An interesting open access paper in Science "Drug-induced phospholipidosis confounds drug repurposing for SARS-CoV-2" DOI points a potential flaw in interpreting in vitro data.

Repurposing drugs as treatments for COVID-19 has drawn much attention. Beginning with sigma receptor ligands, and expanding to other drugs from screening in the field, we became concerned that phospholipidosis was a shared mechanism underlying the antiviral activity of many repurposed drugs. For all of the 23 cationic amphiphilic drugs tested, including hydroxychloroquine, azithromycin, amiodarone, and four others already in clinical trials, phospholipidosis was monotonically correlated with antiviral efficacy. Conversely, drugs active against the same targets that did not induce phospholipidosis were not antiviral.

Phospholipidosis is well known phenomena for those involved in drug discovery, it is based on the physicochemical properties of the molecule and results in excessive accumulation of intracellular phospholipids in tissues, such as the liver, kidney and lung. The resulting accumulation can lead to liver, kidney, or respiratory failure.

Drug-induced phospholipidosis can be determined by measuring the accumulation of specific fluorescent probes in HepG2 cells or primary hepatocytes.

There is a more detailed explanation of the consequences here, "A Strategy for Risk Management of Drug-Induced Phospholipidosis" DOI.