The chatter about a promising drug to fight Covid-19 started, as chatter often does (but science does not), on Twitter. A blockchain investor named James Todaro tweeted that an 85-year-old malaria drug called chloroquine was a potential treatment and preventative against the disease caused by the new coronavirus. Todaro linked to a Google doc he’d co-written, explaining the idea.
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Though nearly a dozen drugs to treat coronavirus are in clinical trials in China, just one—remdesivir, an antiviral that was in trials against Ebola and the coronavirus MERS—is in full-on trials in the US. Nothing has been approved by the Food and Drug Administration. So a promising drug would be great—and even better, chloroquine isn’t new. Its use dates back to World War II, and it’s derived from the bark of the Chinchona tree, like quinine, a centuries-old antimalarial. That means the drug is now generic, and relatively cheap. Physicians understand it well, and they’re allowed to prescribe it for anything they want, not just malaria.
Todaro’s tweet got thousands of likes. The engineer/tech world picked up the idea. The widely-read blog Stratechery linked to Todaro’s Google document; Ben Thompson, the blog’s editor, wrote that he was “wholly unqualified to comment” but that the anecdotal evidence favored the idea. Echoing the document, Thompson wrote that the paper was written in consultation with Stanford Medical School, the University of Alabama at Birmingham medical school, and National Academy of Sciences researchers—none of which is exactly true. (More on that in a bit.) One of Todaro’s co-authors, a lawyer named Gregory Rigano, went on Fox News to talk about the concept. Tesla and SpaceX CEO Elon Musk tweeted about it, citing an explanatory YouTube video from a physician who’s been doing a series of coronavirus explainers. To be fair, Musk wasn’t all-in on the idea absent more data, though he wrote that he’d received a life-saving dose of chloroquine for malaria.
It’s the definition of “big if true.” Part of the story of Covid-19, of the coronavirus SARS-CoV-2, is that it is novel. Humans don’t have any immunity to it. There’s no vaccine, no drug approved to treat it. But if a drug did exist—if a cheap, easy drug can stave off the worst, ventilator-requiring, sometimes-fatal complications of coronavirus infection, or maybe prevent that infection in the first place, what are we all socially isolating for, like suckers?
That if—as the saying goes—is doing a lot of work. The Covid-19 pandemic is causing, reasonably, a worldwide freak-out as scientists and policymakers race to find solutions, not always competently or efficiently. It’s the kind of thing that rankles the engineer-disruptor mindset. Surely this must be an easily-solved problem that’s primarily the fault of bureaucracy, regulation, and people who don’t understand science. And maybe the first two things are true. The third thing, though, is where the risks hide. Silicon Valley lionizes people who rush toward solutions and ignore problems; science is designed to find solutions by identifying those problems. The two approaches are often incompatible.
What happened here, specifically, is that Rigano sought Todaro out. Todaro’s tweet identified Rigano as being affiliated with Johns Hopkins; Rigano’s LinkedIn profile says he’s on leave from a masters degree program there in bioinformatics, but is now consulting for a program at Stanford that does translational drug discovery—finding new uses and commercializable applications for already-approved drugs. (Neither program has returned a request for comment.) “I have a very unique background at the crossroads of law and science,” Rigano tells me. “I have been working with large pharmaceutical companies, universities, biotechs, and nonprofits in the development of drugs and medical products.” He says those contacts told him about the use of chloroquine against Covid-19 in China and South Korea, so he started reading up on it.
It turns out that people have been pitching chloroquine as an antiviral for years. In the early 1990s researchers proposed it as an adjunct to early protease inhibitor drugs to help treat HIV/AIDS. A team led by Stuart Nichol, the head of the Special Pathogens Unit at the Centers for Disease Control and Prevention, published a paper in 2005 saying that the drug was effective against primate cells infected with SARS, the first big respiratory coronavirus to affect humans. That’s an in vitro test, not live animals—just cells.
Nichol didn’t respond to a request for comment, but a CDC spokesperson emailed this: “CDC is aware of reports of various medications being administered for either treatment or prophylaxis for COVID-19, including those demonstrating in vitro activity against SARS-CoV- 2. At this time, it is important to ensure robust clinical data, gathered from clinical trials, are obtained quickly in order to make informed clinical decisions regarding the management of patients with COVID-19.”