Lebrikizumab (INN) is a humanized monoclonal antibody and an experimental immunosuppresive drug for the treatment of asthma that cannot be adequately controlled with inhalable glucocorticoids. It has successfully completed a Phase II clinical trial.[1][2]
[edit] Mechanism of action
Lebrikizumab blocks interleukin 13 (IL-13), a cytokine (cell-signalling protein) that is produced by Th2 cells, a type of white blood cells. IL-13 is thought to induce the expression of another signalling protein, periostin, by epithelial cells of the bronchi. Periostin in turn seems to partake in a number of asthma related problems, such as bronchial hyperresponsiveness, inflammation, and activation and proliferation of airway fibroblasts, which are involved in airway remodelling.[2][3]
This theory is supported by the fact that patients with high periostin levels responded significantly better to lebrikizumab in the Phase II study: the forced expiratory volume in 1 second (FEV1) was 8.2% higher than under placebo in this group (measured from the respective baselines), while low-periostin patients had 1.6% higher FEV1, and the average value for all patients was 5.5%. The FEV1 increase in low-periostin patients was not statistically significant.[4]
[edit] Side effects
In the study, musculoskeletal side effects were more common under lebrikizumab than under placebo (13.2% versus 5.4%). Other side effects were comparable in both groups: infections overall 48.1% versus 49.1%, upper airway infections 12.3% versus 14.3%, and severe side effects overall 3.8% (treatment) versus 5.4% (placebo).[4]
[edit] References
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| Immune system ("-l(i[m])-") |
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Human ("-limu-")
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Mouse ("-limo-")
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Chimeric + humanized
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| Interleukin ("-k(i[n])-") |
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Human ("-kinu-")
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Humanized ("-kizu-", "-kinzu-")
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| Inflammatory lesions ("-les-") |
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Intracellular
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Intracellular
(reception) |
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| Extracellular |
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Serum target
(noncellular)
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Cellular target
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Unsorted
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