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Understanding the Current Biologics in Asthma Treatment
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- In this review article, the authors summarize the current use of biologics for the treatment of patients with asthma. They review the current understanding of different disease phenotypes and endotypes and the pathophysiology of different endotypes. They then describe the currently approved biologics and considerations for choosing the appropriate ones for specific patients.
- This review provides a concise, practical, and comprehensive summary of the rapidly evolving landscape of targeted biologics for the treatment of uncontrolled and/or severe asthma.
abstract
This abstract is available on the publisher's site.
Access this abstract nowUncontrolled asthma and/or severe asthma causes significant impairments in quality of life and is often a huge health care burden. Monoclonal antibodies have been an important addition to the therapeutic management of patients with moderate to severe asthma who do not respond to conventional asthma management. Currently the majority of Food and Drug Administration (FDA) approved biologics target T2 high inflammation. However, with the expanding knowledge of asthma pathogenesis, novel therapeutics targeting T2 low inflammation are in development. In this article we will focus on the current understanding of T2 inflammation and approved biologics for moderate to severe asthma.
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Current Biologics in Asthma Treatment
Semin Respir Crit Care Med 2022 Oct 01;43(5)627-634, D Imanirad, F TabatabaianFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Monoclonal antibodies for asthma
Monoclonal antibody therapy is one of the fastest growing interventions for a variety of inflammatory conditions. The antibody is programmed to take out a messenger of the innate inflammatory cascade.
Severe asthma has been classified as the result of high or low inflammation.
High-Inflammation asthma is associated with eosinophil recruitment stimulated by interleukin (IL)-4, IL-5, IL-13, and thymic stromal lymphopoietin. As expected, high-inflammation asthma benefits more from corticosteroids. The diagnosis is aided by elevated serum eosinophils and elevated serum immunoglobulin E levels.
Low-Inflammation asthma is associated with neutrophil secretions in the airways. It is seen more in older, overweight individuals without a history of allergies. Low-inflammation asthma generally responds better to beta agonists, muscarinic antagonists, and macrolide antibiotics and is less responsive to corticosteroids.
Monoclonal antibody therapies have mainly targeted high-inflammation asthma. Below is a table that summarizes the five monoclonal antibodies approved for high-inflammation asthma and one not yet approved by the FDA that may benefit both high- and low-inflammation asthma.
Medication
Target
Indications
Dosing
Other Uses
Omalizumab (Xolair)
IgE, reducing mast cell activation
>6 yo, total IgE level 30-1500 IU/mL
150-375 mg SC every 2-4 weeks
Urticaria and nasal polyps
Mepolizumab (Nucala)
IL-5
>12 yo in U.S. >150-300 eosinophils/µL
100 mg SC every 4 weeks
Hypereosinophilic syndromes, chronic rhinosinusitis with polyps
Reslizumab (Cinqair)
IL-5
>18 yo, >400 eosinophils/µL
3 mg/kg IV every 4 weeks
Benralizumab (Fasenra)
IL-5 receptor
>12 yo, >300 eosinophils/µL
30 mg SC every 4 weeks, then every 8 weeks
Dupilumab (Dupixent)
IL-4 receptor that reduces IL-4 and IL-13
>12 yo with eosinophilic asthma
400-600 mg SC load then 300 mg SC every 2 weeks
Atopic dermatitis, chronic rhinosinusitis with polyps
Tezepelumab (Tezspire)
TSLP, which can benefit both high and low inflammation asthma
Not FDA-approved
210 mg SC every 4 weeks
A concerning side effect of monoclonal antibodies is the risk of anaphylaxis. The first dose should be administered within a healthcare setting.
Monoclonal antibody therapy has become an effective treatment for severe asthma. However, it does nothing to address the growing incidence of asthma and what may be triggering this worsening inflammatory response. As we use these new tools to better manage this condition, it is important that we keep exploring how we can reduce the need for this rescue therapy that may require dismantling an arm of the immune system.