Celcuity at Leerink Global Healthcare Conference: Promising Cancer Drug Insights

On Wednesday, 12 March 2025, Celcuity (NASDAQ: CELC) showcased its strategic vision at the Leerink Global Healthcare Conference 2025. The discussion, led by Brian Sullivan, focused on the company’s promising cancer drug, getotelisib (GETA), targeting breast and prostate cancer. While the drug’s comprehensive pathway inhibition approach presents exciting potential, concerns about its intravenous administration were addressed with confidence.

Key Takeaways

• Celcuity’s lead asset, getotelisib (GETA), targets both breast and prostate cancer with a multi-node inhibition strategy.
• Promising early phase study results show effectiveness in both PIK3CA wild-type and mutant patients.
• The company is optimistic about upcoming Phase III data readouts, which could establish GETA as a new standard of care.
• Celcuity aims for significant market penetration in a five billion dollar market, with potential blockbuster status.
• Safety concerns, particularly hyperglycemia and stomatitis, are being proactively managed.

Financial Results

• The potential market for GETA is estimated at five billion dollars.
• A 30% to 40% market penetration could position GETA as a blockbuster drug.

Operational Updates

• Celcuity is conducting three Phase III programs, including two readouts expected this year.
• Over 500 patients have been enrolled in studies, demonstrating GETA’s tolerability.
• The dosing schedule for Phase III is three weeks on, one week off.
• Dexamethasone mouth rinse is used as prophylaxis, reducing stomatitis events by 90%.

Future Outlook

• Phase III data for the wild-type population is anticipated in Q2.
• Success could lead to meaningful market penetration with a significant improvement in progression-free survival (PFS).

Q&A Highlights

• PIK3CA wild type includes both ESR1 mutant and wild type.
• The discontinuation rate for GETA is comparable to existing treatments like palbociclib/letrozole.
• Stomatitis is effectively managed with steroidal mouth rinses.
• GETA’s multi-node inhibition is 300 times more potent than single-node inhibitors.

For further details, please refer to the full transcript.

Full transcript - Leerink Global Healthcare Conference 2025:

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Good morning, everyone. I’m Andy Behrens, Senior Biotech Analyst at Leerink Partners. Thank you for joining us on the final day of our Global Healthcare Conference in beautiful and sunny Miami. We’re very excited today to have Brian Sullivan from Cellcuity join us. Thank you, Brian.

You’re

Brian Sullivan, Cellcuity: welcome. It was my pleasure.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Why don’t we start with a brief overview of the company and then we’ll dive right in. There’s been a lot of interesting data in your area that we’re going to talk about, but I think it would help to have an overview of the company for those who may not be familiar with Cellcuity.

Brian Sullivan, Cellcuity: So I started the company a number of years ago initially to focus on development of a platform that could analyze and characterize the activity of signaling pathways in living tumor cells. And so we’ve essentially then evolved over time towards development of our own drug. Our lead asset is getotelisib. It’s a pan PI3K mTOR inhibitor. We have three current programs in process, Phase III program that will have two readouts this year, one in a wild type population, PIK3CA wild type, the next one in PIK3CA mutant patients.

And then we just initiated a Phase III study in first line breast cancer patients. The other study I just alluded to was a second line study. And then we have a Phase 1btwo study in process in castration resistant prostate cancer. And we can go into more detail later.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. Why don’t we talk about the rationale behind bringing in a drug that hits two nodes in the pathway. Other companies have chosen to go very selective or even super selective. What do you think the advantages are from GETTA versus that approach?

Brian Sullivan, Cellcuity: Sure. So while we were developing our platform, one of the pathways of interest to us was the PI3KAKT mTOR pathway. We call it the PAM pathway. And one of the questions that I wanted to answer internally was just how could a pathway that’s so important as an onco driver had the highest proportion of patients with mutations associated with the pathway be so under drugged? At that time that we started looking into this, there was no approved PAM inhibitor or there was one everolimus mTORC1 inhibitor.

And so we started developing a way to characterize signaling activity in this pathway. Along the way, we as part of our development process, we characterized in a bit how good these various inhibitors are. And one thing popped out and one drug in particular stood out to us, and it was gatatilisib. Gatatilisib is actually a pan PIPK mTOR inhibitor. So it actually hit six nodes, the four class one isoforms and then mTORC one and two.

And it was clearly superior as an inhibitor of PAM pathway associated activity. And we thought, wow, this is a fantastic drug, clearly differentiated. And we had a relationship with Pfizer. Pfizer held it at the time. And we thought, let’s collaborate and on development of this drug.

That’s when we found out that they were out licensing it. And so our decision was really fundamentally based on this conundrum of underdeveloped pathway probably reflects the minimal targeting of this pathway. And that reflects the nature of the pathway itself. It’s very complex. Most pathways that are drugged in oncology have a single target.

This pathway has six targets, these class I isoforms and mTORC1 and two. And when the pathway was discovered as an onco driver twenty years ago, because of the understanding of this complex structure, every major pharma had a pan PTH3 mTOR program in place. And none of them made it out of Phase one. And so the reaction was or response was to narrow the focus to inhibition of only single nodes in this complex pathway, pf3 alpha mTORC1 AKT. Problem with that approach is that you essentially are compromising efficacy because the biological imperative requires you to inhibit or to optimize efficacy at least to inhibit the pathway comprehensively, which requires control of all those nodes.

And so on the one hand, these drugs have gotten approved. They got through the therapeutic window because of the challenges with toxicity. But in our view, they haven’t optimized efficacy. And internally, and we published data that has shown that with a pan PI3M4 approach that GETTA takes, the potency and our ability to inhibit cell proliferation is 300 times greater than it is with single node inhibitors. So it really provides a kind of a mechanistic assessment of how important multi node inhibition is relative to single node inhibition.

So the drug we think has solves the riddle that has been challenging to optimize the potential impact targeting this pathway can offer patients, at least initially in breast cancer and hopefully prostate cancer as well.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. And maybe it would help to just broadly go through the data that you’ve demonstrated to date. The drugs in Phase III. There’s a couple of big readouts coming out. We’ll talk about those shortly.

But what have you guys shown with this approach? And I know that some of the narrow drugs that you’ve mentioned, the response rates are usually single digits, low double digits. Some of them have been able to alleviate the hyperglycemia you see with some of the other agents. But what have you guys demonstrated that could support the hypothesis you just mentioned? Sure.

Brian Sullivan, Cellcuity: So in our early phase study, we enrolled 138 patients, four different cohorts based on their prior treatment history. In the treatment naive cohort, patients received GATA and then standard of care, which was Palbo and letrozole, reported forty eight months median PFS, objective response rate of seventy nine percent, which compares very favorably to published data for that reg for the Palbo letrozole regimen. And then with our Phase III dose in patients who had prior CDK, we reported twelve point nine months median PFS and objective response rate of sixty three percent. So again, those numbers compare very favorably to current standard of care. And one of the other very relevant factors is that because of the approach the drug takes by inhibiting it comprehensively, it’s able to at least the preliminary data suggests that we can induce comparable efficacy independent of the status of the PIK3CA pathway.

So PIK3CA wild type patients and PIK3CA mutant patients get about the same response. Whereas the single node inhibitors today, at least, and we wouldn’t expect it to change over time, have only demonstrated activity in patients who have a PIK3C mutation. And so the drug has the potential really to offer an all comer solution for patients and for doctors to prescribe and greatly simplify the treatment paradigm. And more importantly, particularly for wild type patients because there really is very limited options that have an endocrine backbone right now that offer meaningful benefit.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Right. And let’s I just want to define wild type because we have some other drugs that have ran out one yesterday. Your wild type includes ESR1 mutant

Brian Sullivan, Cellcuity: mutations, right? Yes. So essentially, we’re not factoring in ESR1 status. And when we define wild type, it’s PIK3CA wild type, and that include ESR1 mutant and wild type. Similar for mutations of PIK3CA, we’re enrolling both ESR1 mutant and wild type.

We haven’t found our early data we haven’t published this, but we did not see any difference in outcomes based on ESR1 status.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. And that’s irrespective of whatever endocrine therapy is potentially used? Interesting. Okay. And then in terms of some of the concerns I’ve heard about investors is going broader, great, maybe more efficacy, but they’re going to hit they’re going to have more safety toxicity.

So what have you seen with the key events of interest?

Brian Sullivan, Cellcuity: Sure. So one of the great characteristics of the drug is how well tolerated it’s demonstrated, at least in the early studies. So over 500 patients have been studied with the drug and have published results. And in breast cancer, we had cohorts of patients that received the weekly dosing. The discontinuation rate for those patients was around nine percent.

That’s almost exactly the same level as you would see for palocycloblitrazole. So the addition of GETA to that regimen didn’t add incremental toxicity that required patients to discontinue. Whereas with the Phase III dose, for the second line setting and beyond our current studies, It’s a three week on, one week off schedule. The discontinuation rate was less than four percent. And again, below the published data for discontinuation rate for CDK and hormonal therapy.

So our conclusion is, and we’ll see with our Phase III data, is that GEDA has proven to be at least so far or demonstrated at least that it’s well tolerated, doesn’t require people to get off the drug and essentially doesn’t incrementally add toxicity relative to the doubling that it’s added to. And so as we think about the positioning of the drug, we’d say that the safety tolerability is it will actually I mean, again, we’ll see, but indications would be that it would be better tolerated than, for instance, the doublets that have PAM inhibitors today and certainly as well tolerated as CDK4six and hormonal therapy.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Right. And what about adverse events of interest like hyperglycemia?

Brian Sullivan, Cellcuity: So hyperglycemia has been somewhat the third rail on this pathway, and that’s because the PAM pathway regulates glycolic function. That function takes place in the liver and particularly with oral drugs that are processed first pass through the liver. You disrupt that activity and can induce very high levels of hypoglycemia. GATA is an infused drug, IV administered, so you avoid the liver on first pass. And other characteristics of the drug result in optimal exposure for tumor control, but not so great that you are inducing unacceptable levels of hypoglycemia.

So we reported to date about twenty five percent overall hyperglycemia, and that compares with the other inhibitors out there that are sixty percent, seventy percent, eighty percent hypoglycemia when you measure glucose levels. Some of the ALFA inhibitors coming out looks like they’ve figured out how to optimize targeting for mutant versus wild type, and that can create favorable hypoglycemia. But for us, it hasn’t been a reason for either discontinuation or dose reductions in the course of development of that drug. So we think that hypoglycemia is off the table. The one adverse event that we do require that does require management is stomatitis.

Stomatitis is kind of typically induced by this class of drugs. Interesting feature of the our drug though is that it responds even if you don’t have a prophylaxis for it. If you’ve basically given the drug, you experience a somatitis, responds very effectively to steroidal mouth rinses. And so that’s why we haven’t really seen discontinuations due to somatitis because these most patients, great majority respond well and reverse stomatitis with this mouth rinse. But to avoid that and to really hopefully optimize the patient experience For the Phase III studies and the ongoing studies going forward, we’re giving patients the mouth rinse as a prophylaxis upfront for the first couple of cycles.

And there’s some data that suggests you can reduce by ninety percent grade two or greater stomatitis events if patients for the first two cycles use this dexamethasone mouth rinse. So it can be very impactful. So we think going forward, we’ll see when we report our data. But we would expect to report more favorable stomatitis events than what was reported in our early phase data.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. And then I guess just to close the loop on mTOR. You know, that drug there has been a number of mTOR inhibitors for a while. What have they shown in this type of setting?

Brian Sullivan, Cellcuity: Sure. There’s one that’s approved. It’s an mTORC1 inhibitor called Everolimus. Novartis has that drug. And so that drug had challenges upfront when it was launched.

Stomatitis wasn’t very well managed by this dexamethasone mouth rinse. They had twenty four percent discontinuation rate when it was launched. So it had trouble getting much penetration. And that’s likely a function of just daily dosing, high molar amount of drug given to the patient over the course of every month. And they subsequently found though, and they were the ones that ran this randomized study, found that in the case of their drug, if they give the dexamethasone as prophylaxis, patients take it while they’re receiving treatment, it really greatly affects it.

So that’s been very helpful for that drug. But there’s no data right now in the post CDK setting for that drug’s efficacy. There have been a couple of retrospective studies that have looked at chart done chart reviews and found it’s offering three to four months in the wild type setting. But again, it’s not randomized data. It’s not clear really what that drug is doing.

But again, kind of confirmed the importance of mTORC, at least mTORC1. We think mTORC2 is also important as a part of the feedback loops in this pathway and GATA inhibits both. So we think we’re able to optimize mTOR related activity as well. And again, it’s been demonstrated to be very relevant.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. By hitting the pathway in two locations, in two nodes, are you able to lower the amount of coverage you need for each individual pathway? Like in other words, by adding mTOR, does that mean you don’t have to hit the PI3K pathways as hard to get the same level

Brian Sullivan, Cellcuity: of efficacy? So I think sometimes people conflate potency with toxicity. And I think in this pathway, the toxicity is obviously related to potency and on target effect, but more related or asthma related to target organ exposure. So for instance, liver for hypoglycemia, GI for GI related toxicity. And again, as an infused drug, you avoid those two organs in first pass.

But what’s interesting about GETA is that it is equipotent against all six of these nodes, low nanomolar concentrations or subnanomolar concentrations. And when you compare the activity of the drug as an inhibitor of tumor cell proliferation, you need twelve nanomolar to get a half maximal effect. Whereas with the single node inhibitors, to have half maximal effect on their proliferation potential, they need 300 times more drug. And that just reflects the more limited biological potential of inhibiting a single node. But that if you do inhibit this pathway comprehensively and in effect shut off these resistance mechanisms, you subsequently need a lot less drug.

But against each individual target, you’re for instance, our drug, when you assess it biochemically in a cell free assay, is tenfold more potent against alpha nenapalipsoid or the relay compound, as an example. So you actually it’s a get the best of all worlds. By being very potent comprehensively, you ultimately need less drug to induce the on target effect that you’re seeking.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. Why don’t we before we talk about the trial you’re running and the big readout you have coming imminently, why don’t we just talk about a couple of the data sets that have come out recently? I know we’ve chatted about EMBER before. I guess we can start with that one, but I’d also like to talk about SIRENA six, which I thought was a brilliant study. And I’d like to hear your perspective because I don’t think we’ve chatted about that since the top line came.

Brian Sullivan, Cellcuity: So the EMBER three study, I think it’s a confusing study because of the mixed populations they enrolled. They enrolled first line patients and second line. They didn’t break out that data. So very hard to essentially with what they published to know exactly what that drug is doing. When we tease it out, it looks like nominal effect as a monotherapy, no effect on YSR1 mutant wild type patients.

We think nominal effect in that population even with the Abema addition. So we don’t think there’ll be much overlap with that combo, which is a question of whether it’ll get approved because of the trial design. But take that off the table, assume it does. We think there’ll be very limited overlap with what we’re doing. And as far as this SIRENA six study, no, great, very interesting switch strategy for patients who develop these mutations.

I think there’s going to be an operational component associated with deployment of that study. We’ll certainly optimize first line experience for these patients switching hormonal therapy to optimize for patients that develop an ESR1 mutation. I don’t think it will necessarily impact us downstream. I think the PAM pathway is involved intrinsically in this disease. Our first line data really provides a pretty interesting demonstration.

If you were to look at the impact of hormonal therapy in the first line setting with letrozole, you’d see about fourteen months median PFS. If you bolt on Palbo, CDK4six inhibitor, you get a near doubling with that drug. So clearly, CDK4six is important. And our data, which again, you have to be wary of cross dollar comparisons, it’s a single arm study. But nonetheless, we reported forty eight months median PFS, which we think suggests and kind of provides demonstration of the relevance of this pathway in this disease overall, not essentially as a consequence of resistance to the initial treatments they’ve received.

And so that’s why we made the decision to go into the first line as early as we could because we think that the hypothesis the rationale for that is very strong scientifically.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Yes. I almost I’d like to hear your thoughts on this. I mean, I don’t know if there are data out there yet, but I feel like if you can actually bring in a drug that’s active, an ESR1 mutation, to the front line or whatever you want to call it, front line 1.5, it could obviously, it should block the ESR1 mutation from being an escape pathway. And it could put more emphasis on PAM, which

Brian Sullivan, Cellcuity: Exactly. The PAM pathway is involved. And really, when people think of breast cancer, they should think of it as involving three cooperative pathways, uro pathway, CDK46 pathway and the PAM pathway. And optimal tumor control, at least our data suggests certainly, would require comprehensive inhibition of all three of those pathways. And certainly, you can optimize in the case of ESR1 mutation patients a control of the ER pathway, but that doesn’t make the PAM pathway less relevant.

As you said, it suggested it could make it more relevant. And so I think the PAM pathway, in our view, clearly needs to be inhibited to optimize outcomes for patients. And we’ll have data hopefully that confirms that in the Phase III setting, but certainly the preliminary data suggest that.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. So why don’t we talk a little bit about the Phase III pivotal program, the readouts that you have. I know you’ve been asked probably 10 times as many times as I have about the bar that you’re looking for in the first readout and then the second readout. So why don’t we go through the two binary events you had that are very broad catalysts?

Brian Sullivan, Cellcuity: Sure. So we expect to report out next end of Q1, sometime in Q2 data for our wild type. We have three arms. We’re evaluating GATA, palvaciclib and fulvestrant, triplet, and comparing that. And one primary endpoint versus fulvestrant is to control.

And we have another arm that’s GATA fulvestrant, arm B, that we’re also comparing to fulvestrant. We’re testing those hierarchically, so we’re sparing off, so we’re optimizing that analysis. And as far as expectations, if you were to look at the data that’s been generated the past few years with fulvestrant from inpatients who had prior CDK, you’d see fairly consistent results essentially in this two to three month range. And so we think it’s most likely that the control would don’t want to be too precise, but in that range. And so we’ve heard pretty consistently from regulators as well as KOLs that what really will determine or establish a new standard of care is a delta relative to, in this case, this control of three months.

That’s not necessarily what we hope for, but three months delta PFS will essentially, according to the regulators and KOLs and certainly the community docs we’re speaking with, motivate usage of a regimen that offers that and would allow you to get very, very meaningful penetration. The market itself is very, very significant, dollars 5,000,000,000 served market potential with proprietary drugs. So there’s a there there. Even I’m not suggesting and projecting anything from a penetration standpoint. But it does point out that even with just a 30% to 40% penetration, you can build a blockbuster indication.

And so certainly, more than three months is better. So we would hope, but again, the data will be reported and we’ll see soon, to have as maximum a delta as we could. But the delta to be in the game and to be relevant, to be a potential standard of care is about three months.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. And how important is the doublet arm in the readout, do you think?

Brian Sullivan, Cellcuity: Readout so essentially, we added that primary analysis really to give us the potential to submit that for an approval as well as and so we wanted to make it a registrationable endpoint. And if it is registered and so it’s at our option, our discretion. It’s not required for success. If AC is successful, that will carry the day. But the rationale for it is to just provide doctors, if the data bears this out, with an option.

This is not a homogeneous population, and some patients become not only refractory to CDK, but they can’t tolerate them for whatever reason. So if we have an option that allows doctors to prescribe their patients get a fulvestrant, as an example, may not provide optimal tumor control, but for that patient, it may be the best option available to them. And it would provide a way to, we think, maximize overall penetration of the drug in this setting.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. And then the Fluvestrin arm will have patients with ESR1 mutation in it.

Brian Sullivan, Cellcuity: Yes.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: What percentage do you think you will get based on valuations?

Brian Sullivan, Cellcuity: Well, the data to date shows that there’s no difference in outcomes between patients with ESR1 mutations or wild type with fulvestrant. So essentially, the control arm is going to be what it is independent of a mix of patients with that mutation. But if the data is consistent, if the patient population is consistent with what’s been reported with some of the SIRDS studies, you’d expect between thirty percent and forty percent of the patients to have an ESR1 mutation.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. And then subsequent to this readout, you have another Phase III readout

Brian Sullivan, Cellcuity: in mutations? Yes. So, exactly. And so there, we’re comparing our triplet GETTA PAVO FULVESTRAIN to Opalypsob and FULVESTRAIN. And Opalypsob has reported median PFS in the five point five to seven point five month range.

Again, not a huge amount of data. So we have our internal assumptions about what we expect there. And so again, similar delta, I think, is required to be considered clinically meaningful about three months and if we’re able to do that. Now what’s interesting is that another PAM inhibitor was recently approved called Capivasitor AKT inhibitor. It didn’t demonstrate it didn’t directly compare to Opalypsob, but their data, if you just do a cross trial comparison, was comparable or you could even argue maybe a little worse, lower efficacy, but much better safety profile.

And so there’s been a rapid shift away from Opelipsib. And then as they’ve also, because of the better tolerability, been able to expand the penetration of that drug. And so in less than a year, they’re at a $600,000,000 run rate, primarily just because of the safety advantage, which I think highlights how desperate oncologists are to find better solutions for these patients. Obviously, what they’re hoping for is better efficacy and good tolerability. But if they’re not even getting better efficacy, they’ll switch very quickly to a drug that offers their patients better quality of life.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: When we see the first data release in the wild type patients, what would you expect to see as a step up to the mutant population?

Brian Sullivan, Cellcuity: So early phase data suggests that it’s comparable, but there’s a numerical advantage relative to the wild type data. And again, this is preliminary data, but sixty percent of patients in the mutants cohort were progression free at twelve months. With the data published for Opelipsa as an example, I think less than it was about twenty five percent were progression free at twelve months. So we think, again, if you just look at that preliminary data, it suggests we should see, we hope, a meaningful delta. That same number for the wild type patients was around forty nine percent.

And that because of the way the Kilometers curves are shaped, that can create somewhat of a delta. It’s hard to predict because you don’t quite know the slope of the curve. But so we would expect there to be a differential. I don’t want to speculate what that would be. But I would expect it to be higher in the mutant population than in the wild type population of PFS.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Okay. And then just maybe, at the last minute we have, one of the concerns of some investors, and I know we’ve chatted about this before, is the implications commercially of an IV drug in a setting that seems I mean, fulvestrant obviously doesn’t seem to be going anywhere, but a lot of the physicians are hoping to have oral options. So what do you see as

Brian Sullivan, Cellcuity: a Sure. Well, the point of the realm in oncology, as is the case in most diseases, is efficacy, right? The guidelines basically are, for the most part, oriented around recommending regimens that offer superior efficacy relative to the alternatives. The second criteria that they emphasize is tolerability. We want to maintain as long as possible a patient’s quality of life.

And so that’s the benefit risk calculation. The route of administration really isn’t a consideration that’s even taken into account with these guidelines and typical recommendations. Now certainly, all things being equal, if you have two drugs that offer similar safety and efficacy, one has a better route of administration, that’s going to be an advantage. But if you have a regimen that is offering better efficacy and is well tolerated, I think there’s very few and again, based on our internal research, we think it’s very small number of docs that wouldn’t want to make that an option for their patients. And so the other, I think, consideration to understand is that breast cancer, the largest drugs are all infused drugs.

Herceptin was launched as a weekly drug twenty years ago, twenty five years ago now, offering a three month delta in efficacy. Obviously, they built that into a $6,000,000,000 peak revenue drug, added PERJETA, another infused drug. Certainly, the and HER2, the new ADC, has not found any limitations with infusion. So there’s an infrastructure in place. These docs know how to essentially deploy and manage infusion.

And then there’s other advantages in this setting from a managed access standpoint. These docs get to recover costs when they infuse patients. They get capture some of the cost of the prescription for these patients. Because it’s a medical benefit as an infused drug, patients aren’t exposed in the same way they are with the prescription to copay risk. So there’s a lot of actual advantages from a docs perspective in prescribing their patients’ infused therapy.

And then there’s the compliance question. They know their doc, their patients are taking the drugs because they’re showing up and then know if they don’t show up, which is a consideration with some oral therapies. So overall, that’s we just don’t think it’s a relevant factor given what we think the safety and efficacy that we hope to report will be.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Great. Well, we’re waiting for the data, as I’m sure you are and a lot of the investors. So we look forward to when you turn over the cards.

Brian Sullivan, Cellcuity: Yes. Great. Well, thank you.

Andy Behrens, Senior Biotech Analyst, Leerink Partners: Thank you, Brian. Thanks, everyone, for joining us.

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