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Telmisartan as tentative angiotensin receptor blocker therapeutic for COVID-19
Rodolfo Pedro Rothlin1, Héctor Miguel Vetulli2, Mariano Duarte3,4
1Sociedad Argentina de Farmacología Clínica, Asociación Médica Argentina, Buenos Aires, Argentina.
Insights
Telmisartan may be a viable treatment for COVID-19 patients before Acute Respiratory Distress Syndrome (ARDS) develops. This commentary discusses telmisartan
Area of Science:
- Pulmonology
- Infectious Diseases
- Pharmacology
Background:
- COVID-19, caused by SARS-CoV-2, involves viral entry via ACE2 receptors in alveolar cells.
- This interaction disrupts the ACE2/angiotensin balance, increasing pro-inflammatory angiotensin II.
- Elevated angiotensin II can trigger inflammation, apoptosis, and potentially Acute Respiratory Distress Syndrome (ARDS).
Purpose of the Study:
- To propose telmisartan as a potential therapeutic agent for COVID-19.
- To justify telmisartan's use based on its pharmacokinetic and pharmacodynamic properties.
- To present a Phase II clinical trial evaluating telmisartan in COVID-19 patients.
Main Methods:
- Review of pharmacokinetic and pharmacodynamic properties of telmisartan.
- Proposal for telmisartan as an alternative treatment for COVID-19.
- Description of an open-label, randomized Phase II clinical trial (NCT04355936).
Main Results:
- The abstract does not contain specific results from the clinical trial.
- The article makes a case for telmisartan based on theoretical benefits.
- The clinical trial aims to evaluate telmisartan's efficacy and safety.
Conclusions:
- Telmisartan's properties suggest potential benefits in managing COVID-19.
- Further clinical evaluation through the presented trial is warranted.
- Telmisartan may offer a therapeutic option to prevent ARDS progression in COVID-19.
Abstract:
In late 2019, a new coronavirus emerged in Wuhan Province, China, causing lung complications similar to those produced by the SARS coronavirus in the 2002-2003 epidemic. This new disease was named COVID-19 and the causative virus SARS-CoV-2. The SARS-CoV-2 virus enters the airway and binds, by means of the S protein on its surface to the membrane protein ACE2 in type 2 alveolar cells. The S protein-ACE2 complex is internalized by endocytosis leading to a partial decrease or total loss of the enzymatic function ACE2 in the alveolar cells and in turn increasing the tissue concentration of pro-inflammatory angiotensin II by decreasing its degradation and reducing the concentration of its physiological antagonist angiotensin 1-7. High levels of angiotensin II on the lung interstitium can promote apoptosis initiating an inflammatory process with release of proinflammatory cytokines, establishing a self-powered cascade, leading eventually to ARDS. Recently, Gurwitz proposed the tentative use of agents such as losartan and telmisartan as alternative options for treating COVID-19 patients prior to development of ARDS. In this commentary article, the authors make the case for the election of telmisartan as such alternative on the basis of its pharmacokinetic and pharmacodynamic properties and present an open-label randomized phase II clinical trial for the evaluation of telmisartan in COVID-19 patients (NCT04355936).
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