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http://dx.doi.org/10.1016/j.jaci.2019.02.015 | DOI Listing |
Increased production of Prostaglandin D2 (PGD2) is linked to development and progression of asthma and allergy. PGD2 is rapidly degraded to its metabolites, which initiate type 2 innate lymphoid cells (ILC2) migration and IL-5/IL-13 cytokine secretion in a PGD2 receptor 2 (DP2)-dependent manner. Blockade of DP2 has shown therapeutic benefit in subsets of asthma patients.
View Article and Find Full Text PDFDrug Dev Ind Pharm
May 2022
Global Program Management, Portfolio Strategy and Management, Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA.
Objective: This work summarizes select methodology of twin-screw melt granulation (TSMG) and process analytical technology that were used in the successful scaling-up and commercial transfer of high drug load (80.5% w/w) immediate release fevipiprant tablets.
Significance: The unique and compelling learnings from this industry work are (1) insights into Novartis AG's commercial scale transfer using TSMG and (2) rapid, nondestructive NIR methodology as a PAT tool for RTR testing.
Clin Sci (Lond)
March 2022
Department of Medicine, College of Nursing at Augusta University, Augusta, GA, U.S.A.
Respir Res
December 2021
Princeton Center for Clinical Research, Skillman, NJ, USA.
Background: The prostaglandin D (PGD) receptor 2 (DP receptor) pathway is an important regulator of the inflammatory cascade in asthma, which can be stimulated by allergic or non-allergic triggers. Fevipiprant is an oral, non-steroidal, highly selective, reversible antagonist of the DP receptor that inhibits the binding of PGD and its metabolites.
Methods: SPIRIT, a 2-treatment period (52-week, double-blind and optional 104-week single-blind), randomised, placebo-controlled, multicentre, parallel-group study, assessed the long-term safety of fevipiprant (150 mg and 450 mg o.
Respir Res
October 2021
Department of Biomarker Analysis and Development, Clinical Airway Research, Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover, Germany.
Background: Prostaglandin D (PGD) signaling via prostaglandin D receptor 2 (DP) contributes to atopic and non-atopic asthma. Inhibiting DP has shown therapeutic benefit in certain subsets of asthma patients, improving eosinophilic airway inflammation. PGD metabolites prolong the inflammatory response in asthmatic patients via DP signaling.
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