# Remdesivir in COVID-19: pros and cons

**Authors:** Yara Rouhana El Feghali, Layan Rabih, Jad Abdul Khalek, Mariam Arabi

PMC · DOI: 10.3389/fphar.2026.1731244 · Frontiers in Pharmacology · 2026-02-12

## TL;DR

This paper reviews remdesivir's effectiveness and limitations in treating COVID-19, including its use in patients with congenital heart disease.

## Contribution

The paper evaluates remdesivir's role in treating COVID-19 and identifies a research gap regarding its use in patients with congenital heart disease.

## Key findings

- Remdesivir shortens recovery time and lowers mortality risk in early-stage or mild to moderate COVID-19.
- Safety in patients with renal impairment was confirmed, leading to an FDA label update.
- Uncertain effects of remdesivir in patients with congenital heart disease highlight a need for further research.

## Abstract

Beginning in late 2019, the COVID-19 pandemic caused by SARS-CoV-2 rapidly evolved into a global health crisis. High rates of severe illness, hospitalizations, and long-term complications highlighted an urgent need for effective therapeutic agents. This necessity drove unprecedented efforts in drug discovery and repurposing. Remdesivir, developed by Gilead Sciences in 2009, was initially designed as a broad-spectrum antiviral targeting Ebola virus disease. Following observations of broad antiviral activity against coronaviruses, remdesivir was granted Emergency Use Authorization by the FDA in May 2020 for hospitalized patients with severe COVID-19. The FDA subsequently issued full approval in October 2020, expanding remdesivir’s use to hospitalized adults and pediatric patients aged 12 years or older and weighing at least 40 kg.

This paper aims to assess the advantages and limitations of remdesivir in the treatment of COVID-19, drawing on evidence from clinical trials and examining its application in patients with congenital heart disease (CHD).

The literature review was conducted until September 2025 using PubMed and Google Scholar searching for recent clinical trials in addition to relevant reviews.

Remdesivir has been shown to shorten recovery time and lower mortality risk, particularly in patients at an early stage of infection with mild disease severity or requiring oxygen support. Although early guidelines advised against its use in patients with severe renal impairment, subsequent studies confirmed its safety prompting an FDA label update to allow use regardless of renal function. While some trials reported limited effects, the overall body of evidence supports remdesivir’s role in improving clinical outcomes in COVID-19 treatment. In patients with CHD, the uncertain effects of both COVID-19 and remdesivir highlight a key research gap, emphasizing the need to refine existing therapies while following National Institutes of Health (NIH) treatment guidelines.

## Linked entities

- **Chemicals:** remdesivir (PubChem CID 121304016)
- **Diseases:** COVID-19 (MONDO:0100096), congenital heart disease (MONDO:0005453), SARS-CoV-2 (MONDO:0100096), Ebola virus disease (MONDO:0005737)

## Full-text entities

- **Genes:** SLCO1B3 (solute carrier organic anion transporter family member 1B3) [NCBI Gene 28234] {aka HBLRR, LST-2, LST-3TM13, LST3, OATP-8, OATP1B3}, SLCO1B1 (solute carrier organic anion transporter family member 1B1) [NCBI Gene 10599] {aka HBLRR, LST-1, OATP-C, OATP1B1, OATP2, OATPC}, CYP3A4 (cytochrome P450 family 3 subfamily A member 4) [NCBI Gene 1576] {aka CP33, CP34, CYP3A, CYP3A3, CYPIIIA3, CYPIIIA4}, ORF1ab (ORF1a polyprotein;ORF1ab polyprotein) [NCBI Gene 43740578], CTSA (cathepsin A) [NCBI Gene 5476] {aka BSVD6, GLB2, GSL, NGBE, PPCA, PPGB}, CES1 (carboxylesterase 1) [NCBI Gene 1066] {aka ACAT, CE-1, CEH, CES2, HMSE, HMSE1}, SLC47A1 (solute carrier family 47 member 1) [NCBI Gene 55244] {aka MATE1}
- **Diseases:** QT interval prolongation (MESH:D008133), cardiac abnormalities (MESH:D018376), chronic (MESH:D002908), pulmonary hypertension (MESH:D006976), cardiovascular decompensation (MESH:D006333), kidney damage (MESH:D007674), depressed myocardial contractility (MESH:D003866), myalgia (MESH:D063806), cardiac disorders (MESH:D006331), hepatic toxic effects (MESH:D056486), atrial fibrillation (MESH:D001281), COVID- (MESH:D000086382), reduced cardiac output (MESH:D002303), cardiovascular complications (MESH:D002318), infection (MESH:D007239), loss of taste and smell (MESH:D000086582), ACHD (MESH:D006330), impaired tissue perfusion (MESH:D009380), atrioventricular block (MESH:D054537), dry cough (MESH:D003371), lethargy (MESH:D053609), anemia (MESH:D000740), hematological or renal toxicity (MESH:D006402), hypertension (MESH:D006973), immunodeficiencies (MESH:D007153), death (MESH:D003643), fever (MESH:D005334), hypotension (MESH:D007022), renal, hepatic, or cardiac (MESH:D066126), metabolic (MESH:D008659), hypoxemia (MESH:D000860), Ebola virus disease (MESH:D019142), multi-organ dysfunction (MESH:D009102), pulmonary infiltrates (MESH:D017254), obesity (MESH:D009765), rash (MESH:D005076), respiratory (MESH:D012131), hypoalbuminemia (MESH:D034141), acute kidney injury (MESH:D058186), diarrhea (MESH:D003967), hypoxemic pneumonia (MESH:D011014), chest pain (MESH:D002637), fatigue (MESH:D005221), viremia (MESH:D014766), valvular disease (MESH:D006349), diabetes mellitus (MESH:D003920), bundle branch block (MESH:D002037), cyanosis (MESH:D003490), kidney and liver dysfunction (MESH:D051437), dyspnea (MESH:D004417), chronic kidney disease (MESH:D051436), ventricular dysfunction (MESH:D018754), cyanotic defects (MESH:D000013), critical illness (MESH:D016638), sinus bradycardia (MESH:D012804), univentricular hearts (MESH:D000080039), respiratory infections (MESH:D012141), Diseases (MESH:D004194), atrioventricular canal defect (MESH:C562831), conditions (MESH:D020763)
- **Chemicals:** RN (MESH:D011886), baricitinib (MESH:C000596027), uridine triphosphate (MESH:D014544), creatinine (MESH:D003404), dextrose (MESH:D005947), adenosine triphosphate (MESH:D000255), nucleoside (MESH:D009705), phosphoramidate (MESH:C011067), GS-443902 (MESH:C000706175), lopinavir (MESH:D061466), 1'cyano-substituted adenosine nucleotide (-), Na+ (MESH:D012964), hydroxychloroquine (MESH:D006886), triphosphate (MESH:C005692), SBECD (MESH:C093196), GS-704277 (MESH:C000722731), GS-441524-MP (MESH:C000718587), GS-5734 (MESH:C000606551), Ala (MESH:D000409), GS-441524 (MESH:C000710751), oxygen (MESH:D010100), tocilizumab (MESH:C502936)
- **Species:** Coronaviridae (family) [taxon 11118], Nipah virus [taxon 121791], Homo sapiens (human, species) [taxon 9606], Respiratory syncytial virus (no rank) [taxon 12814], Macaca mulatta (rhesus macaque, species) [taxon 9544], Hendra virus [taxon 63330], Severe acute respiratory syndrome-related coronavirus (no rank) [taxon 694009], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Murine hepatitis virus (no rank) [taxon 11138], Gammacoronavirus (genus) [taxon 694013], MHV [taxon 2845560], Ebola virus [taxon 186536], Middle East respiratory syndrome-related coronavirus (no rank) [taxon 1335626]
- **Mutations:** V553L, C799F, D484Y, N198S, V166A/L, F476L, V792I, S759A, E796D, E802D
- **Cell lines:** NL63 — Homo sapiens (Human), Induced pluripotent stem cell (CVCL_1E71)

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12936022/full.md

## References

100 references — full list in the complete paper: https://tomesphere.com/paper/PMC12936022/full.md

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Source: https://tomesphere.com/paper/PMC12936022