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&lt;p&gt;&lt;b&gt;New page&lt;/b&gt;&lt;/p&gt;&lt;div&gt;An &amp;#039;&amp;#039;&amp;#039;antiasthmatic agent&amp;#039;&amp;#039;&amp;#039; is a medicine used in the management of [[wikipedia:Asthma|asthma]], the chronic inflammatory airway disease characterised by reversible bronchoconstriction, airway hyperresponsiveness, and (in many but not all phenotypes) eosinophilic and type-2 inflammation. The category covers the [[:Category:Bronchodilators|bronchodilators]] that relax airway smooth muscle (the beta-2 agonists, the inhaled antimuscarinics, the methylxanthines), the [[:Category:Inhaled_corticosteroids|inhaled corticosteroids]] that reduce airway inflammation, the [[:Category:Leukotriene_receptor_antagonists|leukotriene receptor antagonists]] and the [[:Category:Mast_cell_stabilizers|mast-cell stabilisers]] that modify alternative inflammatory pathways, and the biologics that target the type-2 inflammatory cytokines and IgE.&lt;br /&gt;
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The clinical history of asthma is among the oldest documented in medicine; the Egyptian Ebers papyrus describes inhalation of heated herbs through a reed, and the second-century physician Aretaeus of Cappadocia gave the first detailed clinical description and named the condition for the Greek &amp;#039;&amp;#039;asthma&amp;#039;&amp;#039; meaning panting. The pre-pharmacological era was dominated by inhaled herbal preparations: the leaves of &amp;#039;&amp;#039;Datura stramonium&amp;#039;&amp;#039; (jimsonweed) smoked as stramonium cigarettes, in use from antiquity through the 1950s, contained the antimuscarinic alkaloids atropine and hyoscyamine and produced reliable acute bronchodilation. The injectable epinephrine introduced by [[wikipedia:Jokichi Takamine|Jokichi Takamine]] in 1900 was the first effective parenteral acute medicine; the oral [[wikipedia:Ephedrine|ephedrine]] of [[wikipedia:Ephedra sinica|&amp;#039;&amp;#039;Ephedra sinica&amp;#039;&amp;#039;]] (long used in traditional Chinese medicine) followed in clinical Western practice in 1920. The 1930s addition of theophylline as an oral bronchodilator and the 1940s development of isoproterenol completed the pre-modern pharmacopoeia.&lt;br /&gt;
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The modern era of antiasthmatic therapy began with two parallel developments in the 1960s and 1970s. The first was the introduction of beta-2 selective adrenergic agonists (described in detail under [[:Category:Bronchodilators|bronchodilators]] and beginning with [[Albuterol|salbutamol]] (albuterol) at Allen and Hanburys in 1968), which reduced the cardiac side effects of the older non-selective adrenergic medicines. The second was the introduction of inhaled corticosteroids (described in detail under [[:Category:Corticosteroids|corticosteroids]] and [[:Category:Inhaled_corticosteroids|inhaled corticosteroids]] and beginning with [[wikipedia:Beclometasone|beclomethasone dipropionate]] at Glaxo in 1972), which provided the first practical way to suppress airway inflammation without producing the systemic glucocorticoid adverse-effect profile.&lt;br /&gt;
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The 1990s introduced two new mechanistic classes. The cysteinyl-leukotriene receptor antagonists ([[wikipedia:Zafirlukast|zafirlukast]] 1996, [[wikipedia:Montelukast|montelukast]] 1998) block the LTD4-mediated airway inflammation and have specific utility in exercise-induced bronchoconstriction, aspirin-exacerbated respiratory disease, and the asthma-allergic-rhinitis combination. The mast-cell stabilisers (sodium cromoglycate, nedocromil sodium) prevent mediator release from mast cells; they were widely used as inhaled prophylaxis in paediatric asthma in the 1980s and 1990s but have been progressively displaced by inhaled corticosteroids.&lt;br /&gt;
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The transformative event of the past fifteen years has been the introduction of the biologic medicines targeting the type-2 inflammatory cytokine network. [[wikipedia:Omalizumab|Omalizumab]] (Novartis, 2003), an anti-IgE monoclonal antibody, was the first; it is used in severe allergic asthma with elevated total IgE. [[wikipedia:Mepolizumab|Mepolizumab]] (GSK, 2015) and [[wikipedia:Reslizumab|reslizumab]] (Teva, 2016), both targeting interleukin-5, deplete eosinophils and reduce exacerbations in severe eosinophilic asthma. [[wikipedia:Benralizumab|Benralizumab]] (AstraZeneca, 2017), an anti-IL-5 receptor antibody with afucosylated Fc producing antibody-dependent cellular cytotoxicity against eosinophils, has similar indication. [[wikipedia:Dupilumab|Dupilumab]] (Regeneron/Sanofi, 2017 for atopic dermatitis, then 2018 for asthma), an anti-IL-4 receptor alpha antibody that blocks both IL-4 and IL-13 signalling, has been the most broadly active biologic across asthma phenotypes including the type-2-high subset and is also approved for atopic dermatitis, chronic rhinosinusitis with nasal polyposis, eosinophilic oesophagitis, and prurigo nodularis. [[wikipedia:Tezepelumab|Tezepelumab]] (Amgen/AstraZeneca, 2021), an anti-thymic-stromal-lymphopoietin (anti-TSLP) antibody, acts upstream of multiple type-2 cytokines and works across the entire spectrum of severe asthma, including the smaller but real type-2-low non-eosinophilic phenotype.&lt;br /&gt;
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The contemporary stepwise management of asthma is built on the principle that inhaled corticosteroid therapy, even in mild disease, reduces exacerbations and slow lung-function decline more reliably than as-needed short-acting bronchodilator alone. The Global Initiative for Asthma (GINA) guideline now recommends as-needed low-dose ICS-formoterol combination ([[wikipedia:Budesonide|budesonide]]-formoterol or [[wikipedia:Beclometasone|beclomethasone]]-formoterol) as the preferred reliever therapy in mild-to-moderate asthma, replacing the historical short-acting beta-agonist monotherapy with a combination that addresses inflammation as well as bronchoconstriction (the SYGMA trials 2018 and the related real-world studies). For more severe disease, escalation proceeds through medium- and high-dose ICS-LABA, addition of a [[:Category:Long-acting_muscarinic_antagonists|LAMA]] (tiotropium, the SMART triple-therapy approach with budesonide-glycopyrrolate-formoterol or fluticasone-umeclidinium-vilanterol), then specific biologic by phenotype.&lt;br /&gt;
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== Classes indexed ==&lt;br /&gt;
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By role in asthma management:&lt;br /&gt;
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* &amp;#039;&amp;#039;&amp;#039;Controller (anti-inflammatory) medicines&amp;#039;&amp;#039;&amp;#039;:&lt;br /&gt;
** [[:Category:Inhaled_corticosteroids|Inhaled corticosteroids]]: fluticasone propionate and furoate, [[Budesonide|budesonide]], [[Mometasone|mometasone]], beclomethasone, ciclesonide&lt;br /&gt;
** [[:Category:Leukotriene_receptor_antagonists|Leukotriene receptor antagonists]]: [[wikipedia:Montelukast|montelukast]], [[wikipedia:Zafirlukast|zafirlukast]]; the 5-lipoxygenase inhibitor [[wikipedia:Zileuton|zileuton]]&lt;br /&gt;
** [[:Category:Mast_cell_stabilizers|Mast cell stabilisers]]: cromolyn sodium, nedocromil (largely retired)&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;Reliever (bronchodilator) medicines&amp;#039;&amp;#039;&amp;#039; (cross-indexed under [[:Category:Bronchodilators|bronchodilators]]):&lt;br /&gt;
** Short-acting beta-2 agonists (SABA): [[Albuterol|albuterol]], levalbuterol, terbutaline&lt;br /&gt;
** Long-acting beta-2 agonists (LABA): salmeterol, formoterol, indacaterol, vilanterol (only in combination with ICS for asthma after the SMART trial concerns)&lt;br /&gt;
** Short-acting antimuscarinics: [[Ipratropium|ipratropium]] (limited role in acute asthma adjunct to SABA)&lt;br /&gt;
** Long-acting antimuscarinics (LAMA): [[Tiotropium|tiotropium]] (Respimat formulation approved for asthma), aclidinium, umeclidinium, glycopyrronium&lt;br /&gt;
** Methylxanthines: theophylline (oral, narrow therapeutic window, declining use)&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;Combination inhalers&amp;#039;&amp;#039;&amp;#039; (cross-indexed under [[:Category:Fixed-dose_combinations|fixed-dose combinations]]):&lt;br /&gt;
** ICS+LABA: fluticasone-salmeterol (Advair/Seretide), budesonide-formoterol (Symbicort), fluticasone furoate-vilanterol (Breo Ellipta), mometasone-formoterol (Dulera), beclomethasone-formoterol (Fostair)&lt;br /&gt;
** ICS+LABA+LAMA (single-inhaler triple therapy): fluticasone furoate-umeclidinium-vilanterol (Trelegy Ellipta), budesonide-glycopyrronium-formoterol (Breztri Aerosphere), mometasone-indacaterol-glycopyrronium (Enerzair Breezhaler)&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;Biologics&amp;#039;&amp;#039;&amp;#039; (severe asthma, by phenotype):&lt;br /&gt;
** Anti-IgE: [[wikipedia:Omalizumab|omalizumab]]&lt;br /&gt;
** Anti-IL-5: [[wikipedia:Mepolizumab|mepolizumab]], [[wikipedia:Reslizumab|reslizumab]]&lt;br /&gt;
** Anti-IL-5 receptor: [[wikipedia:Benralizumab|benralizumab]]&lt;br /&gt;
** Anti-IL-4 receptor alpha (blocks IL-4 and IL-13): [[wikipedia:Dupilumab|dupilumab]]&lt;br /&gt;
** Anti-TSLP: [[wikipedia:Tezepelumab|tezepelumab]]&lt;br /&gt;
* &amp;#039;&amp;#039;&amp;#039;Oral systemic corticosteroids&amp;#039;&amp;#039;&amp;#039; (acute exacerbation and bridging severe disease): [[Prednisone|prednisone]], [[Prednisolone|prednisolone]], [[Methylprednisolone|methylprednisolone]], [[Dexamethasone|dexamethasone]] (single high-dose for paediatric acute exacerbation)&lt;br /&gt;
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== Notes on scope ==&lt;br /&gt;
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The boundary of this category is &amp;quot;medicine prescribed for the chronic management or acute treatment of asthma.&amp;quot; The [[:Category:Bronchodilators|bronchodilators]] used in [[wikipedia:Chronic obstructive pulmonary disease|chronic obstructive pulmonary disease]] (COPD) overlap substantially with the asthma bronchodilators but are not identical (the LABA-monotherapy concern of SMART does not apply to COPD; the LAMA tiotropium has had a primary COPD indication for years before its asthma extension; some biologics for severe asthma have not been studied in COPD). The medicines for [[wikipedia:Allergic rhinitis|allergic rhinitis]], [[wikipedia:Atopic dermatitis|atopic dermatitis]], and other type-2 inflammatory conditions overlap mechanistically (intranasal corticosteroids, antihistamines, montelukast, dupilumab) but are listed under their primary indication. The medicines for [[wikipedia:Cystic fibrosis|cystic fibrosis]] (CFTR modulators ivacaftor, lumacaftor, tezacaftor, elexacaftor; dornase alfa; inhaled tobramycin and aztreonam) are not antiasthmatic and are listed under cystic-fibrosis-specific categories. Beta-blockers, particularly the non-selective ones, are relatively contraindicated in asthma and are not in this category but their interaction warrants mention on the asthma medicine pages.&lt;br /&gt;
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== About these pages ==&lt;br /&gt;
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This category page is an encyclopedia article about its subject. The actual index of medicines belonging to the category is generated automatically by the wiki engine, from category-membership declarations on the individual medicine pages, and appears at the foot of the page below the references.&lt;br /&gt;
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== References ==&lt;br /&gt;
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[[Category:Medicines]]&lt;br /&gt;
[[Category:CuratedCategoryPage]]&lt;/div&gt;</summary>
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