[Chloroquine] was synthesized in 1934 by Hans Andersag at Bayer, and the initial evaluation of the drug by Bayer marked it down as too toxic for human use. This was later considered a major mistake (the “resochin error”, using the drug’s German trade name), as it became a major antimalarial drug after World War II. It was considered a major advance in that it had strong antimalarial activity and didn’t actually make people change into various rainbow colors. You can see how this one came from quinacrine, just chopping off that third ring, which also gets rid of the colorful visible-light absorption properties. And it’s also getting back a bit closer to quinine, as a substituted quinoline with aminoalkyl group up at the 4 position. But it still can lead to depression and other effects. Hydroxychloroquine came along in the 1950s, and just has an extra OH group coming off of one of those N-ethyls over at the end of the chain; it’s quite similar to chloroquine itself.
You might wonder how an antiparasitical drug might do that, but the problem is that the mode of action of all these drugs against malaria parasites is still being argued over. And there are almost certainly several modes of action at work, which will go on to have different effects in different human tissues, etc. Both chloroquine and hydroxychloroquine are used off-label for rheumatoid arthritis and for lupus, but how they work in these areas is another shoulder-shrugger, and there are side effects in the eye. It’s been suggested as an adjunct in some cancer therapy regimes, but there are problems there, too, in the kidney.
So if you see someone confidently explaining just how chloroquine exerts whatever antiviral activity it may have, feel free to go read something else. No one’s sure yet. Viruses certainly have fewer moving parts than trypanosomes, so it might be easier to figure out what’s going on, but anyone who’s done “target ID” will tell you to settle in for some work.
From the article: