Ramatroban

Description: Ramatroban is a thromboxane receptor antagonist and a DP2 receptor antagonist. It is indicated for the treatment of coronary artery disease and has also been used for the treatment of asthma.

• Catalog: OFC116649855
• CAS: 116649-85-5
• Category: Fluorinated APIs
• Synonyms: Baynas
• Purity: >98%

• IUPAC Name: 3-[(3R)-3-[(4-fluorophenyl)sulfonylamino]-1,2,3,4-tetrahydrocarbazol-9-yl]propanoic acid
• InChI: InChI=1S/C21H21FN2O4S/c22-14-5-8-16(9-6-14)29(27,28)23-15-7-10-20-18(13-15)17-3-1-2-4-19(17)24(20)12-11-21(25)26/h1-6,8-9,15,23H,7,10-13H2,(H,25,26)/t15-/m1/s1
• InChI Key: LDXDSHIEDAPSSA-OAHLLOKOSA-N
• Isomeric SMILES: C1CC2=C(C[C@@H]1NS(=O)(=O)C3=CC=C(C=C3)F)C4=CC=CC=C4N2CCC(=O)O
• EC Number: 631-428-1

• Molecular Formula: C21H21FN2O4S
• Molecular Weight: 416.47
• Appearance: White to off-white solid powder

• XLogP3-AA: 2.9
• Hydrogen Bond Donor Count: 2
• Hydrogen Bond Acceptor Count: 6
• Rotatable Bond Count: 6
• Exact Mass: 416.12060649 g/mol
• Monoisotopic Mass: 416.12060649 g/mol
• Topological Polar Surface Area: 96.8Ų
• Heavy Atom Count: 29
• Formal Charge: 0
• Complexity: 689

Case Study

Ramatroban in the Treatment of Perennial Allergic Rhinitis: Experimental Application

Ohkubo K, et al. Allergology International, 2003, 52(3), 131-138.

A clinical study evaluated the therapeutic potential of ramatroban, a thromboxane A₂ receptor antagonist, in perennial allergic rhinitis. Ten untreated patients were administered ramatroban orally for 28 consecutive days. Symptom assessment was conducted using self-reported scores for nasal obstruction, rhinorrhea, and sneezing, recorded at baseline and during treatment. To examine mediator involvement, nasal fluid was collected following antigen challenge, and concentrations of histamine and TXB₂ (the stable metabolite of TXA₂) were quantified. Results demonstrated significant improvement in nasal obstruction and overall symptom scores in nine patients. Moreover, post-treatment antigen-induced nasal fluid showed marked reductions in histamine and TXB₂ levels, indicating suppression of inflammatory mediator release. Symptom severity for nasal obstruction correlated positively with TXB₂ concentration, reinforcing ramatroban's mechanistic role in inhibiting TXA₂-mediated pathways. These findings confirm ramatroban's clinical efficacy and pharmacological relevance in allergic rhinitis.

Ramatroban in the Treatment of Eosinophilic Otitis Media

Wada T, et al. Auris Nasus Larynx, 2006, 33(4), 455-460.

Two clinical cases of eosinophilic otitis media were treated with ramatroban, a dual antagonist of thromboxane A2 receptor (TP) and CRTH2. Patients received oral ramatroban as an adjunct to minimal corticosteroid therapy. The therapeutic response was assessed by monitoring middle ear effusion through otoscopic examinations and audiometric evaluations over a follow-up period exceeding one year. Both patients demonstrated sustained suppression of effusion and symptomatic improvement without recurrence. These findings highlight the experimental application of ramatroban in modulating Th2-mediated inflammation, offering a novel therapeutic strategy for this otherwise intractable otologic condition.

Ramatroban for Improving Vascular Reactivity in Hypercholesterolemic Rabbits

Ishizuka T, et al. European Journal of Pharmacology, 2003, 468(1), 27-35.

In this study, ramatroban, a thromboxane-prostanoid (TP) receptor antagonist, was evaluated for its capacity to restore vascular function in hypercholesterolemic rabbits. Elevated plasma levels of 8-iso-prostaglandin F2α, a potent vasoconstrictor acting through TP receptors, were observed in cholesterol-fed animals. Vascular reactivity was assessed in vivo by measuring acetylcholine-induced vasodilation. Hypercholesterolemia significantly impaired this response, an effect further aggravated by exogenous 8-iso-prostaglandin F2α. Treatment with ramatroban effectively reversed the attenuation of acetylcholine-mediated dilation, indicating blockade of TP receptor-mediated vasoconstriction. Importantly, co-administration of the nitric oxide synthase inhibitor l-NG-nitroarginine methyl ester did not diminish the protective effects of ramatroban, confirming that its action was independent of nitric oxide pathways. These results demonstrate the experimental application of ramatroban in mitigating cholesterol-induced vascular dysfunction through targeted inhibition of isoprostane-TP receptor signaling.