombolysis can be enhanced. Protein Binding Approximately 60% is bound to plasma proteins.

[1]. 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]. 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 pro.

[3]. Ridogrel, a dual thromboxane synthase inhibitor and receptor antagonist: anti-inflammatory profile in inflammatory bowel disease. Aliment Pharmacol Ther. 2000;14(6):807-817.

Ridogrel belongs to the (trifluoromethyl)benzene family of compounds. Ridogrel is a dual-action drug used to prevent systemic thromboembolism and as adjunctive therapy in thrombolytic therapy for acute myocardial infarction. However, there is currently no clinical evidence that Ridogrel is superior to aspirin. Ridogrel has only been found in individuals who have taken the drug. It is a dual-action drug used to prevent systemic thromboembolism and as adjunctive therapy in thrombolytic therapy for acute myocardial infarction. However, there is currently no clinical evidence that Ridogrel is superior to aspirin. Ridogrel inhibits thromboxane A2 synthase and blocks the thromboxane A2/prostaglandin intraperoxide receptor. Thromboboxane synthase produces thromboxane in platelets. Thromboboxane is a vasoconstrictor that promotes platelet aggregation. Therefore, by inhibiting thromboxane production and promoting its aggregation, the thrombolytic effect can be enhanced. Drug Indications: For adjunctive treatment of patients with acute myocardial infarction to induce thrombolysis. Mechanism of Action Lidogre inhibits thromboxane A2 synthase and blocks the thromboxane A2/prostaglandin/internal peroxide receptor. Thrombosome synthase produces thromboxane in platelets. Thrombosome is a vasoconstrictor that promotes platelet aggregation. Therefore, by inhibiting and promoting thromboxane production, thrombolysis can be enhanced. Pharmacodynamics Lidogre is a combination of a thromboxane synthase inhibitor and a receptor antagonist, used in combination with streptokinase as adjunctive therapy to reduce thrombus formation and volume. Thrombi can lead to ischemic cardiac events (myocardial infarction). Lidogre has a dual action, inhibiting both thromboxane synthesis and blocking the thromboxane/prostaglandin/internal peroxide receptor. Studies have shown that Ridogrel can accelerate recanalization and delay or prevent re-occlusion during systemic thrombolytic therapy with tissue-type plasminogen activator (streptokinase). Ridogrel is a more effective antiplatelet drug than aspirin, and therefore may be more advantageous than aspirin in thrombolytic therapy for patients with acute myocardial infarction. Aspirin works by inhibiting cyclooxygenase (an enzyme responsible for thromboxane production), while Ridogrel directly inhibits thromboxane synthesis. A recent study comparing aspirin and Ridogrel as adjunctive thrombolytic agents in patients with acute myocardial infarction showed that Ridogrel was not superior to aspirin in enhancing the thrombolytic efficacy of streptokinase, but it may be more effective in preventing new ischemic events. Currently, clinical experience with this drug remains relatively limited.

C18H17F3N2O3

366.3344

366.119

110140-89-1

5362391

White to light yellow solid powder

1.26g/cm3

495.2ºC at 760mmHg

253.3ºC

1.26E-10mmHg at 25°C

1.531

4.124

1

8

8

26

483

0

C1=CC(=CC(=C1)C(F)(F)F)/C(=N\OCCCCC(=O)O)/C2=CN=CC=C2

GLLPUTYLZIKEGF-HAVVHWLPSA-N

InChI=1S/C18H17F3N2O3/c19-18(20,21)15-7-3-5-13(11-15)17(14-6-4-9-22-12-14)23-26-10-2-1-8-16(24)25/h3-7,9,11-12H,1-2,8,10H2,(H,24,25)/b23-17+

5-[(E)-[pyridin-3-yl-[3-(trifluoromethyl)phenyl]methylidene]amino]oxypentanoic acid

R68070 R-68070 Ridogrel, R 68070

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

DMSO : ~100 mg/mL (~272.98 mM)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)