P revious reports have found that in-hospital famotidine use in coronavirus disease 2019 (COVID-19) patients was associated with reduced risk of death or intubation. 1,2 In 1 of these studies the authors proposed that famotidine inhibits the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) protease, 3-chymotrypsin-like protease, that is essential for breakdown of the immature SARS-CoV-2 protein particles that contribute to the inflammatory response seen in some COVID-19-infected individuals, 1 which in turn can lead to acute respiratory distress syndrome, multiorgan dysfunction, physiologic deterioration, and death. 3 In a global pandemic with a lack of US Food and Drug Administration-approved targeted therapeutic agents, identification and repurposing of well-established drugs with a proven track record of safety, affordability, and widespread availability are necessary. 4 The purpose of this study was to evaluate the reported protective effect of famotidine on mortality in hospitalized COVID-19 patients. MethodsRefer to Supplementary Methods for complete details. In brief, admitted adults to affiliated hospitals who tested positive for SARS-CoV-2 by reverse transcriptase polymerase chain reaction between February 11, 2020 and May 8, 2020 were included. Exclusion criteria were death or intubation within 48 hours of admission or if famotidine was received >24 hours after admission. The primary outcome was 30-day all-cause mortality. Primary exposure was in-hospital famotidine use, regardless of dose and route, within 24 hours of admission.To mitigate bias from nonrandomized assignment of treatment, a coarsened exact matching (CEM) 5 technique was used for famotidine users and nonusers on age (by 10-year intervals), sex, race, ethnicity, body mass index, comorbidities, and in-hospital hydroxychloroquine (HCQ) use. A multivariable logistic regression model within the CEM cohort and adjusted for baseline World Health Organization (WHO) severity and use of other medications was performed to evaluate the association between famotidine use and 30-day mortality.

Background Remdesivir is FDA approved for the treatment of hospitalized patients with COVID-19 and has been shown to shorten time to recovery and improve clinical outcomes in randomized trials. Methods This was the final day 28 comparative analysis of data from a phase 3, randomized, open-label study comparing 2 remdesivir regimens (5 vs 10 days, combined for this analysis [remdesivir cohort]) and a real-world retrospective longitudinal cohort study of patients receiving standard-of-care treatment (non-remdesivir cohort). Eligible patients, aged ≥18 years, had confirmed SARSCoV-2, oxygen saturation ≤94% on room air or required supplemental oxygen, with pulmonary infiltrates. Propensity score matching (up to 1:10 ratio) was used to ensure comparable populations. We assessed day 14 clinical recovery (determined using a 7-point ordinal scale) and day 28 all-cause mortality (coprimary endpoints). Results Altogether, 368 (remdesivir) and 1399 (non-remdesivir) patients were included in the matched analysis. The day 14 clinical recovery rate was significantly higher among the remdesivir versus the non-remdesivir cohort (65.2% vs 57.1%; OR 1.49, 95% CI 1.16–1.90; P = .002). The day 28 mortality rate was significantly lower in the remdesivir cohort versus the non-remdesivir cohort (12.0% vs 16.2%; OR 0.67, 95% CI 0.47–0.95; P = .03). Conclusions Remdesivir was associated with significantly higher rates of day 14 clinical recovery, and lower day 28 mortality, compared with standard-of-care treatment in hospitalized patients with COVID-19. Collectively, these data support the use of remdesivir to improve clinical recovery and decrease mortality from SARS-CoV-2 infection.

NCCCP participation had a direct and positive impact on all activities, with enhanced access to expanded types of trials and cancer care services. Our data demonstrate the feasibility of successful implementation of an expanded spectrum of clinical trials and programs in a rural community.

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