But the strongest indicator of efficacy in humans was that it worked in monkey models, both prophylactically and therapeutically, something I wrote about in March. I have no explanation of why the monkey efficacy did not translate into human efficacy. None.
Here what troubles me most. I have just given you the profile of an experimental drug that should be an effective antiviral drug based on what we know about RNA and DNA polymerase inhibitors. Of course, it would have been nice if the drug was 100-times more potent in cell culture experiment. But keep in mind that this drug was “off the shelf” – not a molecule that had been fine-tuned for years for anti-SARS-2-CoV, yet it still looked good.
Why? I have no idea (I worked on HCV polymerase inhibitors for 5 years so I’m more than a little familiar with this topic). This tells me that it is probably going to be VERY hard to develop an antiviral drug for SARS-2-CoV. This is what troubles me the most. If remdesivir fails what in the world is going to succeed? The malaria drugs never had a chance from the get-go. The AIDS drugs were a stretch, but everything about remdesivir makes sense, except the outcome.