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MP29-02* reduces eosinophil survival induced by epithelial cell secretions from nasal mucosa

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Clinical and Translational Allergy20155 (Suppl 4) :P9

  • Published:


  • Rhinitis
  • Allergic Rhinitis
  • Fluticasone
  • Fluticasone Propionate
  • Nasal Mucosa


Recently, MP29-02* (a novel intranasal formulation of azelastine hydrochloride [AZ] and fluticasone propionate [FP]) has demonstrated significant clinical effects in AR compared to these drugs in monotherapy. The aim of this study was to investigate the anti-inflammatory effect of MP29-02* compared to AZ and FP alone in an in vitro validated model of eosinophilic inflammation.


Peripheral blood eosinophils were incubated for 4 days with decreasing dilutions of MP29-02* (from 1:102 to 1:105 times), equivalent dilutions of FP (7.3x10-6M to 10-9M) or AZ (2.4x10-5M to 10-8M) prior to the addition of Epithelial Cell culture Media (ECM) from nasal mucosa (NM). Eosinophil survival was assessed by Trypan blue dye exclusion. Results are expressed as percentage (mean ± SEM) of eosinophil survival compared to control (100%).


ECM from NM at 10% induced eosinophil survival from day 1 to 4. This effect was inhibited in a dose-response manner by MP29-02* and FP alone (from day 2 to 4) and AZ alone (only at day 4). At day 3, MP29-02* significantly inhibited eosinophil survival induced by ECM from dilution 1:102 (13.8±1.5%, N=6) to dilution 1:105 (58.8±10.8%, N=6), compared to ECM (100%). This inhibitory effect on eosinophil survival induced by MP29-02* at 1:102 dilution (13.8±1.5%) was significantly (p<0.05) stronger than that induced by FP alone (36.7±6.3) or AZ alone (70.3±10.4%) at similar dilutions.


These results suggest that MP29-02* may reduce upper airway eosinophilic infiltration more potently than corticosteroids or antihistamines administered alone. This anti-inflammatory effect may account, at least in part, for the stronger clinical effect of MP29-02* on moderate to severe allergic rhinitis when compared to these drugs in monotherapy.

This study has been sponsored by a research grant from MEDA Pharma.

* Dymista

Authors’ Affiliations

IDIBAPS & CIBERES, Barcelona, Spain
IDIBAPS, CIBERES & Universitat de Barcelona, Barcelona, Spain
Medscript, Dundalk, Ireland


© Roca-Ferrer et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.