Therapeutic Status of Famotidine in COVID-19 Patients: A Review

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.

Clinical impact of Candida respiratory tract colonization and acute lung infections in critically ill patients with COVID-19 pneumonia

“…The novel coronavirus SARS-coV-2, which emerged in Wuhan in November 2019, has increasingly spread causing a global pandemic that infected more than 494 million people, resulting in severe social and economic ramifications, and claimed more than 6,183,000 lives by April 6, 2022 [ 1 ]. Coronavirus disease 2019 (COVID-19), which is attributable to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been the cause of global health threats [ 2 , 3 ].…”

SARS-CoV-2 Spike Protein Receptor Binding-ACE2 Interaction Increases Carbohydrate Sulfotransferases and Reduces N-Acetylgalactosamine-4-Sulfatase through Phospho-p38-MAPK and RB-E2F1

“…The potential benefit of the H1 histamine receptor blocker Desloratadine is suggested by the measured decline in phospho-p38 and by inhibition of the SPRBD effects on expression of CHST15, CHST11 and ARSB, as well as by pharmacological studies that identified desloratadine/loratadine as a mechanism-based target [36][37][38]. Several clinical studies of H2 blockers on the response in Covid-19 have been reported and additional studies of antihistamines are ongoing [57][58][59].…”

Expediting COVID-19 Recovery with an Orthomolecular Approach: Two Case Reports

“…The mechanism by which famotidine could improve the outcomes of COVID-19 is currently unknown. 39 It has been suggested that famotidine may reduce COVID-19 severity through antagonism or inverse agonism of histamine signaling. 40 A meta-analysis found no significant association between famotidine use and clinical outcomes.…”