Table 1.
Pharmacotherapy | Mechanism of Action | Metabolism | Mechanism of Interaction | Clinical Manifestation | |
---|---|---|---|---|---|
Interaction With AADs | Interaction With Anticoagulants | ||||
Chloroquine/hydroxychloroquine |
|
CYP2C8, CYP3A4, CYP2D6, and CYP1A1 |
|
|
None |
Azithromycin |
|
MRP2 and ABCB (minimally by CYP3A4) |
|
|
|
Lopinavir/ritonavir |
|
CYP3A4 |
|
|
|
Remdesivir |
|
Mainly by phosphorylation in nonspecific organ and partially by CYP2C8, CYP2D6, and CYP3A4 |
|
None | None |
Ribavirin |
|
Mainly by hydrolase and partially by CYP2C8, CYP2D6, and CYP3A4 | None | None | None |
Favipiravir |
|
Oxidase and renally excreted | None | None | None |
Umifenovir |
|
CYP3A4 |
|
|
None |
Interferon |
|
Proteolytic degradation by lysosomal enzymes, which are excreted in urine | None | None | None |
Tocilizumab |
|
Unknown (expected to undergo catabolism) |
|
None |
|
Sarilumab |
|
Unknown (expected to undergo catabolism) |
|
None |
|
Pirfenidone |
|
CYP1A2 and renally excreted | None | Amiodarone, a CYP1A2 inhibitor, may increase pirfenidone plasma concentration | None |
Bevacizumab |
|
The reticuloendothelial system | None | None | None |
Eculizumab |
|
The reticuloendothelial system | None | None | None |
Lenzilumab |
|
The reticuloendothelial system | None | None | None |
Methylprednisolone |
|
CYP3A4 |
|
|
|
Fingolimod |
|
CYP4F2 |
|
|
None |
AAD indicates antiarrhythmic drug; ABCB, ATP binding cassette subfamily B; ACE2, angiotensin‐converting enzyme 2; COVID‐19, coronavirus disease 2019; CYP, cytochrome P; DOAC, direct oral anticoagulant; GM‐CSF, granulocyte‐macrophage colony‐stimulating factor; ICaL, L‐type calcium channel; IKach, acetylcholine‐dependent potassium channels; IKr, potassium channel; LMWH, low‐molecular‐weight heparin; MRP2, multidrug resistance‐associated protein 2; TdP, torsade de pointes; and VEGF, vascular endothelial growth factor.