Biologic therapies for chronic obstructive pulmonary disease

Matera, Maria Gabriella; Calzetta, Luigino; Cazzola, Mario; Ora, Josuel; Rogliani, Paola

doi:10.1080/14712598.2022.2160238

Cited by 4 publications

(13 citation statements)

References 95 publications

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“…Anti-IL-17A mAbs, collectins, anti-IL-5 mAbs, anti-IL13/IL4 mAbs, anti-TSLP mAbs, and anti-IL-33 mAbs are among the biological therapies that have the potential to treat COPD. 24,76 Anti-IL-17A mAbs Along with IL-22, IL-17A and IL-17F are linked to an increase in neutrophils in the airways, which results in chronic inflammation and increased mucus production and smooth muscle mass in the airways. 76 To reduce neutrophil recruitment and airway inflammation, many anti-IL-17A and anti-IL-17 receptor A (IL-17RA) mAbs are being developed, 77 but CNTO 6785 is the only anti-IL-17A mAb that has been investigated in patients with COPD.…”

Section: Biologic Therapiesmentioning

confidence: 99%

“…24,76 Anti-IL-17A mAbs Along with IL-22, IL-17A and IL-17F are linked to an increase in neutrophils in the airways, which results in chronic inflammation and increased mucus production and smooth muscle mass in the airways. 76 To reduce neutrophil recruitment and airway inflammation, many anti-IL-17A and anti-IL-17 receptor A (IL-17RA) mAbs are being developed, 77 but CNTO 6785 is the only anti-IL-17A mAb that has been investigated in patients with COPD. It caused a small improvement in FEV 1 but did not interfere with the other primary or secondary endpoints.…”

Section: Biologic Therapiesmentioning

confidence: 99%

“…Brodalumab, which is a mAb that targets IL-17RA, secukinumab, a fully human anti-IL-17A of the immunoglobulin (Ig)G 1κ isotype, and CCJM112, a novel fully human anti-IL-17A IgG 1κ mAb that binds with similar affinity to both human IL-17A and IL-17AF, have not yet been tested in patients with COPD. 76 Collectins SP-A and SP-D are termed collectins because they contain collagen and are functional lectins. 79 By competing with LPS for CD14 binding on alveolar macrophages, SP-A and SP-D decrease TNF-α production.…”

Section: Biologic Therapiesmentioning

confidence: 99%

“…89 Patients with eosinophilic COPD and concomitant emphysema had significant levels of sputum matrix metalloprotease-12 (MMP-12), which is produced by alveolar macrophages when IL-13 is present. 76 Furthermore, it has been demonstrated that individuals with stable COPD or during an AECOPD have greater levels of group 2 innate lymphoid cells, which can produce IL-13. 90 Lebrikizumab, a humanized mAb that binds to soluble IL-13 and inhibits activation of IL-4Rα and IL-13Rα1 heterodimers, has been examined in patients with COPD with a history of exacerbations despite using ICS and at least one long-acting bronchodilator inhaler drug (NCT02546700).…”

Section: Targeting Il13/il4mentioning

confidence: 99%

“…90 Lebrikizumab, a humanized mAb that binds to soluble IL-13 and inhibits activation of IL-4Rα and IL-13Rα1 heterodimers, has been examined in patients with COPD with a history of exacerbations despite using ICS and at least one long-acting bronchodilator inhaler drug (NCT02546700). 76 Although the complete results have not yet been made public, early data indicates that lebrikizimab did not affect the AECOPD rate compared to placebo. Consequently, the clinical development of lebrikizumab for the treatment of patients with COPD has been halted indefinitely.…”

Section: Targeting Il13/il4mentioning

confidence: 99%

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Novel Anti-Inflammatory Approaches to COPD

Cazzola¹,

Hanania²,

Page³

et al. 2023

COPD

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Airway inflammation, driven by different types of inflammatory cells and mediators, plays a fundamental role in COPD and its progression. Neutrophils, eosinophils, macrophages, and CD4 + and CD8 + T lymphocytes are key players in this process, although the extent of their participation varies according to the patient's endotype. Anti-inflammatory medications may modify the natural history and progression of COPD. However, since airway inflammation in COPD is relatively resistant to corticosteroid therapy, innovative pharmacological anti-inflammatory approaches are required. The heterogeneity of inflammatory cells and mediators in annethe different COPD endo-phenotypes requires the development of specific pharmacologic agents. Indeed, over the past two decades, several mechanisms that influence the influx and/or activity of inflammatory cells in the airways and lung parenchyma have been identified. Several of these molecules have been tested in vitro models and in vivo in laboratory animals, but only a few have been studied in humans. Although early studies have not been encouraging, useful information emerged suggesting that some of these agents may need to be further tested in specific subgroups of patients, hopefully leading to a more personalized approach to treating COPD.

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