This transcript has been edited for clarity.
Eric J. Topol, MD: Hello. This is Eric Topol with the Medscape podcast Medicine and the Machine. I'm delighted today to have Dr David Fajgenbaum join me from the University of Pennsylvania, Penn Med. He has a remarkable story that will be familiar to some of you in the medical community, but there are a lot more chapters going forward. Welcome, David.
David Fajgenbaum, MD: Eric, thanks so much for having me.
Topol: I recently had a chance to read your amazing book, Chasing My Cure. It is quite a story. Let's go back to 2010 when you picked up that something wasn't right about your health, after having been the picture of health: bench-pressing 375 pounds — friends called you The Beast. But then something went off the track. Maybe we could start at that point.
Fajgenbaum: I was a healthy, third-year medical student, never had any health problems in my whole life. And then out of nowhere, I started feeling more tired than ever before. You remember during training — we were sort of always tired, right? In that context, what is feeling more tired than ever before? But it felt different. Then I noticed some lumps and bumps in my neck, which turned out to be enlarged lymph nodes. I noticed fluid pooling around my ankles, which seemed unusual, and this horrible abdominal pain. It got worse and worse over the course of a couple of weeks. I was on an ob/gyn rotation. I went from taking my medical school exam for ob/gyn to walking down the hall to the emergency department.
They ran blood work, and I'll never forget: My doctor walked into the room and said, "David, your liver, your kidneys, your bone marrow, your heart, and your lungs are shutting down. We have to hospitalize you right away." Within days, I was in the intensive care unit and had my last rites, because my doctors didn't think I would survive. I was on dialysis, and it got even worse from there.
Topol: I know you courted death at least five times.
Fajgenbaum: That's right.
Topol: You were diagnosed with a form of Castleman disease. As I understand it, there are two forms. You had the most serious, multicentric form. Maybe you could explain since you are now the world authority on Castleman disease. What is the difference between the more benign and the more serious form?
Fajgenbaum: The thing that's in common between both forms of Castleman's is that if you cut out a lymph node, they look the same under the microscope. But the form I have — what's called idiopathic multicentric Castleman disease — is a deadly form where the immune system attacks and shuts down the vital organs for an unknown reason. Until recently, the only thing you could treat it with was chemotherapy.
The more benign form behaves completely differently. Patients typically are cured with surgery. This shows the importance of molecular medicine. Something may look the same under the microscope, but molecularly, it behaves very differently and, therefore, patients have completely different outcomes.
Topol: Your presentation told us right from the get-go that you didn't have the form that is easily cured. We're going to get into cures because this is a theme of yours. You went from "chasing my cure" to chasing cures for all.
One of the most memorable quotes about you was in the New York Times profile a few years back, where an Emory University professor said, "I almost wish that every disease had a David to be part of the charge." That says a lot right there.
You discovered something that helped you, having tried many different interventions. But you finally came upon something that made a difference. You've been in remission for about 8 years now. Is that right?
Fajgenbaum: Over 9 years on a drug that you know well and that many have been talking about a lot. Sirolimus, also called rapamycin, is a drug that was never intended for Castleman's and had never been used before for Castleman's. Sirolimus is a potent inhibitor of mTOR. Based on work I did in the lab, and based on the data in front of me that my mTOR signaling pathway was turned into overdrive, I became the first patient with my disease to be treated with this drug. It's been more than 9 years, and we've got patients all over the world who are now on it.
Topol: How did you come to give rapamycin a shot?
Fajgenbaum: After my fourth relapse, I'd gone back to Penn Medical School, got another year of med school under my belt, and relapsed again. That relapse was so difficult because I was on an experimental drug that blocks interleukin-6 (IL-6), and it didn't work. That's when I realized that if I wanted any chance of survival, I would need to get involved in research. I knew it was unlikely that I would find anything that would help me, but it was the only shot I had.
So I started collecting blood samples on myself, storing them in the freezer every couple of weeks. Any chance I got, while I was finishing up medical school, I went into the lab to work on these samples. I relapsed and nearly died for a fifth time while I was collecting these samples.
Thankfully, I was given a combination of seven different chemotherapies. They saved my life. But when I got out of the hospital after those seven chemos, I went into the lab and began performing a series of experiments. First, I assessed serum proteomics where I measured over 1000 different molecules in my blood from multiple time points. I did flow cytometry to look at the status of the various immune cells in my body, and how activated and not activated they were.
From these multiple datasets, there was what's called an mTOR signature. Basically, the proteins that were elevated in my blood were the proteins that are elevated when the communication line called mTOR is turned on. It wasn't proof, but it was a signature. Then I went to a lymph node that had been resected during my last relapse and I did a simple stain. It cost about $17 to run this experiment, which showed, in black and white, that this particular communication line, mTOR, was turned on to overdrive.
I drove down to Washington, DC, and I took the results to a doctor of mine at National Institutes of Health and showed them to him. I said, "What do you think? I've got this deadly disease. I keep relapsing. There's no way I'm going to make it to my wedding day unless we try something new. I'm out of options." And he said, "Sure, let's give rapamycin a try."
Topol: It's remarkable because rapamycin has a multiplicity of effects.
Fajgenbaum: That's right.
Topol: One effect is, of course, that it can help with mitochondrial dysfunction. But also, it can suppress the immune system; it is a standard drug for transplant to prevent rejection. So you came upon this and then you had to find the right dose that wouldn't necessarily knock out your immune response capability. Did you have to explore doses to find a dose that worked? And how would you know? Did you keep doing all of these tests on yourself to figure that out?
Fajgenbaum: It's such an important question because, just as you said, rapamycin is one of those drugs where the dose really, really matters. I know Peter Attia has shared that at a low dose, rapamycin may actually boost the immune system in some ways, as opposed to suppressing it. So you must get the dose right.
In my case, with Castleman's, literally, the immune system attacks the vital organs, almost as though they're foreign organs. My immune system attacks my kidneys and my lungs and liver almost as though they should be rejected like transplanted organs. So, we thought, let's start with an organ transplant rejection dose. Let's start with the dose we give to patients after kidney transplants, and that dose was too high. My immune system was completely wiped out.
So we started dialing it back until we got to a level where my symptoms were controlled. It's now been 9 years without a relapse, and I'm going to knock on some wood on my desk. My symptoms were controlled but my white blood cell count shouldn't be just zero. We wanted to find that middle ground. So it was a bit more trial and error to get that right dose and a bit less quantitative proteomics, but I think we found the right dose.
Topol: Then you took all the lessons you learned to form a Castleman's global network. Tell us about how you went from an N of 1 to an N of thousands.
Fajgenbaum: My book is called Chasing My Cure, but I think that was the wrong title. It should have been Chasing Our Cure because it really wasn't me working on my own. Yes, I was the one doing the experiments in the lab, but I also had this amazing network of people around me from all over the world, just as you mentioned — a scientific advisory board representing nearly every continent in the world, physicians, researchers, patients, all working together with this common mission: We've got this disease that is deadly and relentless. Can we build a team that's also relentless to try to find solutions for it?
We decided to do things differently. Rather than the typical approach of rare disease research where you raise money first and then you invite researchers to apply for it, we said, what if we start out by just asking physicians, researchers, and patients what the important studies are that we should do? Let's come up with that prioritized list, and then let's go out and recruit the best researchers in the world to do those studies, whether or not they'd studied Castleman's or knew anything about Castleman's in the first place. Just what should be done? Let's go recruit someone to do it.
That approach has been groundbreaking. It's been amazing to get patients to participate in the research questions we're asking, to get researchers who had never heard of Castleman disease, but they're the best people in the world at single-cell RNA sequencing to work on our project. It's been a great example of how when you bring the right people together and you have a clear mission and vision, you can achieve so much more than you ever could have on your own.
Topol: Now, in the world of people who have the multicentric form of Castleman's, are they mostly taking rapamycin now?
Fajgenbaum: A lot of patients are on rapamycin and doing very well. There's also an IL-6 blocker which has an incredible backstory and is also used quite a bit for Castleman's. I was given that IL-6 blocker; it didn't work for me, but it does work for between one third and one half of patients. A lot of patients are doing well on IL-6 blockade.
Let me quickly share the story about IL-6, or tocilizumab. Many people have heard about this in the context of COVID. It's the first drug administered to patients in the intensive care unit after they've gotten dexamethasone. But the story behind tocilizumab is an incredible one, and it started with Castleman disease.
Back in the 1990s, Kazu Yoshizaki discovered that IL-6 was important in Castleman's. He developed this drug now called tocilizumab to block the IL-6 receptor. I had heard that Kazu gave it to himself as the first patient ever. And I said, "Kazu, I heard that you gave it to yourself." He said, "No, no, no, I didn't give it to myself; the nurse gave it to me."
So, he discovered the target. He developed the drug, and he gave it to himself as the first human ever, which I don't recommend by any means. But he didn't have a bad outcome. And he tested the drug in patients with Castleman's. He got approval in Japan for Castleman disease. Then, when it was purchased by a large pharmaceutical company, they decided Castleman's was too small a market in the United States, so they studied it in rheumatoid arthritis and juvenile idiopathic arthritis, and now in COVID as cellular immunotherapy. So, tocilizumab, which was made for Castleman's, is now being used for myriad other conditions all over the world.
Topol: Recently, we were discussing the prospects of using it for long COVID, because long COVID has been shown to have mitochondrial dysfunction and an untoward immune activation. So, rapamycin may turn out to be a worthy candidate for long COVID. We need to do a trial for that. Repurposing what you found that helped you and many others may also work for something that millions of people now are suffering from. Do you think there's a chance it will work with long COVID?
Fajgenbaum: I think so. Just as you said, there are multiple mechanisms through which rapamycin may be effective. The dose is going to matter, which is tough when you do a large clinical trial because you must pick the right dose and have sufficient numbers on the right dose to be able to see the right effect and think about duration. Is it 1 month, 6 months, 1 year? What's the right duration to see the effect you're looking for?
There are good mechanistic reasons to believe that it could be useful, like some of the observational data around metformin used during acute COVID and how that lowers the risk for long COVID. This is also circumstantial, but supportive evidence suggests that metformin works in many ways similar to rapamycin. So there's reason to believe that could be useful. As you can imagine, as someone who's alive thanks to a drug that wasn't made for my disease, I think a lot about the drugs that are at our neighborhood pharmacies, that maybe were intended for one thing, but what other things could they be helpful for?
Topol: You're living proof of drug repurposing, if there ever was one. As if that wasn't enough to accomplish at your young age in your career, now you've launched Every Cure.
Tell us about it. You made a major announcement at the Clinton Global Initiative recently. This is taking the lessons you've learned and all the people you've had a chance to work with to yet another mega level.
Fajgenbaum: I'm alive thanks to a repurposed drug. After finding that drug, I joined the faculty at the University of Pennsylvania to continue to study hyperinflammatory diseases like Castleman's, and then to look for existing drugs that are on the pharmacy shelf, to see if they could potentially be repurposed to treat those diseases now — not 10 years from now, not $1 billion from now.
We've been quite successful here at Penn. Our center has identified and/or advanced 16 repurposed drugs for diseases they were not initially intended for. In the course of doing that, with every one of these drugs and with every patient who walks into our center who gets a drug that wasn't intended for their disease, and weeks later is doing better, it is in my face that there are drugs sitting on the pharmacy shelf that could save patients' lives.
The reverse of that is that there are patients suffering when there's a drug sitting on the pharmacy shelf that could have saved their lives. The more I saw this and, frankly, the longer I've lived on this repurposed drug, the more compelled I felt to say that we need to do something systematically. We can't just do it with Castleman disease and then POEMS syndrome, one rare disease at a time. We really need to do this at scale.
A few things came together at once that led to Every Cure. One piece of it is something you've been tracking — the incredible progress with generative artificial intelligence (AI) and the advent of these new tools that can help us do things within seconds that once took a medical student like myself months of working in the lab. That's one big pillar.
Another pillar is that, certainly, we've had a lot of experience and success with repurposing. The third is that I got this phone call on March 31, 2021, so the day before April Fools' Day. And I'm telling you, at the time, all I could think about was repurposing. I got this call from an unknown number. And the person on the other end of the line says, "President Clinton is on the line. He read your book. He wants to talk to you."
I was pretty sure it was a joke. But then on the other line I hear, "David, it's Bill Clinton." And I'm like, Oh, my gosh, this really is President Clinton.
He had read my book, and his question for me was, how many more drugs do you think are out there that could be repurposed? I told him that I believe that there are 3000 drugs that are approved for, on average, between one and three diseases each. But it's no exaggeration to think that each one of those drugs could treat maybe one to three additional diseases. Think about that — that's doubling the impact of the pharmaceutical products within reach.
He said, "What's your dream?" And I told him. I said, "My dream is to create an initiative to do this systematically, to unlock the full potential of every drug for every disease possible." And he said, "Well, if you ever do that, know that you've got my full support. I'd love for you to announce it at the Clinton Global Initiative." He kept calling me every few months to check in to see if I was going to do this. And eventually, I did believe we could build the right team to do this at scale.
So we launched Every Cure. We announced it at the Clinton Global Initiative, and the last year has been all about building the team, bringing together the resources and the funds to create an AI engine that comes up with a predictive score for the likelihood of every drug to treat every disease — all 3000 drugs against all 20,000 human diseases. This is the perfect use case for something like AI. Right? There's so much data that's already out there to train it on.
We're looking for patterns in the data that could connect one drug to a disease. So, basically, we come up with these predictive scores, and then we take the most promising ones into clinical trials to prove whether this drug actually helps patients with this disease, and move it all the way forward, whether or not it's profitable for a company.
Topol: This is kind of the thematic of the Medicine and the Machine podcast: Where and how can we learn from AI and machines what can make for better medicine, better health? One example of that, which I know you're familiar with, is during the pandemic, the JAK kinase inhibitor baricitinib was datamined through AI to say, this drug is being used for rheumatoid arthritis and alopecia areata, but let's try this in patients with severe COVID. And it has, in more than one randomized trial, been shown to save lives. It has full approval, and it is an AI success story in the midst of the pandemic. A lot of people think about vaccines and maybe Paxlovid, but this is saving lives as well. There are many others drugs like this. You mentioned the 3000 drugs; those are approved drugs. There are another 10,000 in the ReFRAME database (reframeDB) here at Scripps Research. These molecules didn't make it as drugs, but they were tested.
So, it could go beyond the drugs that are approved to those that weren't approved but could turn out to be great success stories. You're on to something extraordinary. But it isn't just this that you're doing, because you get to work with Carl June and the people who are doing all of this T-cell engineering who are changing the world. You're also working on cellular engineering. Can you tell us about that?
Fajgenbaum: Sure. I've had the opportunity to be at this great institution, the University of Pennsylvania, where so much great work is being done in cellular immunotherapy and engineering. My focus has been on, when you give patients cellular immunotherapy and they do have a cytokine storm reaction to it, how do we control the cytokine storm so that we can save their lives so the cellular immunotherapy can extend their lives?
I've worked, thankfully, very closely with Carl June and John Wherry and others to think about the tail end of cellular immunotherapy, because if you can't control the cytokine storm when you give someone immunotherapy and they die from the treatment, that's a travesty. Right? So let's get them these life-saving therapies, but let's make sure that in the process of treating them with a lifesaving therapy, we don't cause more harm than good. We've been focused on deeply profiling the cytokine storm that occurs with these immunotherapies.
Topol: I don't know if people are aware that the whole idea of CAR-T — that is, engineering T cells — is going through a revolution, even now, using CRISPR genome editing. Basically, it's about antigens that are specific to an individual's cancer, and revving up the cancer immune response beyond the drugs that we have today, like the PD-1 receptor inhibitor. So, as you said, one of the biggest downsides is the cytokine release syndrome, which can be fatal. Is that now under check? Has that been markedly reduced over time?
Fajgenbaum: It has been. It's been reduced tremendously, thanks to IL-6 blockade. That drug tocilizumab that Kazu made has pretty much been given uniformly to patients all over the world. There are still some challenges, such as individuals getting something called ICANS (immune effector cell-associated neurotoxicity syndrome), which is neurologic and quite progressive and serious. So there are still unmet needs in controlling the immune response in cellular immunotherapy. But it's a lot better than it was.
As you said, the more powerful and the better we're getting with cellular immunotherapies, the more we have to continue to retool how we prevent them from getting out of control.
Typical cancers, solid tumors such as lung cancer or colon cancer, have been more refractory to cellular immunotherapy over the years. Blood cancers have been much more responsive. Now that we're starting to crack the code in solid tumors, I think it may be a different sort of immune response that we're seeing afterwards. So, we're having to pay attention because, one, you need to treat the cancer but, two, you need to make sure you don't cause harm along the way.
Topol: Right. No question. We've seen some small successes but we have a ways to go. One thing that's noteworthy is that you have Every Cure going for all these rare diseases. And on the other hand, you're also working on cancer, essentially by trying to develop the treatments that the group at Penn is mission control for. Making that safer, more effective, and eventually, we hope, charting a path that will be effective in addressing cancers — this whole theory you have about the immune system being a source of why people get cancer and don't respond. For years, that was out there, and finally we started to develop checkpoint immunotherapy agents that have already helped some people with certain types of cancer.
But there seems to be so much more room to rev up our immune system. I wanted to ask you about cancer, which is obviously a genomic disease. But is the ability for it to go on to metastasize because our immune system is defective or just isn't up to the challenge?
Fajgenbaum: I think one part is that it might be defective. Another part is that maybe it's not defective, but we can program it to be more effective. It's not so much that it didn't send something, but it's that there's actually human potential to reprogram these cells, just as we talked about earlier, to actually effectively remove them. I think the immune system — and of course, I'm biased; I am an immunologist and I run an immunology lab — but I think immunology and the immune system play a critical role all across medicine.
Look at the colchicine approval in cardiovascular disease. This is such an incredible concept; 20 or 30 years ago, who would have ever thought that colchicine, a gout drug that is certainly anti-inflammatory, would get an approval for secondary prevention of heart disease? It's because of the role that inflammation plays in cardiovascular disease. I would love to hear your thoughts on colchicine in particular, given your background.
Topol: It's an interesting point you're making, which is, here is another repurposed drug. I never would have thought I'd give colchicine for heart disease. But there are two randomized, placebo-controlled trials that provide compelling evidence of benefit, whether it's post-MI or for people at high risk. I don't think it's even out there in the cardiovascular community, because when a drug is repurposed, people just don't get it that these drugs will help people. And you wouldn't call ischemic heart disease or coronary atherosclerosis rare diseases.
The number of people I see in clinic who have coronary disease or are post-MI who are getting colchicine is next to nil. It's going to take a while to convince people that those two colchicine trials actually provide some compelling evidence. I believe the cardiologists just think of it as inducing diarrhea for treating gout or something. And again, dose is another part of that story. There's a company that's trying to market something that is different from generic colchicine. As I recall, the difference is between 0.5 mg and 0.6 mg, which I can't believe.
Fajgenbaum: That's correct.
Topol: And obviously, that kind of marketing has helped to cloud the issue, because it's not like it's a new drug. It's just a slightly different dose of a very old drug.
So, where do you go now? You're starting to have an impact globally. Are you going to move outside to the galaxy? What's the next step, David?
Fajgenbaum: I'm just so thankful to be here. I mean, literally to be on your podcast with you — what an honor for me. But frankly, just to be alive... I feel like I have this incredible responsibility. I'm alive because of a drug that no one paid attention to, that was just sitting there all these years. And now patients all over the world are alive because of other drugs that were just sitting on the pharmacy shelf.
I feel this incredible drive and mission, which is to say, we need to do everything we can to make sure that we can unlock the full potential of every drug that's on the pharmacy shelf, because no patient should suffer if there's a treatment right there. You brought up a great point with colchicine. A lot of it comes down to incentives, so if the drug is cheap and old and generic, then no one's doing the work to figure out a new use for it. I feel compelled to help fix this problem.
The potential benefit to society is huge — to take drugs that are sitting on the pharmacy shelf that are safe in many cases, that are inexpensive in most cases because they're generic, and to find new uses for them. We know all too well that there are many diseases that still cause so much hardship in this world. You mentioned long COVID but there are many others.
Modern medicine has solved so many problems and we have a lot to be proud of. I think AI is going to continue to help us to make even more of a dent, but there's still a lot of work to be done. It is an incredible honor that I get to spend every day working with scientists and colleagues to try to figure out how we can save lives with cures within reach.
Finally, what's so exciting about this approach is the turnaround time. If I were to develop a new drug from scratch, I would need at least 10 years and somewhere on the order of $100 million — maybe closer to $1 billion — to develop that one drug for a first disease. We can repurpose drugs and discover a new use for a drug and within weeks have a patient on that drug. Of course, the risk-benefit profile has to make sense. I don't think it's a good idea to ever do data-free repurposing; it should always be data-driven repurposing, and in the right context for the right patient.
The ability to reach out and help someone within weeks of discovery and to have drugs now approved for new uses and recommended after just a couple of years vs what would take so much more money and so much more time, it makes everything feel attainable. I think a lot about hope, because there have been many times in my journey where I was out of hope and I leaned on my family and my friends, and they gave me hope for the future and a dream for the future.
When I think about repurposing, at the end of the day, it's about saying, "There are all these drugs; let's create some hope here by actually tapping into these drugs." It may not be that there is a drug for your condition or that of someone you love, but if you look on the pharmacy shelf, trust me — there are a lot of patients who can benefit from those drugs. We just have to look for them.
Topol: That's another question. There are tens of thousands of conditions out there. And by the way, collectively, people with rare diseases like Castleman's account for tens of millions of people around the world. How do you prioritize? Obviously, you have a bent toward immunologic conditions or immunologic bases for conditions, but how would you say, "Okay, Every Cure is going for this one or that one. This drug looks so alluring." How do you make the call?
Fajgenbaum: It's a great question, and it's a tough one. We ran our first version of the algorithm and got 36 million scores, so every drug vs every disease. Of course, you look at the top and you say, "Wow, this makes sense. This drug works for this disease." You start going down the list. And to your point, how do you start choosing out of 36 million? Obviously, you don't want to pick the ones at the bottom because it's unlikely that they're going to work. But how do you pick out the top ones?
We think about it in terms of a number of criteria. But I boil it down to two. The first is the likelihood of scientific success. How clear is the mechanism? You think about long COVID, for example, and how the drug works and, maybe, whether there are some clinical data that already exist. What's the scientific evidence?
But then the second question is, what's the impact?
What's so cool about being a nonprofit organization through Every Cure and being in this position, being armed with all the data, is that we don't have to worry about whether the drug is going to be profitable in the new disease area. We don't have to worry about the cost of it. It's really about the impact. You can think about impact in terms of the impact for a given life. Will it be potentially transformative for a small number of patients? Or will it have a smaller impact across a larger population?
What is the cost of the drug to the healthcare system? You can start to factor in things around impact that drug companies, frankly, aren't able to think about because it's not part of their business model. Is it likely to help? That's where you have to build a great team and bring together a lot of great scientists.
I'll make a shameless plug that right now we're recruiting the best drug developers and the best data scientists in the world to be a part of our Every Cure team. We know we've got this great opportunity, but we need a great team to go through and make these tough decisions. Are we going to go after this disease or are we going to go after that disease?
Topol: I can see that you're creating almost unlimited opportunities by having this systematic approach. Then you want to have points on the board that Every Cure is actually curing some conditions that previously were not approachable or had inadequate types of interventions. What you're on to now is remarkable — this idea that many people have heard about and how AI is the hottest area in the life-science industry for drug discovery.
Fajgenbaum: Right.
Topol: There are 100 AI companies now with partnerships with all the major pharmaceutical companies. Each major pharma has, like, three AI partners. But the difference is that they're not much interested in repurposing drugs; they're interested in coming up with new molecules that can make billions. Is that a fair comparison? Or are some of those AI companies also competing with Every Cure?
Fajgenbaum: You're exactly right. We're using almost identical technologies, but those companies are purely looking for new molecular entities or tweaks to existing molecules. That way, there can be intellectual property. So if you take that approach and you have a new molecule you're going after and it looks really promising, get ready to spend $1 billion on drug development and get ready to wait 10 years.
We say, let's use the same technology, but let's point it at the drugs that are already at the neighborhood pharmacy where we can do a clinical trial for $1 million, for one one-thousandth of the cost, and we can get it to a patient tomorrow. I wonder, why is there this gap? It seems so obvious. The technology is the same, but if you apply it to old molecular entities rather than new ones, you have an incredible opportunity for immediate impact.
Your comparison is exactly right. There's always been this gap in our drug development system, and it's something I've spoken about a lot with Janet Woodcock and others at the US Food and Drug Administration. This thing that's a bit surprising is that that once a drug gets a first approval, surprisingly, that's when R&D starts slowing down for that drug. You would think that, instead, they'd think, We've got an approved drug, it's on the market; let's ramp up R&D; let's find all the additional uses for it.
But paradoxically they think, Now that the drug has its first approval, let's start ramping down R&D and let's go find another drug. As someone who's alive thanks to one of these old drugs, I think that's when we have to start ramping up and focusing on finding more uses. That's what we're trying to do with Every Cure.
Topol: I don't know that anyone could be more of a force or an icon. You are the picture of health. No one would ever believe that you were on death's door five times and went through all that you did. It is extraordinary. We're all indebted to you, David, you and the team you're developing at Every Cure to help accelerate the knowledge base for finding these medications that could help cure people and that, up till now, have not been assessed or identified and proven.
You've been able to get some great funding from key players out there. So, hats off to you. Big-time kudos. We're going to be following your story because it wasn't over when you wrote the book, Chasing My Cure, 4 years ago. Now, you're chasing everybody's cures. Thank you so much for all that you're doing. The team at Penn with John Wherry and Carl June — these are some real heroes. And to have you on as part of that, how does it get any better?
I know you're going to add more to the group. Watch out, folks and fasten your seat belts here, because a lot of good things are going to come out of this. Thanks for joining me today.
Fajgenbaum: Eric, thanks so much for having me. And thanks for those kind words. It's truly such an honor to be with you and to be a part of this podcast. As I said, I'm so thankful to be here, and I'm so thankful that I get to have the opportunity to find drugs so that more people can be here and experience all the amazing things in life.
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