Kymera at UBS Global Healthcare Conference: Strategic Insights

On Monday, 10 November 2025, Kymera Therapeutics (NASDAQ:KYMR) presented at the UBS Global Healthcare Conference 2025. The company highlighted its innovative degrader platform and key assets, including the promising STAT6 and IRF5 programs. While Kymera is well-capitalized with a cash runway into 2028, challenges remain in advancing its pipeline through clinical trials.

Key Takeaways

• Kymera’s STAT6 program (KT-621) is advancing into phase 2B studies for atopic dermatitis and asthma.
• The IRF5 program (KT-579) targets immune-mediated diseases, with phase 1 trials planned for next year.
• Kymera’s cash runway extends into the second half of 2028, supporting key clinical milestones.
• Upcoming catalysts include phase 1B data for KT-621 and phase 1 data for KT-579.
• Sanofi prioritizes Kymera’s next-generation IRAK4 degrader (KT-485) over KT-474.

Financial Results

• Cash Runway: Kymera’s financial position is robust, with funds expected to last into late 2028, ensuring support for ongoing and future clinical studies.
• Funding Usage: The financial resources are allocated to complete phase 2B studies and potentially initiate phase 3 studies for atopic dermatitis and asthma.

Operational Updates

• KT-621 (STAT6 Degrader): Phase 2B study in atopic dermatitis has commenced, with an asthma study planned for early next year.
• KT-579 (IRF5 Degrader): IND-enabling studies are complete, with a phase 1 healthy volunteer study scheduled for early next year.
• KT-485 (IRAK4 Degrader): Sanofi is advancing KT-485 into phase 1 trials, following enhanced preclinical safety measures.
• Pipeline Expansion: Kymera plans to introduce one to two new programs into clinical development annually.

Future Outlook

• Phase 2B Completion: The phase 2B study is expected to conclude by mid-2027.
• Regulatory Strategy: Kymera aims to leverage phase 3 doses from AD and asthma studies for other indications, pending regulatory approval.
• Market Opportunity: With only 1-2% of moderate to severe AD patients accessing dupilumab, an oral alternative could significantly expand patient access.

Q&A Highlights

• STAT6 Degrader Efficacy: The STAT6 degrader is positioned as a potential oral alternative to biologics, offering comprehensive STAT6 degradation.
• IRF5 Indications: Lupus is the primary target for the IRF5 program, with potential applications in IBD and rheumatoid arthritis.
• TARC Reduction: The phase 2B AD trial aims for a 70-80% reduction in TARC, aligning with Dupixent’s performance.

Readers interested in further details are encouraged to refer to the full transcript below.

Full transcript - UBS Global Healthcare Conference 2025:

David, Interviewer: All right, thank you, everyone, for joining us. Our fireside chat with Kymera Therapeutics. Sorry. Yep. I’m told that, you know, if you have questions you want to ask in the audience, please scan the QR code and then you’re able to ask a question. I will be able to pick it up here on the iPad and ask a question. Please feel free to scan the QR code and put your questions in there. All right. With that out of the way, it’s our great pleasure to welcome Jared Gollob, Chief Medical Officer of Kymera. Jared, thank you for joining us.

Jared Gollob, Chief Medical Officer, Kymera Therapeutics: Yeah, thanks, David. Thanks for having me.

Yeah, that’s great. For those probably new to the Kymera story, can you just give a quick overview of the company, your degrader platform, and any key assets that investors should pay attention to?

Sure. Happy to. Yeah. You know, next year we’ll be celebrating. Kymera will be celebrating our 10th anniversary. Since we were founded by Nello Mainolfi and Bruce Booth, we were founded with protein degradation really as our platform and really with the aim being to turn protein degradation into transformative drugs, you know, for diseases with high unmet need. You know, there’s been a real evolution over the past 10 years. Our platform itself has evolved considerably to the point now where we can really address very difficult to drug targets, transcription factors, multifunctional proteins almost at will. You know, based on our chemistry technologies.

You know, we’ve moved five programs into the clinic over the past five years, showing very nice translation from preclinical to clinical and, you know, where we’ve learned to really marry our technology to the sorts of targets and pathways where we think we can be most impactful. You know, several years ago, really pivoting more toward an immunology focus. We feel like at this point we have, we’re on route to having, you know, the hopefully best in industry sort of oral immunology platform right now. Our solely owned programs of greatest interest, you know, to us and others include our STAT6 program, immunology, as well as our IRF5 program. We’ve really made a lot of progress on those programs with STAT6. Just over this past year, we’ve moved it through a phase 1A healthy volunteer study, presented data last June.

We’ve moved it through phase 1B and are presenting data in December on that. We’ve initiated our first phase 2b study in atopic dermatitis and plan on starting an asthma study, phase 2b, early next year. A lot going on with that program and for IRF5, our KT579 program. Very excited about that as well. We planning on moving that into phase one healthy volunteer study next year. Lastly, you know, we’re fortunate to be well capitalized. We have a cash runway that takes us into the second half of 2028, which will enable us to get through key readouts for both of our phase 2b studies in AD and asthma. Also key readouts for the 579 program and our plan to bring at least one additional immunology program into the pipeline each year.

Excellent. That’s a great overview. Thank you so much. Let’s start with the, you know, the lead program, KT621, which is the STAT6 degrader. Maybe just start things off. Can you review why a STAT6 degrader should be more effective than, you know, inhibitor?

Yeah, that’s a really important question. You know, STAT6 has been in everybody’s sort of, you know, target over the last 10 years because it really controls signaling through the IL-4, IL-13 receptors. Those pathways having been well validated by drugs like Dupixent. There has been a real desire to try to develop an oral drug that can block STAT6 and phenocopy what Dupixent can do. You can imagine how transformational that can be for the field where Dupixent right now only really penetrates a very small percentage of all the moderate to severe patients with, say, asthma and AD. An oral drug could really open up that segment. The reason for degrader is degraders have a catalytic mechanism. Degraders are heterobifunctional small molecules that co-opt an E3 ligase.

It binds to an E3 ligase and to a protein of interest, brings them into proximity, leads to ubiquitination and degradation. It’s catalytic because one molecule of a degrader can degrade thousands of copies of its protein. So there’s between PK and PD. Even when the drug is cleared, tiny amounts of drug in the cell are still mediating profound deep degradation. Which is the reason why you can dose once daily with a degrader like KT621 STAT6 and fully suppress that protein round the clock 24/7. That’s the only way you can match both the efficacy and safety of an antibody biologic. Small molecule inhibitors really are very exposure based, right? As the exposure waxes and wanes after a dose, so does the activity against the target.

It’s very difficult, if not impossible, to get 24/7 full suppression of a target like STAT6, usually using an inhibitor. We feel that the only way to match the activity of a biologic by targeting STAT6 is to use a degrader.

Got it. I mean, you recently just provided some healthy volunteer data. Could you maybe just provide a quick overview of the data and what were the most important key takeaways from the initial clinical data?

Yeah, so those SAD MAD data in healthy volunteers from the phase 1A, we presented those this past June. We actually moved through that study very quickly, even though we had over 150 subjects on that study. What we learned from that study is that we can fully, completely degrade STAT6 in blood and skin in relatively low doses, doses as low as 50-200 milligrams a day, complete degradation. That degradation was associated with full pathway blockade of the IL-4/13 pathway, which we showed through impact on circulating biomarkers like TARC and eotaxin. Importantly, it was very safe and well tolerated. The MAD consisted of 14 daily doses of drug and the safety profile was essentially indistinguishable from placebo.

Got it. And then of course, you know, you’re going to be moving two doses for the phase 1b trial right now. Could you maybe just, you know, just help us understand what are the, you know, the expectations for the data readout, atopic dermatitis for, you know, in December assessment expectation around what should we be looking for in the data set?

Yes, so maybe starting with like, what are our objectives? What were our objectives for phase 1B? The main objectives for doing a relatively small uncontrolled study was, number one, to show translation of safety and PD from healthy volunteers to patients. That was very important for us for the study. Number two was through that translation of PK and PD to confirm the doses that we were going to be selecting for the phase 2B dose range finding study. Third, to really show hopefully a Dupixent-like impact on Th2 biomarkers both in the blood and in skin with 28 days of dosing, which was the duration of the phase 1B. Finally, to also be able to show potential impact on a variety of different clinical endpoints in AD, even in the absence of a placebo control.

We think this was an opportunity for us to be able to show initial activity to your point, around the doses. We initially started off with one dose that was selected based on our phase 1A data. You may recall that at doses of 50-200 milligrams. In phase 1A, we saw complete degradation in blood and skin. So we brought one of those doses into the phase 1B. And after enrolling 10 patients and doing that briskly, we felt we saw enough data to allow us to actually bring a second dose into phase 1B so we could show translation across two different dose levels. The aim was not for us in phase 1B to show dose response or to make up with a second dose any deficits we were seeing on safety or efficacy with the first dose.

It was really just to further strengthen the translational database from healthy volunteers to patients and then further, you know, confirm and give us even that much more confidence in the doses that we were bringing into the phase 2b dose range finding study.

Got it. Out of those two doses, what sort of statistics, target degradation should we be expecting of those two doses?

Should be looking for? You know, I think our aim was to bring in, you know, doses that would be, you know, active, obviously highly active, you know, for the first dose. As I mentioned, that dose was chosen from the 50-200 milligram range. We have not really given guidance yet into what the second dose was and we will make that information available when we actually present the data in December. Again, I think the aim was to be able to show translation across two different dose levels. If we move to the phase 2b dose range finding study, where we have already initiated that one in AD this quarter, we just announced initiation of that phase 2b study.

We have three different dose groups and placebo and what we said about those three different dose groups is that it sort of will give us a sort of pharmacologically active and clinically active dose. You know, a higher dose that would be super pharmacologic and then a lower dose that would be sort of maybe submaximal. That is the sort of dose range finding that we want to do within a phase 2b. What we have said about those doses, even though we do not plan on revealing what those doses are for the phase 2b, we have said that those will be. Those were chosen based on the doses that we looked at in the phase 1a healthy volunteer study.

Got it. Just going to the specifics around the endpoints and we should be looking at biomarker data like TARC reduction. Could you help us understand what level of TARC reduction would be considered meaningful in your opinion?

Yeah, I think TARC, you know, is a helpful biomarker to look at in AD. Prior studies with Dupixent have shown greatly elevated TARC levels in AD patients. In that context, Dupixent has shown anywhere from 70-80% reduction of TARC as early as 28 days. Again, keeping in mind that our phase 1B study is 28 days duration. Interestingly, if you look at some of the other Dupixent studies in other diseases like asthma and EoE, where the baseline levels are not as high as they are in AD, you see less of a reduction, reductions that are more in the 35-40-45% range, which is what has been seen in healthy volunteers as well.

I think the expectation is that if baseline levels are high as they were in the prior Dupixent studies, then one should be able to see 70-80% reduction of TARC biomarker even at 28 days. We have set that as the ballpark that we would like to be able to see for KT621 in our phase 1B.

Got it. Besides TARC, of course, you’re going to be potentially showing some clinical endpoints like EASI. Also, pruritus. Just help us understand some of the expectations for what kind of data readout should be expecting in terms of what we consider clinically meaningful.

Yeah, I think if one harkens again back to the Dupixent data and going back to, say, the phase three SOLO 1, SOLO 2 studies, you can take a look at what they saw 28 days for changes in EASI and changes in NRS pruritus and get a sense for. That’s sort of the ballpark that we’d like to be in, you know, in phase 1B, you know, when we think about aspirationally where we’d like to be with regard to activity for 621, we believe that the biology and the preclinical data and the phase 1A healthy volunteer data point to the potential for this drug to be Dupixent-like. And so that’s the reason why we’d like to see impact on endpoints such as EASI and NRS pruritus.

Even in phase 1B in the absence of a placebo control, that are, you know, within the ballpark of what Dupixent saw at 28 days in their studies.

Got it. Okay. And then, you know, for that phase 2B trial you’re planning to start in the fourth quarter in AD, could you just show us over a quick overview of the clinical trial design?

Sure. So that particular study which has already been initiated, it’s a 200 patient study in moderate to severe AD. Typical 16 week duration, primary endpoint % change in EASI over 16 weeks. The study also has a 52 week open label extension period after completion of the 16 week planned placebo controlled period. As I mentioned, you know, three dose levels along with placebo. And again, you know, in addition to EASI looking at, not just EASI as a continuous variable, but also looking at, you know, EASI 50, EASI 75, looking at pruritus, NRS, vIGA, all the typical endpoints that you would see in an AD study.

Got it, got it. How should we think about translation from the AD study into other derm or gen indications such as, you know, PN, EoE, BP and SCU?

Yeah, I think it’s a great question. You know, currently our development plan is an accelerated plan where the centerpiece are really two phase 2b studies. We call them sentinel phase 2b studies. Right? One in AD which has already begun, and the second in moderate to severe asthma that will be starting in Q1 of next year. Both of those phase 2b studies actually will be testing the same three dose levels of KT621. Ideally, what we’d like to have happen is for the AD study, the phase 3 dose that comes out of that phase 2b study could be used not just in the phase 3 study in AD, but also in other skin indications where Dupixent has been active and approved, as well as in GI indications like EoE.

Rather than having to do additional phase 2b studies, we would go directly to phase 3 studies across those other indications. This of course still requires regulatory buy-in, but we think that that’s a reasonable approach. Likewise, for the phase 2b asthma study, the phase 3 dose that comes out of there could be used not just for moving ahead with a phase 3 study in asthma, but then also going into COPD, for example, or CRS with nasal polyps, you know, other respiratory diseases where Dupixent has gone, and also going in and potentially parallel tracking or staggering additional phase 3 programs there again without having to do any additional phase 2b studies.

Got it. Can you just remind us how big is the AD market overall?

The AD market is quite large. I mean there are literally tens of millions of patients. In the U.S. and in Europe and elsewhere, in Asia. It’s important to remember also that this is a disease that affects children, very young children, adolescents as well as adults. It really is a very sizable population. If you look at the moderate to severe segment of patients with AD, what’s really striking is that only about 1-2% of those patients are actually getting access right now to dupilumab, which is a highly successful, active, well tolerated drug. What that means is that there are the other 97-98% of patients with moderate to severe disease.

We are talking of tens of millions of patients who, if we have an oral drug that were potentially as safe and active as Dupixent, you can imagine that that could then be accessed by that many more patients. It could really be a drug that now transforms the lives of many more patients, both young children, adolescents as well as adults.

Got it, got it.

Great.

Now let’s switch gears and talk about your second program, which is the IRF5, the KT579 program. We saw some encouraging preclinical data at ARC recently. Can you just maybe share a quick overview of the mechanism and biology of IRF5 and how do you think it could complement the STAT6 program?

The IRF5 program is another very exciting program for us. KT579 is the name of that program. And again, like STAT6, it exemplifies, we believe, marrying our platform technology to ideal targets and pathways where we think we can really have, you know, a transformational drug that can reach millions of patients and with higher met need. IRF5 has been of great interest for years, you know, for both big pharma and biotech, because it mediates signaling through B cells, it’s involved in B cell activation and autoantibody production, it’s involved in controlling type 1 interferon production and it’s called, it’s involved in controlling the production of multiple different proinflammatory cytokines. It affects B cells, monocytes, plasmacytoid dendritic cells and even neutrophils. It’s essentially activated through all the different toll-like receptors and other innate immune receptors.

IRF5 is unique in that its expression is restricted just to those types of immune cells that I just described. It is also usually disactivated in the setting of sort of pathological. It is a target that has been of great interest because it can affect all these pathways that have been validated indirectly by other drugs that are targeting type 1 interferon receptors, targeting pro inflammatory cytokines, targeting B cells. You could have it all in one drug targeting IRF5, but it is very difficult to drug. It is a transcription factor. There are multiple IRFs and even IRF5 has multiple isoforms. Finding a drug that is highly selective for IRF5 and completely block its activity has been very difficult. Now we have a degrader that can do just that. We have a degrader that is highly selective for IRF5, highly potent, can be dosed once orally daily.

You know, we have these preclinical data that you referred to, David, that we presented at ACR recently, where in two different mouse models of lupus, you know, we see very strong activity that’s equivalent to or usually better than other approved drugs or active drugs, as well as data in rheumatoid arthritis. What’s attractive about this target is that there’s very strong genetic association between IRF5 polymorphisms and susceptibility to lupus, to inflammatory bowel disease, to RA and to other type 1 interferons like Sjogren systemic sclerosis. Now having these powerful data and animal models of SLE and RA just give us further confidence in the potential of this drug across those various indications.

Our plan right now is we’ve completed IND enabling studies for this program and we plan on initiating phase one in healthy volunteers early next year and to have data readout sometime next year as well. Following that, we will then be moving into our first patient studies.

Yeah, this seems like this mechanism is very wide in terms of applicability. I am curious in terms of your thoughts around what would be some of the leading indications you are thinking of.

I think, you know, lupus is certainly, you know, at the top of the list for us, given the very. Probably has the strongest genetic association with IRF5. Obviously a huge unmet need, you know, very little in the way of oral active drugs in lupus. And, you know, the strength of our. Of our animal model data, I think lupus is definitely sort of high on our list. I think at the same time there are also these very interesting genetic associations with IBD in RA. We already have this animal model data in RA, which is also looking very positive. I think, you know, lupus is certainly probably, you know, at the top of our list.

You know, multiple other indications that I think we’re still working on how we might prioritize those, you know, whether there are other type 1 interferonopathies or whether it’s IBD or RA. I think that’s still a work in progress that we’ll sort of share more on that as we get further along in our thinking.

Yeah, so then, you know, help us understand some of the expectations then for. From healthy volunteer data. What are you looking for, to actually determine that you’re, you know, that you want to move into certain indications.

I think, you know, certainly in terms of phase one healthy volunteer study, I think as we get closer to starting that study, we can provide more information on it. It’ll be certainly sort of a SAD MAD standard. And you’ve seen sort of our SAD MAD healthy volunteer studies now across multiple programs. You know, for us it’s going to be important to be able to show that we can, you know, strongly degrade IRF5, you know, in blood and then at least another sort of tissue such as skin, for example, which we can look at in healthy volunteers, showing safety, showing we can do this and get deep degradation 90-95% or greater, you know, at reasonable doses, you know, so those are among the probably most important sort of biomarkers that we’ll be looking at in that phase one study.

Got it. That’s helpful. Great. And then moving on to your IRAK4 degrader, KT, you know, so when you look at, you know, right now the program is being, you know, being partnered with Sanofi and Sanofi has, you know, has prioritized next generation IRAK4 degrader, the 485 over the first generation degrader, you know, 474, you know, due to some subclinical QTc issues. So I’m just curious, could you share some detail around, you know, what have you seen that caused the QTc prolongation?

Yeah, it’s a good question. With KT474, we did see this subclinical QTc prolongation and we investigated that very thoroughly. What we can say is that that was really very compound specific. It was not at all any sort of degrader class effect. It had nothing to do with actual on-target IRAK4 degradation. It was very specific to that particular compound. And we’ve learned a lot from that. We’ve learned preclinically how we can avoid having any HERG impact, having any QT effect. We now use non-human primate cardiovascular studies in order to make sure that any compounds that we’re bringing into the clinic will be fully de-risked around having any QTc prolongation.

I think all those learnings from KT474 have been applied not just to KT485 obviously, which as you mentioned is why Sanofi is now so interested in moving that forward in place of KT474, but also applies to all of our other programs including STAT6, IRF5 and all the other programs to come.

Yeah. Just to kind of follow that, what kind of learning have you were able to gather out of that?

485.

Or KT474 that you can apply to other degraders not only for your existing programs, but also down the road?

Yeah, I think it’s really learning. It’s all about chemistry and learning, you know, what is it about chemistry of any compound that might contribute to having an effect on HERG channels in your earliest preclinical work? And even when you’re then avoiding having compounds that have any impact on HERG, you want to then be even more reassured by putting those compounds into cardiovascular studies in monkey. It turns out that monkey is really more predictive than dog in whether you’re going to have any QTc prolongation with a compound.

Knowing that we can now not just use, you know, in vitro HERG as a way to avoid compounds that can cause QTc prolongation, but now this added step of now putting those compounds, you know, into non-human primates and showing definitively there that there’s no QTc effect with multi-dosing, I think that really strongly, you know, de-risks seeing this sort of an issue with any future compounds.

Got it.

Great.

Okay. I think we’re almost out of time, so maybe just one last question, Jared. What’s the next catalyst over the next 12 to 18 months that we should watch for?

I think obviously for December, our plan is to present phase 1B data. That’s obviously a very important catalyst. We just recently announced initiation of our phase 2B AD study. In Q1 of next year, we’ll be announcing an initiation of our phase 2B asthma study. I think, you know, further catalysts next year will include, you know, phase 1 data for KT579. I think our expectation, although this is beyond our control, this is in Sanofi’s control. The expectation is that Sanofi will be moving KT485 into a phase 1 healthy volunteer trial next year. Our plan is to move at least one or two new programs into the clinic, into our pipeline each year. I think those will really be the main catalysts.

As I mentioned earlier, with our cash run rate that goes through the end of 2028, I think we’re also looking at important catalysts in 2027. We’ve guided that the phase IIb study will complete by the middle of 2027. That will be another important catalyst. That cash runway, I think, gets us through these phase IIb studies, the startup of potential phase 3 studies for AD and asthma, as well as key phase 1 and phase 2 readouts for the IRF5 KT579 program. Great.

Okay. I think with that, I think we can conclude here. Thank you everyone for joining and thanks to Jared for your time coming to the UPS conference.

Yeah, thanks for having us here, David, and thanks for the question.

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