Famotidine associated with improved clinical outcomes in people hospitalised with COVID-19

Simon Collins, HIV i-Base

A retrospective analysis reports a positive association between open label use of antacid famotidine (an H2 receptor agonist with antiviral properties) and better clinical outcomes in people hospitalised with COVID-19, compared to a control group matched by baseline characteristics. [1]

Famotidine had previously been identified from a database of potential compounds screened for repurposing for COVID-19 based on computational analysis of structures encoded by SARS-CoV-2 proteins. [2]

This paper reported on clinical outcomes from 84/1,620 (5%) adults who were given famotodine within 24 hours of admission to a single centre from 25 February to 13 April 2020 with PCR confirmed COVID-19. Comparison to a control group used propensity score matching to balance the baseline characteristics of patients who did and did not use famotidine.

Factors in the analysis included pre-existing diabetes, hypertension, coronary artery disease (CAD), heart failure, end-stage renal disease or chronic kidney disease, and chronic pulmonary disorders; obesity, based on BMI; and age, classified as <50 years old, 50-65 years old, and >65 years old.

Overall, 340/1,620 (21%) met the composite primary endpoint of progression to intubation (n=142, 8.8%) or death (n=238, 15%). In adjusted analysis, famotidine was associated with reduced risk for intubation or death (aHR) 0.43; 95% CI: 0.21 to 0.88) and also for death alone (aHR 0.30; 95% CI: 0.11 to 0.80), both p<0.01. When those who died prior to intubation were excluded, there was no association between use of famotidine and intubation (log-rank p=0.40)

Participants using famotidine received a total median dose of 136 mg (63 – 233 mg) for a median 5.8 days.  28% of all famotidine doses were intravenous; 47% were 20 mg, 35% were 40 mg, and 17% were 10 mg.  Famotidine was used prior to admission by 15% of those who used famotidine while hospitalised compared to 1% of those who did not (p<0.01).

The results were similar in several sensitivity analyses, including use of proton pump inhibitors that had no impact on either endpoint, indicating any mechanism was unrelated to acid suppression.

The study reported that a lower peak ferritin value was observed among users of famotidine, supporting the hypothesis that use of famotidine may decrease cytokine release in the setting of SARS-CoV-2 infection.

A randomised phase study of high-dose IV famotidine with hydroxychloroquine (HCQ) vs HCQ is already underway in 1170 participants with mild or moderate COVID-19. [3]


This report is from a paper that has not yet been peer-reviewed.

This article was first published on 26 May 2020.


  1. Freedberg DE et al. Famotidine use is associated with improved clinical outcomes in hospitalized COVID-19 patients: a propensity score matched retrospective cohort study. Pre-peer review. DOI: 10.1101/2020.05.01.20086694.(19 May 2020).
  2. Wu C et al. Analysis of therapeutic targets for SARS-CoV-2 and discovery of potential drugs by computational methods. Acta Pharm Sin B. 2020.
  3. A multi-site, randomized, double-blind, multi-arm historical control, comparative trial of the safety and efficacy of hydroxychloroquine, and the combination of HCQ and famotidine for the treatment of COVID-19 (MATCH). NCT04370262.

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