Famotidine and Coronavirus Disease 2019

Freedberg, Daniel E.; Wang, Yichen; Abrams, Julian A.

doi:10.1053/j.gastro.2020.12.044

Cited by 4 publications

(3 citation statements)

References 8 publications

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“…As discussed in our previous work on HP5 [ 30 ], we carried out the molecular docking between ACE2 and LL37 peptides on the ZDOCK server ( http://zdock.umassmed.edu/ ) [ 31 ] using the default parameters. The dock site has 20 residues (SER19, GLN24, THR27, PHE28, ASP30, LYS31, HIS34, GLU35, GLU37, ASP38, TYR41, GLN42, LEU79, MET82, TYR83, ASN330, LEU333, LYS353, GLY354, ASP355) as shown in Fig.…”

Section: Theories and Methodsmentioning

confidence: 99%

HD5 and LL-37 Inhibit SARS-CoV and SARS-CoV-2 Binding to Human ACE2 by Molecular Simulation

Chen

Shi

et al. 2021

Interdiscip Sci Comput Life Sci

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Graphic abstract The coronavirus (COVID-19) pandemic is still spreading all over the world. As reported, angiotensin-converting enzyme-2 (ACE2) is a receptor of SARS-CoV-2 spike protein that initializes viral entry into host cells. Previously, the human defensin 5 (HD5) has been experimentally confirmed to be functional against the SARS-CoV-2. The present study proposes a human cathelicidin known as LL37 that strongly binds to the carboxypeptidase domain of human ACE2 compared to HD5. Therefore, LL37 bears a great potential to be tested as an anti-SARS-CoVD-2 peptide. We investigated the molecular interactions formed between the LL37 and ACE2 as well as HD5 and ACE2 tailed by their thermodynamic stability. The MM-PBSA and free energy landscape analysis outcomes confirmed its possible inhibitory effect against the SARS-CoV-2. The results obtained here could help propose a promising therapeutic strategy against the havoc caused by SARS-CoV-2 infections. Supplementary Information The online version contains supplementary material available at 10.1007/s12539-021-00462-3.

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Section: Theories and Methodsmentioning

confidence: 99%

HD5 and LL-37 Inhibit SARS-CoV and SARS-CoV-2 Binding to Human ACE2 by Molecular Simulation

Chen

Shi

et al. 2021

Interdiscip Sci Comput Life Sci

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“…A few studies have begun considering the possible sources of discrepancies and heterogeneities, to which at least some of the inconsistencies in the famotidine/COVID-19 literature can be attributed. Some such sources relate to differences in study designs, or are otherwise methodological in nature—e.g., Freedberg et al's (2020b) description of potential biases from residual confounders in the baseline characteristics of case-matched cohorts. There also exists the possibility of spurious links (or, inversely, masked associations) because of underlying physiological factors, e.g., Sethia et al's (2020a) description of the impacts of 1) potentially great differences in disease severity on treatment outcomes (without adequately accounting for such in case-matching and stratification methods to obtain sub-cohorts), 2) heterogeneity in classification of the severity of illness, 3) whether these variations are factored into the case-matching and stratification stages, 4) variation in the regimen for famotidine treatment, including administration route (oral, intravenous), dosage levels, timings with respect to onset of disease symptoms and duration of treatment [see also Malone (2021) ], and 5) confounding factors from co-medications or comorbidities among patients who do more/less well with famotidine.…”

Section: Introduction: Possible Systematic Approaches?mentioning

confidence: 99%

A Birds-Eye (Re)View of Acid-Suppression Drugs, COVID-19, and the Highly Variable Literature

et al. 2021

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This Perspective examines a recent surge of information regarding the potential benefits of acid-suppression drugs in the context of COVID-19, with a particular eye on the great variability (and, thus, confusion) that has arisen across the reported findings, at least as regards the popular antacid famotidine. The degree of inconsistency and discordance reflects contradictory conclusions from independent, clinical-based studies that took roughly similar approaches, in terms of both experimental design (retrospective, observational, cohort-based, etc.) and statistical analysis workflows (propensity-score matching and stratification into sub-cohorts, etc.). The contradictions and potential confusion have ramifications for clinicians faced with choosing therapeutically optimal courses of intervention: e.g., do any potential benefits of famotidine suggest its use in a particular COVID-19 case? (If so, what administration route, dosage regimen, duration, etc. are likely optimal?) As succinctly put this March in Freedberg et al. (2021), “…several retrospective studies show relationships between famotidine and outcomes in COVID-19 and several do not.” Beyond the pressing issue of possible therapeutic indications, the conflicting data and conclusions related to famotidine must be resolved before its inclusion/integration in ontological and knowledge graph (KG)–based frameworks, which in turn are useful for drug discovery and repurposing. As a broader methodological issue, note that reconciling inconsistencies would bolster the validity of meta-analyses which draw upon the relevant data-sources. And, perhaps most broadly, developing a system for treating inconsistencies would stand to improve the qualities of both 1) real world evidence-based studies (retrospective), on the one hand, and 2) placebo-controlled, randomized multi-center clinical trials (prospective), on the other hand. In other words, a systematic approach to reconciling the two types of studies would inherently improve the quality and utility of each type of study individually.

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“…The interferon-stimulated gene 15 from host cell proteins cleaves the C-terminal end of the consensus sequence LXGG, a process termed deISGylation[ 11 - 13 ]. Freedberg et al [ 14 , 15 ] reported that results from a retrospective study tested associations between the use of famotidine and the outcome of patients with COVID-19. They classified the use of famotidine based on COVID-19 exposure within 24 h following hospital admission and maintained a follow-up for up to 30 d.…”

Section: Discussionmentioning

confidence: 99%

Role of H₂receptor blocker famotidine over the clinical recovery of COVID-19 patients: A randomized controlled trial

Chowdhury¹,

Kamal²,

Abbas³

et al. 2022

WJCC

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BACKGROUND Coronavirus disease 2019 (COVID-19) is a global pandemic putting the population at a high risk of infection-related health hazards, mortality and a potential failure of proper medical therapies. Therefore, it is necessary to evaluate the potential use of the existing drugs that could be used as options for the medical management of COVID-19 patients. AIM To evaluate the role of the H 2 receptor blocker “famotidine” in COVID-19 illness. METHODS This study was done on seriously ill COVID-19 patients admitted to the intensive care unit (ICU) from different institutes in Bangladesh. Patients were divided into famotidine treatment group “A” (famotidine 40 mg to 60 mg oral formulation every 8 h with other treatment as given), and control group “B” (treatment as given). National early warning score (NEWS)-2, and sequential organ failure assessment day-1 score was calculated to evaluate the outcome. Outcomes were evaluated by the time required for clinical improvement, characterized as duration required from enrollment to the achievement of NEWS-2 of ≤ 2 maintained for 24 h; time to symptomatic recovery, defined as the duration in days (from randomization) required for the recovery of the COVID-19 symptoms; mortality rate; duration of ICU and hospital stay; total period of hospitalization; the rate of supplementary oxygen requirement; the computed tomography (CT) chest recovery (%), the time required for the viral clearance and “NEWS-2” on discharge. RESULTS A total of 208 patients were enrolled in this study with 104 patients in each group. The famotidine treatment group had comparatively better recovery of 75% and a low mortality of 25% than the control with a recovery of 70% and a mortality of 30%. Duration of clinical improvement (group A 9.53 d, group B 14.21 d); hospitalization period among the recovered patients (group A 13.04 d, group B 16.31 d), pulmonary improvement in chest CT (group A 21.7%, group B 13.2%), and the time for viral clearance (group A 20.7 d, group B 23.8 d) were found to be statistically significant P ≤ 0.05. However, the Kaplan Meier survival test was not significant among the two study groups, P = 0.989. CONCLUSION According to our study, treatment with famotidine achieved a better clinical outcome compared to the control group in severe COVID-19 illness, although no significant survival benefit was found.

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Famotidine and Coronavirus Disease 2019

Cited by 4 publications

References 8 publications

HD5 and LL-37 Inhibit SARS-CoV and SARS-CoV-2 Binding to Human ACE2 by Molecular Simulation

HD5 and LL-37 Inhibit SARS-CoV and SARS-CoV-2 Binding to Human ACE2 by Molecular Simulation

A Birds-Eye (Re)View of Acid-Suppression Drugs, COVID-19, and the Highly Variable Literature

Role of H₂receptor blocker famotidine over the clinical recovery of COVID-19 patients: A randomized controlled trial

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Famotidine and Coronavirus Disease 2019

Cited by 4 publications

References 8 publications

HD5 and LL-37 Inhibit SARS-CoV and SARS-CoV-2 Binding to Human ACE2 by Molecular Simulation

HD5 and LL-37 Inhibit SARS-CoV and SARS-CoV-2 Binding to Human ACE2 by Molecular Simulation

A Birds-Eye (Re)View of Acid-Suppression Drugs, COVID-19, and the Highly Variable Literature

Role of H2 receptor blocker famotidine over the clinical recovery of COVID-19 patients: A randomized controlled trial

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Role of H₂receptor blocker famotidine over the clinical recovery of COVID-19 patients: A randomized controlled trial