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Pharmacogenomics of COVID-19 therapies
dc.contributor.author | Takahashi, Takuto | |
dc.contributor.author | Luzum, Jasmine A | |
dc.contributor.author | Nicol, Melanie R | |
dc.contributor.author | Jacobson, Pamala A | |
dc.date.accessioned | 2020-09-10T19:14:52Z | |
dc.date.available | 2020-09-10T19:14:52Z | |
dc.date.issued | 2020-08-18 | |
dc.identifier.uri | https://www.nature.com/articles/s41525-020-00143-y | en_US |
dc.identifier.uri | https://hdl.handle.net/20.500.12663/2174 | |
dc.description.abstract | A new global pandemic of coronavirus disease 2019 (COVID-19) has resulted in high mortality and morbidity. Currently numerous drugs are under expedited investigations without well-established safety or efficacy data. Pharmacogenomics may allow individualization of these drugs thereby improving efficacy and safety. In this review, we summarized the pharmacogenomic literature available for COVID-19 drug therapies including hydroxychloroquine, chloroquine, azithromycin, remdesivir, favipiravir, ribavirin, lopinavir/ritonavir, darunavir/cobicistat, interferon beta-1b, tocilizumab, ruxolitinib, baricitinib, and corticosteroids. We searched PubMed, reviewed the Pharmacogenomics Knowledgebase (PharmGKB®) website, Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines, the U.S. Food and Drug Administration (FDA) pharmacogenomics information in the product labeling, and the FDA pharmacogenomics association table. We found several drug-gene variant pairs that may alter the pharmacokinetics of hydroxychloroquine/chloroquine (CYP2C8, CYP2D6, SLCO1A2, and SLCO1B1); azithromycin (ABCB1); ribavirin (SLC29A1, SLC28A2, and SLC28A3); and lopinavir/ritonavir (SLCO1B1, ABCC2, CYP3A). We also identified other variants, that are associated with adverse effects, most notable in hydroxychloroquine/chloroquine (G6PD; hemolysis), ribavirin (ITPA; hemolysis), and interferon β -1b (IRF6; liver toxicity). We also describe the complexity of the risk for QT prolongation in this setting because of additive effects of combining more than one QT-prolonging drug (i.e., hydroxychloroquine/chloroquine and azithromycin), increased concentrations of the drugs due to genetic variants, along with the risk of also combining therapy with potent inhibitors. In conclusion, although direct evidence in COVID-19 patients is lacking, we identified potential actionable genetic markers in COVID-19 therapies. Clinical studies in COVID-19 patients are deemed warranted to assess potential roles of these markers. | en_US |
dc.language | English | en_US |
dc.subject | COVID-19 | en_US |
dc.subject | Hydroxychloroquine | en_US |
dc.subject | Chloroquine | en_US |
dc.subject | Azithromycin | en_US |
dc.subject | Remdesivir | en_US |
dc.subject | Drug Therapy | en_US |
dc.title | Pharmacogenomics of COVID-19 therapies | en_US |
eihealth.country | Others | en_US |
eihealth.category | Candidate therapeutics RD | en_US |
eihealth.type | Published Article | en_US |
eihealth.maincategory | Save Lives / Salvar Vidas | en_US |
dc.relation.ispartofjournal | npj Genomic Medicine | en_US |
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