Name Evidence Type
Remdesivir In-vitro effective against COVID-19; Effective (esp. prophylactically) against MERS in macaque monkeys; More effective than lopinavir/ritonavir against MERS in mice
Chloroquine In-vitro effective against COVID-19; In-vitro effective against SARS; Not in-vitro effective against MERS in monocyte-derived cells
Cinanserin In-vitro effective against COVID-19;In-vitro effective against SARS
Lopinavir/Ritonavir Human retrospective evidence of effectiveness in MERS and SARS but not COVID-19; In-silico predicted effectiveness against COVID-19
Indinavir In-silico predicted effectiveness against COVID-19; Not effective in-vitro against SARS
Thalidomide Improved symptoms in one case study of severe COVID-19


An in-silico study of HIV drugs for their docking affinity to a key enzymes in the COVID-19 virus – RdRp, the main protein for RNA replication – found an almost perfect match in the antiviral drug remdesivir, suggesting it might be a good candidate drug for treating COVID-19.[3]

Remdesivir also inhibits the COVID-19 virus in vitro.[7]

Remdesivir is effective at reducing the clinical signs of infection and viral load from MERS coronavirus in rhesus macaque monkeys; if given prophylactically, it prevents the monkeys from getting any disease symptoms at all and keeps their viral loads negligible.[10] In mice, remdesivir is more effective than lopinavir/ritonavir in improving pulmonary function and reducing viral load from MERS infection.[11]

In 3 US patients treated with remdesivir, 2 patients saw fever drop immediately upon receiving the drug (the third didn’t have a fever); one was able to go off supplemental oxygen; all recovered.

Remdesivir is currently in trials in China and the US for COVID-19.


A brief summary document [1] claims that clinical trials in China including over 100 patients have found the antimalarial drug chloroquine phosphate “superior to control treatment” in treating COVID-19 pneumonia and shortening disease course. The paper provided no documentation about experimental methods.

Chloroquine also inhibits the replication of the COVID-19 virus in vitro,[7] as well as the SARS coronavirus in vitro.[9] It does not inhibit the MERS coronavirus in vitro in a culture of monocyte-derived cells.[13]

Chloroquine frequently causes gastrointestinal side effects (diarrhea, nausea), problems with visual acuity, insomnia, and paresthesias (prickling skin sensations.)[15] More rarely, chloroquine can cause psychiatric symptoms like depression.


Cinanserin is a serotonin receptor antagonist which was also found to inhibit the replication of the SARS virus in vitro. Cinanserin inhibits the activity of COVID-19’s main protease in vitro, and inhibits the virus’s replication in vitro.[5]

Cinanserin also inhibits the replication of the SARS coronavirus in vitro.[14]


Lopinavir/Ritonavir is a combination of two antiviral drugs approved for the treatment of HIV.

In one Korean patient, aged 54, with mild pneumonia and a diagnosis of COVID-19, treatment with the antiviral drug combination of lopinavir and ritonavir diminished coronavirus load to undetectable levels.[2]

Lopinavir/Ritonavir was also used by the Thai infectious disease team to successfully treat patients with severe COVID-19.[3]

Lopinavir also had a high binding affinity to the COVID-19 protein 3CL-PRO in an in-silico screen of 3118 FDA-approved drugs.[4]

Lopinavir is a protease inhibitor, effective in vitro against the main protease of the SARS coronavirus; it also has in vitro antiviral activity against SARS-CoV. Lopinavir reduced viral load and clinical symptoms of the MERS coronavirus in mice and marmoset monkeys.[6]

In human SARS cases, treatment with lopinavir was associated with lower death rate (2.3%) and intubation rate (0%) compared with standard treatment (11% and 15.6% respectively.). Another case-control study of SARS found a lower rate of ARDS in patients treated with lopinavir (2.4% vs 28.8%). [6]

A retrospective study of 40 patients found that post-exposure prophylaxis including lopinavir/ritonavir reduced the spread of MERS-CoV by 40% in healthcare workers. However, a retrospective study of 134 COVID-19 patients found no significant difference between lopinavir/ritonavir treatment, Abidol treatment, and control treatment.[6]


Indinavir is an antiviral drug used to treat HIV.

In an in-silico screen of the binding affinity of 3118 FDA-approved drugs to several key enzymes of the COVID-19 virus, the highest-affinity drug for the protease PDB-6LU7 was indinavir, an antiviral drug approved for use against HIV. (Even higher affinity were human proteins that closely resemble the enzyme’s ligand – ACE2 and GHRP-2.) Indinavir also had a high binding affinity to another COVID-19 protein, 3CL-PRO.[4]

However, in an in-vitro test against the SARS coronavirus, indinavir did not block replication.[12]


Thalidomide is an immunomodulatory drug used to treat cancers.

A 45-year-old woman with a severe case COVID-19, with fever, pneumonia, dyspnea, nausea, and vomiting, improved and went into remission after being treated with thalidomide, which has anti-inflammatory effects, reducing the “cytokine storm” responsible for the severe symptoms of COVID-19.[7]


[1]Gao, Jianjun, Zhenxue Tian, and Xu Yang. “Breakthrough: Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies.” BioScience Trends (2020).

[2]Lim, Jaegyun, et al. “Case of the Index Patient Who Caused Tertiary Transmission of COVID-19 Infection in Korea: the Application of Lopinavir/Ritonavir for the Treatment of COVID-19 Infected Pneumonia Monitored by Quantitative RT-PCR.” Journal of Korean medical science 35.6 (2020).

[3]Chang, Yu-Chuan, et al. “Potential therapeutic agents for COVID-19 based on the analysis of protease and RNA polymerase docking.” (2020).

[4]Contini, Alessandro. “Virtual screening of an FDA approved drugs database on two COVID-19 coronavirus proteins.” (2020).

[5]Jin, Zhenming, et al. “Structure-based drug design, virtual screening and high-throughput screening rapidly identify antiviral leads targeting COVID-19.” bioRxiv (2020).

[6]Yao, Tian‐Tian, et al. “A Systematic Review of Lopinavir Therapy for SARS Coronavirus and MERS Coronavirus–A Possible Reference for Coronavirus Disease‐19 Treatment Option.” Journal of Medical Virology (2020).

[7]Wang, Manli, et al. “Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro.” Cell research 30.3 (2020): 269-271.

[8]Chen, Chengshui, et al. “Thalidomide combined with low-dose glucocorticoid in the treatment of COVID-19 Pneumonia.” (2020).

[9]Vincent, Martin J., et al. “Chloroquine is a potent inhibitor of SARS coronavirus infection and spread.” Virology journal 2.1 (2005): 69.

[10]de Wit, Emmie, et al. “Prophylactic and therapeutic remdesivir (GS-5734) treatment in the rhesus macaque model of MERS-CoV infection.” Proceedings of the National Academy of Sciences (2020).

[11]Sheahan, Timothy P., et al. “Comparative therapeutic efficacy of remdesivir and combination lopinavir, ritonavir, and interferon beta against MERS-CoV.” Nature Communications 11.1 (2020): 1-14.

[12]Tan, Emily LC, et al. “Inhibition of SARS coronavirus infection in vitro with clinically approved antiviral drugs.” Emerging infectious diseases 10.4 (2004): 581.

[13]Cong, Yu, et al. “MERS-CoV pathogenesis and antiviral efficacy of licensed drugs in human monocyte-derived antigen-presenting cells.” PloS one 13.3 (2018).

[14]Chen, Lili, et al. “Cinanserin is an inhibitor of the 3C-like proteinase of severe acute respiratory syndrome coronavirus and strongly reduces virus replication in vitro.” Journal of virology 79.11 (2005): 7095-7103.

[15]Martins, Antonio Camargo, et al. “Side effects of chloroquine and primaquine and symptom reduction in malaria endemic area (Mâncio Lima, Acre, Brazil).” Interdisciplinary perspectives on infectious diseases 2015 (2015).