Kymera Therapeutics Inc. Q1 2023 Earnings Call

To push the boundaries of our signs expand our capabilities to support the rapidly maturing company and build a culture that enables us to achieve what may have seemed impossible.

We look forward to sharing exciting updates on our clinical programs platform company in the coming months at this point I'd like to thank the <unk> team as well as our partners and the patients participating in our clinical trials for sharing this journey with US finally, thank you all for participating in our call and I look forward to your questions.

I will now hand, the microphone back to the operator, so that we can take your questions.

We will now begin the question and answer session.

Again to ask a question you May Press Star then one on your telephone keypad.

If youre using a speakerphone please pick up your handset before pressing the keys.

Anytime your question has been addressed and you would like to withdraw your question. Please press Star then two.

We ask that you please limit yourself to one question and one follow up for today's call.

At this time, we will pause momentarily to assemble our roster.

And our first question here will come from Vikram <unk> with Morgan Stanley . Please go ahead with your question.

Good morning, everyone. This is gospel on folks Vikram, we have one question. So for fall <unk> three on the KC 303, you have mentioned that you would expect those level III for a niche programs to demonstrate clinical activity.

When does that is available what do you think is going to be the best way to interpret that data to gauge the strength of the clinical activity for each molecule.

As your benchmark for Determinate code outcome first a more mixed one thank you.

Thanks for the question. So first I would like just due to to to be clear. We said in December that we expect those level III and dose level would be.

And clinically active exposures and level of big relation obviously the question will be at the at those doses do we see clinical activity just just to be clear so.

So just to remind everybody. This is our first in class mechanism.

And for both mechanisms for <unk>, III and <unk>, we've shown some really compelling preclinical data remind you for <unk> III. We've shown that if you degrade direct core eagerness denials for about 72 hours anywhere between 50% and 90% across the three protein we can drive my view.

<unk> mutant tumors to complete remission.

For 333, we've shown that if you degrees that three.

For about 90% for about 48 hours, we're able to drive some subset of liquid tumors, we've talked about <unk>.

Ptca NGL leukemias.

<unk> at least in some preclinical models that we were able to to run to complete remission.

The question that we as we always look at clinical translation from two perspectives. The first one is the molecule able to translate what it was designed to do and so we ask of these two molecules to replicate our preclinical degradation profile. So as I mentioned, what we believe it to be clinically relevant.

This is Steve.

50% to 90% degradation for one 3% and 90% degradation for 3334 as I said 72 hours for one program in 48 hours for the second so as we continue to explore PK PD and safety in the clinic and in fact, what we said is that we're going to give you an update on <unk> on that we want.

To make sure that our molecules are able to reach those degradation profiles at tolerated doses and exposures and we did tolerated profile.

And then the second part of the clinical translation de risking is is that particular degradation profile.

As you had done in the preclinical studies translating into antitumor effect and Thats going to be the question that we're going to try and answer and show data in the later this year I think we said.

So it's hard for us to set a bar because just to be clear.

We're running a relatively broad.

One dose escalation studies in terms of patient population. So we will have that.

A handful of patients that fit the right.

Criteria in terms of the disease and type of tumor types.

So we would like to see in those patients is the ability of translation of antitumor effect and so I think we're staying away right now on comparing in setting the bar just because we're still early in the clinical development Jared anything you want to add to that no I think that covers it. Thank you.

And our next question will come from Michael Schmidt with Guggenheim. Please go ahead with your question.

Hey, guys. Good morning, Thanks for taking my questions just a follow up on 333413 as you think.

Think about this upcoming update at the ICR conference.

Can you talk about a bit how far you are in two phase one studies now beyond delta over one or two how many patients worth of data.

You have at this point or how are you tracking towards identifying a recognized.

Yes.

And our next question will come from Mike <unk> with SVP. Please go ahead with your question.

No.

We're working on a manuscript that will have.

Even the lower dose levels will have the potential ability to.

Where we can dose intermittently as we can with AML. Once every three weeks in tumor models and see profound tumor regressions and so we have identified various solid tumor cell lines.

<unk> four it was sub clinical across all the four doses in this study so again, saying that this was a different mechanism that a.

Can you share how your thoughts on positioning of <unk> 474 has evolved in light of the recent development.

In this space.

Typically has any of the recent competitor data being.

<unk> factored into the phase two trial design.

The choice the selection of efficacy endpoint et cetera. Thank you.

Yes, no. Thank you it's a great question talking about patients.

So.

Hs is.

High unmet need we all know.

Don't believe that Hs is driven by a single cytokine.

So I am pleased to see that IL 17 agents work.

I don't believe that <unk> is the solution to Hs.

But it is going to be a great tool in the arsenal of tools that.

Doctors and patients will have so I think it's great to see this evolving class of anti.

Antibodies and the likes that are being developed in this space.

This is a.

Abroad inflammatory disease, local and systemic that we believe requires a broad anti inflammatory agents and we believe that Iraq for is uniquely positioned to be both active and well tolerated and have and obviously be an oral agent.

So.

Our view of the unmet need.

And the opportunity for an oral active agents has not changed they are still high unmet need and we believe we can have an opportunity to have a broad impact in this disease in terms of how we think about trial design.

I think that we have learned.

What we've seen from from <unk>.

<unk> studies that have been run is really validation of.

What are the key primary and secondary endpoints that one wants to see to confirm activity of drugs and I don't believe we've learned anything that has changed.

<unk> on how we want to design, a clinical study, which.

We have done in collaboration with Sanofi on phase two so.

I think it's great to see again other agents being asked is.

The opportunity.

This is total is still there for a normal active drug in the space that is again active in west tolerated.

And we have time for one more question, which will come from rich <unk> with credit Suisse. Please go ahead with your question.

Hi, This is Greg on for rich. Thank you for taking my question. The first one is.

Goldman path and timelines for this.

Program in combo with PD, one and do you see any other combo regimens that will make sense.

Yes, no. Thank you so yes the answer to the second question is yes, we we see several combo opportunities here and this is a bit what I was referring to earlier.

The beauty of working with a new mechanism we are learning.

Also with our some of our academic collaborators that have published and we will continue to publish on this.

Start three biology can be combined with to drive synergistic.

Tumor effects.

With regards to timing. So we're now focused as you know on dose escalation is single agent <unk>.

We're obviously learning.

Also when we can.

Yes.

When patients allow for biopsies also what's happening in the tumor microenvironment at least that's one of the goals that we have.

And any combo will be part of laser expansion cohort, which will open after we conclude phase one.

Operator, we probably can take one or two more so if you want to.

Go to the queue that'd be great.

Absolutely. Our next question here will come from Geoff Meacham with Bank of America. Please go ahead with your question.

Good money and this is how cutting in forecast Anita and thank you. So much logically staffing for the question. So I think you've touched on this I guess a follow up for <unk> could you talk about the choice of the Q3 <unk>.

We see recovery of April with Io and to some extent Iraq floor.

It is helpful for the neutral opinion could you talk about the data maybe some implication on the efficacy side. They have seen thank you.

I mean, we've shown in our preclinical models and we've run multiple preclinical xenograft models of both CTX in Pdx models of <unk> 88, mutated <unk> and very consistently in those models. We have shown that a once every three week IV infusion.

<unk> in complete responses that are durable. So I think we're feeling fairly confident in the ability of a once every three week regimen to illicit activity in the target patient population and that comes back to what we've learned even in vitro and wash out experiments, where we know that is <unk> 88 mutant cell lines. If youre not these targets down for about 72 hours that commit these cells to <unk>.

Ptosis and Thats why we think we are seeing these profound anti tumor responses in the geographic models with regard to the every two week dosing and safety we've learned from our GOP Tox studies that when we do see.

Drop of neutrophil counts, which is really driven by the <unk> activity of the drug we can see a nice recovery of those accounts prior to the next dose three weeks later and Thats why we think that we anticipate having an acceptable therapeutic index with an every three week dosing regimen, while at the same time, so being able to maximize clinical activity, even with that sort of intermittent dose.

<unk> schedule.

And our last question here will come from cockpit Patel with B Riley. Please go ahead with your question.

Yeah, Hey, good morning, Thanks for taking the question.

Maybe one for Iraq for <unk>.

The greater the landscape there has been other recent collaborations in the industry for developing IraQ40 graders.

Yes from the available information for these other molecules are there any specific points of differentiation that you want to highlight and maybe what early metrics do you think it might be crucial to focus on when making comparison. Thank you.

Thanks Scott.

I'll say, we're very proud of having initiated a new field here with Eric for and I'm being serious so I think it's good to see that the mechanism has been.

Rick and I finally recognized.

Once you have the right approach and in this case, we did see greater approach.

We have.

Drag there is quite exceptional we can degrade the target at 95% plus.

We can have degraded in the scheme in the blog, we've seen some really exciting.

Early data in both HSN.

It's a profile that is going to be hard to match I don't know, which molecules others are advancing I know.

There is a collaboration.

In which a molecule with option at D. C. So clearly a couple of at least a couple of years behind.

I think there are also other molecules. We just don't know what those molecules look like we haven't seen any presentations of any type of data. So it's hard for me to point to something besides seeing.

We have a really really good molecule would be hard to match PJ.

PK PD activity and safety.

And obviously, we're also further ahead than competition.

And this concludes our question and answer session I would like to turn the conference back over to <unk> for any closing remarks.

Well, thanks, I want to thank everybody for joining our call today, it's been an exciting first.

First quarter for 2023, starting from early in the year when we.

Announced some of strategic choices that we've made.

In terms of where we're taking our discovery engine and platform.

With some t's on the new program.

Also we've been talking about where and when we will be disclosing our oncology data across our pipeline both preclinical and clinical we have in the next seven weeks.

Presentation across the whole clinical pipeline for <unk> for the B.

Then we'll have <unk> preclinical in this case the Ehealth and then we have both TC for one three and 333 at <unk>.

Then we have more data in the second half of the year and this is really what this company will continue to be.

Producing.

Clinical data.

First in class mechanisms with broad clinical potential.

And I expect that in the next two to three years, we will have a large pipeline with continued Kate.

Cadence of.

Clinical readouts. So it's an exciting time for seven years of camera theme.

In a fund right, but the more exciting will be the next seven so thank you very much for being on the call and looking forward to more interactions in the next few weeks.

The conference has now concluded. Thank you very much for attending today's presentation. You may now disconnect your lines.