Kymera at Goldman Sachs Conference: Pioneering Oral Protein Degraders

On Tuesday, 10 June 2025, Kymera Therapeutics (NASDAQ:KYMR) presented at the Goldman Sachs 46th Annual Global Healthcare Conference. The company’s strategic focus was on its oral protein degrader programs, with a particular emphasis on the STAT6 program for immunology applications. While the discussion highlighted promising advancements, it also underscored the challenges associated with resource allocation and market competition.

Key Takeaways

• Kymera’s STAT6 program (KT-621) shows promising Phase 1 results, advancing to Phase 1b in atopic dermatitis.
• The company achieved a $20 million milestone from Sanofi for the IRAK4 program.
• KT-621 aims to outperform existing treatments like Dupixent in the Th2 disease market.
• Kymera plans to initiate a Phase 1 study for its IRF5 degrader program targeting lupus.
• The company is focused on rapidly advancing its pipeline into Phase 3 studies.

Financial Results

• Achieved a $20 million milestone payment from Sanofi related to the IRAK4 program.
• The focus remains on pipeline development and partnership milestones, with no specific revenue or profit figures disclosed.

Operational Updates

• STAT6 Program (KT-621):

- Phase 1 data revealed significant STAT6 degradation with a strong safety profile.

- Phase 1b study in atopic dermatitis is underway, with Phase 2b studies planned for late this year or early next year.

• IRAK4 Program:

- Partnered with Sanofi, Phase 2b studies in HS and AD are ongoing, with Chimera retaining the option to opt into global development before Phase III.

• IRF5 Degrader Program (579):

- Focus on lupus and interferon-mediated pathologies, with a Phase 1 study planned for early next year.

Future Outlook

• KT-621 Development:

- Plans to advance into Phase 3 studies, addressing multiple indications.

- Phase 2b studies in AD to feature a traditional placebo-controlled design with around 200 patients.

• Partnership and Growth:

- Strategic resource allocation and potential partnering after Phase II studies.

- Aims to become a global commercial-stage company, leveraging partnerships for growth.

Q&A Highlights

• Trial Design:

- Phase 1b study in AD focuses on biomarker impact with approximately 20 patients.

- Phase 2b studies will be placebo-controlled, involving around 200 patients over 16 weeks.

• IRAK4 Program:

- Managed by Sanofi, with Chimera’s option to participate before Phase III.

Readers interested in a deeper dive into Kymera’s strategic plans and clinical advancements are encouraged to refer to the full transcript below.

Full transcript - Goldman Sachs 46th Annual Global Healthcare Conference:

Nella Manolfe, Founder, President, and CEO, Chimera: Hi,

Andrea Newkirk, Biotech Analyst, GS: everyone. Good afternoon. Thanks so much for joining us. I’m Andrea Newkirk, one of the biotech analysts here at GS. And I’m really pleased to be joined by Nella Manolfe, founder, president, and CEO of Chimera.

Thanks so much.

Nella Manolfe, Founder, President, and CEO, Chimera: Thanks for having us.

Andrea Newkirk, Biotech Analyst, GS: Yeah, of course. So maybe before we dig into the data that you just presented last week for your STAT6 program, I thought maybe we could start with a overview of your small molecule oral protein degrader program. Talk to us about why you believe in this opportunity, and why you believe this approach is so particularly well suited in I and I.

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah, so again, thanks for inviting us. So I will start with the concept of oral degraders in immunology, and the opportunity to have orals with biologics like efficacy. So at Chimera, we’ve always been focused from the early days on marrying the power of protein degradation with the right target. I always am a big believer that all platforms or all kind of technology based companies live or die by their target selection. So we really have to be thoughtful about what type of target we can apply the technology against and what is the application and the end use.

So for us, what we’ve learned along the way is the ability when you use a degrader against the right target to block that target and that pathway with the same level of saturation that an injectable biologics can have. And so we started to learn this concept early on, especially when we were working on the AREC4 program in immunology. And so it was a bit of a moment for us where we thought if these drugs are really so potent and they can completely remove these proteins, then we should expand the concept and go after these pathways that have been validated by upstream biologics but do not have an intracellular oral solution to the same biology. And so the concept of this again, orals with biologics like efficacy is coming from the ability of using these catalytic degraders to remove proteins and block pathways with the same efficiency as biologics. So when we think about STAT6, when we stop and say let’s look at all the pathways that have been validated but lack a real best in class small molecule, IL4N13 jumped out, right?

It’s one of the most well validated piece of biology out there, have tremendously impacted patients with Th2 diseases going from asthma to atopic dermatitis, COPD and other EOE and other indications. So there is, based on our calculation, more than one hundred patients in the even just the seven major markets with these diseases, but there is really no small molecule solution to this. And clearly this small molecule not only is there to provide a convenient option, but it’s also there to actually provide an option to patients that are not now on biologics. And so the Bilibustat6 sits right downstream of a DI4 receptor, and it’s a specific selective transcription factor for the receptor upstream, and is able, by blocking STAT6, we’re able to block as effectively IL4 and IL13 as you can with an upstream biologic. So that’s kind of the fundamental thesis behind the program.

Andrea Newkirk, Biotech Analyst, GS: So obviously the target is important, STAT6 is important, but when you think about degradation of that versus inhibition, what are the pros and cons of both approaches?

Nella Manolfe, Founder, President, and CEO, Chimera: Yes, I think this concept applies to all targets. So maybe I’ll take a step back and say we’re a big believer that, again, we need to go after targets that have not been drugged or drugged fully before. When we’ve taken this approach and looked at these pathways, you know, what surfaces out of this Venn diagram is transcription factors that have been historically difficult to drug, multifunctional proteins, some people call them scaffolding proteins, which have been drugged but poorly. An example is IRAK4, I would say another example is TYK2 and others. From the transcription factor STAT6, IRAK5 and others that we’re still working on in the preclinical space.

So when you think about what small molecules can do versus degraders, have to think about what target class you’re going after. If you’re thinking about multi functional proteins, you know that a small molecule inhibitor of a catalytic function of a protein is only going to block that catalytic function. If the protein has also another function, let’s call it scaffolding function, let’s say receptor interaction function like TYK2 or IRAK4, you need to remove the protein completely to elicit the full biology. For a transcription factor, it’s a bit more nuanced. It’s extremely difficult to inhibit a transcription factor, because this class of proteins have evolved to do two things: bind to another protein and then bind to DNA.

So they don’t have a conserved binding site that one can target. Sometimes what seems to be a conserved binding site is similar across the whole family of proteins. For example, the SH2 domain for the STAT protein class. And so with regards to STAT6, we discovered that chimaera, and obviously others in the space, you can actually inhibit this protein. The case that we make for degraders against STAT6 is really the type of target product profile that we’re after.

Our target product profile is to have an oral DUPI, right? The pathway blockade that dupilumab has is basically almost complete blockade of IL-four and IL-thirteen, for sure 90% plus. And we can do it, I would also say if you look at our clinical data quite easily with a once a day oral drug that has again a catalytic effect, so with low nanomolar concentrations we’re able to block this pathway completely by degrading the target at steady state 90% plus. We show we can get to complete degradation. With a small molecule inhibitor, because of the concentration of STAT6 in the full compartment and because it’s a stoichiometric inhibition, so you need to have as much drug as you have off target, you need to have high, in our hands, micromolar concentration to cover the target 90% plus all the time.

And that is, we believe, extremely difficult to do with a once a day oral drug. So that’s, maybe it’s more in detail than I’ve ever gone into, but that’s where the rationale is coming from.

Andrea Newkirk, Biotech Analyst, GS: Super helpful, thank you. Let’s dig into the data you had last week, the phase one healthy volunteer. What were you most surprised to see from this data set?

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah, you know, great question. So when we started the study in, I believe it was October of last year, feels like a lifetime ago, but when we started the study, the goal, based on our preclinical studies, we knew that if we degraded STAT6 90% plus, in quite high bar preclinical studies like the HTM mouse asthma model, we could replicate the level of pathway impact and clinical endpoint that dupilumab had. So with our target was 90% plus degradation in blood and skin with a good safety profile. Obviously what we saw is that all doses above one point five milligrams per day achieved 90% or more degradation. What we also saw that we were able to see complete degradation at doses of fifty milligrams and above in both blood and skin.

We were able to see that we had undifferentiated safety whether you were at 1.5 or you were at two hundred milligrams, and this safety was undifferentiated from each other and from placebo. So placebo like safety. And so I think the, what I was surprised is that we actually had to go back and dose the one point five milligrams MAD cohort, because to that point we had not seen any dose cohorts that had more than less than 90% degradation. And actually the one point five milligrams cohort was one of the last cohorts that we run, again to establish the lower end of the dose response curve. Another, I would call it maybe upside scenario was what we saw with the Th2 biomarkers in healthy volunteers.

We spent the past nine to twelve months explaining that these were going to be noisy biomarkers to read in healthy volunteers where the baseline level were very low as well as the dynamic range was small and the pathway was not activated. And all of that was actually true, but I think what we were pleasantly surprised with is that for example if we use TARC as a biomarker of reference, all our dose cohorts were able to reduce TARC at different levels, but consistently, which was not seen with all the dose cohorts, for example, with dupilumab. Actually the nice thing we were able to see that was not seen again with the biologics that at day seven we had more robust inhibition at day four, day 14 we had more robust inhibition at day seven, telling us that we had a really nice dose and time dependent blockade that didn’t seem to have plateaued even in just two weeks. And then what we did, and I give credit only to my team, I would like to but I cannot take any credit for it, was going in and looking for biotoxin-three as a biomarker. This is something that was only seen, was only measured by the developer of dupilumab in asthma and chronic rhinosinusitis, and they saw a reduction of about 40 to 50% at week fifty two in the phase three study.

We knew that this is a highly sensitive biomarker to IL4 and IL13, much more than TARC, way more than IgE, and in fact if you look at the data we had really tight error bars, reduction up to 60 plus percent, and it’s actually a hint of those responsiveness to it that just speaks to the fact that it’s a highly sensitive biomarker. So, sorry I went too long here, but the bottom line why what was really exciting was probably more potent than we anticipated in vivo in humans, an exceptionally pristine safety profile, as expected I would say, and then really a biomarker profile that I would say was clearer in terms of output than we had anticipated.

Andrea Newkirk, Biotech Analyst, GS: When you think about the level of stat six degradation, the goal going in was 90%. You clearly saw above that, I think, you know, potentially even higher than the 95%, though that was probably a limit based off of the assays you were using to measure degradation. Is more always better here?

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah, so it’s a great question. It’s really hard actually to know, and this is why we’re going run more studies, to really know what 90% versus 95 versus 99 will mean. And actually I think that the goal of our phase study where it’s going to be a large dose ranging study versus placebo. I think that’s really the goal of this study, establishing a correlation between depth of degradation, safety and efficacy. I think if you speak to people that have worked in this pathway for a long time and we’re fortunate to being able to do that here and there, they would tell us that you are required to have really deep pathway blockade.

And I think what I would say to that is that we’re fortunate if you look at the doses that we’ve explored, that we have all the doses, we have all the learnings to being able to ask that question. I would also say that the data that we reported, you know, we said from fifty milligrams and above we have complete degradation. The way we reported it probably underestimates what the actual levels of STAT6. In reality, if you look at the fifty mg dose, more than fifty percent of subjects were below the lower limit of quantitation. At the one hundred mg dose, one hundred percent of subjects were below the lower limit of quantitation.

So probably others would say 100% or 99% degradation. We have a very conservative estimate on how we make this calculation, which I can bore you with, but I thought I’d share that message.

Andrea Newkirk, Biotech Analyst, GS: And as you think about the biomarkers, you’ve touched upon them a little in your previous remarks, what is specifically the relevance that you see there as you see the response here in healthy volunteers?

Nella Manolfe, Founder, President, and CEO, Chimera: Yes, so again, I’ve been saying this for many, many months. We have to be really careful what we do with the biomarker data. To us and to me, what biomarker data are telling us is that we’re blocking IF4N13 optimally. And blocking optimally, even in healthy volunteers, is giving you a response you know, with all the noise and the caveats we talked about that is in line with another drug that turns out to block IL4N13 optimally, which is dupilumab. And that’s all we can say.

I think the relevance of biomarkers in patients will be important. So, you know in a 1b study in atopic dermatitis patients, there we need to see a very robust biomarker impact in blood and skin because here is where it really matters. We know that, you know, TARC, for example, in blood and transcriptomic profiles in the skin are highly correlated for drugs in this pathway to clinical endpoints. And so we want to establish that.

Andrea Newkirk, Biotech Analyst, GS: Great. You just touched on this, that Phase 1b that you’ve initiated for atopic derm. Maybe just remind us the setup of this trial, what can our, what expectations should we have as the data readout later this year?

Nella Manolfe, Founder, President, and CEO, Chimera: Yes, so as I’ve said in the past, our main goal for the development plan of KT621 is to get to market ASAP and have a development plan that can address as many indications in parallel as possible. And so, what that means is we want to get into these Phase III studies as quickly as possible and what’s on critical path to go into Phase three is to have those ranging studies where you establish safety efficacy versus placebo. And so these are the Phase 2b studies that we’re starting end of this year, early next. So we had a window of opportunity between the end of the phase one healthy volunteers and the beginning of this phase 2b studies to establish what we call an early proof of concept. We decided to power, tailor this early proof of concept to a biomarker signature.

We know really well what the biomarker signature of IL-four and IL-thirteen blockade is in both blood and skin with the extensive elegant work that Sanofi and Regeneron did with dupilumab, so we know what we need to look like for a successful drug even in a handful of patients with AD, with moderate to severe atopic dermatitis. And so, we decided to select roughly 20 patients in a novel label study. We know that biomarkers are not affected by any meaningful placebo effect. And so we can hopefully replicate or reproduce what has been seen with upstream biologics with an oral once a day drug in terms of pathway blockade and biomarker impact. Then obviously twenty eight days other drugs in the space have initial clinical benefits.

So, we will measure also easy, itch, IgA, but really focused on the correlated nature of degradation to biomarker to early signs of efficacy versus trying to compare efficacy with in other studies that are placebo controlled. So, really focusing on biomarker and then showing that the biomarkers have a clinical benefit, I think will be important, But it’s clearly not powered to show clinical benefit and compare it to dupilumab study given the short duration, the lack of placebo, and the small end.

Andrea Newkirk, Biotech Analyst, GS: Got it. And given the profile that emerged from the healthy volunteer data, how derisked or how much read through do you see to this Phase 1b study?

Nella Manolfe, Founder, President, and CEO, Chimera: So, you know, I always go back to when we started the program. I don’t want to revisit what I said twenty minutes or fifteen minutes ago, but our investment thesis has always been if you degrade SAT6 you should be able to replicate an upstream biologics effect. So, we spent many years, I won’t say exactly how many, working on the program preclinically. We identified KT6:one, we characterized and we showed that what we thought was going to happen, happened. We went into the clinic and our goal was to show that statics degradation can be achieved and it’s safe and has a very strong pathway impact.

So we’ve shown that. So I mean our expectation is that this translation will continue to happen. I think we’ve completely de risked the fact that we can degrade the target safely, at least in a short duration study. We’ve also de risked, I think to a large extent that degradation of STAT6 has meaningful impact in the pathway. And I think it’s not a great leap of faith to expect that we should be seeing impact in patients.

Andrea Newkirk, Biotech Analyst, GS: As you think about being able to establish this correlation that you mentioned, stat six degradation to the biomarkers, to the EC score. Why do you not need to run a similar 1b study for asthma? Why can’t you just kind of skip over that and go to the phase two?

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah, I mean, so the important thing for us was choosing an indication that is representative of Th2 diseases. I think experts will tell me that atopic dermatitis is the most Th2 skew disease. And showing that we have a positive biomarker impact, we have good degradation and good safety, I think telling you that the drug is operating under the paradigm that we understand and I think provides an amazing opportunity with patients that have other diseases outside of AD to explore clinically. So, we don’t believe we had to repeat the same study in asthma to build that confidence. We believe AD, while it’s obviously a different disease, speaks to the Th2 component of it and that’s why the biomarkers are so important because those will be shared all the Th2 diseases.

Andrea Newkirk, Biotech Analyst, GS: Got it. So that provides you see it once and then you have confidence as you think about the other potential indications. How are you thinking about your planned Phase 2b studies here?

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah, I mean we’ve in a way selected the Phase 2b doses. The Phase 1b is actually a good kind of sanity check, right? Are we everything is translating the way that we anticipate? The team is already working on of course if we say we’re going to start a large global Phase 2b studies in 4Q, we’re actively operating to being able to do that later this year. We’ll have multiple doses.

We’ll share more about the clinical trial design later in the year, but you can imagine for AD to be let’s call it traditional placebo controlled randomized study, sixteen week readout with multiple, probably 200 patients plus or minus. And we’re excited about being very close to that.

Andrea Newkirk, Biotech Analyst, GS: And do you think about the potential to expand, not just into asthma, but other indications, both in dermatology as well as respiratory? You’ve talked about this really interesting strategy to take the phase three dose for both derm and respiratory and be able to expand that to additional indications. Talk to us about what gives you the confidence that the regulatory agencies are on board with that approach. Clearly there’s been so much noise in the recent weeks and months around the regulatory flexibility and the agency. But what gives you confidence that that’s a strategy you can take?

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah, I mean, I think what I’m going to be able to speak to is the fact that some of this strategy was adopted by the companies that developed dupilumab, learning from asthma applying to COPD or learning from other derm indication and applying to others. So this is a playbook that has been used already in the space. Obviously, we need to generate data to being able to support this point plan. I think this is as long as the efficacy safety relationship is supportive of this plan, believe this is a patient friendly and very, very kind of strategic plan to expand the development to as many indications, to as many patients as possible.

Andrea Newkirk, Biotech Analyst, GS: And if six twenty one looks promising here in AD and in asthma, other indications, where does it fit into the treatment paradigm?

Nella Manolfe, Founder, President, and CEO, Chimera: I mean, we’re a strong believer that if we’re able to deliver on the target product profile of oral drugs with biologics like profiles, some KOLs tell us, look, you don’t even have to be as effective as dupilumab. But anyway, if we continue to deliver on that, our vision is that this is going to be the line drug for all indications, for all people with Th2 diseases. I think it’s the right thing to do for patients, it’s the ethical thing to do for patients, and it gives patients the flexibility, the convenience, and the efficacy that cannot be found with any other technology. So, obviously it’s still early to talk about market access strategy, I’m talking more philosophically. I find it hard to imagine that that profile will not be the profile that will expand finally this market that is still, you know, by the biologics, you know, that still has little penetration.

Andrea Newkirk, Biotech Analyst, GS: Maybe to that point, when you think about the potential opportunity here, you’ve called this an oral DUPI. Is there the potential to exceed Dupixent’s commercial opportunity?

Nella Manolfe, Founder, President, and CEO, Chimera: So there’s two things, right? There is one, the kind of the biological profile, one is going be the clinical profile, and one is the commercial profile. So on the, let’s say, to clinical, all the data that we’ve gathered so far is that the biology is coherent, so we should be able to see a similar profile. That’s why we like to say Dupixent in a pill or the oral dupi. With commercial, I think the even if you look at AD and asthma are 85% of the revenues, I believe.

We’re talking about very still very small penetration into those markets. So I’d love to believe that Dupixent is going be a $25,000,000,000 drug in a few years. I’d to believe that if we expand this market, six:one could surpass that. But, know, time will tell.

Andrea Newkirk, Biotech Analyst, GS: Goal for the future. Yes. Maybe switching over to the IRAK4 program here that’s partnered with Sanofi. Just to level set, talk to us about IRAK4 as a target. What makes this so attractive?

Nella Manolfe, Founder, President, and CEO, Chimera: Yes. So IRAK4 is the obligate so let’s go to the mitosome complex, where there is MID-eighty eight, IRAK4, IRAK1, and other partners, is the obligate complex through which IL-one, IL-eighteen, IL-thirty three, IL-thirty six, TLR4, TLR7, TLR8 have to signal through. So, it’s a quite kind of broad inflammatory cascade. IRAK4 small molecule kinase inhibitors have really shown that by inhibiting the kinase function, you’re not really able to block this inflammatory cascade, especially when there are multiple stimuli. And you can imagine diseases like HF, you have locally systemic inflammation, you have TLR and IL-one, and we’ve shown even in cell system that when you have multiple stimuli inhibitors are not able to accomplish pathway blockade.

We have some exciting proof of concept in this pathway. We have an IL-one beta biologics from AbbVie that has shown some quite impressive data And we have other agents that have shown early data in other indications including atopic dermatitis and others. So, the opportunities to have a broad anti inflammatory agent that is really most focused on Th1, Th17 with some impact on Th2. We’ve shown KT474 can block this pathway effectively, pre clinically, in the clinic.

We had really exciting phase one data, complete degradation in the blood, robust degradation in skin. We went into a phase one, let’s call it 1B study in HSN AD with some intriguing early efficacy data as well as biomarker data. And then Sanofi was excited enough to want to take this program into two parallel Phase 2b studies, one in HS and one in AD that are ongoing. I think we reported in the last quarter that we had a milestone from $20,000,000 milestone from Sanofi and this was related to a generation molecule that achieved a preclinical development milestone. So obviously there is continued investment and excitement about this program and we’re obviously waiting to see the next data readout.

Andrea Newkirk, Biotech Analyst, GS: Talk to us about how you’re thinking about potentially bringing IRAK4 because there is an opt in clause There is. Bringing IRAK4 degrader in AD versus six twenty one in AD, how do you think about those two opportunities?

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah. So maybe just to level set on how the collaboration operates. So right now Sanofi from the Phase II on are responsible for both financial as well as for the operations of the program. So they’re running phase two studies where in the event of transitioning into the next phase of development we’ll have milestones and we have royalties down the road. But we do have, as you’re seeing, an opportunity to opt in right before Phase III into the global development of IREC4.

So if Sanofi decides based on data that atopic dermatitis is the right indication to go into Phase III and beyond, we have an opportunity to opt in and share cost of profits. No operational responsibilities. So I think obviously it’s important to think about the also Sanofi has, as you know, investments into the stat six phase. Obviously, they’re behind us. But I think the beauty about the opportunities here is that STAT6 is a pure Th2 drug and serves patients with Th2 inflammation.

IRAK4, it’s more, I guess I say, the Th1, Th17 drug. And so I believe that if it’s successful in AD, it will be probably successful in a subset of patients that might be complementary to what STAT6 is going to be operating against. So obviously time will tell and data will tell, but I could see them to be complementary drugs and not competing drugs.

Andrea Newkirk, Biotech Analyst, GS: Got it. So one wouldn’t cannibalize the opportunity or the other?

Nella Manolfe, Founder, President, and CEO, Chimera: I think it’s early to tell. Don’t think it will have to depend on how it’s developed. But I think it’s going to be complementary drugs.

Andrea Newkirk, Biotech Analyst, GS: Is there a path forward for Chimera to be involved in both?

Nella Manolfe, Founder, President, and CEO, Chimera: Look, think that’s a resource allocation question. If you think from a kind of science and strategy and desire, obviously, in the event that there is positive data, we would love to be part of the fifty-fifty co development than co. In reality, the decision would be made based on resource allocation. I think if six twenty one continues to show the profile that we’re seeing so far, it’s going to be a very resource intensive program. And given that it’s a wholly owned program, I would imagine that we would prioritize that.

But time will tell. We’ll have to see how the rest of the pipeline evolves. And those decisions fortunately don’t have to be made in the near future.

Andrea Newkirk, Biotech Analyst, GS: Maybe on that point in the last couple of minutes we have here, we’d love to hear about your newest asset that you just unveiled on your earnings call, $5.78. What makes you so excited about this one?

Nella Manolfe, Founder, President, and CEO, Chimera: Yes, so RF5 degrader 579. The beauty about this program is the ability to be cell specific. So, IRA5 is really mostly, it’s not only expressed in macrophages, monocytes, B cells, and it’s also really activated by particular stimuli, mostly TLR seven eighty nine as well as B cell receptor to some extent. And so, we can be targeting IRAD5, I like to think of it in a kind of disease, almost disease specific manner. What we’ve shown pre clinically that where you look at, let’s call it more traditional immunology, and if you’re guided by human genetics, we know that IRF5, there is GWAS studies showing association with, you know, in lupus, in IBD, in RAI think the stronger one are in lupus.

If you’re guided by that, you’ll know that this drug could be really disruptive in lupus with an oral drug in a space that has really limited option now. There is some like other drugs in development, but no really oral drug I think that has the opportunity that we have with IRF5. So, I think that’s high level the opportunity and the molecule is extremely well behaved, large safety window, no adverse events in preclinical studies, and excited to start a phase one early next year.

Andrea Newkirk, Biotech Analyst, GS: And as you think about potential indications, you mentioned evidence in lupus, is that a fair assumption that would be an indication of interest for you?

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah, I think I would say where we are all on the same page, at least at Chimera is lupus and all these interferon mediated pathologies like Sjogren’s disease and others. And then what we’re trying to nail between now and the end of our Phase I healthy volunteer study is RA IBD, we want to generate a bit more preclinical data, overlap it with the genetic association, and then decide which of the two, both, one or neither, we want to advance in parallel to a lupus study to, you know, again create as much optionality as possible.

Andrea Newkirk, Biotech Analyst, GS: And as you think about your pipeline, I think you’ve also you’ve talked in the past about being still open for partnerships. How are you thinking strategically about which assets, which programs, maybe even which indications you’d like to keep in house versus out licensing or partnering?

Nella Manolfe, Founder, President, and CEO, Chimera: Yeah, think one thing we’ve learned along the way is obviously partnerships can be highly value creating when done in the right moment and with obviously the right partners and we have examples that we’ve done at Chimera. We feel pretty strongly that partnering before a solid proof of concept, let’s say before Phase 2b studies, it’s probably done only if you have probably no financial capabilities or you don’t want to invest in that particular disease area. But we’re really well capitalized and we have these studies in front of us funded already. So it’s unlikely, if not impossible, that we will be partnering any program in our pipeline, in our immunology pipeline before a Phase II study. I think after that it becomes again a resource allocation decision.

We want to be a global commercial stage company, but if all the programs in our pipeline are successful, it’s going to be hard for us to do all of it on our own. And I think at that time we can make resource allocation decisions and decide when we grow up, which program we want to continue to have wholly owned versus partnered.

Andrea Newkirk, Biotech Analyst, GS: Perfect. Well, with that, thank you so much, Nelo.

Nella Manolfe, Founder, President, and CEO, Chimera: Thank you.

Andrea Newkirk, Biotech Analyst, GS: Thanks, everyone.

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