| Size | Price | Stock | Qty |
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| 5mg |
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Purity: ≥98%
| Targets |
Asapiprant targets the prostaglandin D2 receptor subtype 1 (DP1). It acts as a potent and selective antagonist with a Ki of 0.44 nM for the human DP1 receptor. The compound exhibits approximately 3.6-fold higher affinity than S-5751 (Ki = 1.6 nM) and 1.3-fold higher affinity than laropiprant (Ki = 0.57 nM). By selectively blocking the DP1 receptor, Asapiprant inhibits the PGD2-DP1 signaling axis, which is involved in allergic inflammation.
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| ln Vitro |
In vitro, Asapiprant demonstrates high affinity and selectivity for the DP1 receptor in receptor binding assays. In direct binding assays on the human DP1 receptor, it shows a Ki of 0.44 nM. This high affinity is maintained in functional assays where it antagonizes DP1-mediated signaling. These in vitro activities confirm its potent and selective DP1 receptor antagonist profile, which is the basis for its potential therapeutic effects in allergic airway diseases.
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| ln Vivo |
Oral treatment of 1 mg/kg and 3 mg/kg of asapilan to sheep significantly (P<0.01) decreased the increase in nasal resistance by 82% and 92%, respectively. Oral injection of 5 mg/kg Asapiprant to sheep decreased prostaglandin (PG) D2 (PGD)2-induced nasal resistance by 86%. Asapiprant (3, 10 and 30 mg/kg) suppressed immediate airway responses (IAR) by 52%, 57% and 96% and late airway responses (LAR) when taken orally 1 hour before antigen challenge to pigs ) are 67%, 50% and 79% respectively. Asapiprant (5 mg/kg) was taken orally for 4 days. Asapiprant significantly (P<0.01) decreased sheep antigen-induced nasal resistance by 73%. Treatment of pigs with 3 and 30 mg/kg Asapiprant significantly (P<0.01) decreased nasal secretions by 53% and 72%, respectively. Treatment of rats with 10 mg/kg Asapiprant significantly reduced airway hyperresponsiveness (AHR), inflammatory cell infiltration, and mucus formation in bronchoalveolar lavage fluid (BALF) despite treatment with 0.1 mg/kg Asapiprant. (P<0.05) had no significant effect on any response [1].
In vivo, Asapiprant has demonstrated efficacy in animal models of allergic airway diseases. In a sheep model, oral administration at 1 and 3 mg/kg significantly suppressed the increase in nasal resistance by 82% and 92%, respectively. In a guinea pig model of allergic rhinitis induced by ovalbumin, Asapiprant reduced nasal secretion and antigen-induced cell infiltration in nasal lavage fluids. In rats, it significantly reduced airway hyperresponsiveness, inflammatory cell infiltration, and mucin production at 10 mg/kg. |
| Enzyme Assay |
The in vitro receptor binding assay for Asapiprant typically involves radioligand displacement studies using membrane preparations from cells expressing the human DP1 receptor. The compound's affinity (Ki) is determined by measuring its ability to displace a specific radiolabeled ligand from the receptor. These cell-free assays provide a direct measure of the compound's binding affinity and selectivity for the DP1 receptor over other prostanoid receptors. This data is critical for characterizing its pharmacological profile.
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| Cell Assay |
In vitro cellular assays for Asapiprant assess its functional antagonism at the DP1 receptor. Cells expressing the DP1 receptor are stimulated with PGD2, and the compound's ability to inhibit downstream signaling, such as cAMP accumulation or calcium flux, is measured. These assays confirm that the compound acts as an antagonist at the DP1 receptor, blocking PGD2-mediated signaling. The potency of the compound in these functional assays correlates with its receptor binding affinity.
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| Animal Protocol |
In vivo animal studies for Asapiprant have been conducted in sheep and guinea pig models of allergic airway diseases. In the sheep model, nasal resistance is measured after antigen challenge. In the guinea pig model, allergic rhinitis is induced by ovalbumin, and endpoints include nasal secretion and cell infiltration in nasal lavage fluids. In rat models, airway hyperresponsiveness, inflammatory cell infiltration, and mucin production are assessed. These studies demonstrate the compound's in vivo efficacy in reducing allergic airway inflammation.
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| ADME/Pharmacokinetics |
Specific pharmacokinetic data for Asapiprant are not extensively detailed in the available literature. However, the compound is orally active, as it has been administered orally in animal models and clinical trials. Its oral bioavailability supports its development as an oral therapeutic agent. The compound's pharmacokinetic properties, such as half-life and Cmax, would have been evaluated in clinical studies, but specific data are not provided.
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| Toxicity/Toxicokinetics |
Specific toxicity data for Asapiprant are not extensively detailed in the available literature. As a DP1 receptor antagonist, its toxicity profile is likely related to its pharmacological activity. However, the compound has participated in Phase II and III clinical trials, indicating that it has been evaluated for safety in humans. The specific adverse event profile from these trials is not detailed in the search results. Preclinical toxicology studies would also have been conducted as part of its development.
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| References | |
| Additional Infomation |
Asapiprant (S-555739) is a potent and selective DP1 receptor antagonist that has been investigated for the treatment of allergic airway diseases, including allergic rhinitis. It has participated in Phase III clinical trials in Japan and Phase II trials in the USA. The compound selectively blocks the PGD2-DP1 signaling axis, which is involved in allergic inflammation. It has demonstrated efficacy in animal models of allergic airway diseases. It is not approved for clinical use and remains an investigational agent.
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| Molecular Formula |
C24H27N3O7S
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| Molecular Weight |
501.5521
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| Exact Mass |
501.157
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| CAS # |
932372-01-5
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| Related CAS # |
932372-01-5
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| PubChem CID |
59232326
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| Appearance |
White to off-white solid powder
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| LogP |
4.186
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
10
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| Rotatable Bond Count |
9
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| Heavy Atom Count |
35
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| Complexity |
789
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
ZMZNWNTZRWXTJU-UHFFFAOYSA-N
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| InChi Code |
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)
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| Chemical Name |
2-[2-(1,3-oxazol-2-yl)-5-[4-(4-propan-2-yloxyphenyl)sulfonylpiperazin-1-yl]phenoxy]acetic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~11.11 mg/mL (~22.15 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 1.11 mg/mL (2.21 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 11.1 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 1.11 mg/mL (2.21 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 11.1 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. 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. View More
Solubility in Formulation 3: ≥ 1.11 mg/mL (2.21 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.9938 mL | 9.9691 mL | 19.9382 mL | |
| 5 mM | 0.3988 mL | 1.9938 mL | 3.9876 mL | |
| 10 mM | 0.1994 mL | 0.9969 mL | 1.9938 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT01651871 | Completed | Drug: S-555739 Dose 1 Drug: S-555739 Dose 2 Drug: Cetirizine HCl Dose 1 |
Seasonal Allergic Rhinitis | Shionogi | 2012-07 | Phase 2 |
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