Conference Transcript - CELC 2026-06-04

Maury Raycroft, Analyst — Jefferies

My name is Maury Raycroft, and I'm one of the biotech analysts at Jefferies. I'd like to welcome Brian Sullivan, the CEO of CellCuity. We're doing a fireside chat format. So Brian, thanks for joining us. Maybe for those who are new to the story, if you can give a brief intro to the company. You just had a big update recently. So talk about that as well.

Brian Sullivan, CEO

So I started the company about 12 years ago. Our focus initially was to develop a cellular analysis platform that could analyze intracellular activity quantitatively. We subsequently migrated towards development based on our research of a drug that could target the PI3K-AKT mTOR pathway called PAM. And based on our research, we identified, A, what we thought the required mechanism was to address this pathway, and then we found a drug that corresponded to our supposition called gadatilisib. And as it turns out, Gadotsalissib was zoned by Pfizer. We had a relationship with them because of the other research we were doing. They had decided to out-license it, and we raised our hand and said, well, if we were ever going to get into the drug development business, it would be for a drug that hits this pathway and this drug. And so now we have had two Phase III readouts in the second-line setting in breast cancer. We have two current ongoing Phase III studies in the front-line setting for advanced breast cancer. We have an early phase study. It's ongoing in prostate, metastatic castration-resistant prostate cancer.

Maury Raycroft, Analyst — Jefferies

Great. Yeah, it's a great overview. You just said the mutant top-line data reported at ASCO on Tuesday. Can you give a quick recap of the presentation of the most important efficacy and safety signals you're seeing?

Brian Sullivan, CEO

Sure. So ultimately, we had a three-arm trial design. We had GETA combined with palaciclib, which is a CDK4-6 inhibitor, and fulvestrin, which is an ER inhibitor, tested against alpalipsib, and fulvestrin alpalipsib is a PI3K-alpha inhibitor, and then we tested gaditalisib by itself, rather, just with fulvestrin. And so this provided the first head-to-head comparison of a drug, two drugs hitting the same pathway, this PI3K-AKT-MTOR pathway. The triplet and doublet each showed over 11 months median PFS, each showed a doubling of the likelihood of survival without disease progression or death. So very, very favorable results. The hazard ratios were 0.5, essentially indicating that we were significantly exceeding our internal estimates, and also I think the implied estimates out there, but I think there's been some misinterpretation of those analyses.

Maury Raycroft, Analyst — Jefferies

What were your internal estimates for HR?

Brian Sullivan, CEO

So we had between 0.56 and 0.6, 0.56 and 0.6, based on an assumption of about seven and a half months for the control arm, which is Alpalipsib, and then about 13 months for the triplet. And as it turns out, it was 5.6 and 11.1 for that primary analysis.

Maury Raycroft, Analyst — Jefferies

Right, yeah. Yeah, it's pretty impressive data. one of the observations, which you mentioned, is that the PFS for the doublet and the triplet were similar. Why do you think the adding CDK4-6 isn't driving incremental benefit?

Brian Sullivan, CEO

Well, so I think you have to think of it in two ways. We showed that there's a significant contribution in the wild-type setting with the CDK addition to getta and fulvestrin. And we think in the wild-type setting, these three pathways play a more co-equal role. Clearly in the mutational setting, PIC3CA mutant setting, the PAM pathway plays a more important role, it's probably a primary driver, CDK is less important, and so we don't see a benefit on a median PFS basis or hazard ratio basis. But there was a higher objective response rate, you know, nearly 50 percent with the triplet, you know, 36 percent with the doublet. So clearly some additional anti-tumor activity, very strong duration of response. And you'd say data is immature for overall survival, but you'd look at the overall survival curves and the data that's more favorable with the CDK4-6 edition. So we think there may be more of a latency effect or more, again, more of a passenger effect than a driver effect, but still relevant when you dive into the data.

Maury Raycroft, Analyst — Jefferies

Got it. Yeah, it makes sense. You've got the response rate difference, and then it could potentially translate into OS benefit. Do you think the lack of separation could be driven by small numbers in the doublet?

Brian Sullivan, CEO

It could be a factor. I think sometimes PFS can hinge on a few patients. What was interesting to us was that half the patients had an objective response in the triplet. The duration of response was nearly 16 months. And so we had half the patients, the duration of response of 16 months, and an overall PFS of 11 months. So it indicates that half the patients getting the triplet are getting very, very extended duration of treatment beyond the PFS.

Maury Raycroft, Analyst — Jefferies

Right. Yeah. Interesting. And in the mutant core, median PFS came in below phase one at the 14.6. Should we attribute this to baseline differences or are there other factors?

Brian Sullivan, CEO

There were baseline differences. I mean, I think a quarter to a third, I forget exactly, of the patients in that early phase study hadn't had prior CDK. So that's a big difference. You can see a doubling of outcomes in non-CDK treated patients in this setting. So, you know, So that added some, not distortion, but just some difference in the results. We also had a very, I don't want to say tough to treat, but the patients with significant tumor burden, 80 percent, had liver lung mets. We had 15 percent that were endocrine resistant. Many of the studies done these days, particularly with the SIRDS, exclude the endocrine resistant because they're just not responsive at all to estrogen receptor inhibition. And we included those patients. They showed a very meaningful benefit. And so, you know, those factors can result in a divergence of results from an early smaller sample size study relative to a global phase three.

Maury Raycroft, Analyst — Jefferies

Got it. For the endocrine resistance population, are you saying more what the benefit was in those patients?

Brian Sullivan, CEO

We have. It's in the subgroup analysis. I forget the hazard ratio, but it's still a very favorable hazard ratio.

Maury Raycroft, Analyst — Jefferies

Got it. Okay. And when should we expect final OS data from the mutant data set, and is WildType still on track for first quarter of 2027?

Brian Sullivan, CEO

I don't know if we've said first quarter. I think first half would probably be a better characterization of WildType, and then probably sometime in the second half. Less predictable OS, smaller number of events, and it's event-driven, not time-driven.

Maury Raycroft, Analyst — Jefferies

Got it. And in real-world practice, especially in the community setting, how do you see doublet versus triplet being used, and would PICC-3 testing be required to guide CDK4-6?

Brian Sullivan, CEO

So in the wild-type setting, we expect the doublet and triplet to both be approved. We're nearing the purduffman date, which is July 17th. And, you know, our research indicated that there's, based on, you know, quantitative assessment from a survey, about an 85-15 split between preference for the triplet versus the doublet. And that was consistent with what we saw when patients were crossed over, a similar proportion by doctors deciding that. There'll clearly be a less heavily weighted preference probably for the triplet, but we think there's still an argument for the triplet, or rather I think doctors could still believe that, particularly for patients, let's say you're a premenopausal woman, younger, you probably want to make sure, or at least we've gotten this feedback, that you want to essentially control all these pathways. And the benefit to them of making that decision is that it's not a binary decision. They can ultimately decide, look, Paabo, my patient's not tolerating it well for whatever I can discontinue that and continue on with this regimen. So I think ultimately what we've created with two regimens to enable physicians to potentially improve the tailoring of an option based on the patient's profile. And oftentimes drugs, you know, most of them are one size fits all. Some patients may not be suitable for it, and so they're not treated. In our case, for instance, you'll have subgroups of patients who are particularly aggressive disease. You absolutely would probably want to have the triplet. But you may have other patients, a 75-year-old woman with indolent, more indolent disease. You may not include polycyclic. And the fact that, you know, we're giving the doctor flexibility to tailor, also the flexibility to modify the regimen without affecting the positive benefit that could be induced is actually, we think, will accrue in the long term to, you know, higher penetration than we might otherwise be able to get.

Maury Raycroft, Analyst — Jefferies

Yeah, it makes sense. Yeah, it definitely makes sense. And so for the wild-type data, you saw some differences based on geographic split. You're not seeing that in the mutant setting. I guess what drove the regional differences, and if CDK4-6 use was a factor, what specifically differed across the geography?

Brian Sullivan, CEO

So in the wild-type setting, so these were patients lacking PIC3CA mutations, we saw U.S. patients get 19 months meeting PFS. U.S., Europe, European countries, Western European countries and Japan, overall, when you aggregated that data, which was about two-thirds of the patients, or 60 percent, was about 16.6 months. And then as we dug into the data, we saw that there were differences probably associated with CDK46 usage, polycyclic usage, in terms of dose reduction or interruption. There was also interruption of GEDA-Talysib or dose reduction that occurred in these countries disproportionately. GEDA doesn't, for instance, introduce any myelosuppression like neutropenia. But in these countries, you saw significant alignment of reduction of palibociclib and GEDA for those reasons. Well, they shouldn't have. And we think that, in fact, affected the results because we saw kind of a correlation in the countries with palbociclib penetration. In the mutant population, we didn't see that variance, and it probably relates, I mean again, this is speculation, but I think it's sensical, is that the palbociclib played less important role. So independent of how you may have managed the palbociclib, to the extent you maybe didn't have an optimal management, it would have had less effect. And so there's just less dispersion potential based on the less significant role CDK 4-6 was playing.

Maury Raycroft, Analyst — Jefferies

Got it. Okay, that all helps make sense. And given the efficacy and safety profile to date, how do you expect Uptake to look in the second-line mutant setting? And how do you think the physician decision tree will evolve versus standard of care?

Brian Sullivan, CEO

Well, we think the reaction, you know, we were at ASCO just this week, so coming from Chicago to here. And it was a great meeting for us. I mean, it was great data, in our view, and also in the view of the KOLs we met with. You know, we presented many of these KOLs. You know, these are important docs doing a lot of research. On a confidential basis, we previewed the data with them, just get their take, you know, see if we were missing anything. And it was universally positive. They just thought, you know, this is great data. I mean, it's unequivocal. You guys should be the standard of care. Some of them actually got more specific and said, well, I was hoping you could do .65 hazard ratio. If you did that, that would be a home run. Obviously, we did 0.5, so that's better. Lower is better with this metric. So we came out of ASCO just feeling, oh, this is great. You know, the reaction will be very positive, obviously. Some investors had different expectations, but ultimately, I think that'll resolve because this data really is outstanding. And you really rarely see in a study that compares two drugs of the same class head-to-head, a hazard ratio of that low, a 0.5 hazard ratio, a doubling of efficacy.

Maury Raycroft, Analyst — Jefferies

Yeah, makes sense. And I guess maybe just digging deeper into the question, though, as far as market research goes, what percent of the mean population do you think you can capture versus standard of care?

Brian Sullivan, CEO

A lot. No, I do think we'll establish a new standard of care. I mean, we don't want to get too specific in our forecasts. But, you know, again, it's not often you have such a wide separation. The drugs are also better tolerated. So we win both on the efficacy standpoint. We also think we win on the tolerability from the tolerability perspective. That would certainly seem to translate to significant preference for our regimen over the other guys. And so we think we'll be the ultimate winner in that segment.

Maury Raycroft, Analyst — Jefferies

Yeah, makes sense. I guess another way to look at it is that our penetration estimates that we have in our model are pretty conservative. Would you agree with that or disagree?

Brian Sullivan, CEO

Not your conservative penetration assumptions, no. I think how you model it needs to be thought about because essentially you have to take into account what is a reasonable penetration assumption and then factor in what's the time to achieving that penetration, peak penetration, and then you assume kind of a linear achievement of those penetration targets. So if you work backwards from those assumptions, you'll come up with, assuming your penetration target's accurate, a reasonable estimate of kind of revenue potential over time.

Maury Raycroft, Analyst — Jefferies

Got it. Yeah, it makes sense. And for the wild type approval, coming up soon, July 17th, where does the review stand today, and are you already in labeling?

Brian Sullivan, CEO

Do you want me to give you the kind of play-by-play here? So we're approaching the end. We have a priority review. They're still reviewing it. That's good, right? We haven't been kicked out yet. So, no, we're very optimistic, and again, we had breakthrough designation, which gave us the opportunity to interact with the agency on a regular basis, you know, asking questions along the way about, you know, topics that are relevant for a new drug submission. And so we came into the process and incorporated in our NDA kind of a resolution to the extent there were any questions up front. So we really, we think, minimize the risk of getting surprised because we asked all the hard questions, tried to get alignment to the extent there was anything else that the FDA would have wanted. We resolve that up front.

Maury Raycroft, Analyst — Jefferies

Got it. Okay. And as far as the label goes, what are the items you're focused on there as far as population, dosing, safety language?

Brian Sullivan, CEO

Yes, we are focusing on all of those. No, I mean, obviously, you know, the FDA's responsibility is to create a label that communicates effectively to doctors what they should expect and how they should think about managing patients on the label. So, and that's totally, you know, as expected and appropriate. And so, you know, we expect a label that will be informative and appropriate.

Maury Raycroft, Analyst — Jefferies

Makes sense. And can you update us on launch readiness, what's been completed so far, and what still needs to be done?

Brian Sullivan, CEO

So we began the commercialization preparation process a couple years ago when we brought on our chief commercial officer, subsequently built out senior people in the marketing, commercial operations, market access, sales areas, medical affairs, and then completed build-out of those organizations except for the sales force last year, last fourth quarter, And then brought on our sales force, and today we have all of the sales reps. They're all trained. They've all been released into the wild. They're not able to market or sell, but they are able to profile and doctors understand what their practice habits are, their perspective on patients and potential patient subgroups, just to essentially get familiar with the doctor and their general clinical approach to treating these patients, which is, you know, a good way to lay some foundation going into a launch.

Maury Raycroft, Analyst — Jefferies

Right. Yeah, it makes sense. And for the first 90 days of the launch, what are the key milestones that you want to achieve there? Maybe talk about access, accounts, patient starts.

Brian Sullivan, CEO

Sure. So you've got a lot of different variables that we're focused on. Obviously, from a market access standpoint, we want to have submitted and have moving forward forward dossiers at all of the national accounts of payers from a strategic account standpoint. We've been having these discussions, again, for 18 months with them. We can't move forward specifically, but we essentially are making sure the constituency that is going to ultimately make decisions about the formulary or the pathway, preference, et cetera, is fully informed. So we want to get all those dossiers submitted. We want to get NCCN submitted immediately. from a strategic account standpoint, similar to the payers, and then from a sales standpoint. And that's all groundwork that's required to support your sales efforts. So from a sales standpoint, we want all of our reps to have obviously met with all the doctors in their territory. Each of the docs, each of the reps have roughly 80 docs or so that they're responsible for. And we want them to hit certain targets for number of doctors prescribing, number of doctors, you know, repeating prescription, writing scripts, and overall level of interaction. There's some other activities that are relevant that we expect the reps to perform, and those will also be tracked.

Maury Raycroft, Analyst — Jefferies

What are the targets?

Brian Sullivan, CEO

I'll get back to you on that, Maury.

Maury Raycroft, Analyst — Jefferies

I'll make sense. And based on the market research, how do you expect uptake to differ between community versus academic settings? And given this is IV infusion, what are the initial bottlenecks you expect that should ease over time?

Brian Sullivan, CEO

So our research doesn't indicate wide separation and usage between an academic center and a community setting. Community setting will account, though, for roughly 80% or so or more of the patients So obviously, that's where we need to make sure we do a great job. So many of them are affiliated, or a good chunk of them are affiliated with larger networks like U.S. Oncology, you know, Florida Oncology, Texas Oncology. So you work with them because there's a bit of a top-down component to that decision process. And then, you know, work accordingly.

Maury Raycroft, Analyst — Jefferies

And at ASCO, one of the doctors we spoke with mentioned that for the community setting, there could be capacity issues.

Brian Sullivan, CEO

Yeah, it's interesting they mentioned that. But just one thing to point out, you know, in the breast cancer setting as well, as many other settings, infused drugs are a very important component of their practice. In the breast cancer, Herceptin, Bridgetta, $10 billion revenue drugs at peak, Pembrolizumab and HER2, Tredelvi, all billion-dollar drugs. Every patient ultimately will get chemo that is often weekly infused. So they've built practices around infusing patients with drugs. It's a well-worn operational procedure that they have. We can essentially plug and play into that. I haven't heard one person talk to me about capacity, so I don't think it's a problem.

Maury Raycroft, Analyst — Jefferies

And for launching in second line, are there subpopulations of patients that you think could be early adopters?

Brian Sullivan, CEO

Well, I think certainly patients with aggressive disease. You know, again, doctors, I think it's more a function of the doctor and, you know, their comfort launching new, or rather, prescribing new drugs. I mean, you know, doctors are somewhat like consumers. You have early adopters or experimenters. You have mainstream, and then you have the skeptics. And so, you know, there's a continuum of folks you work with. Certainly, as we're doing work profiling accounts, to the extent we can characterize whether these people seem to fall in the early adopter category versus the skeptical category. You focus on the early adopters. Part of it is understanding based on their individual preferences, who they think are the first patients to treat. And so it's really going to be territory by territory, doctor by doctor, targeting.

Maury Raycroft, Analyst — Jefferies

Got it. Yeah, it makes sense.

Brian Sullivan, CEO

By patient subgroup, yeah. And a lot of it will just be a function of where the doctor's preference is. But one of the advantages of GEDA, initially, you know, the drug will be, you know, we expect to be approved in patients lacking mutations. And we've now demonstrated that the drug is very active and superior in the mutant setting. And so, you know, ultimately our position will be that we are giving doctors, you know, clinical oncologists, the medical oncologists, the ability to provide, you know, have us utilize a single treatment that's suitable for all patients who've progressed after their first line of therapy.

Maury Raycroft, Analyst — Jefferies

Yeah, with having both data sets and the wild type of mutant kind of builds out the value proposition of the drug. Doctors theoretically wouldn't have to test in second line.

Brian Sullivan, CEO

And it's self-reinforcing because I think as doctors typically get more experience with the drug, they get more comfortable with it. And once they get comfortable with the drug, they tend to stick with it. And we saw this in the first-line setting with palvociclib versus rabiciclib. Palvociclib was by far the preferred CDK4-6 inhibitor in the first-line setting, probably had a 60, 30, 10 split between the three drugs with palbo being the lead. Now it's probably a 50, 40 with ribo in the lead. Ribo flipped the script because they got favorable OS data, But Palbo is hung in there because it's a good drug, it's a great drug, patients tolerate it well and they're comfortable with it. And so I think over time by having this broad, this ability to treat essentially an all-comer population will lead the doctors to use this drug very frequently and in turn feel very comfortable with it. And our goal will, for them to consider this their go-to option for all of their patients who've progressed after their first treatment.

Maury Raycroft, Analyst — Jefferies

Makes sense. And when you think about the value proposition, how does that translate to how you're thinking about pricing for the drug? Could it be more in line with CDK4-6 inhibitors or alpalisib or something different?

Brian Sullivan, CEO

I think the second-line drugs, which were launched later, and if you look at the second-line drugs in this setting, you'll see them in this $25,000 to $27,000 wholesale acquisition cost range. And that certainly sets a benchmark. I'm not saying that's our price, but that gives you a perspective or a frame of reference for, you know, what to expect for drugs of this type in this setting.

Maury Raycroft, Analyst — Jefferies

Got it. And how do you view the competitive landscape and wild type over the next approximate five years? Are there any specific mechanisms you're focused on?

Brian Sullivan, CEO

Well, I mean, I think, you know, fundamentally by addressing all three critical drivers of this disease, you know, ER, PAM pathway, CDK4-6, you're optimizing the potential outcome you can offer patients because these three pathways are linked and you're going to optimize benefit by hitting all three. PAM pathway plays an outsized role, clearly, in particularly the mutant setting. So we think over the next five years we'll be well positioned to have, you know, essentially the superior regimen that's going to offer the best potential outcomes for their patients.

Maury Raycroft, Analyst — Jefferies

Yeah. Makes sense. And I wanted to talk about the frontline setting as well, which could be an even bigger market opportunity. You recently updated that you're going to include endocrine sensitive patients. What are your expectations for enrollment timelines in endocrine resistant versus endocrine sensitive?

Brian Sullivan, CEO

Sure. So we've set up Victoria 2. Victoria 2 is essentially two studies in one endocrine resistant patients. These are women who progress almost or recur very quickly after they were diagnosed with early breast cancer and developed metastatic disease. Endocrine sensitive, which is two-thirds of the population, are women who recur much later. And that's relevant because they respond differently to current standard of care therapy. We're enrolling these patients, you know, essentially simultaneously. We're intaking patients, and if they are endocrine resistant, they would get assigned to study And then if they're endocrine resistant. assigned to study two, and we think we'll enroll proportionately. So essentially endocrine-sensitive is about two-thirds of the total number of patients resistant about one-third. And then we've got more patients, though, in the endocrine-sensitive population, I think 740 versus 440. So it'll just be naturally, you know, it may balance out where they can enroll somewhat proportionately to completion, roughly the same period of time, but there'll be a much longer follow-up. The duration of treatment for current standard of care in the endocrine-sensitive population is around 24 months, two years, only seven in the other indication. So we think, you know, today current estimates would be around end of 28 for data from the resistant population study, study one, and then, you know, late, you know, in 2030 timeframe for the patients in the sensitive population.

Maury Raycroft, Analyst — Jefferies

Got it. Makes sense. And in the endocrine-resistant front-line setting, there's no clear benchmark from GEDALASIV. How are you framing expectations for activity in this population?

Brian Sullivan, CEO

Well, I mean, again, with the first line, rather the second line data we've shown, the GEDA in the wild-type population improves outcomes relative to fulvestrin monotherapy by nearly fourfold. So it's clearly active, you know, five-plus months just on a duration of time off of a two-month delta. And so if we are able to achieve similar deltas, we'll create a statistically significant clinically meaningful result for these patients. Got it.

Maury Raycroft, Analyst — Jefferies

And Invalisib is approved in frontline endocrine-resistant but only in the mutant setting. Is that data, is it a relevant benchmark for your frontline endocrine-resistant outcome?

Brian Sullivan, CEO

I think it's a relevant benchmark. Mark, that drug, because of the hypoglycemia it induces, is really only appropriate, as it turns out, for patients who are, you know, not appropriate, rather, think of it this way, for patients who are pre-diabetic or diabetic, which, unfortunately, includes about half of women diagnosed with breast cancer. So it's a very narrowly targeted drug. Ultimately, you know, we're, you know, positioning our drug as an all-comer independent of your HbA-C1 status, your glucose level status, or your PIK3CA status. And so, you know, our study endpoints are all-comer, you know, tend to treat. They're not separate endpoints by PIC3CA mutational status.

Maury Raycroft, Analyst — Jefferies

Yeah, yeah. And you reported 48 months meeting PFS from the data listed Phase I-B study in the endocrine-sensitive data set. How should we interpret that versus what's achievable in the Phase III given the baseline differences and inclusion-exclusion?

Brian Sullivan, CEO

No, I mean, I would like to think we could do 48 months, but I think that's kind of dreaming a little bit. But I think the benchmark is pretty clear. All three of these current CDKs deliver similar results, about 25 months for these patients. You know, a clinically meaningful benefit in that setting is probably at least five months. And so if we've shown in an early phase study 48 months, and to be clinically meaningful, we need to maybe hit 30. You know, we think that that's enough margin for error to have a lot of confidence. that we think gives us the kind of margin for error that makes it highly – or at least in our view, a high probability of success.

Maury Raycroft, Analyst — Jefferies

Got it. Okay.

Brian Sullivan, CEO

So about a five-month – That would translate to both, we think, statistically significant and clinically meaningful. Got it.

Maury Raycroft, Analyst — Jefferies

Okay. And you also announced a sub-Q formulation for gadolizib. How materially could that change the commercial uptake and what do you need to do there? Anything more on timelines for doing that?

Brian Sullivan, CEO

So sub-Q formulation is really designed almost and intended to be developed in parallel with the development of the indication for the endocrine-sensitive patients. We don't think penetration will really be affected by IV administration. Certainly sub-Q, when it's available, would be a preferred, but absent its availability, it won't, we think, limit our penetration. However, in the endoconsensitive population, where these patients, if the data bears this out, you know, is on for two and a half to three years, we think sub-Q would be important to optimize penetration of that. And so, you know, we expect the data and an approval, potentially, if everything shakes out the way we'd like, in the 2031 timeframe. And so that's when we think we will have, and that's what we're targeting, is to have that sub-Q available in that 2031 timeframe. It's typically a five-year development cycle. If you look at some other programs done in other companies, it's a four- to five-year development process.

Maury Raycroft, Analyst — Jefferies

Yeah, okay, makes sense. And also I wanted to ask on, there's been discussion around the relay data where they should 11-month data in the phase two. You guys have two phase three readouts. I guess, what are your views on how to contextualize?

Brian Sullivan, CEO

Well, I mean, it's hard to, in general, it's hard to, you know, place as much weight on a phase one B study as a phase three study. I also think in these studies it's really important is to analyze the baseline characteristics of the patients because there are some variables that can, you know, yield significant differences in these characteristics. And one characteristic that can, you know, significantly affect the results is the inclusion of patients with nonmeasurable disease. It was interesting in our study we saw that patients with nonmeasurable disease who got fulvestrant responded four times as well if they had bone-only disease versus those who had measurable disease. So, you know, if you have 40 percent of your patients, let's say, or a significant proportion of non-measurable disease, you're going to create an upward lift in your overall number. Typically in phase three studies, you're enrolling patients who have measurable disease because you need to assess PFS very reliably. Secondly, I think in general, what we've found certainly with the SIRDs, is that if you have a similar mechanism, even if you have different ways of achieving it, which a number of these SIRDs are different, you find that there's only so much biological potential out of a target. And so, you know, there's other drugs under development, alpha inhibitors, PFK alpha inhibitors. You know, our data, as it turns out, is 10 times more potent than a couple of the, like alpalipsum, for instance, or the relay compound. And so we do a good job of inhibiting alpha. But what's more important is that we're shutting down the pathway by inhibiting all the other components of this, or critical components of this pathway. And ultimately, that's what we think is important. You know, the SIRDS really haven't shown very significant differentiation, even though they have different potency, different mechanisms, you know, to address your target. And so, ultimately, you know, the biology will win out, and there's only so much, you know, juice you can get out of the squeeze. You can't inhibit more than 100%.

Maury Raycroft, Analyst — Jefferies

Yeah, makes sense. We're pretty much out of time. Maybe in closing, if you still want to comment on cash runway assumptions and key updates that investors will focus on.

Brian Sullivan, CEO

So, you know, we just closed a convertible note offering, and we think that convertible note gives us cash, you know, certainly, you know, through 2029. We raised $500 million as a green shoe where we could take down another $75 million. We'll pay down about $130 million of debt. So we will net, if the Greens use exercise, around $420 million. So that's a good addition to the coffers. And we had $380 million at the end of the first quarter. So on a pro forma basis, $900 million. And we think that will carry us quite a bit, quite a ways.

Maury Raycroft, Analyst — Jefferies

Okay, thanks so much for joining us today, Brian.