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Infect Disord Drug Targets . Therapeutic Status of Famotidine in COVID-19 Patients: A Review

tetano

Editor, Senior Moderator
Infect Disord Drug Targets


. 2022 Jan 7.
doi: 10.2174/1871526522666220107125511. Online ahead of print.
Therapeutic Status of Famotidine in COVID-19 Patients: A Review


Moein Mohseni[SUP] 1 [/SUP], Vahid Raissi[SUP] 2 [/SUP], Yasamin Sharifan[SUP] 3 [/SUP], Kimia Barikro[SUP] 1 [/SUP], Sasan Amiri[SUP] 4 [/SUP], Maedeh Sadat Mohseni[SUP] 5 [/SUP], Farid Raeisi[SUP] 6 [/SUP], Kimia Masoumi[SUP] 1 [/SUP], Sina Khodakarami[SUP] 1 [/SUP], Omid Raiesi[SUP] 7 [/SUP]



Affiliations

Abstract

The novel coronavirus, SARS-coV-2, which emerged in Wuhan in November 2019, has increasingly spread worldwide. More than 272 million cases of infection have been identified. COVID-19 affects 223 countries and territories across the world. The principal target of the SARS-CoV-2 infection is the lower respiratory tract. Series of moderate to non-specific severe clinical signs and symptoms that appear two to fourteen days after exposure to SARS-CoV-2 can occur in patients with COVID-19 disease. There is cough, breath deficiency, and at least two of these symptoms: headache, fever, chills, repeated rigor, myalgia, oropharyngitis, anosmia, and ageusia. No therapeutic agents have been validated to have substantial efficacy in the clinical care of COVID-19 patients in large-scale trials, despite worsening infected rates in COVID-19. Early clinical evidence from many sources suggests that treatment with famotidine may decrease COVID-19-related morbidity and mortality. The mechanism by which famotidine could improve the outcomes of COVID-19 is currently unknown. A more recent postulated mechanism is that the effect of famotidine is mediated by histamine-2 receptor antagonism or inverse agonism, inferring that the SARS-CoV-2, resulting in COVID-19 infection at least partially leads to the abnormal release of histamine and perhaps dysfunction of mast cells.

Keywords: COVID-19; SARS-coV-2; famotidine; histamine-2 receptor antagonism; respiratory syndrome disease; therapeutic.
 
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