Kymera Therapeutics Inc KT-621 BroADen Phase 1b Atopic Dermatitis Trial Results Call Transcript

The following is excerpted from the question-and-answer section of the transcript.

Question: Judah Frommer - Morgan Stanley - Analyst : Congrats on the update here. I guess, first, one of the questions we've been getting over time is just can you help us with dose selection in the Phase 1b, which dose came first? I guess, given the STAT6 degradation you were seeing in TARC reductions, why they need to add the second dose? What do you think you learned from it? And then second, I would just say on itch reduction, that seems to be a real differentiator here. I guess, how does that make you feel about market opportunity in itch prevalent conditions outside of AD and also that rapidity of itch reduction. What does that do in terms of the potential in AD specifically?

Question: Derek Archila - Wells Fargo Securities LLC - Analyst : Congrats on the data here. So just first question for me. I'm not sure if I missed this, but I just wanted to understand maybe the level of efficacy you might be seeing in the Dupi and trial experienced patients. That would be interesting. And just as a follow-up, I guess these FeNO changes that you guys highlight today, they not only look competitive relative to Dupi, but some of the other biologics in development or on the market. So I guess, how do you think oral STAT6 could kind of reshape the kind of emerging treatment landscape in asthma?

Question: Tazeen Ahmad - Bofa Merrill Lynch Asset Holdings Inc - Analyst : Congrats on the positive update. I have a couple of quick questions. You didn't see any instances of conjunctivitis. It's a small line of patients, but I think that could be a positive indicator of further differentiation from Dupi. Can you talk about what your expectations might be for Phase 2b on side effects specific to conjunctivitis? And then does this data, albeit early, indicate that there could be other indications beyond which you've already discussed wanting to go into as potentially available to explore?

Question: Brian Cheng - JPMorgan Chase & Co - Analyst : Just to touch on the trend in improvement across multiple measures over time. Can you speak to the response out to day 43 once patients are off drug at day 28? How does that line up with your understanding of the PK/PD and also target engagement? And then for the second question, as we think through the BroADen 2 setup for atopic derm, that will look into efficacy out to 16 weeks. How should we think about the step-up in efficacy over time?

Question: Kripa Devarakonda - Truist Securities - Analyst : Apologies. My Internet is a little bit slow in the hotel here, but congrats on the data, fantastic data. So a couple of questions. One on TARC reduction. Just can you remind me, I might have missed the data, but if the data that you showed was from all patients or if you took a cut of the patients? And also, if you can comment on the dose effect, I know small numbers, but dose effect on EASI-75, what could be the reason that you saw

Question: Andrea Newkirk - Goldman Sachs Group Inc - Analyst : Congratulations on the data this morning. Jared, just thinking ahead, I know we're a little ways off from this. But as you think about a potential Phase 3 trial, would you expect to need a head-to-head trial versus Dupi, either in order to support approval or physician adoption? And then just one for Nello, Bruce. You've referenced now the potential utility for 621 or STAT6 degradation across a range of type 2 diseases. But how are you thinking strategically about internal versus external development for those programs and prioritization of resources?

Question: Thomas Smith - Leerink Partners LLC - Analyst : Congrats on the data. Just in the patients who had prior biologic exposure, I appreciate the color on the one patient who responded after prior response to Dupi. I was just wondering if you could expand on the background and maybe the narrative for the other four biologic experienced patients. Were there any nonresponders or suboptimal responders that subsequently responded to 621? Or were these patients all prior responders? And then maybe as a follow-up, you talked about the slope of the EASI pruritus curves here suggesting we could see some greater benefit of longer dosing. Also appears to be some durability and response on some of these measures out to that two-week follow-up period. Just curious how you're thinking about the potential durability of effect. And for patients that seem to have more of an extended response, are there any common features among those patients?

Question: Geoffrey Meacham - Citi Infrastructure Investments LLC - Analyst : Okay. Good. Awesome. Congrats on the data, guys. I wanted to ask you about the speed of onset. The release mentions a pretty rapid onset by day eight in EASI and pruritus. Just curious if you could tie clinical responses to the mechanism and biomarkers more specifically. That's the first question. And the second one is just another one on FeNO, really impressive data there, obviously, just a few patients, but maybe does the baseline in this study in comorbid patients with asthma look like what you want to explore in Phase 1b and future studies. Just wanted to put maybe that in context.

Question: Joseph Catanzaro - Mizuho Securities USA LLC - Analyst : Actually, I think, a good follow-up, maybe just to the last question in terms of asthma in those four patients, given their comorbid with AD, is it fair to assume that they had high baseline levels of eosinophils, so eosinophilic asthma and then I guess, relatedly, thinking about 621 and its mechanism and utility in asthma, how should we think about it relative to phenotype eosinophilic versus non-eosinophilic, whether it will behave like Dupi or not? LSEG STREETEVENTS | www.lseg.com | Contact Us consent of LSEG. 'LSEG' and the LSEG logo are registered trademarks of LSEG and its affiliated companies.

Question: Mayank Mamtani - B. Riley Securities Holdings Inc - Analyst : Congrats on the fantastic results. If I could ask one more asthma question. If you could clarify the treatment duration that you might be looking to explore in the Phase 2b. Dupi had a bunch of different trial designs initially that were conducted. So if you're able to give any information what you've learned by FeNO and the eosinophil comment you had earlier. And then on the sort of the safety AE table, I'm sure we'll get at a future medical conference, combining exposure across healthy volunteer. Now, I think of 150 subjects. Could you just confirm if you've established the safe minimally effective dose threshold? Or is that going to be a key Phase 2b objective? I was just curious about the details there.

Question: Mayank Mamtani - B. Riley Securities Holdings Inc - Analyst : Any AEs that were dose dependent you can comment on, Nello?

Question: Andy Chen - Wolfe Research LLC - Analyst : Just one question from my side. Curious if your Phase 1b here has generated additional confirmatory evidence that degraders are better than inhibitors. And I'm hoping that you can help us quantify how much better a degrader is compared to an inhibitor. Or in other words, if a STAT6 inhibitor were to produce TARC or IgE data, where do you think they will land?