title: Stratified medicine in selecting biologics for the treatment of severe asthma.
abstract: OBJECTIVE
  Despite optimal treatment, asthma symptoms in about 5-10% of patients remain poorly controlled. Apart from having an impact on their asthma-related quality of life and adverse effects of the medications used (especially corticosteroids), their severe symptoms also impact healthcare resources due to frequent admission and requirement for intensive medications use. The last decade has seen an improved understanding in the pathophysiology of the complex cellular and molecular networks involved in the inflammatory and immunological phenotype of severe asthma. This knowledge may help providing strategies by which these phenotypes operate and pave the way for drug development and individualized treatment.
  
  
  RESULTS
  Here we review the current evidence of biological agents in patients with severe asthma recently assessed for safety and efficacy. Some of these agents have shown to be useful in specifically targeted subpopulations of patients with severe asthma, whereas others have proven to be unsafe and/or unsuccessful. In addition, we discuss recent data on clinical and pharmacokinetic-pharmacodynamic aspects of omalizumab, the only licensed anti-IgE therapy for severe atopic asthma.
  
  
  CONCLUSIONS
  More basic science work is required to improve the current understanding of severe asthma pathophysiology and proof-of-concept clinical studies are required to explore relevant biomolecular targets in this small subset of patients. At present, only one drug is licensed for allergic asthmatic patients with severe disease, omalizumab. Novel therapies in the form of oligonucleotide therapies and other biological agents are also being investigated in the difficult-to-treat asthmatic patient group.
authors.affiliation: IIR Division, School of Medicine, University of Southampton, Southampton General Hospital, Southampton, UK.
authors.forename: Jaymin B
authors.initials: JB
authors.lastname: Morjaria
authors.forename: Maria
authors.initials: M
authors.lastname: Proiti
authors.forename: Riccardo
authors.initials: R
authors.lastname: Polosa
mesh_terms: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D001249:Asthma / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D001549:Benzamides; D001688:Biological Products / Q000627:therapeutic use*; D000077561:Daclizumab; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D000069444:Omalizumab; D010880:Piperidines; D011725:Pyridines; D019948:Receptors, Interleukin-4 / Q000037:antagonists & inhibitors; D013844:Thiazoles / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D001549:Benzamides; D001688:Biological Products; D007074:Immunoglobulin G; D010880:Piperidines; D011725:Pyridines; D019948:Receptors, Interleukin-4; D013844:Thiazoles; D014409:Tumor Necrosis Factor-alpha; D000069444:Omalizumab; C434107:mepolizumab; D000077561:Daclizumab; C526575:masitinib