All right. Let's kick off our next session. Good morning, everyone. I am very excited to host Alcuity, and with me is Brian Sullivan, CEO and co-founder of the company. We have a lot to go through, a lot happening in the company, but before we get there, I'm going to turn it to you for opening remarks.

Oh, sure. So I guess the most important thing to understand about cell acuity is that we're focused on treating diseases that involve the PI3K-AKT-MTOR pathway, or which we refer to as the PAM pathway. Our lead candidate is a multi-target inhibitor of that pathway, and it's able to comprehensively shut it down. And the pathway itself represents probably one of the most important oncogenic pathways overall, but also one of the most challenging to drugs. And the real advance that GEDA-Tilisib has demonstrated so far, and I'm sure we'll get into that, is the superior efficacy and better tolerability you can achieve with the approach GEDA takes relative to the approved drugs in this class that have essentially narrowly targeted the inhibitor, or rather this pathway, in a less efficacious way.

Fantastic. So the FDA granted priority review, and you guys have a PDUFA Day coming up very soon in July. in that wild-type population. How is the commercial PrEP going for that, and what does it take?

So you're referring to our Phase III study in second-line breast cancer where essentially we evaluated patients who HER2, you know, HR positive, HER2 negative, advanced breast cancer, lactic 3C mutations, showed fantastic results, really unprecedented results. And, you know, we've anticipated success in this business. You have to plan for success. So we began building our commercial organization over two years ago. We've since completed the build-out of that organization as well as the other infrastructure that's required. Salesforce has been hired, trained, and ready to go.

All right, fantastic. And then you guys have the mutant that you guys presented, the data. What is the BLOA submission timeline for that?

So this will be an NDA where we have a small molecule, and our plan is to submit what will be a supplemental NDA sometime in the third quarter. Okay, great.

And in addition to breast cancer, I know GEDA is also being evaluated for prostate cancer. Can you talk about the rationale for prostate and what is that opportunity, the phase 1B2 trial design and the status for that, and also when can we see data?

So prostate cancer has a similar underlying biology as breast cancer. They're both hormonally-driven diseases. A lot of non-clinical work, as well as some clinical studies have shown and demonstrated that this pathway, the PAM pathway, is involved. But optimizing treatment of this pathway is critical to really inducing what we think is a necessary and clinically meaningful benefit. And so we have a Phase I, B2 study that's ongoing. It's essentially dose-finding. We've reported out results, preliminary results for the first two doses that we evaluated, very encouraging results. We hope to provide updated data with results from additional doses later this year at a medical conference. And so overall, we're optimistic. The population that we're treating are men who have metastatic castration-resistant prostate cancer. They've progressed on a prior androgen receptor inhibitor. represents a population that's similar in size as those, as a woman that we're targeting and hoping to treat in breast cancer. So a very sizable population. If you think about breast cancer and prostate cancer, they're two of the three largest populations that are available to treat. And we think Gada Tolisib has an opportunity to essentially improve the standard of care in both.

Got it. You guys got it one way into 2027.

What does that include and not include well we actually just raised some additional money we raised about 575 million um recently and so combined with the current cash we think that takes us through you know 29 and you know at least through 29 so we think we have a long runway i think that funds obviously our commercial launch but also funds you know some two additional phase three studies that we have and you know we can talk about those uh in the advanced breast cancer space right and also the commercialization. In the commercialization, exactly.

Okay, fantastic. Let's dive deeper into GETA in that second line setting. So in that Victoria 1 study, in that study 1 for the wild type patients, you guys performed, I think, subgroup analysis for that GETA triplet and also the doublet. And then when you look at the MPFS, across the different subgroups, like geographic areas and then time for or the disease progression, and various other metrics. There seems to be some mixed data in terms of the consistency across different attributes. How should we interpret the mixed results for this group, and how would it affect you commercially when you go and try to sell the drug across different regions and things like that?

Right. So it was interesting. We saw in patients who were enrolled in the U.S., Canada, Western Europe, Asia PAC, that median PFS was about 17 months, almost 17 months, whereas in countries, Latin America, Eastern Europe, patients enrolled there, the results weren't as favorable. And we think, just based on analysis of dose reduction interruptions that were triggered for polycyclob, the CDK4-6 inhibitor, that are probably related to those countries' less frequent or less use of CDK4-6 inhibitors. And so we think CDK4-6 pathway is important to inhibit, particularly in the wild-type setting. And so as far as the countries that have a lot of experience using CDK4-6 inhibitors, we saw 16 months in the second-line setting. It's unbelievable. So that's great. And so I think in those other countries, which, again, represent, if we just look at it from a commercial standpoint, relatively, probably less than 5% of the potential. So we don't think that will have a big impact. We would want to commercialize there, make the drug available. But certainly, we would focus on helping them understand better how to manage probably sick, but not dose reduce how to essentially manage patients according to the label. And I think if that happens, you'd see more similar results across these different regions.

I see. Okay. Got it. And then at ASCO, very exciting. You guys presented that phase three, Victoria one, in the study two population, the PIK3, the mutant population. Can you summarize the results there and then the key learnings? And it seems like the market did not seem a little disappointed and then hope to see a higher benefit. Is that a fair expectation?

Well, two things. One, the data was, you know, the first head-to-head trial of a drug comparing two PAM inhibitors. Ours is a multi-target inhibitor. We compared to the PF3K alpha inhibitor called alpalypsib that Novartis has. We showed the highest median PFS ever reported in the second-line setting for therapies that include an endocrine backbone. So that's obviously fantastic. And then we also showed the highest objective response rate in breast cancer in the second-line setting for therapies, regimens, including an endocrine therapy. So the results were, to be frank, great. We doubled PFS benefit for these patients. I think what the market got wrong, and I think over time we'll pay more attention to, is that actually we exceeded the expectations, implied expectations people had. But as you know, people can zero in on a single number when they need to dial into two. There were some assumptions made about what the study arm could do, 12, 13 months, but again, they also were assuming about seven and a half months for the control. Implied hazard ratio, if you do that analysis, is in the 0.6 range. Well, we reported a hazard ratio of 0.5, actually significantly better. The reason why they, I think, have not quite understood how good that is is because Alpalipsib only did five and a half months, 5.6 months. You know, we reported 11.1 and 11.3 months. And ultimately, you do phase three studies to show the comparative benefit and show how on a relative basis when you control for all the other factors that could influence outcomes, how much difference there is between one therapy and another. And so to show double the benefit between, you know, two drugs of the same class is typically actually very unusual, and it really highlights how important the mechanism of Geta is and when it's used, how much improved the outcomes will be for patients.

Well, I think another way to see it is that if you compare study one result and study two, should there be a higher benefit because now you're study two is targeting the mutation that the drug is designed to target, whereas the wild type is not excluded.

Well, I mean, the results were better in the mutant, so I'm not quite sure I'm tracking here. The results were better in the mutant population. They were 11.1 months versus 9.3, double. In the case of the PIK3CA mutation patients, they actually have worse prognosis. They're only getting five and a half months from existing approved therapy, whether it's an AKT inhibitor or whether it's a PF3K alpha inhibitor, and then to offer those patients who really have no other options double the benefit. But, you know, in oncology, if you're offering double the benefit relative to standard of care, that's generally considered to be a home run. And that's certainly how the KOLs interpreted the data. So, you know, we were able to meet with, you know, obviously a lot of KOLs over the course of the ASCO meeting. And we previewed the data with them on a confidential basis just to, you know, get their reaction and get their thoughts. And it was overwhelmingly positive. We thought, wow, you know, we were hoping for 0.65 hazard ratio. And the fact that you were .5 is great, and so this will clearly establish a new standard of care. So the feedback from the clinical community has been unequivocally positive. I see, okay. And sometimes that's what matters. Well, not sometimes. That is what matters.

Yeah, exactly. So in that study, too, the triplet and the doublet show similar median PFS and also the hazard ratio. Why didn't the triplet show more benefit compared to the doublet? And then at this point, how would you look at both regimens from the submission, from the NDA filing? How do you think about that?

So I think what was surprising to us, we didn't have data for the doublet going into the study, so it was an unknown for us. I think what was surprising, and I think it really surprised to the good, was the fact that GEDA, when combined with Fulvestrin, carried the weight in effect. It doubled the benefit relative to opalipsib in a pure head-to-head setting. And I think our interpretation, then, is that the PAM pathway plays a particularly important role, as you'd expect, in patients in tumors that have this mutation. And the CDK4-6 still involved, because if you look at some of the additional data that we reported, clearly CDK4-6 is playing a role, but less prominent. You think of it as more of a passenger rather than a driver of the disease at that point. Whereas in the wild-type setting, where you don't have the mutation, you have these three pathways, ER pathway, CDK4-6 pathway, the PAM pathway, that each are probably playing, I don't want to say co-equal, it's hard to tease that out, but playing a very important role, more balanced, I guess you could think of, and less balanced maybe in the mutant setting, which just highlights how important, to be frank, having a multi-target inhibitor is for these patients. Okay, got it.

And then in that subgroup analysis for study two, patients who received ribo in the prior line seem to benefit more compared to those who received palpal. What's the implication there in terms of that ribo-palpal dynamic?

Sure. Well, two things. One, really both sets of patients benefited significantly, regardless of which CDK4-6 they had. And so in these subgroup analyses, you'll see somewhat minor differences in hazard ratios, and you don't want to tease too much out of that. What really we think is most important is the fact that, irregardless of what prior CDK4-6 you had, you're getting a very meaningful benefit. And we saw this in the wild type as well, where patients who had prior palbo, prior ribo got almost exactly the same benefit. I would say in mutant, you would say that they basically got essentially the same benefit. And that, we think, highlights the benefit that occurs just by keeping the pressure on that pathway and then when you comprehensively inhibit it, so that essentially doctors can approach this and say, okay, independent of what this patient may have received prior in their first-line setting, whether it was ribo or palbo, my patient is going to get a very meaningful benefit when I combine getta with palbociclib and, in this case, fulvestrin.

I see. Okay. So now with study one, study two, you're kind of able to capture that entire second.

Exactly. And so essentially I think our positioning is that now doctors will have, I mean, we have a ways to go to get our submission for the mutant. But, you know, if we fast forward, let's say, a year from now, we fully expect that doctors will have an approval for these regimens and doctors will have the option of selecting and optimizing, really, selection between the doublet and the triplet because it's a very heterogeneous population. You know, typically drugs have one option, one size fits all. And in the case of breast cancer, it's probably more heterogeneous than many diseases, where you can have a woman who's 35, premenopausal, with very aggressive disease, and you can also have a 75-year-old woman who has more indolent disease. And so giving doctors the option of selecting between a triplet, let's say, and a doublet, and factoring in, you know, the clinical characteristics of their patients, will actually be hugely helpful to them because it allows them to more precisely dial in what they think the best treatment will be for those patients. And that overall to us from a penetration standpoint is that we think it will actually help us expand or certainly optimize the potential penetration because we won't have this dilemma where doctors are concerned about potentially continuing on a CDK4-6 for patients who may have essentially a more compromised immune system. They can have confidence that the doublet, to get a doublet, will give a fantastic outcome for these patients. Or they can start off with the triplet, and to the extent that there's some myelosuppression that they're concerned about, back off the palbo and continue with the doublet. And, again, have confidence that the regimen will still offer a meaningful benefit.

I see. Have you seen those patients, the ones that were on a triplet and then maybe in the trial at some point they come off the CDK4-6 or something like that? Have you seen how those patients compare to patients who did not come off?

So essentially you don't really see a very significant difference. I think that if you get some initial treatment with CDK4-6, you don't see, again, these are small sample sizes. I mean, for instance, pavocyclib discontinuation is in the small percentages numbers When you're trying to tease out too much information from these small sample sizes, you can kind of get a misleading interpretation. But you do know how well patients did who just got the doublet, and the results are very favorable. For instance, the doublet in the wild type, for instance, if it weren't for the triplet, would have been the most favorable results relative to endocrine monotherapy ever reported in breast cancer. So, you know, by itself, the doublet would have been just unbelievably historic results, and the triplet was even better. So, again, those are two good options for these docs to have and the patients to have.

So in that second-line setting, there's a lot of other therapies also being developed. And we have seen in the past where these next-gen serp like palacestrin, when you add that to a CDK4, it's like ribo, it shows like 13-month PFS in that medium PFS. in that all-comer setting. How do you view GEDA's doublet competitive position for the next generation third that could be recommended on top of a C2K4 in the second line setting? Even if it's not approved, it could be recommended in the NCCN guideline based on some of the use.

Maybe. I think the drug you're referring to is an investigational, so it's only phase one data. We don't know. The five studies have reported out phase three data, though. that are for oral SIRS have not shown a benefit relative to fulvestrin in patients lacking mutations. And so their approvals to date, and we think going forward, are going to be limited to treating patients who have ESR1 mutations. And that's an important subgroup. Patients who have ESR1 mutations and are PIC3CA wild type represent about 20% of the population. So there'll be some overlap in populations. We think we offer a clinical benefit relative to them, but that'll will be probably a more competitive segment in that 20%. 40% of patients are ESR1 wild type, PIC3CA wild type. And again, we don't think they're fantastic options for patients today. We think Geta will be positioned well as the clear standard of care. And then with the mutant data, we think we've established a new standard of care for patients that have a PIC3CA mutation, and that's about 40% of the patients. So if we think about the 80% of patients that I just described, we think we've set a significantly higher new bar for standard of care, and that in the patients that have ESR1 mutations, PIC-3C wild type, it'll be more competitive, but that's fine.

Right, okay. And then have you thought about doing any combination studies with GEDA and these next-gen SIRT instead of Fulvestrin, given the limitation for ESR1 mutations of Fulvestrin? If you were to do a combo, which cert would you use for that partner?

Well, ultimately, we think GEDA thalissib, because of its two things. This pathway is involved in the disease, independent of whether or not the patient has a mutation. That's our data has clearly shown that. And secondly, GEDA is able to address it effectively and more favorably than has ever been reported. And so we think GEDA will be a core backbone to any regimen that wants to offer standard of care benefit to their patients. And so it does make sense for us to evaluate these other therapies or classes of drugs, you know, oral SIRS, for instance, or other ones that might come up. And that will be just part of our life cycle plan is to evaluate those. As far as, you know, which of those SIRS would be optimal, I think there's very little differentiation between them. If you look at the results on a comparative basis, You'd see that they all offer hazard ratios in this mid 0.5 or 0.55, 0.57 range. And then, you know, essentially you're going to get to physician preference. You'll see some differences in toxicity profiles that are, on the scheme of things, relatively small. Certainly, Lestestrin was the first drug that was approved, has done a great job of developing, from what I can tell, the market to their credit. The other companies are following. But, again, from an efficacy standpoint, you really don't see differentiation. The only differentiation I think you'll see is just in potentially the indications where they're trying to develop their drugs.

I see. Okay. And have you done any subgroup analysis in that ER-SR1 mutation versus wild-type setting? And do you see any differences between these two subtypes? And then also, what is the, like, in the Victoria 1 study, between the study 1 and 2, how do these patients compare the ESR1 mutations?

So in our study, we did not break out subgroups and did not end up, unfortunately, generating data for ESR1 mutational status. We enrolled ESR1 mutant wild-type patients just because they're part of the population, typically defined between 35%, 40%. But we started the study before ESR1s had been a validated biomarker, so it wasn't an area of focus. And that actually is what occurred with the other drugs evaluating in our class, this population. So our results represent an agglomeration of results that include both ESR1 mutant patients as well as those who have a wild type.

I see. But was ESR1 mutation measured? Could you do that in the future?

Going forward, yes, certainly we can. We just need to incorporate it in the protocol and have that analysis done. But we wouldn't expect, just because ultimately we found this with CDK4-6, it tends to be a class effect. If you're inhibiting all three pathways, essentially, as comprehensively as Geta does, good can be good enough. We saw, for instance, no difference between ribo and palbo in outcomes. Patients had prior ribo or palbo when patients got retreated with palbo. In studies that had evaluated patients who had received prior palbo and then were subsequently retreated with palbo but with a different endocrine therapy, saw no benefit. And so in our case, we saw a fantastic benefit with patients who had received prior palbo because you were controlling this pathway, and essentially as long as that pathway was controlled effectively, you were going to get the benefit. And so we think the relative benefit may be more muted when you comprehensively shut down the pathway of PAM than when you're not. And so the mutation will play a more important role when the other pathways are not controlled.

I see. Yep. That makes sense. What is your view of this emerging class of the CAF-6 inhibitors? So it seems to be complementary to the CERT. I think we saw some data from Pfizer. I think Lima is going to have this combination data coming out later this year or 2027. how do you see CAP6 as a potential emerging competitor?

Well, it's another target. We think the biology is well understood in breast cancer. You have three cooperative pathways, ER pathways, CDK4-6, PAM pathway, and that directly inhibiting those, in our view, is likely to yield the most favorable benefit. Hitting a different target that's more downstream It may be a successful strategy to get something that could be better relative to endocrine therapy, and so it may be an approvable approach. I'm not sure it will be a better approach.

Or potentially it could be another combination agent for Geta, too.

I mean, again, I think it's early days on that target.

And you mentioned that you guys are developing a subcutaneous formulation for Geta. What is that timeline and the status for that?

And that program is essentially running in parallel with a Phase III study that we're running in patients, first-line breast cancer patients, who are considered to be endocrine-sensitive. And these are women who, on the current standard of care therapies, are getting roughly 25 months median PFS. We reported in that segment, in an early phase study, median PFS of 48 months. So a very, very long duration of benefit, early phase, single-arm study. so you have to take it with a bit of a grain of salt, but very encouraging. So clearly at least demonstrating in our view that this pathway is intrinsically involved irregardless of mutational status or prior treatment, or independent of prior treatment. And so given the duration of treatment that these patients could potentially be on with our drug, we wanted to offer a sub-Q alternative, and so the development timeline will run in parallel with our plan. with the development and performance of that study. And so that at the time things go the way we hope, we get favorable results and get an indication to treat those patients approved, we would have a sub-Q alternative formulation available to those patients. And we think it makes sense. That would certainly help optimize the penetration potential for that patient population.

I see, okay.

In the other settings that we're in, we found our research indicates The current IV formulation doesn't create a barrier to infusion, or rather to achieving what we think are the appropriate penetration targets in those segments.

So with that formulation, would that work for the second-line setting and also the first-line setting?

So typically the FDA wants you to demonstrate in one setting if you're using the same molecule equivalence, non-inferiority. And if you do that, then the approval will allow you to use the formulations interchangeably and other indications.

For all settings. For all settings. So let's switch gears to the front line. There's a lot of things happening there, too. You have the Victoria 2 study. And then you also have study 1 and study 2, one for endocrine resistant and one for endocrine So when I look at this Victoria 2, it's almost like two studies. Two different phase 3 studies. So, and then when you look at that, the study population, I think for the study one is around 440, and then the other one is 740. So these are smaller. If I look at it individually compared to the front line, like Persevera, like Serenifor, I mean, how do you think about the size of the study? Is it too small? No, no, it's actually appropriately sized.

Essentially, the number of patients you enroll is a function of what your underlying assumption is about the effect size difference you'll see, i.e., what do you see in this case, our regimen versus the control. The larger the projected effect size is, that difference, smaller number of patients required to detect that difference in a statistically significant way. In the case of these other studies, essentially they're replacing one therapy of a particular class for another, like one hormonal therapy versus another. Typically, the effect size potential is much smaller, and as we found, unfortunately, with the study with gerogestrin, it wasn't meaningful enough. When you're adding a new class of drug to address an untreated disease mechanism, the potential benefit is much greater, and as we showed in our early phase study, it would potentially double the outcomes for these patients. Well, if you're offering that magnitude of benefit, the number of patients required to detect it, again, is correspondingly smaller. And so, to be frank, we're relatively overpowered, we think, in the endocrine-sensitive population relative to the benefit we expect, and similarly in the other study. So we're very confident that these studies are powered appropriately and essentially reflect what we think is the clinical benefit of controlling this pathway versus not compared to control.

Okay, got it. And then you guys use palbo plus fulvestrin or palbo plus AI in the study one and two, respectively. But then you swap out the palbo for ribo in the comparator arm. What is the rationale for that?

So ribo is the standard of care because it had no S-benefit. And so that was clear from a comparator standpoint that we need to offer patients the standard of care. Now, when you combine a CDK4-6 inhibitor with a drug like GEDA, we think the differences that are potentially available to patients are essentially not going to be meaningful. If you look at a PFS standpoint, palbocyclib and ribocyclib offer identical profiles in terms of hazard ratios, even duration of benefit. And palbocyclib is generally considered and almost very widely considered than ribocyclib. And so, given the duration of treatment, we're optimistically hopeful that patients experience in the triplet, in the first-line setting, we think tolerability is actually more important and that essentially we'll be getting equivalent efficacy that we would otherwise have gotten if we had used ribo. And so, we elected to choose the more tolerable CDK4-6 inhibitor for our study arm.

And then what is the bar for efficacy and safety in that frontline population given that the quality of life is important to patients who can run that trial for a couple years? And then maybe remind us about your prior phase 1B result in those 41 patients and how translatable are they to phase 3?

Well, certainly, you know, small phase, you know, a sample size of 41 is not necessarily 100% translatable. But what it provides is an important signal. The patients had 100% measurable disease, and so they had essentially a significant tumor burden for that setting. When you see a delta of 2X relative to what has been reported for historical studies with the same population, that's obviously encouraging. The GEDA has been very well tolerated to date, we found in the second-line settings. Discontinuation rates, which is kind of an uber metric for assessing tolerability, was between 2% and 3%. So that's actually historically, if you were to look at other drugs evaluated in breast cancer, that's actually very low. So we think net-net patients can stay on GEDA. We have still patients. We have patients who've been on GEDA from our early phase studies for over five years. And they're continuing to come in. and continuing to receive benefit, which is great for them. And so if you can offer a clinically meaningful benefit, it's probably in the five- to six-month range relative to control in this setting, proportionately hazard ratio 0.75, just as an example. I think the challenge for the oral surge that we're evaluating this population is that the clinical benefit was not achieved, and as a result, again, that just reflected the lack of benefit of replacing one drug with a different, rather, having an alternative from the same class of drug might not be the way to optimize outcomes for those patients. You need to inhibit what is an untreated disease mechanism, in this case the PAM pathway, to take the leap in improvement for these patients.

So when we look at Persevera, it did show about five-month benefit in PFS, but that did not translate to statistical significance.

But if you look at the hazard ratio, it was 0.89 hazard ratio, and so that's the number that matters. And, again, that's, to be frank, not even close. Right, yeah.

So how many months of benefit do you think it takes to get that?

Well, STAT-SIG typically can be achieved less than what's clinically meaningful in these studies. That's always the trick is to make sure you're not just powering a study to detect a statistical difference when it's not going to be clinically meaningful. So we design our studies to make sure that we're going to be able to detect a clinically meaningful difference. And, again, in this setting, probably five to six months, you know, that's statistically significant, i.e. hazard ratio in that 0.75 range plus, I think would be considered clinically meaningful.

Okay, fantastic. We probably have time for one more question. So I want to ask you a more blue sky question. So as the adjuvant continues to trend to it, the CDK4-6 combination compared to just AI monotherapy, and then you saw the gerodestrin success with Lidera, how do you see the treatment paradigm changing in the next three or five years and the effect from that, the changes in that adjuvant setting percolating to the front line, to the second line plus.

It's going to have, the short answer is it will have a nominal effect. You know, the women who are getting treated in the adjuvant setting can typically expect most of them to not have the disease recur. You know, 75%, 70% won't have the disease recur. And so these drugs are going to lower their recurrence rate by a few percentage, which is great for these women. But the downstream effect will take a decade. And unfortunately, as the incidence of breast cancer increases, I think the number of women that get ultimately diagnosed with metastatic disease will probably, even with the benefits from the use of these adjuvant therapies, will be offset by just the increase in overall incidence. For instance, roughly 40% of women who are diagnosed with metastatic breast cancer are diagnosed de novo. They did not have diagnosis of early disease. Essentially, it was diagnosed with metastatic. And that number has been increasing. I don't think scientists understand what's driving that. But that's a patient population that isn't at all affected by potential treatment in the early disease setting. So, again, it's a very good option for patients to have the reduction of likelihood of recurrence. But, again, it's going to be almost an intangible, or rather not a significantly detectable difference in the populations that we'll be treating with our drugs.

Fantastic. Well, we're out of time. It's been a very interesting conversation. Really appreciate having you here at the GS conference, Brian. and then I'll turn it to you for a final remark.

No, we're very excited. I mean, we're kind of a few weeks away from what we think will be a positive approval decision from the FDA. We're really excited about being able to offer our drug to patients. And we have two additional phase three studies to treat roughly 90,000, we hope, to develop the therapy for the 90,000 women a year who are diagnosed initially and require that first-line treatment. And data we've received in the second-line setting certainly gives us a lot of encouragement and optimism that we could potentially extend get a solicit to offer a very, very meaningful benefit to those women. And, again, that would be great. Fantastic.

Thank you again.