TABLE 1 | Biological drugs in asthma treatment

From the following article:

The potential of biologics for the treatment of asthma

Girolamo Pelaia, Alessandro Vatrella & Rosario Maselli

Nature Reviews Drug Discovery 11, 958-972 (December 2012)


DrugMechanism of actionEffectsDevelopment*
OmalizumabBinds free IgEReduces exacerbations, improves symptoms and quality of lifeFDA- and EMA-approved
MepolizumabBlocks IL-5Decreases the number of eosinophils and frequency of exacerbations, as well as prednisone consumptionPhase II/III
ReslizumabBlocks IL-5Decreases the number of sputum eosinophils and enhances FEV1Phase II
BenralizumabInhibits binding of IL-5 to IL-5RαDepletes the number of peripheral blood eosinophilsPhase I/II
PascolizumabBlocks IL-4No significant clinical efficacyPhase II
AltrakinceptSoluble IL-4RNo significant clinical efficacyPhase II
PitrakinraInhibits binding of IL-4 and/or IL-13 to IL-4RαMay prevent a decrease in FEV1 after allergen challengePhase II
TralokinumabBlocks IL-13Reduces airway eosinophiliaPhase I/II
AnrukinzumabBlocks IL-13Inhibits allergen-induced late-phase asthmatic responsesPhase II
LebrikizumabBlocks IL-13Enhances FEV1 in patients with high serum levels of periostinPhase II
MEDI-528Blocks IL-9Reduces airway inflammation and hyperresponsiveness in micePhase II
MT203Blocks GM-CSFDecreases survival and activation of eosinophilsPhase II
SecukinumabBlocks IL-17Data not yet availablePhase II; NCT01478360
GolimumabBlocks TNFαMay increase the risk of infections and malignanciesSuspended
InfliximabBlocks TNFαReduces PEF oscillations and asthma exacerbationsPhase II
EtanerceptSoluble TNFα receptorConflicting data; see main textPhase II
*Unless given in the table, details of identifiers or publications are given in the main text. EMA, European Medicines Agency; FDA, US Food and Drug Administration; FEV1, forced expiratory volume in 1 second; GM-CSF, granulocyte–macrophage colony-stimulating factor; IgE, immunoglobulin E; IL-4, interleukin-4; IL-4Rα, IL-4 receptor-α; PEF, peak expiratory flow; TNFα, tumour necrosis factor-α.

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