Asapiprant

• CAT Number: R034200
• CAS Number: 932372-01-5
• Molecular Formula: C₂₄H₂₇N₃O₇S
• Molecular Weight: 501.55
• Purity: ≥95%
• Target: DP1 receptor antagonist
• Storage: -20°C
• InChI: InChI=1S/C24H27N3O7S/c1-17(2)34-19-4-6-20(7-5-19)35(30,31)27-12-10-26(11-13-27)18-3-8-21(24-25-9-14-32-24)22(15-18)33-16-23(28)29/h3-9,14-15,17H,10-13,16H2,1-2H3,(H,28,29)
• InChIKey: ZMZNWNTZRWXTJU-UHFFFAOYSA-N
• SMILES: O=C(O)COC1=CC(N2CCN(S(=O)(C3=CC=C(OC(C)C)C=C3)=O)CC2)=CC=C1C4=NC=CO4

Asapiprant, also known as S-555739, is a the potent and selective DP1 receptor antagonist. Asapiprant exhibited high affinity and selectivity for the DP1 receptor. Significant suppression of antigen-induced nasal resistance, nasal secretion, and cell infiltration in nasal mucosa was observed with asapiprant treatment. In addition, treatment with asapiprant suppressed antigen-induced asthmatic responses, airway hyper-responsiveness, and cell infiltration and mucin production in lung. These results show that asapiprant is a potent and selective DP1 receptor antagonist, and exerts suppressive effects in the animal models of allergic diseases. Thus, asapiprant has potential as a novel therapy for allergic airway diseases.

Reference

1:Eur J Pharmacol. 2015 Oct 15;765:15-23. doi: 10.1016/j.ejphar.2015.08.003. Epub 2015 Aug 12. Effect of the potent and selective DP1 receptor antagonist, asapiprant (S-555739), in animal models of allergic rhinitis and allergic asthma.Takahashi G,Asanuma F,Suzuki N,Hattori M,Sakamoto S,Kugimiya A,Tomita Y,Kuwajima G,Abraham WM,Deguchi M,Arimura A,Shichijo M, PMID: 26277322 DOI: 10.1016/j.ejphar.2015.08.003 Abstract: Prostaglandin (PG) D2 elicits responses through either the DP1 and/or DP2 receptor. Experimental evidence suggests that stimulation of the DP1 receptor contributes to allergic responses, such that antagonists are considered to be directed therapies for allergic diseases. In this study, we demonstrate the activity of a novel synthetic DP1 receptor antagonist termed asapiprant (S-555739) for the DP1 receptor and other receptors in vitro, and assess the efficacy of asapiprant in several animal models of allergic diseases. We determined the affinity and selectivity of asapiprant for the DP1 receptor in binding assays. In the animal models of allergic rhinitis, changes in nasal resistance, nasal secretion, and cell infiltration in nasal mucosa were assessed after antigen challenge with and without asapiprant. Similarly, in the animal models of asthma, the effect of antigen challenge with and without asapiprant on antigen-induced bronchoconstriction, airway hyper-responsiveness, mucin production, and cell infiltration in lung were assessed. In binding studies, asapiprant exhibited high affinity and selectivity for the DP1 receptor. Significant suppression of antigen-induced nasal resistance, nasal secretion, and cell infiltration in nasal mucosa was observed with asapiprant treatment. In addition, treatment with asapiprant suppressed antigen-induced asthmatic responses, airway hyper-responsiveness, and cell infiltration and mucin production in lung. These results show that asapiprant is a potent and selective DP1 receptor antagonist, and exerts suppressive effects in the animal models of allergic diseases. Thus, asapiprant has potential as a novel therapy for allergic airway diseases. Copyright © 2015 Elsevier B.V. All rights reserved.