Great to see you guys. The last time was over a pizza.
It was in Chicago.
Indeed. Okay, let's get underway here, and welcome to the Goldman Sachs conference presentation this afternoon with Boundless Bio. We are very happy to have you guys here with us. It's your debut presentation since the recent IPO, CEO Zach Hornby and CFO Jami Rubin. Thank you to both of you for joining us. Let's tell a story. I think let's create an opportunity for people to go on this journey that you have been, because there's some novel, actually, it's really cool science that is trying to endeavor in ways that I think have not been precedented, and therefore that's a challenge, but investors, that is an opportunity.
And when you have this, you have to have people who have a certain mindset, and a dedication, and a relentless understanding of the pursuit of the scientific genesis, which is really where this company comes from when you think about the founders, and we'll talk a little bit about that as well. But at the same time, public equity investors wanted to be equipped with folks who have sat in these roles, public company C-suite, and know how to wear the hats but also walk the walk, have been through difficult decisions and times, made those difficult decisions, navigated through that. And so I think that is a really relevant and important aspect of what should hearten investors as they take this combined quest of going after something very novel, very innovative, potentially very transformative, but essentially, who's behind the wheel?
It's a couple of folks, and there's some people on your team as well who are not here, who are very equipped to do that. So maybe as an introduction, Zach, tell us about yourself and what brings you to this moment on the stage, but really as CEO of this company.
Great. Well, first of all, thanks, Chris, for hosting today at the conference. So yeah, Zach Hornby, CEO of Boundless Bio. I've been working in the biotechnology industry for about 25 years, various operational roles, everything from business development, to regulatory, to finance, to commercial. But I've spent about the last 15 years in oncology and, in precision oncology specifically. And so prior to Boundless, I was with a company called Ignyta from its inception, ultimately through its acquisition by Roche, including, the development of a now globally approved precision oncology drug called Rozlytrek. And so I have an extensive background in precision oncology, and I'll, I'll come back to that in a minute with further questions, but I'll leave it there for a moment and have Jami introduce herself as well.
Yeah. You look really familiar somehow. But Jami, you know, I think you look really familiar to so many different people in different domains, and it is almost a source of fascination. And I have to ask you then, you can do kind of so many different things that you would want to do. You chose Boundless.
Mm-hmm.
Talk about that decision-making for yourself, and also why are you here with us?
Yeah, sure. And again, thank you so much, Chris, for having us. It's a real pleasure to be here. Why Boundless? I chose Boundless for a, a handful of reasons. Number one, I am very attracted to solving big problems. My whole career on Wall Street was... I was attracted to big ideas, and transformative ideas, and shaking things up, and, you know, Boundless, the science at Boundless, which we'll get into ecDNA, is very novel, but really interesting and exciting and explains so much about what we don't really understand about cancer, why tumors develop resistance. And ecDNA represents a root cause as a driver of that big problem that the industry has not really solved. I was very attracted to the science. If we're successful, we have the potential to create a whole new class of cancer therapeutics. That's pretty cool.
Mm-hmm.
Nobody else is in this space.
Mm-hmm.
And it's, you know, oncogene amplified cancers is a big unmet medical need, and we're really the only company addressing that big white space in the market. So big TAM, if we're successful, really interesting science. And as you said so eloquently, we have a strong, experienced management team, and who's been there, done that, has, you know, seen understands that developing drugs is not easy, it's not linear, and, and they've been there, they've done that before. These are the group of people who have sold companies before, so I was very attracted to that. And lastly, the syndicate of investors. Very sophisticated investors attracted to the story. So all these things came together for me to make sense, and, and Zach's a pretty good guy, too.
Pretty good.
Exactly. Yeah, no, I think it takes a certain amount of boldness and smart money, which you've had throughout the journey for the company to be able to understand and nurture some of the ambitions that you have here. And is the reason why in a, you know, the fourth year of a certainly imperfect tape for companies to go public-
Mm-hmm
... you guys got out there and you're here with us and continuing to, you know, advance the pipeline and pursue. So ecDNA, I felt badly that I had no idea what this was before I met you guys. But it turned out during investor education that there were a lot of really smart people who had no idea either.
Yeah.
So Zach, tell us about ecDNA.
Sure. And, and maybe I'll just rewind one minute before I even get into ecDNA. So I mentioned my background in precision oncology, and the reason that's relevant is I think probably most people at this conference have borne witness over the past couple decades to the power of precision oncology.
Mm-hmm
... the ability to advance targeted therapies and the substantial benefit they can have on certain types of cancers. What we've observed, if you look a little bit more carefully at where targeted therapies work and where they don't, they work exquisitely well in patients whose tumors are driven by gene fusions. So think ALK, ROS, RET, TRK, FGFR, talking 60%-80% response rates, long durability. They also work very well in patients whose tumors are driven by activating point mutations, insertions, skipping deletions, things like EGFR, L858, BRAF V600E-
Mm-hmm
... most recently, KRAS G12C.... but there is another more frequent driver of tumor than all of these fusions and point mutations combined, which is oncogene amplifications. And so these are tumors where there isn't a mutation to the gene sequence of an oncogene, but instead there's too many copies. That's what amplification constitutes. And now, these exact same targeted therapies that work really well for fusions and targeted therapies suddenly don't work for amplifications. And actually, with the sole exception of HER2 inhibitors, there has never been a single drug approved for any oncogene amplification in any tumor type. We're talking 25% of all cancers, more than 1 million patients per year. So we start with this huge unmet need.
Yep.
Our scientific founders and really led by a gentleman named Paul Mischel, who's vice chairman of research in the pathology department at Stanford, he was really motivated to try to understand why don't targeted therapies work in these patients with amplifications? The amplification is a strong driver. One would think intuitively that if you inhibit that protein product from the driver, that that would cause the cells to die. But when he tried this in multiple different tumor models, what he realized was there was something different about oncogene amplification biology relative to other types of mutations. And that, that distinction is that generally, when gene mutations or gene fusions occur, that is on chromosomal DNA, the DNA that we all learned about in high school biology. But in cancer, where there's amplifications, frequently that is not a chromosomal DNA event.
Instead, those amplifications are occurring on these cancer-specific units of DNA that are circular. They reside inside the nuclei, but they're not on the chromosome. They're adjacent to the chromosome. And so these circles of DNA are called extrachromosomal DNA or ecDNA. So to your question, what are ecDNA? They are cancer-specific circular units of nuclear DNA that are the primary site and mechanism for high copy number oncogene amplification. And these ecDNA have a couple unique properties that really help explain why they are so oncogenic in nature, and also why they are resistant to traditional targeted therapies. And those two key features are, one, that these little circles of DNA are highly accessible to the transcriptional machinery, meaning that they give rise to a high level of gene expression and ultimately to a lot high level of oncogenic protein.
So they're very active in spewing out oncoprotein. That's one. And number two, perhaps even more importantly, is that chromosomes all have centromeres, so that when cells go through division or mitosis, they first align to the center of the cell, and then they get evenly pulled to the poles. And so when two new cells are created, they each have the same number of chromosomes. And that's how, in a multicellular organism, every cell is identical in genetic code. But these circles of ecDNA, they lack centromeres, so that when mitosis occurs, they do not get evenly lined up and then distributed to the daughter cells. Instead, they get asymmetrically or randomly distributed, such that some cells get more copies, some get fewer, and that compounds over time with each successive cell division.
And so what this ultimately gives rise to is you can get exponential increase or decrease in copy number of any genes encoded on these ecDNA. And so when you have a bulk population of tumor cells, of thousands of cells, each cell is genetically different than the one next to it, meaning that each cell has a unique fitness advantage, where under selective pressure, be that chemotherapy, radiation, targeted therapy, some cells are gonna have a natural ability to survive better than others, and those that do become dominant resistant clones. And so these features of ecDNA explain why they're so oncogenic in nature and why they are so difficult to treat, because they can become resistant through their genomic heterogeneity.
That's a fantastic explanation of the science. Now, let's take it to the journey of thinking about turning this into an enterprise and the structure around that. You did bring up precision oncology, and we often think about needing to have a framework. You have a proprietary framework for that, and then there are also tools that help you prosecute that and almost become harbingers to the way you may commercialize with the diagnostic component. Tell us a little about the proprietary Spyglass-
Yes.
as well as the tools.
So Spyglass is the moniker for our platform, and because this is a new area of biology, we knew as we set up the company that we needed to really understand this biology. How, when, where, why do these ecDNA form and perform? But this wasn't an academic exercise. We really had an end goal in mind, which is, if we can understand how these culprits work, we could also potentially identify vulnerabilities that accompany them, because as I mentioned before, they are unique to cancer cells. These are not a feature of healthy cells. And so we set up our Spyglass platform to try to answer a simple question, which is: targets, which when inhibited or knocked out, would kill cancer-bearing cells that have ecDNA, but would spare cells that do not have ecDNA?
Platform to identify unique targets that kill cancer cells with ecDNA.
And then there is this process of thinking about turning this into a molecule that you select, go after patient populations. It seems the scope is extremely broad, as you talked about, in terms of amplified oncogene-related conditions. Talk about the targets that you've chose. We have a proprietary pipeline here. The first one goes after CHEK1, BBI-355.
Yep.
What enabled this to be the lead asset?
Great. Now I'll drill a little bit more into how the platform works. Spyglass consists of a unique library of cancer models that we have assembled or acquired, and then exquisitely characterized, alongside a set of proprietary tools that we have built to identify them, monitor them, quantify them, characterize them. These models, which are now hundreds of in vitro models and dozens of in vivo models, they all have oncogene amplification, but some of them are on ecDNA, and some are not. We basically bin the models into ecDNA positive versus ecDNA negative.
We then apply our tools, and with the goal to run controlled experiments, where we can, for instance, go across the entire genome with a CRISPR screen and knock down every single encoding gene one at a time and ask, "Okay, which genes, when knocked down, kill only the ecDNA positive cells and not the ecDNA negative cells?" So that is one type of screen we run, but we run multiple different modality screens, always asking that same question. And of course, as we ask that question in an unbiased way, we start to see patterns in the answers. Certain targets arise again and again as being common to always synthetic lethal in the ecDNA-bearing cells. And so a few of the targets that have arisen, we have ultimately validated across multiple different in vitro and in vivo models, representing different onco drivers.
For instance, EGFR, FGFR, KRAS, MYC, CDK4, CDK6, et cetera, and also different tumor types: sarcomas, glioblastoma, colorectal cancer, lung cancer, gastric cancer. And so we identify these targets through these unbiased... But we ultimately validate them only if their effect is reproducible across multiple tumor types, multiple drivers. Three of the targets that have worked their way to the top and, and are the, components of, of the pipeline that we featured publicly so far. The first is called CHEK1, which is actually a known historical cancer target, but to this date, has never been successfully drugged through to market. The second target is called ribonucleotide reductase, also a known target, but there are no approved oral selective RNR inhibitors. And then our third target is a kinesin, where we haven't revealed the specific one yet, because it's a first-in-class target. It really identified on this.
But each of these targets impacts a different component of the ecDNA. You might think about ecDNA in terms of formation, transcription, replication, repair. These are all potential intervention points in the life cycle of ecDNA, and we're agnostic as to where or how we intervene, so long as it ultimately dismantles the functionality of the ecDNA and their oncogenic processes. So CHEK1, the lead program, BBI-355, we have found is involved in the replication and transcription of ecDNA. And when we inhibit CHEK1, it renders ecDNA transcriptionally inactive, so they can no longer express oncogenic protein. The second target, RNR, which is the target of our second clinical program, BBI-825, is involved with the assembly and repair of ecDNA. So when we inhibit this target, it actually depletes the ecDNA themselves.
And then the third target, the kinesin, is involved with the segregation or localization or movement of ecDNA during cell division. And what we found is that when we inhibit this target, the ecDNA don't properly move to the right spot. They aggregate, which ultimately leads to death of those ecDNA-bearing cells. So this gives you a sense that we're impacting different areas of biology, but with the ultimate end goal of rendering the ecDNA non-functional.
I recommend that people listening to this webcast turn to the corporate deck, because so much of this, very helpfully demonstrated in terms of the visualization of the cell cycle and bears how you're, you know, looking to attack this from all the various angles. You talked about being agnostic to whatever path that is chosen, and therefore, you're attacking it from all these different ranges. CHEK1, unprecedented. Talk a little bit about the science and industry's efforts. What has been the challenge?
Yeah. So many companies historically, over the past couple of decades, have identified CHEK1 as a potential target. It, it is known to be a cytotoxic target, and companies ranging from Merck to AZ to Genentech, Pfizer, have all tried to develop CHEK1 inhibitors. Most of them have failed. That said, CHEK1 inhibitors have demonstrated single-agent antitumor activity in the clinic, and sometimes actually quite robust or durable. But the problem is, those single-agent responses were somewhat few and far between, and historically, nobody was able to link who the responder patients were, or more importantly, be able to predict and therefore enrich for a high response rate. Meanwhile, if you dose a CHEK1 inhibitor high enough, you will ultimately get toxicity-
Mm.
hematological toxicity, neutropenia.... So all of the prior developers ultimately discontinued their programs because that risk-benefit ratio in an unselected population, they are going up to MTD, encountering toxicity, but were having relatively low response rates. So that's the history of the industry. For us, as I mentioned, CHEK1 arose organically through our screens, and a light bulb went off for us, which is, if we know CHEK1 inhibitors can have activity, and if we're seeing that ecDNA is a root cause of replication stress, which is CHEK1's role to intermediate, then perhaps ecDNA becomes the predictive biomarker. Perhaps we can identify patients whose tumors are characterized by ecDNA, and therefore have high replication stress, and therefore would be exquisitely sensitive to CHEK1 inhibitors.
Maybe this will now be the angle to identify the responders and no longer need to dose up to toxic levels of this agent. So that's the overarching thesis, is that with the right biomarker, you can enrich the response rates, but you can also identify a population whose tumors are more exquisitely sensitive to this mechanism, and therefore don't require such high doses that might be associated with toxicity.
So let's take it now to where you are. You're in the clinic. I do wanna also ask you to make mention of the diagnostic ECHO-
Yeah
Because this threads into some of the design strategies that you have for the study. So tell us about ECHO.
Great. So ECHO is an acronym for our diagnostic assay, internally developed. It stands for ecDNA Harboring Oncogenes, so that's the ECHO. ECHO is a proprietary algorithm in a software that we developed. And the reason I use those words is it does not involve any kind of new machinery or wet lab techniques. But what ECHO does is it takes standard sequencing data that's being generated on targeted oncology panels. Think something like a Tempus panel, a Caris panel, a Foundation Medicine panel, where when those panels are run on patient tumor biopsies, they generate an output data, which is a BAM file or a FASTQ file. Our ECHO software ingests that data and interprets those data in a different way that has not historically been done, such that we can see whether the DNA reads are constituting these circles of ecDNA.
So we use this software to find ecDNA in standard sequencing data. The reason that's important is we made a strategic decision that we wanted to be able to adopt into standard patient care. Today, in the developed world, many patients' tumors are sequenced on these targeted panels. So we are not disrupting any kind of patient flow, pathology flow. We're not introducing any kind of new biopsy or anything like that. We simply have a software that can sit on top of these diagnostic workflows that already exist.
And that acknowledgment is a real flex in terms of what we talked about at the very beginning, having executives who sort of can understand having the end in mind and are not just sort of just being beholden to the science. The practical aspect of thinking about the application and understanding the workflows is just really essential for thinking about mapping out how this could be utilized as a tool in the real world for these very real problems. So I think that's important. So we've already established that Boundless is a group of people who... You know, I guess there's an expression, "We can do difficult things." I would argue that your expression is more like, "We thrive on doing difficult things." So let's talk about the clinical trial, because basically, maybe the mantra for that is, "We thrive on multiplexing.
Right.
It's a couple of different groups. Help us understand that. As much as it's gonna take work to understand what these are, the investors should feel good about the fact that there's not a binary event, that there's actually a, a range of optionalities from which you will learn, and therefore the probability of success, success being defined by finding paths to continue to go further. Talk about the trial design.
Sure. Thanks, Chris. So the trial design for our BBI-355 program, this is a first-in-human, Phase I/II study in cancer patients. It has a 3-part design. The first part, which is called Part I, is your classic single-agent dose escalation to identify the safety, tolerability, pharmacokinetics, pharmacodynamics, maximum tolerated dose, and recommended Phase II dose of BBI-355. Once we have the recommended Phase II dose, Part I also expands to evaluate single-agent efficacy in patients with either high-grade ovarian cancer or endometrial cancer with an oncogene amplification. So that's Part I. That's solely looking at single agent. We have also now entered Part II of the study, which is co-evaluation of combinations. And within Part II, there are three cohorts.
The first cohort is patients whose tumors are driven by a wild-type EGFR amplification, and in this setting, we are administering BBI-355 with a wild-type EGFR inhibitor, and specifically, the best wild-type EGFR inhibitor is erlotinib. Sometimes people say: Well, why wouldn't you give, like, osimertinib or a later EGFR inhibitor? Because those agents have been specifically designed to be mutant selective and not inhibit wild type. But amplifications are of the wild-type gene, and therefore you need a wild-type inhibitor. That's Cohort I, EGFR amplifications administered with erlotinib.
The second cohort is patients with FGFR amplifications, which actually could be FGFR one, two, three, or four, and therefore we are co-administering with a pan FGFR inhibitor, which is futibatinib, an approved agent that's being supplied to us under a supply agreement by Taiho. And then the third cohort, which we have not initiated yet, but this will be looking at patients with either CDK4 or CDK6 amplifications, where we are co-administering with a CDK4/6 inhibitor, abemaciclib, which is supplied to us by Eli Lilly under a supply agreement. So within Part Two, we will dose escalate our agent, plus these combo agents, to come up with a recommended Phase II combination dose that's well tolerated with both agents. And then we will go into Part III of the trial, which is a dose expansion under a Simon two-stage design, where we will be looking for efficacy.
These are tissue-agnostic baskets, so a patient with EGFR amplification could have gastric cancer, esophageal cancer, colorectal cancer, head and neck cancer. For FGFR, it's similar. And then in this Part III, we are also going to be enriching for patients whose tumors not only have amplification, but specifically have amplification on ecDNA as detected by our ECHO diagnostic.
Clearly, the task at this stage is to think about dose, dose selection, identifying what is optimal. I almost used that, that word in terms of, like, Project Optimist and the, the necessity of trying to really establish what is as correct as possible, where you can be. But also, we talked about CHEK1 and the, you know, the, the known risks. And then when you're immediately talking about combinations, CDK4/6 as well, the potential for overlapping hematologic toxicity.
Right.
So talk to us about how you're thinking and your confidence in finding that therapeutic window, because I think that's one of the learnings that'll be key from the dataset that's coming.
Right. So one of the things we publicly disclosed through our S-1 process and IPO roadshow is that as predicted, as we dose escalated, we encountered on-target toxicity for this class, which, as I mentioned before, is hematological toxicity or neutropenia. So we dose escalated. And by the way, we administer our agent every other day because it's got a long half-life of 40 hours. So by administering every other day, we actually get constant target suppression. We dose escalated from 20 mg to 40 to 60 to 80. At 80, that's where we encountered dose-limiting toxicity. But our 60 mg dose was well tolerated and gave good pharmacokinetic exposure that was in the range associated with activity in our preclinical models. Also showed signs of on-target pharmacodynamic engagement. So we determined 60 mg every other day to be the maximum tolerated dose.
And so that is the MTD with 60 mg. And then, as we went into the combination arms, to be safe, we stepped down 1 level.
Mm-hmm.
We started escalating the combination arms at 40 mg every other day.
Okay. And remind us when we're going to actually see some cards turn over, and very importantly, and I think relevantly and smartly, what the N in the denominator of patients that you're studying?
Right. So for this program, what we've stated is that we expect to have preliminary clinical proof of concept data by end of this year, and that could be from any of the arms I've just mentioned. It could be either from the single-agent expansion, it could be from the EGFR combo, or from the FGFR combo. We have not stated the end.
But in terms of just the study design-
Yeah
... you're not talking about very small numbers that Wall Street will love to jump to inadequate con-
In terms of the study design-
Mm-hmm
... the way it's written is that the dose expansion of the single agent in-
Mm-hmm
Ovarian, endometrial would enroll 20 patients. And in terms of the combo arms, there's kind of a classic... It, it's like a 3 + 3, but it's actually what's called a modified BOIN design in the escalation. And then we get into the Part 3 expansion. That's a Simon 2-stage, where we would initially enroll 23 patients, and then if we meet certain passing criteria, that would expand to 40 patients for each cohort.
Okay. We spent a lot of time on the first asset, but let's make sure we include 825.
Yes.
Because it's going to be an important player in season two-
Correct
... of Boundless Bio, the story that we're telling here. Tell us a little bit about BBI-825 oral RNR inhibitor.
Right. So, Chris is correct. It's an oral selective RNR inhibitor. RNR stands for ribonucleotide reductase. That is an enzyme that plays a rate-limiting role in one of two pathways for nucleotide production. So the two pathways are called the salvage pathway and the de novo pathway. And by the way, nucleotides are the essential building blocks for DNA, including ecDNA. So healthy cells primarily rely on something called the salvage pathway. So they basically, they reuse, they recycle their nucleotides as they're forming DNA. Cancer cells cannot sufficiently rely on the salvage pathway. They're creating more DNA, they have a higher need, and so they starve if they rely only on the salvage pathway. And so they require something called the de novo pathway, so they're basically making nucleotides anew. This enzyme, RNR, is the rate-limiting enzyme for the de novo pathway of nucleotide production.
So that when we inhibit RNR, we inhibit the de novo synthesis pathway, we starve the cancer cells of the nucleotides required to form their ecDNA, and so that ultimately is synthetic lethal in ecDNA cancer cells.
We're also in the clinic. STARmap-
Correct
... is the name of the trial here. Just outline for us, I think there's monotherapy, obviously very logical, but then-
Right
also combination prospects.
Right. So there's some similarities with the STARmap study, as with the prior study I described, the POTENTIATE study. So similarity is that this, again, is a first-in-human, Phase I and II study design that's got three parts. As Chris mentioned, the first part, part one, is your classic single-agent dose escalation to once again characterize safety, tolerability, PK, PD, define a dose. Then we roll into Part II, which once again, is combo arms. But here's the key distinction. 355 in the POTENTIATE study goes after patients whose tumors are driven by an oncogene amplification. This program, 825, is going after tumors who initially are driven actually by a point mutation like KRAS G12C or BRAF V600E, but when treated with targeted therapies, they develop amplification as a mechanism of resistance. So now we're going after a resistant population, not a primary population.
So part two will enroll 825, plus either a BRAF inhibitor or a KRAS inhibitor in patients with colorectal cancer that's driven by either by BRAF V600E or KRAS G12C, but has also developed amplification-mediated resistance to targeted therapies. Part II is gonna be dose escalation of the combos. Part III is dose expansion of the combos.
That season two card turning over, this is a 2025 kind of timeline, right?
That's what we've said, yes.
Yeah. Okay. Given the context of where we're at, let's talk about some of the necessary oxygen for all of these endeavors. Jami-
Let's go to the CFO.
Exactly. Talk a little bit about-
Oh, the money question.
Yes, you know, where did we end up after the IPO?
Mm-hmm.
What do you envision in terms of the runway here, since we have some ambitious clinical work to go ahead?
Right, we do. Well, first, we were delighted to get our IPO done when we did. We raised... We now have just under $200 million as of our March 31st earnings report. That $200 million will take us into the second half of 2026, and most importantly, through our early preliminary proof of concept for both 355 as well as 825.
Yeah.
So well-financed through those two very important clinical data points.
Right. And this circles back again to this notion of an experienced C-suite, as well as a thoughtful board of understanding how to read the room. In this current environment and where we're at, where we're all armchair interest rate economists, thinking about what does it take to be a public company at this stage of the game, the novelty and ambitious science, the potentially transformational kind of clinical contribution and the significance of the TAM is, I think, something that often gives people pause, and you have to digest it a little bit. And so I, hence my sort of metaphor for telling a story here, because really good stories are worth retelling, and I think we're gonna be learning so much more about this.
Still in the context of thinking to close about, you know, the cash and the oxygen that you're gonna need to continue to fuel this machine, strategic optionality here is always part of the playbook to consider. Actually, the source of your FGFR pan inhibitor comes from Taiho. Taiho has also been a company who's been down some of these paths as well. You have sort of supply arrangements with them, as with Lilly. You know, you guys are kind of a cool shop. You're knocking next door and saying, "Can I borrow a cup of sugar?" If I'm lending you that cup of sugar, I'm thinking, "Well, can I have a slice of this cake that comes from this?" So what are you guys thinking as you're mixing and mingling and clearly being watched by other players, how you would contemplate, you know, engaging strategic partners?
We're early days, but that means you have a lot of time to think.
Mm-hmm.
Share us your thinking now.
Right. Right. Well, you're absolutely right. There's a huge amount of optionality as we continue to prosecute our programs. We are. Big Pharma is interested. They've taken interest. We've continued to educate, and they've continued to show interest in what we're doing. They, too, wanna see the data like everybody else. But I think what's exciting is that we have not, you know, our first two programs in the clinic now, but we've got a very deep, potentially very deep, discovery program. And, you know, so all options are really on the table. We're not looking to do anything right now. We don't need to, but we have a lot of optionality.
To be clear, even as I admit how much this was a discovery for me and for many investors, it is a lot of the smart leaders in industry are well aware, in terms of, I think, you know, when you're intersecting with some of the scientists who are part of the larger organizations, the leading organizations, people who work for Susan Galbraith, for instance, they will acknowledge, it's like, "Oh, yeah, I'm part of the ecDNA squad. That's part of my purview.
Mm-hmm.
I think that that's fair to say.
Mm-hmm.
As I was just tromping around, I saw you in San Diego at AACR, also in Chicago at ASCO. It's been an expanding truth, an awareness for that.
That's right. Yeah, so when we present at conferences posters, we've noticed the uptick in people from pharma coming to our posters and saying-
Mm-hmm
... "We're now responsible for ecDNA within company XYZ." So that's been nice to see. It's been encouraging to see the field take note, and I think that really is a testament to the high-quality work being done in academia that's really elucidating this biology in the highest peer-reviewed journals. That it's becoming a mainstream field of oncology.
Fantastic. Boundless Bio, upward and beyond. Take care.
Thank you.
Thank you.
Thank you very much for joining us.
Thanks, everyone.