Related Experiment Video
Updated: Jul 5, 2026

Dry Powder and Nebulized Aerosol Inhalation of Pharmaceuticals Delivered to Mice Using a Nose-only Exposure System
Published on: April 6, 2017
Frontrunners in novel pharmacotherapy of COPD
1National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse Street, London SW3 6LY, UK. p.j.barnes@imperial.ac.uk
Abstract:
The mainstay of current drug therapy is long-acting bronchodilators; several longer acting inhaled beta(2)-agonists and muscarinic antagonists (and combinations) are now in development. No treatments reduce the progression or suppress the inflammation of COPD. With better understanding of the inflammatory and destructive process, several new targets have been identified. Several mediator antagonists tested in COPD have been disappointing, but of CXCR2 antagonists that block pulmonary neutrophil and monocyte recruitment may be more promising. Broad spectrum anti-inflammatory drugs may be more effective, and include inhibitors of PDE4, p38 MAPK and NF-kappaB, but side effects will be a major limitation so that inhaled delivery will be necessary. Perhaps the most promising approach is reversal corticosteroid resistance through increasing HDAC2 activity. This may be achieved by theophylline-like drugs, more effective antioxidants and non-antibiotic macrolides.
Insights
Current COPD treatments focus on symptom relief with long-acting bronchodilators. New therapies aim to target inflammation and disease progression by exploring novel pathways and drug classes.
Area of Science:
- Pulmonary Medicine
- Pharmacology
- Inflammation Research
Background:
- Current treatments for Chronic Obstructive Pulmonary Disease (COPD) primarily rely on long-acting bronchodilators.
- Existing therapies do not halt disease progression or suppress underlying inflammation.
- Recent advancements offer a deeper understanding of COPD's inflammatory and destructive mechanisms.
Purpose of the Study:
- To review emerging therapeutic targets and strategies for COPD.
- To evaluate the potential of novel anti-inflammatory agents in managing COPD.
- To explore methods for overcoming corticosteroid resistance in COPD treatment.
Main Methods:
- Review of current and developing COPD pharmacotherapies.
- Analysis of novel molecular targets, including CXCR2, PDE4, p38 MAPK, and NF-kappaB.
- Investigation of strategies to enhance corticosteroid efficacy, such as increasing HDAC2 activity.
Main Results:
- Long-acting inhaled beta2-agonists and muscarinic antagonists are in development.
- CXCR2 antagonists show promise in blocking neutrophil and monocyte recruitment.
- Broad-spectrum anti-inflammatory drugs (PDE4, p38 MAPK, NF-kappaB inhibitors) face challenges with side effects, necessitating inhaled delivery.
- Reversing corticosteroid resistance by increasing HDAC2 activity is a promising approach, potentially achievable with theophylline-like drugs, antioxidants, and non-antibiotic macrolides.
Conclusions:
- Novel therapeutic strategies are needed to address COPD progression and inflammation.
- Targeting specific inflammatory pathways and enhancing corticosteroid sensitivity represent promising avenues for future COPD treatments.
- Further research into inhaled anti-inflammatory agents and HDAC2 activation is warranted for effective COPD management.
Related Concept Videos
COPD: Management Using Bronchodilators and Corticosteroids
Chronic Obstructive Pulmonary Disease-V: Management
Smoking Cessation
COPD: Pathogenesis and Clinical Features
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
Drugs Used in Lower Respiratory Disorders: Overview
Bronchodilators, the first step of respiration enhancement, come in various forms, each with its own mechanism...
Chronic Obstructive Pulmonary Disease-I: Introduction
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...