Kymera at BofA Conference: Strategic FDA and Manufacturing Insights

On Wednesday, 14 May 2025, Kymera Therapeutics Inc (NASDAQ:KYMR) participated in the BofA Securities 2025 Healthcare Conference. Led by CEO Nelo Minolfi, the discussion focused on the company’s strategic interactions with the FDA, plans to enhance U.S. manufacturing, and the anticipated data from their STAT6 degrader, KT-621. While the company shows promise with its innovative approaches, it also faces challenges in a competitive landscape.

Key Takeaways

• Kymera is committed to sourcing commercial materials in the U.S., enhancing domestic manufacturing infrastructure.
• The company expects to release healthy volunteer data for KT-621 in June, with Phase Ib data in atopic dermatitis patients anticipated in Q4.
• Kymera’s cash position of $775 million is projected to sustain operations into the first half of 2028.
• The STAT6 program aims for significant degradation of STAT6 in blood and skin, potentially replicating the effects of dupilumab in an oral form.
• The competitive landscape for oral atopic dermatitis drugs includes safety concerns with existing JAK inhibitors.

Operational Updates

During the conference, CEO Nelo Minolfi highlighted Kymera’s commitment to enhancing U.S. manufacturing capabilities. The company plans to source commercial materials domestically, reflecting a strategic shift towards strengthening local biopharma infrastructure.

Minolfi confirmed ongoing interactions with the FDA, stating that there have been no significant changes despite structural shifts within the regulatory body.

Clinical Development

Kymera is advancing its STAT6 program, which targets a 90% or greater degradation of STAT6 in blood and skin. The company has initiated a Phase Ib study for KT-621 in atopic dermatitis (AD) patients, with results expected in Q4.

The STAT6 degrader represents a novel approach, potentially offering an oral alternative to dupilumab by addressing inflammation through the Th2 pathway.

Competitive Landscape

The market for oral AD drugs remains competitive, with Kymera positioning its STAT6 degrader against existing JAK inhibitors, which carry safety concerns. The company anticipates that its oral solution could achieve success even if slightly less effective than current treatments, provided it maintains a favorable safety profile.

Future Outlook

Looking ahead, Kymera expects to report healthy volunteer data for KT-621 in June, followed by Phase Ib data in AD patients in Q4. These developments are part of an aggressive plan to advance their pipeline across multiple indications.

With a robust cash position of $775 million, Kymera is well-positioned financially to continue its operations and research initiatives into 2028.

Conclusion

For a detailed account, readers are encouraged to refer to the full transcript of the conference call.

Full transcript - BofA Securities 2025 Healthcare Conference:

Tazeen Ahmad, Senior SMID Biotech Analyst: America conference. I am Tazeen Ahmad, one of the senior SMID biotech analysts at the firm. It’s my pleasure to have with us our next presenting company, Chimera. Sitting next to me on stage is CEO Nelo Minolfi. Nelo, thanks for making the trip out west to see us.

Nelo Minolfi, CEO, Chimera: Thank you, Tazim, for having us.

Tazeen Ahmad, Senior SMID Biotech Analyst: So we’re going to just start off with a couple of macro questions because I think it’s topical and you’ve probably had to answer this a couple of times anyway, so let’s just get it out of the way. Can you talk to us about your interactions with FDA? More importantly, the more recent ones, let’s say over the last couple of months, has there been any change that’s noticeable either in who you’re speaking with, topics of discussion, etcetera?

Nelo Minolfi, CEO, Chimera: You know, I will say that this is too loud,

Unidentified speaker: no? No.

Nelo Minolfi, CEO, Chimera: It feels too loud. I will say so first, again, for having us here today. So we’ve obviously, we have several ongoing interactions with the agencies both in The U. S. And outside of The U.

S. We have not seen any material changes in our interactions. So I obviously I hear that obviously, and I see that there are structural changes and different hires, but we haven’t seen that, at least so far in our direct interactions, we haven’t seen that change materially.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay, that’s good to know. And then in terms of, we’re thinking ahead, but in terms of where you plan to have manufacturing be, can you share with us any details?

Nelo Minolfi, CEO, Chimera: Well, know, we do everything that we do is done in different countries. We do obviously a lot at Chimera in Weathertown, Massachusetts, if anybody wants to come and visit. We source also some of our raw materials globally. And obviously, what we do for our we’re not a commercial stage company, we’re a clinical stage company. But we are committed to making sure that we source our commercial material in The U.

S, at least the material that will eventually be commercialized will be done in The U. S.

Tazeen Ahmad, Senior SMID Biotech Analyst: And for that, that’s for any portion that’s not done in The U. S, do you have any, I guess, redundancy plans if needed to bring that onshore?

Nelo Minolfi, CEO, Chimera: Yeah, look, I think this is a much bigger conversation. If we want to get there, the question we need to ask ourselves, do we have the infrastructure in The U. S. To support the biopharma industry in terms of manufacturing of drugs? The answer is no.

It’s a simple no. So if we want to go there, Chimera will be at the forefront of the investments, and we’re all in. Until then, we will continue to do what we need to do to protect our shareholder investments and manufacture where there is capacity. Right now, it’s all over the world, including U. S.

And again, I’ll say it again, I’m a huge fan of bringing manufacturing in The U. S, assuming we make investments in basic research and in infrastructure.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay, good enough. So let’s talk about some upcoming catalysts that the company has in the second, let’s say second half of the year. We’re almost done with the first half. So maybe set the summary for us and we can go into detail.

Nelo Minolfi, CEO, Chimera: Yeah, so I think June is still first half, so the first start

Unidentified speaker: of the year.

Nelo Minolfi, CEO, Chimera: Just checking.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay.

Nelo Minolfi, CEO, Chimera: Okay. So our first, the upcoming catalyst is obviously the healthy volunteer data for our KT621 that is still in June. And obviously, this is a study that we’ve said has been completed recently. We completed dosing in March actually of the last MAD cohort, And we are in the process of collecting the remaining data to being able to then present it. We’ve always committed to presenting the totality of the SADEMMAD data.

We could have obviously presented some majority of the data already, but we feel like we’re at the stage of the company where, you know, I think we want to do a good job, and we want to have one presentation instead of more than one. So that’s in June. And obviously, STAT6 is, you know, a very unique program, I would say, in this industry. I think very rarely we’ve seen that one of the best blockbuster drugs in the world, in this case dupilumab and alpha receptor alpha, has an intracellular target that has the potential to replicate the same profile. And so STAT6 being the selective transcription factor for alpha receptor, targeting STAT6 has the potential to have a dupi like effect in an oral drug.

So it’s expected that there is a lot of excitement and focus on it. You know, we’ve talked extensively about our target product profile for our STAT6 degraded KT6:one. I remind everybody, this is the first STAT6 directed agent to be in the clinic. And our target product profile is a molecule that is able to degrade STAT6 and 90% plus in blood and skin and safely. And we believe if we’re able to show that kind of profile, we would have de risked the opportunity set for this asset tremendously given how well the biology and the human genetics speaks to the relationship between IL-four 13 and STAT6.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay, can you just remind us what dosing regimen you’re testing in this healthy volunteer study?

Nelo Minolfi, CEO, Chimera: So as we’ve done pre clinically, the drug is dosed once a day, and the is a single ascending dose, and then we’ll have multiple ascending doses. So the drug is dosed once a day for fourteen days at different dose levels to evaluate, as I said, again, the safety, the PK, and the degradation of STAT6.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay, so the topic of biomarkers has come up, and so can you just remind us about which ones are being used, and when the data comes out, how to interpret that?

Nelo Minolfi, CEO, Chimera: Yeah, so the beauty about protein degradation that I think I want to make sure I spend a minute, if I may, on it is, you know, we’ve been used generally in the industry to look for a proximal biomarker to demonstrate target engagement. And so for small molecules or even biologics, usually a proximal biomarker can be a downstream chemokines, cytokines, transcript in the nucleus. And that, you know, the inhibition of that particular downstream effect is a proxy for the target inhibition. That’s historically how drug development has worked. The innovation that comes with target protein degradation, and that’s true also for, for example, RNA interference drugs, you can actually measure a direct target engagement.

Direct target engagement in our case is how much STAT6 do we degrade. So unlike, again, unlike other programs, we have a direct way to measure target engagement. We know the association between STAT6, IL4, and IL13, so the most important biomarker for this program is STAT6 degradation because it’s the most direct and significant biomarker. Now, from other studies, from other drugs, especially dupilumab, and this has been done a bit retrospectively, because actually they couldn’t measure a direct biomarker, they looked at what can we look at in healthy volunteers that might be impacted by the drug. And I think what probably the biomarker downstream of IL-four receptor alpha that is a bit of a window to measure is TARC that dupilumab has shown activity on.

They’ve also looked at Ig, but I would say TARC has a bit of a bigger window. The problem with these downstream Th2 biomarkers is that they are a biomarker of pathway activation. So if you’re in healthy volunteers, you don’t have Th2 disease, so these biomarkers are a baseline in the normal level. So when you give dubilumab and your top dose has a 30% reduction of biomarker, and that’s not even dose responsive, you understand that it’s noisy, difficult to interpret biomarker. So the reason why it’s been discussed a lot is because there is data out there from dupilumab that shows that you can impact TARC in a range between 035%, depending on the dose.

And so what we’ve said, we’re going to look at those biomarkers, we’re going to report on the data, and we expect it to be in the same ballpark. I think what we’re trying to caution against is trying to draw conclusions between these two drugs in two different studies with two different assays with, you know, different patient subjects when the baseline’s level and the assay window is so noisy. So I like to think about this drug as an oral dupi like drug. And so our expectation is that it’s going to look like dupilumab.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay.

Nelo Minolfi, CEO, Chimera: With all the caveats that I tried to explain maybe not well.

Tazeen Ahmad, Senior SMID Biotech Analyst: So, no, I thinking about translating the results from healthies into actual patients.

Nelo Minolfi, CEO, Chimera: Yeah, so that’s the beauty of our development program is that while we’re still talking about healthy volunteers data in June, we’ve already started a Phase Ib study in April. So we’ve already dosed our first patient in April, and we expect to have completed this study in the fourth quarter of the year. And now the beauty about our study or any study in AD patients is AD is a highly Th2 skew disease, which means that the biology of IL4N13 is very relevant in AD patients. So dupilumab in AD patients has shown that after twenty eight days of dosing, you can see a robust reduction, for example, of TARC. Now it’s not 30, it’s actually, depending on the study, between seventy percent and eighty percent.

So it’s a very robust and reproducible signal. Even more importantly, in the skin of patients, in the lesions of AD skin of patients, you can actually look at pre and post dose series of genes that are modulated by dupilumab. And that signature of dupilumab in AD lesions of patients is actually well characterized, and I think there is an appreciation that there is a high level of correlation between the depth of these transcript changes to EASI score. And given that these biomarkers have little or no placebo effect, we’ll be able to actually now generate a robust data set in patients and being able to compare now with some level of confidence to the dupilumab data in twenty eight days. So we’ll be able to show, hopefully, biomarker changes in blood, in skin, and then tie them to clinical endpoints that are usually measured in AD patients, which are EZH as well as IgA.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. I have a couple more questions on this topic, but I’m going to briefly jump ahead to the actual patient data that we might be able to see. Is it by year end?

Nelo Minolfi, CEO, Chimera: Yeah, 4Q.

Tazeen Ahmad, Senior SMID Biotech Analyst: Based on this data that you present, if you were to try to think about likelihood of success of your patient study, would the likelihood of success increase if you saw stat six reduction or lockdown, degradation? And does there need to be a minimal amount of that?

Nelo Minolfi, CEO, Chimera: Yeah, so what, thank you. So what we’ve shown preclinically is that if you have more than 90% degradation, 90% plus of STAT6 in every model that we’ve run, both in human cells or in preclinical mice model, mouse model, we’ve seen an effect on both biomarker and disease endpoints that are at least as good as dupilumab. So our healthy volunteer data, if we’re able to show that we can degrade the target robustly and hopefully safely, I think in my view, it’s going to tell us that we’re going to see some robust efficacy in patients.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay.

Nelo Minolfi, CEO, Chimera: Because that’s what the biology tells us.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. And then just going back to what we were talking about, does it matter the level of degradation per indication? So would you expect to see, have a minimal threshold for AD versus let’s say asthma?

Nelo Minolfi, CEO, Chimera: Yeah, I mean, it’s a great question. The reality is that nobody knows the answer to that. I think the reason why we want to be able to reach ninety percent plus and safely is because we like to explore that profile in our Phase IIb studies in both AD and asthma, and probably go below and then assess whether in AD and or asthma there is a different threshold of degradation that leads to maximal efficacy. My guess is that it’s going to be the same because I think it’s about pathway blockade in Th2 diseases. And I don’t believe that in order to achieve maximal efficacy, you can get away with less than maximal pathway blockade, but I think time will tell.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. And then I also wanted to touch upon safety. We’ll presumably get an update on the safety profile. I think the questions that are coming up on safety are more really about IRAK4 as opposed to STAT6 and whether or not you should expect to see anything similar for STAT6.

Nelo Minolfi, CEO, Chimera: In which way?

Tazeen Ahmad, Senior SMID Biotech Analyst: Any kind of observation of safety concerns, at least initially?

Nelo Minolfi, CEO, Chimera: Well, so, you know, if we go back to IREC4, the you know, this is KT474, now this is back three, four years ago, We had a very good safety profile. The I think we had mild AEs mostly. I think the most common adverse event was headache, you know, their phase one study. Obviously these are different drugs, different mechanisms. I don’t expect that there’ll be any overlap of AEs because they’re, again, different drugs and different mechanisms.

I think the only thing I would say is that our translation of our preclinical into clinical for April was quite good, and we hope that they will be the same with STAT6.

Tazeen Ahmad, Senior SMID Biotech Analyst: Is there anything inherent to STAT6 that you would be on the lookout for?

Nelo Minolfi, CEO, Chimera: Well, you know, we’ve run extensive preclinical safety studies, talk studies, I should say, And we haven’t seen any adverse events in those studies. We’ve also looked closely at all the human genetics. If you look at gain of function of STAT6, the only phenotype is allergic diseases. So it’s telling you that’s the job of the protein. We’ve also looked at heterozygous loss of functions of humans that were identified a few months ago.

Also they were completely normal. Mouse knockout, normal. So we don’t have a particular thing that we’re going to look out for. We would obviously look out for anything and everything, but we don’t have a particular concern.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay, so no concern like for QT prolongation or anything?

Nelo Minolfi, CEO, Chimera: No, so the QT, it’s a good, sorry, reminded me. For April, we did see a subclinical QT effect in the five to ten milliseconds. This was tied to an off target effect for a really small mild binding to a HER channel, we were able to actually replicate this signal preclinically. We did not see that signal in our IND enabling studies because the, let’s say, FDA recommended models that we used were not sensitive enough to see the subclinical signal. We actually built a new model to measure that, and so we haven’t seen that with any other drugs.

So, we have zero expectation that we see it for six to one in the Okay.

Tazeen Ahmad, Senior SMID Biotech Analyst: You talk about what the competitive landscape looks like for orals for AD outside of Chimera and how you think it could be differentiated?

Nelo Minolfi, CEO, Chimera: So I mean, the only oral approved drug in AD is, I mean, it’s a JAK inhibitor, which actually works quite well, but comes with the known both safety flags and the need for testing ahead of initiating dosing. So that adds several layers of complexity. I haven’t seen any robust data yet on any other oral drug. Obviously, have our IRAK4 degrader that will have the ADA, placebo controlled randomized ADA next year. Obviously, was recent data on the ITK, but it’s like on eight patients, so it’s a bit difficult for me to comment on.

I think that there is no drug though that has a Th2 specific profile. And so STAT6 degrader is the only drug that is going to address only the inflammation driven by this pathway. I don’t think there is any other drug that can do that.

Tazeen Ahmad, Senior SMID Biotech Analyst: Yeah, so the ITK, I think you were mentioning is the Corvus data,

Nelo Minolfi, CEO, Chimera: Yeah.

Tazeen Ahmad, Senior SMID Biotech Analyst: So it had a sixty three percent EASY seventy five score, and you mentioned it’s in eight patients. So, based on your response, I think probably more data is needed to really understand how that could, you know, end up in the competitive landscape.

Nelo Minolfi, CEO, Chimera: Yeah, I mean, yes. I mean, I’m not dismissing the data. I just feel like it’s early data and we’ll see. It’s a very different mechanism. And when we are blocking the inflammation driven by IL-four and IL-thirteen, we’re not killing T cells.

So it’s just a bit of a mechanism. You know, it’s a BID drug. So it’s, I don’t think that that’s going to be, you know, like our direct competitor. But obviously, you know, it’s a big space, so hopefully there is an opportunity to expand the market by having, you know, multiple other drugs. So I think it’s all good for patients as long as they’re safe and effective.

Tazeen Ahmad, Senior SMID Biotech Analyst: How important will it be for onset of action of your drug in order for it to be a competitive product?

Nelo Minolfi, CEO, Chimera: Yeah, no, it’s another great question. So I think if you look at the biology of this pathway, you know, you see that the onset of action is driven by, I assume, the pharmacology of IL-four thirteen and by the biologics kind of onset of full target engagement. I think it’s a question that we’re curious as well. I think our expectation is that it will be a doopy like effect, but, you know, that’s why we’re running the studies. We’ll see.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. So as we kind of move forward to looking at patient data, just remind us, is that going to be at the end of this year or would that roll into next year?

Nelo Minolfi, CEO, Chimera: 4Q, yes, 4Q. Our expectation in fourth quarter of this year, we’ll have the Phase Ib AD data.

Tazeen Ahmad, Senior SMID Biotech Analyst: And how many patients would that be?

Nelo Minolfi, CEO, Chimera: We are targeting about 20 patients.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. And this is open label?

Nelo Minolfi, CEO, Chimera: Yes.

Tazeen Ahmad, Senior SMID Biotech Analyst: And so what would be good there, and how should we interpret it?

Nelo Minolfi, CEO, Chimera: I think the expectation should be that it’s going to perform like dupilumab in both biomarkers as well as efficacy. It’s always difficult, obviously, to compare a small dataset. I just mentioned another company. You know, there’s always going to have to be a bit of mental flexibility to absorb data from different studies of different drugs with different ends. But we feel that’s why it’s very rooted in biomarkers because biomarkers have little or no placebo effect.

It’s a very robust signature for dupilumab, and we don’t have any reasons to believe that our drug will have a different type of biomarker signature. So once you have degradation biomarker and then a clinical endpoint, it’s a really good story that can be used to evaluate the activity of the drug in early clinical development. I actually like to think about this as the conclusion of the clinical translation, right, of you’re taking a stat six profile that I would say it’s widely accepted that preclinical is quite impressive. I think it’s difficult to disagree with that. And then doing a phase one healthy and a phase 1b patients to kind of tie it all together and say, this looks like dupilumab in people too.

Now let’s go and run a few large phase two and phase three studies to evaluate the full extent of the efficacy and the safety. I think that’s how I like to think about it.

Tazeen Ahmad, Senior SMID Biotech Analyst: Does it have to look exactly like Dupi because it would have a way of dosing advantage, right, an oral advantage? Yeah. So sometimes when it’s an oral, the bar doesn’t necessarily have to be that high.

Nelo Minolfi, CEO, Chimera: Yeah, and you know, only reason why we say that we believe based on the biology of what we’ve seen, I think it’s widely accepted that, I think if you’re, I’ve heard that if you’re 30% less active than Dupi and you’re an oral safe drug, you’re going to be wildly successful. That’s probably true, but I’m not going to set a bar that is totally artificial. I mean, where is 30% coming from? I have no idea. All I know is that based on our preclinical data, I think it’s going to look like it.

It could look slightly better, slightly worse, and that’s why we’re going to run the studies.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. And then can you talk just theoretically about whether you think there’s a real difference between STAT6 degradation versus STAT6 inhibition?

Nelo Minolfi, CEO, Chimera: Great question. So what is the goal of blocking STAT6, right? The goal of blocking STAT6 is to block the translation of the signal from the receptor into the nucleus. So if you have a small molecule inhibitor that can stop the translation of the STAT6 signal from the receptor to the nucleus, you should be able to do it whether you’re inhibiting the protein or you’re degrading the protein. Now in our hands, in order to block this signal completely, you need to remove the protein, right, 90% plus.

And we can do it with, at least based on our preclinical data, if you look at our data in preclinical species with relatively low doses in dogs and in monkeys, we haven’t shared that data, but it’s quite similar. With a dose around one mg per kg, we can get between one and three, we can get to ninety percent plus degradation with a single daily oral dose. The reason why we can do that because we have a catalytic degrader that degrades the protein very quickly in the first few hours, and then we don’t need to have the drug hang around for much longer because it takes twelve to twenty four hours for the protein to come back. So we can dose the next day and we can degrade whatever is left. And so that’s why we get to this 90% plus steady state.

With a small molecule inhibitor, in order to block the translation of the signal completely, you need to have an exposure of your drug that is superior to the expression of the protein 20 fourseven. And that is extremely difficult to have a PK and a safety profile that will allow you to have an exposure that is above the target expression in every cell, in every tissue. And we haven’t been able, we’ve done quite a bit of work with small molecule inhibitors in our own labs, and we are not able to generate that same signature with once a day oral drug.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. So one of the scenarios, obviously, is you see the data that’s convincing to you that this is a real drug, it’s got good activity, good chance of having similar efficacy to dupi. But in this scenario where you don’t see a trend or the numbers are not in line with what you would like to see, then what? Do you continue to look at different molecules? Do you think about different dosing?

What would be the next step?

Nelo Minolfi, CEO, Chimera: Doctor. Well, that scenario is not considered in my mind. Okay. But I will say that this is a chemistry problem, right? Is the molecule performing the way it’s supposed to perform, which means is the PK alive for degrading the target well and effectively.

If you’re not able to do that, obviously because we’ve done it so well preclinically, then I would say that it’s probably a molecule problem. And then, you know, we believe at Kymaera across the whole pipeline that we’re not a once and done on each program. We have multiple molecules. We have next generation molecules. So should that unlikely event ever happen, you know, we will make sure that we have other tools in our toolbox to deliver on the promise here.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. And then the flip side of it, which is if you do see good data and you move this indication forward, does it open up other indications for you?

Nelo Minolfi, CEO, Chimera: Yeah, I mean, we’re setting up the development program to develop this drug in all the indications which dupilumab has been approved in, which is seven, almost eight. And so these initial phase 2b studies in AD and asthma will allow us to then go into multiple phase three studies in parallel, because we can use the AD phase three dose to go into other derm indication, and the phase three respiratory dose to go into other respiratory indications, asthma dose to go into other respiratory indications. So at that time, would be more of a capabilities and capital question, and I don’t think it would be a scientific question. And we’re building a team to execute on a pretty aggressive, I would say probably one of the most aggressive development plans I’ve seen. And, you know, I think we’re already paid.

We’ve already paid with our runway, the two large Phase 2b studies. Well, actually now with the extended runway, we’re going to go well beyond those. And so that’s it would be an interesting time for Phase 2b studies to kind of see where we are as a company and see what we do for phase 3s.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. And then let’s just quickly talk about oncology. Yes. That’s also a focus for the company. You’ve talked about searching for potential partners there.

Where are you in that process? And when do you think is the right time?

Nelo Minolfi, CEO, Chimera: Yeah, I would say that, yeah, oncology has been a focus of the company in the past few years. We made a decision a couple of years ago now to really focus, at least internally actually, much earlier than that, but externally we’ve made a decision to focus only in immuno, or primarily in immunology. We have, you know, we’ve had some assets in the clinic with actually some really interesting early data. And, you know, partnering those assets is one possibility. I think it’s hard for me to say when and how.

I think when it will happen, if and when it will happen, we’ll share it.

Tazeen Ahmad, Senior SMID Biotech Analyst: But it’s not a near term necessity?

Nelo Minolfi, CEO, Chimera: It’s not a necessity, obviously. But it will be a great thing for patients that they can benefit from drugs that have clinical activities.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay. And then just remind us your current cash position and how far that takes you.

Nelo Minolfi, CEO, Chimera: Yes. So we have $775,000,000 as of end of Q1. That will take us into the first half of twenty twenty eight, so roughly about three years. And as I said earlier, this is going to be well beyond many data readouts, including the Phase IIb on six:one.

Tazeen Ahmad, Senior SMID Biotech Analyst: Okay, perfect. So we’ll be looking out for the data next month, and we’ll talk to you then.

Nelo Minolfi, CEO, Chimera: Excellent.

Tazeen Ahmad, Senior SMID Biotech Analyst: So we’re out of time for today. Thanks, everyone, for joining us, both live here and on the webcast. We’ll talk soon.

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