How Breakthroughs Get Built: A Conversation with Steve Potts

Speaker A: Welcome to the Commons podcast featuring researchers, innovators, artists, entrepreneurs and community builders who are improving the human condition in your own backyard and around the globe. I'm your host, Tom Oshun. Today we're stepping into a part of the innovation economy where the stakes could not be higher and where the timelines test even the most patient builders. Biotech is one of the few domains where you can spend a decade, invest hundreds of millions, even billions of dollars, and still not know if you succeeded until the very end. And yet it is also where some of the most transformative breakthroughs improving the human condition are happening. My guest today is Steve Potts, CEO of Breakthrough Medicine, a company that's moving quickly into that high stakes arena with both ambition and credibility. Steve is not new to this. He is a serial biotech entrepreneur with multiple FDA approved therapies under his belt, which in this industry is about as real as it gets. You don't stumble into that kind of track record. You build it through pattern recognition throughout the through failure, and through an ability to see around corners that most people can't yet see. What makes this moment particularly interesting is that Breakthrough has just raised $60 million in Series A funding, one of the largest early stage biotech financings in the history of Phoenix. And that's just not a milestone for one company. It is a signal for the entire greater Phoenix bioscience industry. It tells us that investors are increasingly willing to to bet on new geographies, new teams, and importantly, new scientific approaches. And Steve is taking exactly that kind of approach. Breakthrough Medicine is built around what they call a patient first tumor agnostic model. Now, that may sound like insider language, but at its core, it reflects a fundamental shift in how we think about treating cancer. Instead of organizing therapies strictly around where a cancer originates, or lung, breast, colon, for instance, the idea is to understand and target the underlying biology that cuts across those categories. It is a move from classification to causation. And if it works, it has a potential to unlock therapies that can reach far more patients far more effectively. What's also compelling is the breadth of science they're pursuing. Molecular glues, small molecules, next generation antibody drug conjugates. These aren't incremental tweaks. They represent entirely new ways of engaging disease at a cellular level. And with that comes both enormous promise and very real risk. But here's where I think Steve's experience becomes particularly relevant. In a world increasingly driven by data and AI, biotech still depends heavily on judgment, on knowing which signals matter early, which programs to double down on and. And which to walk away from before time and capital are lost. That ability to pattern recognize success, or at least the potential for it, is something you only earn over time. So today we're going to explore that journey. Not just the science, but the mindset. What does it take to build a company in a field where failure is common, timelines are long, and the impact, if you get it right, is measured in lives changed and lives saved? We'll talk about Steve's path into biotech, the lessons he's carried forward from previous ventures, and the moment that led him and his co founders to believe breakthrough medicine need to exist. Right now we'll dig into the science, what new therapeutic approaches actually mean, and what they could matter in ways that go beyond the lab. And we'll step back and look at the broader system, the role of startups versus large pharma, the bottlenecks that still slow innovation, and where the next real breakthroughs might come from. Because ultimately, conversations like this aren't just about one company. They're about how innovation happens, how ideas move from hypothesis to therapy, from lab to bench, and from bench to patient bedside. I hope you enjoy this. Episod. Steve, welcome to the commons.

Speaker B: Great to be here, Tom.

Speaker A: Before we dive into breakthrough medicine, I want to start with your journey. What is one thing that might surprise people about the path that brought you here?

Speaker B: Thanks for that question. Um, you know, when we, I'm a cancer drug developer, um, we're a drug hunter. You know, we put companies together, we really work hard to develop cancer drugs. And when we, um, add new employees, we always ask them two questions. You know, the first is what's the earliest memory you have of cancer? And hopefully it's not a parent or a sibling. Um, but, you know, everyone I think can look back and think about when did they first hear this word cancer, you know, in a very negative, painful way, you know, whenever it came. And the second question is, we ask is, you know, who currently that has cancer or that, you know, hopefully not, but passed away of cancer is going to motivate you in our daily jobs because this stuff is hard and you're fighting cancer and you get a lot of scars doing this. You get a few successes and a lot of scars. Why I got into cancer, random walk is a common thing. I did an undergrad in physics, uh, Wheaton College in Chicago, spent six months in Central America, uh, doing healthcare in a rural area of Honduras, then went back to grad school, did a PhD in bioengineering, university Of California, Davis, um, actually in the biosensing area. Got super interested in bioinformatics, which was very new at the time, and just gradually got more and more into cancer. And I certainly had people, loved ones who had had cancer like we all have. And, you know, I came out in 1999 and even since then, so it's been 25 years. It's really interesting. What you see is, you know, when I grew up, like, there were no quote, unquote, you know, better than bad cancers or good cancers, where it's like, oh, you have that, but don't worry, there's plenty of drugs for that. You're probably going to die of something else. Or, you know, you've got 10, 20 years and a whole lot of. A lot of things you can do for everything was kind of a death sentence within a few years. And, um, you know, you look at something like multi myeloma that, you know, 99, when I finished my PhD, I mean, patients were lucky to live a few years, you know, and now, I mean, there are patients that will, um, you know, that will beat the disease will pass away or something else in 20, 30 years later. So it's been amazing to watch lung cancer in some extent. All cancers are like that. And so, you know, that's motivating for us. You know, the only good thing about cancer is that there's nothing good about it. And what I mean is that, you know, it wants to evolve. It doesn't care. It doesn't care if you're Republican or Democrat. You know, it wants to just eat and grow and take over your body and ultimately kill you. And so, you know, from that standpoint, it's good to have an enemy that's kind of the perfect enemy. You're not going to find anything. When you ever feel sorry for it

Speaker A: as a country, it seems like we're better when we have a common enemy that we.

Speaker B: Yeah, it is. I mean, you know. Yeah. I think Americans especially, you know, I've lived in three countries, um, in probably about six or seven years of my life overseas. And I definitely. Americans love the black and white enemy. We like to have an enemy that's easily identifiable, is entirely evil, and you can kill it and then move on.

Speaker A: Cancer is that. I think it was just a, uh, couple of days ago, your latest company came out of stealth mode with a, uh, $60 million raise. I think I saw. So tell me a little bit about breakthroug medicine. I think you emphasized patient first tumor agnostic targeting approach. What does that mean? For lay people not in the industry,

Speaker B: cancers are kind of identified by where you first see them, where the primary is, and whether it's lung cancer, breast cancer, colon cancer, prostate cancer. So that's how they get their name. What's happened is that these cancers, they're typically a mutation or something's gone wrong in the wiring and then that gives it an advantage and it just starts growing. So you have a nice lawn and you got a weed and it just starts taking over your lawn. So those weeds often are not specific to a given tumor type. They often will have kind of a genetic signature in them. And we're learning more about this every day. And frankly, we look back on this in 30 years, we're going to realize there's just a ton of weaknesses or genomic type signatures in these cancers we didn't know about. So think of it like you hear about the human genome. Well, tumors have a genome as well. They evolved and they just come up with different mutations, genes that are different than what is in your body. And then they're tricky enough they do just a little bit, enough to hide from your immune system, but not enough to keep them from growing like crazy and just, you know, taking over. So we will sequence these and we're looking for like, you know, things that are abnormalities, differences. And so it's not a whole gene sequence. By the way, if you're listening to this and you haven't heard and you have a loved one with cancer and they have not gotten a next gen sequencing report or a tumor genome, talk to your doctor, make sure they do. Or go to a center that's doing this, because that's really helpful. It's like a, it's like a blueprint for weaknesses. But those weaknesses are not tumor specific. Oftentimes, sometimes they are, sometimes they're not. But you can imagine there might be a weakness in a prostate cancer that might also show up in a sarcoma or bone cancer. If you think about that and you run it through, well, why are we only developing drugs for certain kinds of tumors? Why wouldn't we just do molecular driven cancers? So if you come up with a drug that works really well for some gene that is only expressed in one kind of cancer, but it shows up in lots of different tumor types, that's. You can then develop a tumor agnostic approach, where basically you're developing a drug for that gene defect, that mutation, then you just apply it across all the tumors. It's a little tricky to run because you might have, you know, breast cancer, lung Cancer, colon cancer, bone cancer, you know, altogether. But it's called a pan tumor approval. So, um, this is something that's grown a lot. There's about a dozen or so approvals this way. And it's been a really, um, you know, a really remarkable step forward. Um, so we're certainly big on that area. One of the challenges we see is that you'll have kind of a roadmap, some possible mutations, but there's no drugs for them. And the reason there's no drugs is because, you know, not everything is druggable. In fact, most things, about 90% of the protein, the machinery in the, in these cells are not druggable. Well, why aren't they druggable? Why can't you just, you know, this is 20, 25, develop a drug for anything? Well, if it's on the cell surface, so the, you know, the surface of the cell is. You can develop an antibody for that. It's accessible. Develop an antibody, goes in and binds to it. If it's internal in the cell, the antibodies aren't gonna work, the biologics aren't gonna get in. But you can do a small molecule. You know, think these are things like aspirin drugs, things you take pills. But it only works in a very small subtype of proteins that actually will bind that. And that's things like a, uh, kinase, typically. And so you have kinase inhibitors. So the cancer area is a lot of very successful drugs that are kinase inhibitors. It's a kind of protein inside the cell we can target. The challenge is there's a whole lot of other kinds of internal buried deep inside the cell. You can't hit with a regular, um, drug. So we're doing something breakthrough really, to, um, go after some of these novel modalities with kind of new approaches, um, to develop new drugs.

Speaker A: So one of the things I think you talked about in the release was molecular glue.

Speaker B: Yeah.

Speaker A: So that was very intriguing. What's that all about?

Speaker B: Typically, a small molecule will go in and it's looking for a cave. So you have a large protein, it has a cave, and the molecule just kind of fits right in that cave. That's how most of the kinase inhibitors work. That's how most of the small molecule drugs work. But the challenge is a lot of these things don't have these nice little accessible little caves to have the molecule go in. So a glue, what it does, it actually has two sides to it. One side will bring a partner or a presenter protein. And then with the presenter protein, it then binds to the cell. So what we're doing is actually gluing um, things together with using, leveraging what is already known in the human body. Um, the best example of this is really a remarkable set of drugs that revolution medicines is they're in late stage trials with uh, pancreatic cancer. It'll probably be one of the best pancreatic drugs in history. It's just a fantastic drug. But shutting down a target called Kras or Ras, and it's a glue. So half of it glues Kras and the other half, um, glues a very highly expressed protein that's just naturally in these cancer cells and also in normal cells. So it gets help from a presenter protein, binds it to the target and then shuts it down. So it's a non degrader glue. Super, um, exciting area, hot area. And we have a team that is very experienced at this.

Speaker A: Oncology is such a tough field. Right. The timelines are so long. How do you really balance this ambition of wanting new approaches with the reality of clinical and regulatory hurdles?

Speaker B: Yeah, I mean there's an answer for my specific company, what I'm doing, and then there's also just a, like a take a step back. So, you know, in this field we're like any field, there's sort of this everyone knows thing, you know, and it's right 90% of the time. So at that time in 1999, everyone knew, every investor, every good drug hunter, that there was no point going after lung cancer. Lung cancer is where biotech companies go to die because lung cancer was just too tough. We didn't understand the targets. We didn't have people getting molecular sequence for their tumors. We didn't have that information. We didn't know what the weaknesses were in lung cancer. But they came out with one drug, Tarceva, uh, back in 1999, the first really good lung cancer drug. And so since then, the last 25 years, there's a ton of lung cancer drugs and there's areas of lung cancer, um, certain subsets where you can live for, you know, a long time with, without the chemo, chemo side effects of these drugs. So from, if you zoom, you zoom out on this and you look at various tumors over decades, they go from everyone knows there's no point developing a drug for this. And the corollary for a patient is this is a bad cancer, this is pancreatic cancer, this isn't prostate cancer. You know, you have months, um, and you know, there's been some amazing leadership here in uh, in Arizona. Dr. Rafael Fonseca. Mayo talks a lot about this and just paints the history of um, in the, in the area of multimyeloma. That's a blood cancer that was, that was a death sentence. You know, when I was PhD time or earlier, that was a death sentence. You had a couple years and now, I mean it's amazing what we've done. And so people just now just say, well, that's a better cancer to get than like aml, which is really just still a nasty, nasty blood cancer, super aggressive. Why is it different? Well, because a whole bunch of people like me, investors believed in us drug hunters got together and worked really, really hard to take shots on goal over, you know, decades. And then you get a whole arsenal of drugs. So we forget that this concept of like, well, it's a better cancer than that cancer. It's because a whole lot of drugs have been developed against that. Investors took bets and we had a really good biotech ecosystem to make those bets. So they knew they could get their, they could make an investment and get a possible return even in a very risky area. So when you take a step back on this, it's really amazing that you have this ecosystem in place that is by the way, very American driven. I am, I am massively proud of this industry. Um, it is an American, American driven industry. We obviously have great work from all over the world, but this has been a, an American contribution to the world, um, for what we've done, you know, in, in drug development. So that's kind of the high, you zoomed out picture. Right? You know, and so zoom in. A little optimistic. So then you zoom in here and I sit with investor. I say look, we're going to bring this team together. Um, you know, if you look at our group, we have about 10 full time employees and a whole, a whole, you know, amazing set of, of about 40ish people of our various connections and partner labs, things like that. But of the 10, you know, we added it up and we have about 13 either approved or late stage drugs, you know, somewhere in our career. It's actually pretty good. I mean I've been involved in kind of one and a half drugs and I kind of sort of use the criteria like if you didn't exist, would the drug have gotten over the line? And you know, there's always someone else that maybe you don't know, but might have done it better if you weren't there. But I think that's the kind of criteria I'm looking for. Like, you know, um, and so we have 13 approved drugs. And then, and then eight of those are actually breakthrough designation, which is kind of where the word comes from. And I'll explain that a little bit, what that means, why that matters. And um, you know, you, you, you basically pull a team together, you have a mission of what you're going to do, and then you have to go to investors and say, look, you know, we, we want you to invest in this. There's, um, a huge unmet need. You know, you're going after these areas where there are not good, you know, enough good drugs. Um, you think about pancreatic cancer, you think about colon cancer, you think about gbm. I mean, and even the ones where there are good drugs, there's still lots of areas. So much work to be done. Um, so you get an investor and you make a pitch and um, I call it Shark Tank for nerds. You really have to have very good story. You have to have hopefully a track record and a very well thought out plan. But the investors are the ones that have to lay out capital now. And it costs, it's over a billion dollars. It's more than that. You can debate exactly the number. It depends if you include all the failures or not. But it can be over $2 billion to actually get a drug fully approved.

Speaker A: Um, but how long does that take? What's that timeline? From bench invention to in a patient,

Speaker B: there's two points on there that are basically FDA driven. And there's a third point that I think is really important for the audience to know. It's what we all talk about. We're trying to teach drug development to others. The two points that are really driven by the FDA are the NDA, which is you have the authorization. You make claims that are demonstrated in hundreds of patients of cancer patients who've taken this drug. And you're carefully controlled, carefully regulated, that you're making a claim that this drug does this to this cancer. And then they give you an approval, an authorization to market that drug. For a, uh, small molecule, it's called an NDA. And for a biologic, like an injectable, it's called a bla. So that's kind of the end. And then if you work backwards, it can take you 5. It can be anywhere from 3 to 10 years of clinical development work before you have an approval. I was lucky to work on a drug, a tumor agnostic drug, um, in the Trek space, um, that was actually very, very fast to get approved because the response rates were so high and also because the pan tumor approval approach. But that Was like three or four years from. In the clinic before we got approved. Um, the other key point before that is called an ind, and we probably should have easier nomenclature for the American living room, but you're stuck with it. Um, the I stands for initial new drug application. It should be called inda, but it's not. It's called ind. We all call it that. And what that means is. And that's actually a really big bar. It means that for the first time, you're going to request to the fda, are you. Is it okay to give this to patients to test inpatients? It's actually a super high bar because that drug has never been in patients before. And so we will do before that. You'll test it in cells, you'll test it in a number of animal models preclinically. And that's really where you learn what the drug is doing. And the whole way through here, you're balancing two things. You're looking at efficacy. Does the drug do what it should do? And then toxicity. How bad are the side effects? Um, and every cancer drug has to be incredibly. It has to kill cells. Otherwise, the worst thing we can do is not have the courage to develop a drug that's really lethal against cancer. The last thing you want is you're a patient, and you've been. Say you're a breast cancer patient, and you've been through 15 lines of technology of all these really good drugs that work for a certain period of time, but then the cancer keeps evolving. So you might kill 10 million breast cancer cells, but there's just a few that have the right mutation to kind of escape that drug. And so those all reproduce. And then six months later, you have an immunity to that kind of drug. So then you move to the next therapy. So you have whole lines of therapies. But after you exhaust those efforts, you then turn. If you're at a good cancer center, you will then turn to clinical trials. And so the last thing you want is to be testing in clinical trials something that isn't super lethal against the cancer. So the efficacy bar has to be really high. But the question is, like, how much room do you have between that and the toxicity? And people all chemo. You know about toxicity. These targeted agents are really cool because you typically are looking for. For things that are in the cancer that are not in the normal cell. So you can get a higher. We call it a therapeutic index, but something that's very highly expressed in the cancer you don't see in any normal cells. So it's just going to wipe out cancer and leave all your normal cells alone. That would be a very high therapeutic index. So the whole way through, we're balancing efficacy. Toxicity takes a long time. Um, the other thing, like, you know, it's easy to say, well, why do these drugs cost so much? And where does all the spend go? Well, most of the money actually goes in a clinical trial. And I remind people of this. You know what we spend per patient in cancer, on average? Um, you think about it might take several hundred patients to develop enough data to prove the efficacy claims in a drug. Um, we spend about $250,000 per patient. That $250,000. I mean, it goes to. We have amazing centers here in Arizona, but it goes to things like Barrow Neurologic Institute. They've been pioneering brain research for decades. Mayo Clinic in Scottsdale. Um, um, I mean, there's Honor Health. Um, I'm missing a few other good ones, but there's just some great history. But these are the centers that basically are. And it's because they have to check everything after very careful. You get actually better care on a clinical trial than you do even in regular care, because we're having to be so careful whether you're getting standard of care or our drug. You're getting scans every month. So a lot of the cost of our drug development is actually back to clinical. You think about how expensive when you get cancer. You know, you have MRIs, CT scans, so many different things. Hospital visits, infusions. Um, all of that we have to pay for too, if we're going to, you know, for each of these patients. So honestly, for us, the cost of healthcare is actually a big part of why our drug development costs are expensive.

Speaker A: Makes sense when you follow that logic. My wife was part of the, uh, clinical trial for Keytruda when, uh, used against triple negative breast cancer. Remember, every time she went in, there were this long process that she had to follow so that they could track her very successful outcomes.

Speaker B: And that's been a great thankful for

Speaker A: these kinds of Tara.

Speaker B: And that's a great example so that you forget quickly when something works. Everybody knew for decades immunotherapy wouldn't work. Everybody knew. And there were a few warriors that kept at it. And, you know, there was even pharmas that had whole drug programs that they shut down that, you know, we're almost there, but not quite. It's a fascinating story. You can, you know, there's. People have written about it much better than I'm going to speak about. But it's another example of we now are like, well, of course you can try immunotherapy. It can work really well in up to 20%, you know, of certain tumor types, and it doesn't work well in others. And when it works, it can often be curated, which is amazing. But you're turning your own, you're getting, you're basically just waking up your immune system, you know, to fight the cancer.

Speaker A: With these long timelines that it takes to bring these drugs to market, how was it that we were able to shorten that timeline considerably for the development of the COVID vaccine? About 18 months, I think, or so.

Speaker B: It was amazing. I mean, there was a reason why it was called Operation Warp Speed, uh, some of it serendipity. I mean, there was several companies. And again, you can find some really good resources. The story is worth hearing, I think on actually your podcast. I think you talked to someone that had been fundamental to this. So I refer you to that if you want the full details, not just the potshot on it from me. But, um, the long and short of it is that there's companies have been working on this for more than a decade. It was kind of ready and actually wasn't working in other vaccines. And Covid just happened to be a really good fit for it. To do something like that in 18 months was crazy. And I know people, I know some Arizona people that worked. They say, steve, I was working like 247 to get this done. You think of all the logistics, it was cold chain. It kind of breaks my heart when I see people say, you hear people talk about needle rape. It's amazing. People listen to them. It's amazing. And give them m. Any airtime when you know what an impact these vaccines can have. And so for me, the best thing we could possibly do, uh, is a vaccine because a drug you keep taking. And our goal is to of course have a drug that's curative, but the cancer often finds ways to evolve. So some of these, some of these vaccines, like the, um, HPV vaccine that gets seven to 11 different kinds of cancers that are caused by HPV virus, to have a vaccine that is. And you see some data for some of the Scandinavian countries where they track millions, these are million patient data sets and they're tracking them and they see just jaw dropping numbers in terms of how much, um, those vaccines are going down. You see the shingles virus recently, that seems to be, it wasn't developed for this, but it seems to be having a real, real, a real major impact on dementia, which is kind of like, huh, huh, interesting. So for me, like, vaccines represent really the pinnacle of drug development. And so, yeah, I do get a little upset when I see people talking about them. Also, I'm a polio. Polio on our family, um, it decimated, you know, two generations back. And they know what a difference polio vaccine make. What's really interesting is that the same problem we have with cancer, we have with vaccines. Whereas if you do a great job and you completely eradicate multiple myeloma, for example, we're almost there. Or the work we're doing on, um, prostate cancer, some flavors of breast cancer, if it's gone, people are like, well, what was that? What are you talking about? Why is molding women? Haven't heard of it. Same thing with these polio rubella mumps. We're like, that doesn't. Because none of us have seen it because they work so well.

Speaker A: So do you see that? Do you think the pace of innovation is accelerating? Or will regulatory, scientific, or maybe I will even put in cultural challenges still be limiting factors to where we go?

Speaker B: It doesn't take much to kill innovation. Forget we benefit from the tree, the shade from the tree, than the tree that was planted by somebody before us. And I think that's true in this space. I am super grateful for the work that a lot of other people, a lot of the volunteers did to ensure that we had an environment where investors could make an investment and know that they would get a return that is not based on politics. I mean, imagine if you're not only you're trying to bet on me, my team, all of us trying to develop a drug, but you're also having to bet that the right party would be in office with the right set of politics to get that particular drug over the line or that particular area, you know, in flavor or not in favor. So, you know, we've done a good job historically of like keeping the partisanship out of cancer drug development, out of cancer funding. Um, but, you know, and I want, you want to see that continue. So, yeah, I think that the changes in the policy really have a huge impact, um, on whether things get funded. I first got involved in policy not because I wanted to, but because I really could not get a small molecule drug funded a couple years ago as Arizona company. And normally it would have gotten funded, but there was a, um, there was a clause in the ira, the Inflation Reduction act, that basically really was. It's still there today. It means you have a much lower return if you have a pill than if you have an infusion? Well, infusions are in hospitals and they're a lot more expensive than taking someone at home or in a clinic. And so you completely rewarded the wrong behavior. And anyway, it was a nine year return instead of 13, but it just up blew. Big picture shows you that if you really start to encroach on free enterprise and pricing and the patent life that has been set up, investors are smart. They're like, well, why would I invest in that?

Speaker A: Yeah, they'll chase the returns.

Speaker B: Yeah.

Speaker A: What motivates you to take on these hard problems?

Speaker B: Right.

Speaker A: Where while we are making progress, there's so much progress to go. How do you stay motivated? And, and what would your advice be for aspiring bio science and biotech entrepreneurs to keep pushing, uh, so that, so that in 20 years we've made strides equal to what we've done in the last 20, hopefully accelerated.

Speaker B: It's patience. Right. And a few times in your career you have something, you go, I'm going to remember that story my whole life. And I had one. I was at uh, I was at Barrow Neurologic Institute. One of the top, it's Ivy Brain Center. It's just a great, you know, for decades it's been one of biggest, the best brain center research areas of the country. And they do both neurodegenerative as well as cancer research. And we had put a drug there that was a pan tumor, pan agnostic drug. And it was going against the gene called track. And it was truly like a. This week the doctors call this kind of a Lazarus patient where you see great responses if um, they have a certain kind of gene. But the problem is it's very rare. But one of the doctors stopped me in the hall and he said, oh my gosh, I had a patient with a brain cancer and I've, you know, we had that mutation. We gave him that, you know, the drug. He said, my drug. Which isn't fair. I'm probably like, if it was, this is a, if this is a movie, I'm like page five of the script of the credits. There were certainly some Steven Spielbergs on that drug, but I'm on, I was probably the key grip on page five. But I was certainly on the, you know, on the script. I did my role, but he stopped me and said, hey, your drug, um, I've never seen a tumor shrink like that. This patient, the brain went from this massive swelling, it shrunk down the pain and the patient had like, you know, another couple years, a year and a half of like, really good quality life that they would not have had, um, you know, otherwise. So that's the kind of thing that that keeps you going.

Speaker A: So, final question, uh, that I've been asking this season, uh, tell me, what are you reading currently that you're enjoying, that you think you'd like to share with others? And is there anything that you're listening to or to or watching, uh, that you suggest others take a look at now?

Speaker B: That's great. Um, I really have always enjoyed, um, Derek Lowe's in the Pipeline blog. He's a guy who's a med chemist. He's buried deep within a large pharma company in Boston, but he's a great writer. And so if you want to learn drug development, I encourage you to start reading that blog.

Speaker A: I'll put a link in the show notes.

Speaker B: Um, the other one is there's a group called no Patient Left behind, and, um, that's most of volunteers and really trying to work hard to help Americans understand drug development better and also just really fight for preserve the ecosystem that we have.

Speaker A: Well, thank you so much for spending time with us today, taking us through what some might consider a hard topic, but certainly one that has so much promise and has already delivered so much value both to our country, as you rightly point out, and to families, to patients, to everybody touched by cancer. The future continues to look brighter because of folks doing the great work that you're doing. So thank you so much.

Speaker B: Thank you. We have a ton of work to do and, you know, think the best if we can just continue to preserve a pro business, pro medicine, pro science environment here in Arizona. It just helps all of us do our jobs.

Speaker A: Amen to that. My guest this morning has been Steve Potts. He is a serial entrepreneur and currently the CEO of Breakthrough Medicine. I'm Tom Osha and this has been the Commons. The Commons is a production of Wexford Science and Technology, llc. Views and opinions expressed are solely those of the host and guest. To view additional material about today's episode, submit questions or story ideas or learn more about Wexford Science and technology, please visit www.wexfordscitech.com thecommons. I'm your host, Tom Osha. Thanks for listening, Sam.