Then he spends most of the next 14 hours leading dozens of fellow researchers and volunteers in a systematic review of all the drugs that physicians and researchers have used so far to treat Covid-19. His team has already pored over more than 8,000 papers on how to treat coronavirus patients.
The 35-year-old associate professor at the University of Pennsylvania Perelman School of Medicine leads the school's Center for Cytokine Storm Treatment & Laboratory. For the last few years, he has dedicated his life to studying Castleman disease, a rare condition that nearly claimed his life.
Against epic odds, he found a drug that saved his own life six years ago, by creating a collaborative method for organizing medical research that could be applicable
to thousands of human diseases.
During a cytokine storm, the body's overactive immune response begins to attack its own cells rather than just the virus. When that inflammatory response
occurs in Covid-19 patients, cytokines are often the culprit for the severe lung damage, organ failure, blood clots or pneumonia that kills them.
Having personal experience tamping down his own cytokine responses gives him a unique insight.
"I'm alive because of a repurposed drug," he said.
Now, repurposing old drugs to fight similar symptoms caused by a novel virus has become a global imperative.
A global repository for Covid-19 treatment data
Researchers working with his lab have reviewed published data on more than 150 drugs doctors around the world have to treat nearly 50,000 patients diagnosed with Covid-19. They've made their analysis public in a database
called the Covid-19 Registry of Off-label & New Agents (or CORONA for short).
It's a central repository of all available data in scientific journals on all the therapies used so far to curb the pandemic. This information can help doctors treat patients and tell researchers how to build clinical trials.
The team's process resembles that of the coordination Fajgenbaum used as a medical student to discover that he could repurpose Sirolimus, an immunosuppressant drug approved for kidney transplant patients, to prevent his body from producing deadly flares of immune-signaling cells called cytokines.
The 13 members of Fajgenbaum's lab recruited dozens of other scientific colleagues to join their coronavirus effort. And what this group is finding has ramifications for scientists globally.
Based on their database, the team published the first systematic review of Covid-19 treatments in the journal Infectious Diseases and Therapy in May.
In that first analysis of the data, the team reviewed 2,706 journal articles published on the topic between December 1, 2019, and March 27, 2020. Just 155 studies met the team's criteria for being included in the meta-review based on standards such as the size of the cohort, the nature of the study and the end points researchers chose for concluding their inquiries.
"It's frustrating because we all want a drug that works for everyone," he said. But that isn't happening because the coronavirus affects people in ways that are much more complex.
They're sorting through oceans of data
The first key thing to consider, Fajgenbaum said, was the huge variety of Covid-19 patient experiences. It's hard to zero in on one particular therapy because there can be such significant differences in the timing of when the drug is administered, how severely Covid-19 strikes a given individual and the stage at which the disease has progressed.
Any change in one of those variables can render an otherwise effective drug impotent. But with massive amounts of patients, the clinical data was bearing out a few noticeable themes, he said.
First, the Covid-19 patients with more severe cytokine storms were more likely to need drugs targeted toward suppressing the immune system. Those with less severe cytokine storms were likely to benefit from an immune-boosting drug.
Outside of drugs designed to boost or suppress the immune system, another major category is antiviral therapies. Various antivirals hit the "viral cascade," Fajgenbaum said. Some work by stopping the virus from infecting cells, others by halting replication within cells. Other antivirals act in between cells and the virus.
Keeping the database is a huge undertaking, given how stunning the pace of global scientific progress and collaboration has been in the face of the disease's human toll.
"We set the really ambitious goal of just getting this started," Fajgenbaum said.
In the three months since the cutoff date for their firs