Kymera at H.C. Wainwright Conference: Strategic Moves in Immunology

On Thursday, 27 March 2025, Kymera Therapeutics (NASDAQ: KYMR) participated in the H.C. Wainwright 3rd Annual Autoimmune & Inflammatory Disease Virtual Conference. The company showcased its progress in targeted protein degradation technology, emphasizing its potential to match biologics’ efficacy with oral treatments. While the focus was on innovation and strategic advancements, challenges in traditional targeting methods were also discussed.

Key Takeaways

• Kymera has advanced five programs into clinical stages over four years.
• The STAT6 and TIK2 programs are pivotal, aiming for biologics-like efficacy with oral degraders.
• A new program announcement is expected in May.
• STAT6 trials for atopic dermatitis and asthma are set to launch in late 2025 and early 2026, respectively.
• The TIK2 Phase 1 readout is anticipated by the end of 2025.

Operational Updates

• Pipeline Advancement: Five programs have entered clinical trials in the past four years, with a focus on immunology and inflammation.
• Program Focus: STAT6 and TIK2 are highlighted for their potential to replicate biologics’ effects with oral treatments.
• Upcoming Announcements: A new program is set to be unveiled in May.
• Trial Readouts: TIK2 Phase 1 results are expected by year-end, while Sanofi’s IRAC4 Phase 2b data is anticipated in mid-2026.
• STAT6 Trials: A Phase 2b trial for atopic dermatitis will start in Q4 2025, followed by an asthma study in Q1 2026.

Future Outlook

• Pipeline Expansion: Kymera aims to introduce at least one new program annually.
• Prioritization Strategy: The company focuses on clinically and genetically validated pathways to minimize biological risk.
• Clinical Development: Accelerated development of the STAT6-621 program is aimed at reaching Phase 3 trials.
• Indication Focus: Larger indications like atopic dermatitis and asthma are prioritized, with plans to explore smaller indications subsequently.
• TIK2 Program: Potential Phase 2 trials in psoriasis, with considerations for IBD, lupus, and other conditions driven by TH17 and interferon pathways.

Q&A Highlights

• STAT6 Program: Kymera plans to demonstrate 90% or greater degradation of STAT6 in blood and skin, ensuring safety and tolerability.
• Biomarkers: Biomarker strategies have been tested in healthy volunteers, showing promising results for TARC and IgE.
• TIK2 Program: The company expects significant degradation over time, with good tolerability in Phase 1 trials for healthy volunteers.
• IRAC4 Program: Sanofi is conducting two ongoing Phase 2b studies, ZEN and ADVERNTA.

For a deeper understanding, readers are encouraged to refer to the full transcript.

Full transcript - H.C. Wainwright 3rd Annual Autoimmune & Inflammatory Disease Virtual Conference:

Ananda, Interviewer: Autoimmune and inflammatory disease virtual conference. Very pleased to have with us doctor Jared Golub, the chief medical officer of Chimera Therapeutics. Jared, good morning and welcome. Maybe we can start with a brief introduction of Chimera before we delve into the pipeline questions.

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Sure. Absolutely. So Chimaera, you know, we were established back in 2016. You know, we are a targeted protein degradation, you know, company. You know, we have now moved, five programs into the clinic, you know, over the last four years in both oncology and inflammation.

You know, we think we’ve been very successful in showing, the translation of PK and PD and efficacy from our preclinical programs into the clinic across the first four programs where we have data, including IRAC4 and in our oncology programs. You know, we are have pivoted now toward a focus that’s largely on inflammation and immunology. You know, and that focus, you know, which is exemplified by the STAT6 and TIG2 programs, for example, comes in part from our early success with IRAC4, but also comes from how we’ve evolved our TPD platform over time to a point now where we can access these high value targets like STAT6 and TIK2, which are really critical signaling nodes within highly validated pathways within immunology and inflammation diseases, be it TH2 diseases, you know, for STAT6 or IL-seventeen interferon driven diseases for TIK2. And the unique pharmacology of our degraders, you know, it now enables us not just to access these targets, but to degrade these targets in a way that can allow for full pathway blockade with oral degraders. So now we’re in the, I think, incredible position of having oral degraders that can block pathways to the same extent as upstream injectable biologics and achieve the same sort of activity potentially in safety, with oral drugs, which really can be transformative now, we believe, across multiple different indications within immunology and inflammation.

You know, STAT6 and TIK2 are sort of the tip of the iceberg, two programs we’re incredibly excited by. We’re going to be announcing another program, you know, in May, and more to come after that, again, focused on going after these highly validated high priority pathways in inflammation and immunology and being in the unique position of being able to access these signaling nodes, with the unique pharmacology of degraders that can give us that biologics like activity.

Ananda, Interviewer: Great. Thanks. Maybe, you know, since 2025 is all about STAT6 and TIC2, can you tell us what got Chimera into these two programs and why, are these of were of high interest

Jared Golub, Chief Medical Officer, Chimera Therapeutics: for the company? Look, I think STAT6 has been of high interest, not just to kind of narrow but to, you know, the big pharma and biotech in general for, you know, a decade. You know, ever since, you know, it was clear that targeting the IL-four or IL-thirteen pathway with, drugs like DUPI were, you know, highly successful and really transformative for patients with TH2 diseases. There’s always been a great desire to try to find other ways of targeting those pathways, especially with oral drugs to try to make it more accessible to a much larger fraction of patients. And so, once we got our technology to the point where we were able to actually, you know, develop degraders to a target like STAT6, you know, that really represented, I think, a real sea change in the ability to target STAT6 and to be able to target it in a way with potency and selectivity and with the de greater pharmacology that would allow us to fully block that IL-four 13 pathway to the same extent as biologics.

And we see that as a tremendous opportunity, not just to transform the space into patients, but also a very tremendous commercial opportunity. And likewise for TIC2, I think, you know, a real aim with TIK2 targeting has been to try to recapitulate, you know, the TIK2 loss of function phenotype where patients are protected from multiple autoimmune diseases. And TIK2 small molecules have tried to do that, but they really have come up short. And we believe that the degrader technology, our degrader against TIK2, you know, is the way to be able to sort of phenocopy TIK2 loss of function and realize the full potential of hitting the TIK2 pathway to treat autoimmune diseases that can really differentiate substantially from what’s been achieved so far with TIK2 small molecule inhibitors. So I think these two targets really exemplify Chimaera’s approach in the immunology and inflammation space and how we’re trying to take advantage of our deGrader technology to really push the envelope and develop transformative drugs.

Ananda, Interviewer: Great. Maybe that might be a segue for historical, you know, what were the challenges with respect to developing a STAT6 inhibitor and you know, what differentiation approach does degraded brings to a STAT6 program?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Well, I think, you know, when we think about proteins that are particularly amenable to the the greater technology to find the right solution. I think we think about transcription factors, which are notoriously difficult to drug potently and selectively, and we think about multifunctional proteins with scaffolding function. You know, TIC2 is an example of a ladder, you know, STAT6 of the former. So I think one of the real challenges in drugging STAT six was to try to come up with novel ligands that could enable one to develop degraders that would be potent and highly selective for STAT six. And I think it’s taken a while to develop that technology and evolve that capability, you know, and at Chimera, you know, we have been in the forefront of developing degraders against these difficult targets and evolved our platform in a way that now allows us to do this quite effectively.

And so I think for, you know, for STAT6, I think that’s been the main challenge. And what you need to do for STAT6 is not just sort of temporarily or partially inhibited, but you want to be able to sort of fully block STAT6 sort of 20 fourseven if you’re going to try to match the efficacy of biologics. And, you know, STAT6 inhibitors can have problems sometimes with selectivity and potency and, you know, usually are not able to sort of fully block and inhibit STAT6 20 fourseven. And so it will probably be very difficult for those sorts of drugs to obtain biologics like activity, whereas with degraders, we’ve shown preclinically, we can degrade STAT6 95 plus percent, you know, 20 fourseven and result in full blockade of the pathway that’s comparable to what DUPI can do but with greater potency. I think that’s what’s going to be needed, to be able to develop an effective, you know, STAT6 targeted approach to treating these sorts of TH2 diseases.

Ananda, Interviewer: Got it. You know, let’s dig into some data. The preclinical data showing comparable efficacy with 2P were perhaps the most important data apart from the picomolar degradation efficiency. Can you tell us the major takeaways from the preclinical datasets and also how good are the atopic dermatitis models with respect to translation, in human clinical trials?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. I think it’s a great question. I think that the models, you know, for which we’ve shared data include the house dust mite asthma model, which is really sort of gold standard TH2 inflammation model, that, you know, doopy, you know, has used and and shown efficacy in. That’s probably one of the best TH2 models out there for showing proof of concept in a TH2 disease. Within that so called HDM model, we’ve been able to show that when we give our degrader at a dose that leads to at least 90% knockdown of STAT6, we’re able to show activity that’s comparable, if not even superior, to what is achieved with dupilumab, which we compare head to head within those experiments.

And so for us, you know, that that is extremely encouraging and that’s why we sort of set the bar at at least 90% for the sort of degradation we want to be able to achieve in the clinic in order to potentially enable us to match the activity of, of dupilumab. Now in terms of atopic dermatitis, you know, there aren’t really very good models of atopic dermatitis that really, you know, reflect what happens in humans. You know, there are various AD models that one uses. We use the NAD model that’s similar to one that DUPI has used that we went head to head with with DUPI in that model And looking at, for example, impact on IgE in that model, we showed again that we have activity that’s at least comparable to DUPI. So I think those models where they’re not absolutely, predictive of what you’re gonna see in the clinic, they give us, you know, a very powerful way of showing what sort of knockdown we need to have activity in those models and also allow us to compare our activity to DUPI to give us a setting to where that bar needs to be in the clinic for the degree of knockdown, the sort of pharmacology we need to be able to reach doobie like activity.

Ananda, Interviewer: Got it. You know, look, given the, you know, the upcoming data, you know, let’s talk about some of the biomarker aspects. You know, historically, IgE and TARC have been used, for two p trials, but have but have only seen modest changes in both, the biomarkers for healthy volunteers. What are your expectations with respect to these biomarkers? Now can baseline biomarker levels predict treatment response?

And finally, you know, what are the expectations from the HP trial data?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. Look, I think it’s important to understand what the limitations are for various biomarkers that you’re looking at in healthy volunteers versus patients. I think for us, you know, from the very beginning, even before we started enrolling onto the Phase 1a healthy volunteer study, we were very clear that for us, the number one biomarker is STAT6. And for us, it’s to show that we can degrade STAT6 by at least 90% or greater in blood and skin at doses that are safe and well tolerated. Given our preclinical data showing that 90% is where we see, activity comparable to DUPE, we believe that if we can show in healthy volunteers that we can achieve that level of degradation at doses that are safe and well tolerated, that greatly derisks the program and should predict for our success once we move into patients.

Now, you know, you mentioned TARK and IgE. Yes, those are biomarkers that have been looked at in healthy volunteers. They tend to be at normal levels in healthy volunteers, but, you know, Regeneron, you know, in their paper looking at DUPI and Healthies and looking at those biomarkers was able to show some clear signal from noise, within those assays, you know, for TARC and IgE. They were able to show for TARC, for example, that you could see anywhere from, you know, 15 to 35% reduction, you know, within the first, say, week after dosing, but with no clear dose response. I think that was important, you know, no clear dose response, but you could see a signal, for IgE in that same sort of timeframe, seven to fourteen days, they weren’t able to see much of an effect on IgE, maybe 100% at best or even less really because there’s a longer half life for IgE.

So when we look at those data, you know, from the beginning, we’ve guided that we do expect to see hopefully a DUPI like effect on those biomarkers, something comparable to DUPI, in addition to showing, you know, the hopefully, you know, profound, hopefully impact on stat six in blood and skin. I think, you know, patients, you know, when we move into phase 1B in AD patients with moderate to severe disease, that will be a much better you know, platform for showing, we believe, more robust effects on TH2 biomarkers in blood as well as in skin. And, you know, when DUPI has looked at that, they’ve seen very robust effects on those biomarkers that can then potentially predict for or correlate with clinical outcomes. And so that’s why I think that phase 1b study, which is a single arm open label study, is going to be very heavily focused on those biomarkers because these biomarkers, you know, rarely move much in placebo groups in randomized studies. And so we don’t really need a placebo arm to be able to show a robust effect or DUPI like effect on biomarkers in that phase 1b study, where we’ll also be looking at clinical endpoints, you know, at four weeks because that study only is only going to be with twenty eight days of dosing in Phase 1b.

But again, we think that that will allow us an even more robust opportunity to show doobie like effect on biomarkers.

Ananda, Interviewer: Got it. Given several indications planned for the STAT6 program, how are you thinking of running those trials post POC trial in patients?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: So I think, you know, the, as I mentioned, you know, the for us what’s most important is accelerating development for the STAT6-six 21 program, ultimately to get to Phase three as soon as we can, because we believe we have a drug that’s going to be transformative in the space. So our Phase oneeight data is going to allow us to choose the doses that we need for these critical Phase 2b studies, in AD and in asthma, the AD Phase 2b starting in Q4 of this year, the asthma study in Q1 of next year. And we think of these as sentinel Phase IIb studies, meaning these are going to be the critical dose range finding studies that will allow us to pick the doses that are going to go into Phase III. So for example, you can think of the AD study, the dose that comes out of that phase 2b will enable parallel phase 2b phase three studies, not just in AD, but in other skin diseases where DUPI has gone before as well as in a disease like EOE, you know, a GI disease. Whereas the asthma phase 2b will allow us to select the dose not just for asthma Phase III, but also for COPD and maybe CRS with MP, you know, and other diseases of that sort.

So in terms of how we prioritize indications, you know, there are many places we can go where DUPI is gone, right, in various TH2 diseases in the derm, GI, and respiratory space. We are prioritizing the larger indications first. That’s why these two Phase IIb studies, which we think are the only Phase 2b studies we’ll need to do, are going to be an AD and an asthma. And then we also anticipate, you know, having Phase three programs, not just an AD and an asthma, but also in COPD to start. So really focusing on the largest indications first and then being able to then also move then into somewhat smaller but still very important indications, either, you know, in parallel with those or staggered.

You know, we haven’t decided on the exact approach there, but I think that gives you an idea of how we’re thinking about prioritizing indications.

Ananda, Interviewer: Got it. You know, let’s switch gear to the TIC two program. I like you know, even though, TIC two remains a critical, regulator considering, inflammation, what do loss of function TIK2 experiments tell us about the safety and tolerability profile?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. I think, you know, I mean, we’re fortunate to have human genetics, you know, to guide us here. And TIK2 loss of function, complete loss of TIK2 in humans, not only protects, you know, from a variety of different autoimmune diseases, especially, you know, TH seventeen and interferon, driven diseases. But, these patients also have a fairly minimal phenotype when it comes to risk of infections. You know, you may see some mild viral infections or some mild intracellular infections that are readily treated with antibiotics.

But these patients don’t come down with, you know, life threatening infections. That’s probably because even with TIC two loss of function, there’s still some small residual amount of signaling through IL 12 and IL 23 and even interferon receptors. That’s been shown in various publications, that probably does protect against, you know, severe life threatening infections or even moderate infection. So we’re expecting, you know, again, from the human genetics and from that experience that, you know, deep, you know, tick to degradation over time should be well tolerated.

Ananda, Interviewer: Got it. And again, similarly, you know, what advantage, does degraders have over the current approaches prevalent in the TIP two landscape?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. I think that’s that’s a really important question. Right? Because I think there has been some sort of TIC2 fatigue in the sense that, you know, small molecule inhibitors have clearly been active and have clearly provided, you know, proof of concept and validation for the pathway, but they sort of all come up short, you know, these various TIC2 small molecule inhibitors when it comes to, you know, trying to reach biologics like activity. And we think the reason for that is that, you know, they lack the depth and breadth of inhibition that one is trying for if you’re trying to phenocopy TIK2 loss of function.

So for example, inhibitors are only able to inhibit the pathway maybe 60 to 70%. They’re not able to get sort of twenty four seven inhibition even at that level. It’s more cyclical inhibition that you get with typical small molecule inhibitors. And that’s translated into these inhibitors all sort of coming up short with regard to reaching biologics like activity and diseases like psoriasis. We think the real advantage of our TIC2 to greater two ninety five is that we’ve shown pre clinically in rodents and in monkeys that we can knock this target down ninety five percent or greater, round the clock.

So 20 fourseven. So no let up, 95% degradation, and it’s kept there, and we believe that that should enable us to phenocopy TIK2 loss of function, and to do that in a way that is hopefully safe and well tolerated, but importantly, we believe it’s that level of degradation and pathway inhibition that will be needed in order to achieve biologics like activity. So our plan for the TIC2 program is, you know, we’re going to be starting phase one in healthy volunteers in the second quarter of this year, and we’ll have a readout by the end of the year. That readout should be able to tell us, you know, can we achieve, you know, 95%, you know, degradation of the target sort of round the clock. If we can, that’s telling us where we’re getting pharmacology that should, you know, sort of phenocopy potentially TIC2 loss of function.

But I think the next important step after that would be, next year then to have a, you know, probably a placebo controlled Phase two study, probably in a disease like psoriasis where one can readily, you know, assess activity relative to placebo in a reasonable timeframe. And there, we would wanna see that we have biologics like activity, you know, IL twenty three injectable biologics like activity and psoriasis to really say, okay, we’ve got a drug that really is differentiated from small molecule inhibitors, potentially even differentiated from the J and J IL twenty three, you know, peptide, inhibitor. And if we’re able to reach that biologics like activity, which even the J and J compound has not been able to attain, that for us, would tell us to want to then move forward probably a multiple phase three campaign. It’s not necessarily in psoriasis. I mean, maybe psoriasis, but I think we’re thinking also about you know, IBD and lupus and other PH seventeen and and, type one interferon driven indications.

Ananda, Interviewer: Got it. You know, you mentioned psoriasis. You know, for psoriasis, the standard endpoint has shifted from, I think, PASI 50 to 75 to even hundred, raising the efficacy bar for these therapies. Plus, there are, you know, 10 other drugs which are approved. Where do you see TIC2 program being a value add to the landscape?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. I I think that’s a fair question. I I think as I just alluded to, you know, essentially for this drug, I think to add value, you know, we believe we need to be able to show biologics like activity. Again, I think, you know, even the J and J compound, which is a highly active drug and has shown activity recently, not just in psoriasis, but also in IBD, you know, is perhaps a new sort of gold standard, you know, for oral drugs. But I think it’s still coming, falling short.

You know, if you look at a disease like psoriasis, you look at PASI 90 levels, it’s not quite achieving what you can with, you know, they say anti IL twenty three injectable biologics. And so I think, you know, if we end up wanting to sort of be in that psoriasis space, I think we’re gonna have to be an oral drug that is able to achieve, you know, biologics like activity. This is something which has still not been achieved yet, you know, even with the best, you know, small molecules. But with that said, as I mentioned earlier, you know, even though it’s possible that our proof of concept phase two study might be in psoriasis, we’re not necessarily committed to developing first in psoriasis. You know, we might then want to take the drug and maybe it’s possible we could prioritize inflammatory bowel disease, you know, or lupus or other indications.

So we haven’t decided yet how we’re going to prioritize development beyond initial phase two proof of concept. You know, it may or may not include psoriasis initially.

Ananda, Interviewer: Got it. You know, going back to, KTE six twenty one and IRAC four program, the biological variability has been cited to be one of the biggest, you know, limiting factors in AD. And with respect to your six twenty one and IRAC four program, how have you kind of thought about, you know, tackling the variability in the trial design?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. I think if if by biologic variability, you’re alluding to the sort of placebo effect that you can see within within these AD studies, which which maybe, you know, attest to that. Right? I I think it’s all about, you know, how important it is to select the right patients for your study and to select the right sites and the right investigators to be running your studies and to have, you know, again, you know, the right eligibility criteria, you know, for your studies to try to do all you can to minimize placebo effect. You know, having very milder patients, you’re more likely to see a higher placebo effect than with more severe patients.

And so I think for us, it’s gonna be important, you know, again, the eligibility criteria that are already out there for the, you know, KT four seventy four, you know, phase 2b study in AD. And, you know, again, you know, for phase 2b with six to one, that’s still a work in progress. But when we think about approaches that can try to minimize that variability or try to minimize that placebo effect, it is gonna be about making sure that we bring patients who really have AD, you know, onto the study, because AD is a clinical diagnosis, it’s not a histopathologic diagnosis, so you really need clinicians who know how to diagnose AD to make sure we have the right eligibility criteria, to make sure we get moderate to severe patients and to make sure we have, you know, clinicians and research teams at the sites who are able to stringently apply those criteria to make sure we are only getting moderate to severe patients on the study and to make sure we have, you know, clinicians investigators at these sites who are very adept at doing the clinical endpoint measures, whether it be EASI or pruritus and RS, you know, whatever it is that we’re looking at to make sure they’re adept at doing those measures and doing them consistently and having, you know, an investigator consistently seeing the same patient over time.

All of these, I think, can be important factors that one needs to pay very important attention to in order to try to get the best study possible and try to minimize the sort of placebo effect you’re gonna see within the study.

Ananda, Interviewer: Got it. Very helpful. Maybe, you know, we can we can kind of go back to the IRAC four program. If you can briefly talk about the ZEN and ADVERNTA, in terms of trial design, endpoint selection and dosing? And also, you know, what are the key learnings from the historical trials in ADNHS with respect to the four seventy four program?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. I mean, both of these studies, these are ongoing Phase 2b studies, you know, that Sanofi is running. You know, these studies, you know, following an interim analysis, a blinded interim analysis of safety and efficacy last June were converted from smaller Phase IIa proof of concept studies to more expansive Phase IIb dose range finding studies to get us more quickly, you know, ultimately to Phase III, you know, for both HS and AD. So both of these studies were expanded. You know, the, patient numbers were almost doubled across both studies.

Additional dose levels were added to make sure that these were full dose range finding studies. Now, both these studies have all of the classic standard, primary and secondary endpoints for HS and AD and the appropriate eligibility criteria to make sure we’re getting, you know, moderate to severe patients. You know, these studies are, the current guidance is for these to read out, you know, sometime in the middle of twenty twenty six. You know, I think in terms of other elements of design, you know, just going back to your prior question, right, in terms of, you know, how do you try to minimize, you know, biologic variability to try to, you know, make sure the placebo rate, you know, whether it’s for HS or AD, isn’t too high, it sort of comes back to those same principles, you know, that I just spoke to earlier, you know, that that Sanofi is also following, as they, you know, not not just in the design of these studies, but also how they operationalize the study.

Ananda, Interviewer: Got it. And that kind of brings us to the last question for today’s fireside. You know, with the promise of one target a year, how do you, you know, prioritize where to put the focus on as the company expands and the pipeline expands?

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. Yeah. Yeah. Look, I I think with our with we’re we’re we’re fortunate that we have a platform technology that we’ve spent, you know, a lot of time and money and have brought in amazing people to really evolve that platform into something that we think is sort of unprecedented in the field, which gives us an incredible multiplicity of opportunities to go after high priority targets, with our focus now being on inflammation and immunology. So you mentioned, you know, one new program a year.

I think we say at least one new program a year. So I think we have the ability to go beyond even one program a year. But if we stick to that for now, you know, I think the sort of targets and pathways that we’re gonna go after, you know, are going to maintain the sort of approach and philosophy that we’ve taken for stat six, for example. We we don’t wanna take a lot of biologic risk, you know, in the pathways we’re going after. We want pathways that are highly clinically validated, you know, and or genetically validated, within inflammation and immunology so that we’re not taking on biologic risk.

We then want to take full advantage of the degraded technology and pharmacology to go after key signaling nodes within those pathways, where we’re confident that if we fully degrade those targets, we can fully block these pathways to the same degree that upstream injectable biologics can block these pathways. And therefore, we’re very confident we can develop oral small molecule degraders that will have the activity and safety of injectable biologics. And by doing that across multiple pathways and multiple indications, you know, can truly be know, transformative. I mean, we truly believe that at Chimera, we have the potential to have the best oral immunology, you know, pipeline, you know, in in industry. We have to obviously, you know, work for that.

But I think where where we are now with Iraq Four, STAT six, and TIC two, and a new program we’ll be announcing in May, I think this gives you an idea of our sort of our ambition and our philosophy and our approach and where we expect to go in the future.

Ananda, Interviewer: Alright. Very helpful, Jared. As usual, great great speaking with you. And, thanks for giving us time, and, you know, good luck with the stat six program readout.

Jared Golub, Chief Medical Officer, Chimera Therapeutics: Yeah. Thanks so much, Ananda. Appreciate the opportunity and and and all the great questions.

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