Kymera at Leerink’s Global Healthcare Conference: Strategic Insights on Drug Development

On Tuesday, 11 March 2025, Kymera Therapeutics (NASDAQ: KYMR) took the stage at Leerink’s Global Healthcare Conference 2025. CEO Nel Manolfi outlined the company’s innovative approach to targeted protein degradation (TPD) and its ambitious pipeline, focusing on STAT6, TIK2, and a forthcoming program. The discussion highlighted both the potential breakthroughs in immunology and the challenges of achieving high target degradation rates.

Key Takeaways

• Kymera aims to develop oral drugs with the efficacy of biologics, focusing on unmet needs in immunology.
• The STAT6 program is a priority, with plans to advance rapidly to Phase III trials.
• Achieving 90%+ target degradation is crucial for matching the efficacy of existing drugs like Dupixent.
• The company is not seeking partnerships for STAT6 until post-Phase IIb studies.
• CEO Manolfi emphasized overcoming challenges related to oral bioavailability and molecular size.

Operational Updates

STAT6 Program:

• Phase 1 SAD/MAD data is expected in June, focusing on target degradation, safety, and biomarkers.
• The goal is to achieve 90%+ degradation in blood and skin, with Phase 2b studies planned for late this year and early next year.

TIK2 Program:

• Healthy volunteer data is anticipated this year, aiming to demonstrate complete TIK2 degradation.

New Program:

• Details will be disclosed in early May, expanding the pipeline’s focus on immunology.

Future Outlook

STAT6:

• Plans to rapidly progress to Phase III trials, potentially pursuing multiple indications.
• Aims for Phase 2b to be the only Phase 2 studies required before Phase III.

Partnership Strategy:

• No partnerships for STAT6 before Phase IIb completion, with evaluations to follow for value maximization.

Pipeline Expansion:

• Continued exploration of immunology targets with potential multi-billion dollar opportunities.

Q&A Highlights

• The company confirmed comprehensive STAT6 degradation across cellular compartments.
• Safety concerns are linked to the pharmacology of the target, not the degradation modality.

For further details, please refer to the full transcript below.

Full transcript - Leerink’s Global Healthcare Conference 2025:

Unidentified speaker, Interviewer: morning, everyone. Welcome to day two of the Lending Partners Global Healthcare Conference. Very pleased with us, very pleased to have with us today Doctor.

Nel Manolfi, CEO of Chimera Therapeutics. So Nel, could you provide us a quick intro to the company and kind of frame what’s ahead for twenty twenty five?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. Thanks for the invite. Thanks for giving me the doctor. I’m nobody does that anymore, but I’ll take it. PHD will do it.

Yeah. Yeah. Yeah. So, so, you know, Chimera was founded almost nine years ago with the goal and the ambition to create a whole new generation of medicines using targeted protein degradation. Our strategy has been consistently focused on trying to marry the power of the technology, which just to remind everybody, it’s a small molecule that can give a phenotype that is as powerful as genetic knockdown.

So you remove a protein with a small molecule, so huge potential. So the strategy has been marrying the power of TPD with the right target. And for us, the right target has always been a target that has not been drugged or drugged fully before in pathways that have been validated clinically by other agents, usually upstream biologics, where they target as human genetics data targeting ideally large patient populations. And so historically, we’ve once you build that Venn diagram, we found that where it’s best suited in terms of target types is multifunctional proteins or scaffolding proteins like TIK2 or IRAC4 for example or transcription factors that have been historically undrugged. So we’ve seen with us working on STAT3, now STAT6, you’ll hear about a new program soon in early May.

And I think with that strategy, we’ve been able to generate some unique profiles. I think our when we started our broader communication on immunology about a year, almost and a half ago, our goal is really to build for the first time in industry oral drugs with biologics like efficacy. And that’s only, I think a profile that an oral degrader can give. The fact that we can block the pathway in a saturated manner with an oral degrader that can mimic upstream biologic. So and that’s how our pipeline has been refined, I would say, right?

I think we learned along the way what are the best targets, what are the best pathways. And if we were the same company that we were nine years ago, we shouldn’t be here, right? We continue to refine and learn, and I think we have right now, I would argue, one of, if not the best oral immunology pipeline. If you look at again, IREQ4, TIK2, STAT6 and again the new program, it’s a very exciting time. So this year is a big year for many programs in our pipeline, I would say for STAT6 first.

This is the probably the best example of going after a target that is directly downstream of a highly validated receptor, I have four receptor alpha. We’ve shown pre clinically that by degrading STAT6, we can phenocopy dupilumab in all contacts that we looked at. So this year we’ll have a hefty volunteer data, we’ll have patients data, we’ll start Phase 2b studies. So it’s going to be a great year for us. Hopefully, it will be a great year for us and for patients that soon would be able to have a completely different treatment option.

We have a TIK2 data also in healthy volunteer this year. And as I said, for the third time now, we’ll also disclose a new program.

Unidentified speaker, Interviewer: Great. Well, thank you for framing that for us. I think a lot of the investor interest on your stock right now is on STAT6, just given the potential, as you mentioned, like downstream of IL-four, kind of dream of being in oral Dupixent. Let’s start with that Phase one. You have SADMAT data coming up in June.

Can you kind of talk through I guess, you’ve guided that the three things to look at are the target degradation, safety, biomarkers. Can you kind of guide us on that first one on target degradation? What should we expect to see? Or what will be a good outcome to see on that?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. So when we set up this clinical expectations, we do it based on extensive PKPD studies that we do pre clinically. We’re probably the company that does most PKPD studies across species, across tissues, so that we can refine our target product profile. And so if you look at our preclinical data with STAT6, which I think is one of the most robust preclinical package that I have seen, you’ll see that when you even degradation profiles of 70% to 85% are able to give you a pretty compelling phenotype that can in many instances match dupilumab. But I think only once you reach that 90% degradation, 90%, ninety % plus is where you consistently see in any type of readouts whether it’s efficacy endpoints or TH2 biomarkers, you see consistently that we’re either equal or numerically superior to dupilumab.

And so for that reason, given that we’re trying to build that first and best in class here, our target is being able to reach 90% plus in blood and ideally in skin.

Unidentified speaker, Interviewer: Yes. So if you don’t reach 90% plus, one, like what does that mean, like biology, like how could that happen? And what do you think sort of like the downstream clinical impact of that would be? Just more of like a curiosity.

Nel Manolfi, CEO, Chimera Therapeutics: Yes. So I’ll answer your question in two ways. The first one, just to the question directly, as we’ve said, even 85%, eighty % degradation in our preclinical model gave us some quite interesting phenotype. And as I said, I think when you evaluate STAT6 agents, you have to look at the totality of at least so far the preclinical data. If you choose one endpoint, let’s say, I don’t know, IgE in preclinical models of asthma or AD, you’ll see that, you know, it can be more or less sensitive.

If you look dark, it can be more or less sensitive to the degrees of degradation. So I think you can develop a drug and likely that’s where the small molecule inhibitor we’re going to land, right, in a suboptimal pathway inhibition profile that might still be clinically relevant. Right. But I think the profile that we’re going for is a Dupi like profile. So I think if we have less than ninety percent, it would not be an ideal case for us to have a best in class profile.

I would also say that this is the fifth molecule we put into the clinic. And I’m not previewing any data. I’m just looking back. We’ve never seen a molecule that stopped degrading below 90%. So it would be the first time.

Unidentified speaker, Interviewer: Yes. Let’s talk about the skin degradation because in your IRAC4 program, I think you had well over 90% plasma degradation, but and it was pretty homogeneous. But in the skin degradation, it was like almost 30 percentage points lower and quite heterogeneous. So how should we think about skin degradation just as a concept?

Nel Manolfi, CEO, Chimera Therapeutics: And

Unidentified speaker, Interviewer: is there a different benchmark to think about there?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. So I would start with why do we want to degrade the target in skin? We have actually no pharmacology from other agents that show direct target engagement in skin, right? We know that if you look at other upstream biologics, you look at skin transcriptomic, for example, in AD patients, and you see a pretty profound impact. But we don’t know whether that’s from target engagement in the skin or it’s just a systemic, these are TH2 diseases or systemic diseases with local manifestations.

So I would say that the reason why we’re pretty bullish about wanting to have skin degradation is because we don’t want to leave any potential kind of value on the table. It is unclear, to be honest, whether we need it, but I think we want to have it just to make sure we have the best profile possible. Now your question is very valid. Obviously, it’s a question we’ve been dealing with for a few years, which is IREQ4 in healthy volunteers and in patients showed, I would say, a degradation of between 5060% at the relevant doses, where in blood we would see 95% plus. So there is two potential explanation for that.

One is that we see less degradation. I think it’s unlikely, but it’s possible. The other one is ARAC4 levels in skin are extremely low. The dynamic range of the assay is very narrow. So it’s really hard to robustly measure a percent reduction.

Unidentified speaker, Interviewer: How Is STAT6 different?

Nel Manolfi, CEO, Chimera Therapeutics: STAT6 levels in skin are much higher. And as we’ve also shown pre clinically, we can measure and reduce STAT6 levels in the skin of many preclinical species quite effectively, including non human primates. So and also the compound distribution profile is slightly different. So we have confidence that we’ll be able to see robust degradation in the skin as well.

Unidentified speaker, Interviewer: Got it. Interesting. So let’s talk about safety then. So I’m curious on STAT6 as a target. What are the safety attributes you should watch out for?

And then are there anything else on safety with regards to just degraders as a whole or just this molecule in general that we should look out for as well?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. So first, I would say that degraders have been actually an exceptionally well balanced have had exceptionally well balanced safety profile. If you look in the industry across all programs, all the safety that has been seen in the clinic were safety that one could explain based on target biology. For example, with ARAC4, we’ve seen really good safety because we know that human genetics tell you that not having ARAC4 should be relatively well tolerated. And other programs from other companies including ours in oncology, what we’ve seen in terms of adverse events were all associated with well understood biology of that particular target.

So telling you that as a modality is a very, very well tolerated modality. There is not a degrader safety profile. With regards to STAT6, we stand on like three important pieces of information, right? I would start with pathway clinical validation. We’ve shown robustly that STAT6 degradation as much as we can tell a one to one relationship with IL-four receptor inhibition and we know that obviously dupilumab is a drug that has been you know those two million patients actually now with including children with a very good safety profile.

I would also say that there is STAT6 human genetics that says if you have a gain of function of STAT6 the only phenotype that you see is severe allergic diseases. So it’s telling you that’s the function of the target. There has been a heterozygous loss of function, humans that have been identified recently also with a no phenotype actually, no adverse phenotype. And then I would say our preclinical talks has shown no adverse events at any doses or concentration. So we’re going into the study expecting a very good safety profile.

I mean, if when we say that we want to have a dupe like molecule, we mean that from both the efficacy and safety.

Unidentified speaker, Interviewer: Yes, yes, I love that. So there’s some investors that kind of have what I think are misconceptions around degraders that degraders are larger, small molecules, they break rule of five, they struggle with oral bioavailability, they might have increased risk for GI or liver tox because of these molecular attributes. How do you what’s your kind of response to that kind of conception that some people have?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. I mean, look, first of all, there are no rule of fives. I think that’s kind of a lazy observation, if I may say. I think what I would say is that these are generally larger than your traditional small molecule inhibitor. The reason why degraders and that’s good for companies like Chimera haven’t been commoditized completely is because it does require different rules on how you build them into being like a pharmaceutical agent.

And companies like Chimera and others, I would say, we’re not the only ones, I think were the very good one. We’ve learned how to effectively make these molecules behave like traditional small molecule from a pharmaceutical perspective. And to be honest, we’re well past that question. That question used to be discussed at Chimera four years ago maybe, but not now. We’re more focused on making drugs against targets that we like.

And I think that particular question is for the kind of naive of the space.

Unidentified speaker, Interviewer: Yes. Appreciate that. So in terms of biomarkers, I think you’ve talked about TARIC and IgE as biomarkers that you’ll look at both in the healthy volunteer setting and then your Phase 1b in patients. At least in the healthy volunteer setting, acknowledging that those outcomes are often pretty noisy, is there a minimum bar that you want to see on TARAC and IgE even in the healthy volunteer setting to feel comfortable with the molecule?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. No, I love how this has become a controversial topic. I’m not sure how that happened. I was told that I’ve changed the narrative around it. So I’m going to say what I’ve been saying for months, which is, if you just look at the publications, I think Regeneron has done a great job and Sanofi, they’ve done a great job publishing signs, not just drug development.

So there is a paper on healthy volunteer. There is several papers on biomarkers on patients across all the indications. So we have all the data out there. Like it’s not about what I say. It doesn’t matter what I say.

It’s actually what’s in the publication. So if you look at the dupilumab in healthy volunteer publications in where they have, when they have like those response over time, As you’ve said, you don’t really see a clear dose response. And you see a measurable effect in TARQ. I would say in IG, if you look at the first two weeks, it’s not easy to see a real measure. And so I think what I’ve been saying all the time is that we given that we believe we can phenocopy in a broad sense, dupilumab that you should expect from us a profile that is going to look like that.

What I keep saying, which is only a fact, is that if a drug within its own dose response is not it doesn’t have a clear dose response, what I’m saying is that it’s not trying to compare two drugs. If an individual drug doesn’t have a clear dose response and I’m talking about dupilumab, I don’t want to get into comparing drugs across two different studies. So the bar, you asked the question about the bar. It’s hard, right? I don’t know what the bar is.

I just would say that I’ll be surprised. I think we would all be surprised if there was no measurable changes in these biomarkers because they’ve been shown by dapilumab and also Adelai-thirteen drugs. And I don’t know that there is a bar there. I mean, if you look at the TARQ data, they go anywhere from, I don’t know, ten percent to thirty five percent within the first two weeks, right? So I don’t know where the bar is.

Unidentified speaker, Interviewer: Okay. Makes sense. So let’s talk about another controversy then. Can you defend your decision to do a Phase 1b, single arm, no placebo, single dose in atopic derma? Yes.

Nel Manolfi, CEO, Chimera Therapeutics: Now that’s an easy one. So the goal of our development plan is to get to market ASAP. Like we are committed to actually developing this drug because I think this is a I said it on the call, this is a once in a generation drug, hopefully, right? I mean, we still have a lot of long way to go. But I think the setup is this is one in a generation drug, one in a lifetime drug for people like me.

So we’re committed to do the right thing by the drug first. And so if we want to get to Phase III ASAP, we need to get to Phase IIb ASAP, which as you know, we are starting hopefully if everything goes according to plan, the first Phase 2b will start in 4Q, the second Phase 2b will start in 1Q. We believe those Phase 2b might be the only Phase two studies we’ll ever have to run. And we can do a series of Phase three studies after that. So what we wanted to do before the start of Phase IIb, which we want to do SAP is to build the dataset that will show us robustly that we behave like and we know in AD patients the strongest data set of is looking at biomarkers in blood and more importantly in skin.

And we know that for example, there is a strong correlation of biomarker changes in skin with extent of clinical response. We know that actually reduction in PARCC has been associated with reduction in pruritus in dupilumab’s Phase II and Phase III studies. So we know really well that if we inhibit and block these biomarkers, we can easily make a correlation between biomarkers and clinical endpoints. Given that this is a four week study, we don’t think we need placebo to show that. Placebo and biomarker, you can look at it, the papers are everywhere, are very, very minimal.

There is no really placebo rates in biomarker. And so for a four week study to move quickly in a Phase 2b without running 100 patients four week study because that’s probably what it will take to do a placebo controlled study, we thought we can show degradation in blood and skin, biomarkers in blood and skin that correlates to we believe that it would be a robust dataset that will not need any conversation.

Unidentified speaker, Interviewer: Yes. And it’s interesting because I think when we last spoke you mentioned, you said this phrase, you’re like biomarkers don’t lie.

Nel Manolfi, CEO, Chimera Therapeutics: I know. Some people love that. Some people didn’t, but Oh, okay.

Unidentified speaker, Interviewer: Interesting. Well, I mean, because the investor controversy was that in AD studies, placebo has such a huge variability on an EZ score reduction. So I think people actually kind of don’t appreciate that biomarkers. So we pulled the data.

Nel Manolfi, CEO, Chimera Therapeutics: You’re easily surprised. Yes. The biomarkers is really very little placebo effect. We’re talking about biomarkers in patients, right, not to confuse the previous conversation. I would also say that it’s true that the placebo rates in AD have increased a bit over time.

I think that’s mostly due to the fact that it’s extremely competitive and patients may be that might not meet all the entry point or included some of these studies. But I think if you run-in a highly controlled study, be able to reduce the placebo rates.

Unidentified speaker, Interviewer: Yes. And then how do you choose which dose you put into the Phase 1b?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. So how we choose the dose, I mean, without going into the details, but we talked about what is the profile we’re looking for, which is we want to have a degradation profile that degrades the target around 90% plus at a dose that is well tolerated. And that’s the dose that is going into the Phase 1b, which as you probably gather, it’s likely to start before we release the healthy volunteer data.

Unidentified speaker, Interviewer: Got it. Makes sense. So I want to talk about another topic. I know you might not comment too much, but I’m going to try. So we noticed that you published some, I think it was 3,000 pages worth of patents on STAT6 graders a few days ago.

Can you comment on the structure and what that means for the kind of the future of the molecule?

Nel Manolfi, CEO, Chimera Therapeutics: It’s funny. We’re trying to do all these under the radar. Now you want to bring it in front of everybody. No, we have a we’ve been working on this target for multiple years. We have multiple patents out there.

Yes, some I believe were published a few days ago. I don’t remember exactly when. Some were published earlier. I think your comment about a number of pages, maybe the only comment I would make is we take our IP very seriously at Chimera. We have a very, I would say, good strategy that is forward looking, and we’re very proud of the chemistry we built.

Unidentified speaker, Interviewer: Makes sense. All right. So I want to spend a few minutes on your other pipeline candidates. You said you’re going to disclose your next candidate in May. Yes.

I think you’ve made some allusions to what it might be. I guess you’re not going to tell us what it is, but can you just talk a little bit about your philosophy on what went into the decision of what you were going to work on next after the stat statistics?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. Look, it goes back to the same principles I’ve outlined before. There are I think the reason why a few years ago we decided to go in immunology almost fully is because there has been so much validation of immunological pathways with especially biologics in the past few years. And there has been such an underwhelming sets of data from traditional small molecule inhibitor that the way I think about it, the time of the graders in immunology is now. And so we have a lot of activities on a variety of targets that I think each could be multibillion dollar opportunities.

And there are so many of them, to be honest, that if you think about target strategy well and you have the right platform to prosecute and we have a unique ability to find binders to undrugged protein right now at Chimera that I think the target is going to be one that is on everybody’s list because it’s one of those transcription factors that you don’t have to think about long to kind of appreciate where to position clinically. And I don’t want to raise expectations too much, but I think it’ll be appreciated broadly. And it’s another amazing molecule.

Unidentified speaker, Interviewer: Got it. Interesting. And I guess, as you think about your pipeline development, like, you have like STAT6 and TIC2. STAT6 goal is to drug an undruggable transcription factor. TIC2 is to drug something better than how it’s drugless with, in traditional small molecules or allosteric small molecules.

How do you think about, like, what comes next and kind of like leading, you know, between these two different types of approaches?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. As I said, if you think about marrying the power of the technology with the right target, we’re not limited by the type of target. I think what I said is we’ve ended up working in these couple of classes of the scaffolding proteins and transcription factors, but I wouldn’t say that those are limiting. We have another early program that is going after a totally different target type. So I would just say that the key what I think would stay consistent is validated biology are saving the potentially best in pathway drug where you don’t compromise on efficacy with an oral drug.

So you capture both most efficacy and most convenience with an oral drug with biologics like efficacy or even biologics superior efficacy, which I think will happen in some of our programs.

Unidentified speaker, Interviewer: Got it. Makes sense. So I want to just talk quickly about TIK2. As you know, investors don’t love TIK2 for a few different reasons. But can you kind of defend why you chose that as a target to go after and why you feel good about your program?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. I mean, I think it’s fair to say there is a bit of fatigue around TIC2, which, I mean it’s understandable if you think about TIK2 inhibitors, right? How many TIK2 inhibitors are needed to drug a target? This is a pet peeves of mine. How many drugs do we need?

There are so many targets that are way over drugged at this point, right, with hundreds of companies. TIC2 is probably close to that, not as bad as the PD-one or the CD-nineteen, the CD-twenty, but it’s getting there. But I think we’re talking here about a different modality with different pharmacology. We’re trying to replicate the human genetics data that has made this target one of the most compelling target in immunology. This target should work in dragging this target properly should work in IBD, should work in psoriasis, in psoriatic arthritis and in many other indications.

I think inhibiting the function of TIK2 is not going to be enough. And we’re going to derisk it in two different way. In the Phase one, which hopefully will have data this year already show that we can degrade this target fully, which is the phenotype that nobody has ever shown. And then show that this full degradation of TIK2 is going to drive a biologics like efficacy profile, let’s say in an indication like psoriasis or others as a proof of concept. So I’m totally comfortable for this program to be a show me the data program, but I we have the utmost confidence this is going to be one of the another big program for us.

Unidentified speaker, Interviewer: Got it. All right. So we’re at three minutes left. I have two questions. So obviously with step six, you spoke about the huge potential going after large mass market opportunities.

You guys are first in class with this molecule. How are you guys thinking about the kind of strategic path forward for the molecule? Like, does it make sense for a company with your skill to be developing this forward? How are you thinking about the potential partnership strategy there?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. So I think what I can say with Comfort right now is that there is no scenario where partnering this program between now and the end of this big Phase IIb studies will accelerate or expand the potential of this program. We are likely going to be able to do it faster and better than any other company given the investments we’ve made already and are continuing to make. I think at the end of those Phase IIb studies where in front of us, we would have potentially eight indications or more that we could in theory parallel track in Phase three. We’re talking about 21 Phase three studies, if one wanted to parallel everything.

The question would be is, are we positioned to maximize value? I think it’s a fair question to us then, and we can address it then.

Unidentified speaker, Interviewer: Okay. Sounds good. I’ll put it on the list. So just one last one to wrap us up. What do you think investors misunderstand most about the Chimera story?

Nel Manolfi, CEO, Chimera Therapeutics: Yes. Look, I do my job. Investors do their job. It’s hard for me to say, especially missing. I think I hope that investors that invest in the signs of companies in the fundamentals because not everybody does that, right?

But for the ones that actually invest in the signs and the fundamental of the company, I think there is a strong appreciation of the quality of work that we do, the strategy that we have and the targets that we have. Again, not everybody likes every target. That’s okay. I think there is a I think right now, I feel like there is an under appreciation of what monumental what of the monumental potential of degrading STAT6 safely mean and getting hung up on a relatively unscientific readout, which is the biomarker readout instead of understanding that if we integrate STAT6 safely, this has the potential to be one of the biggest drugs in immunology.

Unidentified speaker, Interviewer: Yes. That’s great. We have just a little bit of time left. Just want to check if anyone in the audience has any questions.

Nel Manolfi, CEO, Chimera Therapeutics: Look at that. You’ve got multiple. Go ahead. Have you looked at sub cellular localization with any of your protein degraders and have your limitations on the cellular context in which your protein can be degraded effectively? That’s a great question.

We have looked at that extensively, especially with transcription factors that as you know are activated in the cytoplasm, usually by phosphorylation and then go to the nucleus to bind to DNA. And so we have shown I’m not sure if we’ve shown with STAT6, but I know we’ve shown internally that we can degrade STAT6 and we remove it from every compartment. And actually we’ll show also data from this new program because it’s another transcription factor. Yes. I didn’t say.

I actually said that there the safety of the degraders are based on the mechanism of the pharmacology of the target. So obviously, in that particular case, there are some substrates that are degraded that have a particular pharmacology, but nothing to do with the actual degradation modality, but it’s the pharmacology of that particular drug.

Unidentified speaker, Interviewer: And so as it’s true

Nel Manolfi, CEO, Chimera Therapeutics: I think we’re way past time. Maybe we can do it after. Okay.

Unidentified speaker, Interviewer: Well, now thank you so much for joining us and thank you for folks in the room and folks who dialed in as well.

Nel Manolfi, CEO, Chimera Therapeutics: Thank you.

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