COPD Medication

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The aim of pharmacological handling of chronic obstructive pulmonary disease (COPD) is to control and prevent symptoms, decrease the frequency, decrease exacerbation severity, up-surge the general mental and physical well-being of the patient and improve exercise tolerance. However, no drugs to date deployed for the management of COPD are capable to amend the progressive deterioration in the functioning of the lungs that is the hallmark symptom of the disease (Izquierdo et al., 2021). Additionally, to date, smoking cessation is one of the effective tactics to decrease COPD progression. To attain the above-stated aim, pharmacological treatment including bronchodilators, nicotine replacement therapy, and behavioural therapy have proven effective to deal with COPD symptoms (Izquierdo et al., 2021). Hence, this section will include the three selected drugs (Salbutamol, Formoterol, and Theophylline) as a treatment modality for COPD. Additionally, adverse drug reactions, pharmacokinetics and pharmacodynamics of the selected drugs will be illustrated. 

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Currently Recommended Drugs 

Medications that are currently deployed for COPD treatment include bronchodilators (methylxanthines, selective β2-agonists, and anticholinergic antimuscarinic agents), glucocorticoids, and other medications (antibiotics, mucolytic agents, vasodilators, and immunoregulators).


Salbutamol is a beta-2 adrenergic receptor agonist, which is a short-acting bronchodilator (Jacobson et al., 2017). This drug is mainly deployed for the treatment of COPD and asthma. To be more specific, this drug is mainly recommended for the acute frequency of bronchospasm, which is common in both COPD and asthma. The chemical formula of the Salbutamol is C13H21NO3 and other names of this drug are Salbutamolum and Albuterol (Jacobson et al., 2017).

Mode of action

Salbutamol has a greater influence on the beta 2 receptors. Beta 2 receptors are chiefly situated on the bronchial smooth muscle and are adrenergic receptors. Though, 10 to 50% of the beta 2 receptors are located in the cardiac tissue. Salbutamol has some binding capacity to beta 1 receptors, which are situated on the heart tissue (Wang et al., 2020). Beta 2 receptors get activated after drug administration by activating the adenyl cyclase. Furthermore, the drug causes up-surging of the intracellular concentration of cyclic-3′, 5′-adenosine monophosphate (cyclic AMP).  Cyclic AMP activates the Protein Kinase A, which is responsible for muscle relaxation. Hence, salbutamol causes airway relaxation from the tracheal tissue to terminal bronchioles. Additionally, cyclic AMP is also associated with the inhibition of mast cells that lead to air spasms and bronchoconstriction (Jacobson et al., 2017; Wang et al., 2020).

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Pharmacodynamics can be defined as the action of the medicine on the body. It is essential to reflect on the receptor mechanism through which at the cellular level, any medicine can bind to give pharmacodynamic effects.  Salbutamol can be given orally or through the parenteral route. This drug’s action on the body is associated with its racemic mixture nature. Racemic mixture implies that this drug consists of R isomers and S isomers (Heuberger et al., 2018). After drug administration, R and S isomers get bind to the specific beta receptors. Parenteral/oral administration of the drug can cause a high accumulation of medicine in the beta receptors area. Therefore, R isomers have more affinity for the beta 2 receptors, though; beta 2 receptor selectivity is not absolute (Heuberger et al., 2018). In contrast, S isomers are more affinity for the Beta 1 receptors as compared to R isomers.  Beta 1 receptor activation causes cardiac tissue activation and Beta 2 receptor activation leads to hypotension, skeletal muscle tremors, vasodilation, and uterine muscle relaxation. Parenteral/oral administration of the drug also causes some metabolic effects, for example, hyperinsulinaemia and hyperglycaemia can also occur, though the mechanism is not clear (Sottas et al., 2016).

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Pharmacodynamics can be illustrated as the action of the body on the medicine/drug, which emphasises on absorption, distribution, metabolism and elimination of the drug. After drug inhalation, it affects the airway’s smooth muscle. Initially, the drug traces are not detectable in the bloodstream.  However, followed by 2 to 3 hours on drug administration, very low drug concentration traces can be detected.  The cause of low traces detection is associated with the small dose swallowing that gets absorbed through the gut and the drug’s systematic level is small followed by consuming recommended dose (Sottas et al., 2016).

156 +/- 38 L is the drug’s volume of distribution. However, the protein binding capacity of the drug is low. The drug is not processed in the lungs. Although, the drug gets converted into 4′-o-sulphate ester in the liver, which has minimal pharmacologic activity. Additionally, salbutamol 4-O-sulphate can fully be metabolised by oxidative conjugation and/ or glucuronide deamination. Within the 24 hours of the drug administration, 60 to 80% of the drug dose is secreted in the urine as the free drug. 2.5 to 5 hours is the half-life of the drug and plasma half-life is around 4.6 hours. The drug’s clearance rate after oral and intravenous administration is 272 +/- 38 ml/min and 291 +/- 70 ml/min respectively. Lastly, the sulphate metabolite clearance rate is 98.5 +/- 23.5 ml/min (Heuberger et al., 2018). 

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Side effects 

This drug is categorized under schedule 3 therefore, only registered practitioners or pharmacists can advise this drug.  Salbutamol is indicated for therapeutic usage hence needed monitoring throughout the treatment course. Some of the side effects are seizures, dry mouth, hyper/hypotension, palpitation, headache, hypokalaemia, Arrhythmias, tachycardia, and hyperglycaemia (Heuberger et al., 2018).


Mode of action

 It is a secretive long-acting beta 2 adrenergic receptor agonist; however, this drug has some degree of impact on the beta 1 and beta 3 receptors also.  Beta 2 receptors are chiefly situated on the bronchial smooth muscle and are adrenergic receptors. And, beta 1 receptors are situated on the heart tissue. Therefore, for the treatment of COPD, it is essential that the drug has beta 2 selectivity. Formoterol shows 200-fold superior action at beta 2 receptors above beta 1 receptors. This drug stimulates the intracellular adenylyl cyclase at the molecular level. The rest of the mechanism is the same as Salbutamol (Mostafa et al., 2021).


Drugs act on the lungs at the local level and act as bronchodilators causing the opening up of the airways and smooth muscle relaxation. Furthermore, this drug has a rapid action onset (around 2 to 3 minutes) and long action duration (approximately 12 hours).  Drug administration can cause a high accumulation of medicine in the beta receptors area. Beta 1 receptor activation causes cardiac tissue activation and Beta 2 receptor activation leads to hypotension, skeletal muscle tremors, vasodilation, and uterine muscle relaxation (Tashkin, 2020).

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Formoterol pulmonary and total systemic bioavailability is approximately 43% and 60% of the delivered drug dose respectively. It is rapidly absorbed in the plasma after inhalation. Formoterol Time of maximum (Tmax) ranged from around 0.167 to 0.5 hours in a healthy individual. However, in an asthmatic patient, Tmax is approximately 0.58 to 1.97 hours. Around 31 to 38% of the plasma binding of the drug is evident. This drug gets metabolised through direct glucuronidation and O-demethylation of the initial drug after glucuronidation. Drug elimination is depending on the route of administration.  Around 50 to 60% of the drug gets eliminated through urine when administrated orally. Additionally, approximately 30 to 35% of the drug can be eliminated through faeces when orally administered. 7 to 10 hours is the terminal half-life of the drug. 157 mL/min is the renal clearance of this drug when inhaled by the patient (Tashkin, 2020).

Side effects 

3130 mg/kg is oral LD 50 of Formoterol in rats. Some of the side effects are seizures, dry mouth, hyper/hypotension, palpitation, headache, hypokalaemia, Arrhythmias, tachycardia, and hyperglycaemia (Tashkin, 2020)


Mode of action

Theophylline is the methylxanthine derivative having diuretics, bronchial dilation, stimulation of the central nervous system, and smooth muscle relaxation property. It functions as the blocker of adenosine receptor, inhibitor of phosphodiesterase and activator of histone deacetylase.

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It is a xanthine derivative having chemical properties similar to theobromine and caffeine. This drug has two distinct functions; suppression of the stimuli which can lead to airway constriction and relaxation of the smooth muscle (bronchodilation). Moreover, this drug competitively obstructs type 4 and type 3 phosphodiesterase, this enzyme breaks the smooth muscles’ cyclic AMP, possibly causing bronchodilation.  This drug also binds to the adenosine A2B receptor and causes stoppage of bronchoconstriction mediated by adenosine (Sohn et al., 2017).


Theophylline gets readily and thoroughly absorbed followed by oral administration. The volume of distribution of this drug is 0.3 to 0.7 L/kg with 40% of the protein binding capacity, chiefly to albumin. It is metabolized in the liver, biotransformation occurs through demethylation to 1-methylxanthine, 3- methylxanthine and followed by 1, 3-dimethyluric acid by hydroxylation reaction. Moreover, approximately 3% of the drug dose gets N-methylated to caffeine.  Theophylline gets metabolised in the liver and it does not undergo much pre-systemic elimination.  The half part of drug life is around 8 hours. 0.65 mL/kg/min is the clearance of the drug in non-smoker healthy individuals (Jilani, Preuss, & Sharma, 2020).

Side effects 

The drug-associated side effects are vomiting, diarrhoea, insomnia, shaking, restlessness and irritability. The overdose symptoms are GI effects, arrhythmias, and seizures (Jilani, Preuss, & Sharma, 2020).

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Heuberger, J. A., van Dijkman, S. C., & Cohen, A. F. (2018). The futility of current urine salbutamol doping control. British journal of clinical pharmacology84(8), 1830-1838.

Izquierdo, J. L., Morena, D., González, Y., Paredero, J. M., Pérez, B., Graziani, D., … & Rodríguez, J. M. (2021). Clinical management of COPD in a real-world setting. A big data analysis. Archivos de Bronconeumología (English Edition)57(2), 94-100.

Jacobson, G. A., Raidal, S., Robson, K., Narkowicz, C. K., Nichols, D. S., & Haydn Walters, E. (2017). Bronchopulmonary pharmacokinetics of (R)salbutamol and (S)salbutamol enantiomers in pulmonary epithelial lining fluid and lung tissue of horses. British journal of clinical pharmacology83(7), 1436-1445.

Jilani, T. N., Preuss, C. V., & Sharma, S. (2020). Theophylline. StatPearls [Internet].

Mostafa, M. M., Rider, C. F., Wathugala, N. D., Leigh, R., Giembycz, M. A., & Newton, R. (2021). Transcriptome-Level Interactions between Budesonide and Formoterol Provide Insight into the Mechanism of Action of Inhaled Corticosteroid/Long-Acting β2-Adrenoceptor Agonist Combination Therapy in Asthma. Molecular Pharmacology99(3), 197-216.

Sohn, J. A., Kim, H. S., Oh, J., Cho, J. Y., Yu, K. S., Lee, J., … & Park, E. A. (2017). Prediction of serum theophylline concentrations and cytochrome P450 1A2 activity by analyzing urinary metabolites in preterm infants. British journal of clinical pharmacology83(6), 1279-1286.

Sottas, C. E., Anderson, B. J., & Holford, N. H. G. (2016). Salbutamol has rapid onset pharmacodynamics as a bronchodilator. Acta Anaesthesiologica Scandinavica60(9), 1328-1331.

Tashkin, D. P. (2020). Formoterol for the Treatment of Chronic Obstructive Pulmonary Disease. International Journal of Chronic Obstructive Pulmonary Disease15, 3105.

Wang, S., Liu, F., Tan, K. S., Ser, H. L., Tan, L. T. H., Lee, L. H., & Tan, W. (2020). Effect of (R)salbutamol on the switch of phenotype and metabolic pattern in LPSinduced macrophage cells. Journal of cellular and molecular medicine24(1), 722-736.

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