Yahoo Finance Kymera Therapeutics, Inc. (NASDAQ:KYMR) Q1 2024 Earnings Call Transcript
Kymera Therapeutics, Inc. (NASDAQ:KYMR) Q1 2024 Earnings Call Transcript May 3, 2024
Kymera Therapeutics, Inc. isn’t one of the 30 most popular stocks among hedge funds at the end of the third quarter (see the details here).
Operator: Good day, and welcome to the Kymera Therapeutics First Quarter 2024 Results Conference Call. All participants will be in the listen-only mode. [Operator Instructions] After today's presentation, there will be an opportunity to ask questions. [Operator Instructions] Please note that this event is being recorded. I would now like to turn the conference over to Justine Koenigsberg. Please go ahead.
Justine Koenigsberg: Thank you. Good morning, and welcome to Kymera's quarterly update call. Joining me this morning are Nello Mainolfi, President and CEO; Jared Gollob, our Chief Medical Officer; and Bruce Jacobs, our Chief Financial Officer. Following our prepared remarks, we will open the call to questions. To have enough time to address everyone's questions, we ask that you please limit your questions to one, and a relevant follow-up. Before we begin, I would like to remind you that today's discussion will include forward-looking statements about our future expectations, plans, and prospects. These statements are subject to risks and uncertainties that may cause the actual results to differ materially from those projected.
A description of these risks can be found in our most recent 10-Q filed with the SEC. Any forward-looking statements speak only as of today's date, and we assume no obligation to update any forward-looking statements made on today's call. With that, I'll now turn the call over to Nello.
Nello Mainolfi: Thank you, Justine. Good morning, everybody. It's been a very productive beginning of 2024, starting in January with an extensive update at our Immunology R&D Day, and a subsequent financing to provide capital that we will invest in our expanding clinical development efforts and growing pipeline. Past quarters we focused on execution on both our preclinical and clinical pipeline, as well as external engagement across the variety of business and medical conferences. Today, our plan is to share a brief update on our programs, as well as timelines for new [indiscernible] we're expecting through the rest of this year, and early '25. As we shared earlier this year, we believe we have a significant opportunity to address and expand the existing treatment paradigms within immunology by developing compelling oral small molecule degrader medicine with biologics-like activity.
As has been the case all the way back to the starting of the company, we have taken a differentiated approach to target selection and focused on critical molecular pathways that are well validated through human genetics, clinical evidence, and/or the success of approved drugs. Many of these pathways play a key role in immune-mediated disease pathology. And while injectable biologics dominate these markets, often due to their strong clinical activity, they're not without limitations, which in many instances can limit penetration. As a result, we believe developing convenient oral options with biologics-like activity and good safety profile represents an enormous opportunity to expand patient access in many of these markets that are currently dominated by injectable agents.
Our IRAK4 program, which was our first program to enter clinical development that simplifies a target and a pathway that has the potential for a broad patient impact. We have talked in the past about our reasons for enthusiasm around IRAK4 as a target, and our rationale for pursuing it. IRAK4 is an obligate node in IL-1R/TLR signaling, and believe its degradation is the only approach to fully block the pathway, creating multiple development opportunities in large [indiscernible] indications. In the KT-474, IRAK4 Phase 1 trial we observed deep and well-tolerated degradation, early signs of clinical efficacy, and high fidelity of translation from preclinical models to patients, which provide key insights for our growing immunology pipeline, and position future programs such as our STAT6 and TYK2 degrader programs for success.
In March, we had the opportunity to showcase our proprietary immunology programs, KT-621, our STAT6 degrader, and KT-294, our TYK2 degrader at the American Academy of Dermatology Annual Meeting. The poster presentations, which marked the first data from a STAT6 targeted agent and the TYK2 degrader to be shared at a major medical meeting highlighted our robust preclinical packages, and support the significant potential of our oral degrader in this pathway. In our KT-621 AAD poster, we highlighted the preclinical efficacy studies comparing KT-621 to dupilumab in a preclinical atopic dermatitis model. Importantly, KT-621 shows robust activity in vivo in this model, equal or superior to dupilumab. KT-621 degradation STAT6 was well tolerated in multiple preclinical safety studies at dosage and concentration up to 40-fold above the projected human executions concentration.
If we can indeed deliver biologics-like activity and good safety profile at oral once-daily dosing, we believe KT-621 could change the treatment paradigm for millions of patients suffering from Ph2-driven information. In terms of timing, KT-621 is currently IND enabling studies, and is on track to enter Phase 1 testing in the second-half of 2024. It's our intent to conduct a Phase 1 healthy volunteer study to assess single and multiple ascending doses of KT-621, and move quickly from there into patients. We have finalized our clinical development plans and strategy, and we look forward to sharing more details as we move closer into clinical data. Moving to TYK2, we shared a poster in AAD that demonstrated [indiscernible] inhibition of the IL-23, IL-12, and Type 1 interferon pathway, showing KT-294's potential to recapitulate the biology of human TYK2 loss of function in patients.
The biological differentiation of KT-294 from [indiscernible] small molecule inhibitors will demonstrating through [indiscernible] compared to [Supra] (ph), which is important in inflammatory bowel syndrome, as well as was shown through superior inhibition of Type 1 interferon pathway compared to TAK-279, which is relevant for the treatment of several diseases including interferon-related diseases. Additionally, KT-294 demonstrated decent sustained TYK2 knockdown in vivo with low daily oral doses. We believe that this data demonstrates that a TYK2 degrader has the potential to deliver best-in-class TKY2 pathway blockade with productivity across multiple IL-12, 23, and Type 1 interferon-driven immune-inflammatory diseases. We intend to continue to share updates across our pipeline in medical meetings in 2024.
In fact, later this month, we present poster highlighting KT-621 and its potential to treat Ph2 allergic diseases at both the American Thoracic Society International Conference, in San Diego, as well as at the Digestive Disease Week, in D.C. These presentations which build on what was previously shared at the R&D Day will include new exciting additional preclinical data. To sum up my intro here, since our founding day, years ago, a milestone which we will commemorate just in a few days, we have demonstrated consistent and scalable innovation, including strong preclinical to clinical translation of degradation safety and activity across the whole pipeline. We have also achieved early proof of concept in both immunology and oncology, which we believe is a significant accomplishment for the new modality.
As we are transitioning from early to mid-late development across our pipeline, we remain committed to building on our early success and expanding our team and capabilities to deliver on the substantial clinical and commercial opportunities that our programs offer, to ultimately become a global commercial stage medicines company. In the meantime, we look forward important and near-term data readouts in this year in oncology, and multiple readouts from our immunology pipeline in '25. I'll pause here, and ask Jared to provide an update on our clinical programs. Jared?
Jared Gollob: Thanks, Nello. I'll round out the immunology discussion this morning with IRAK4, and then give an update on our two clinical oncology programs. Our first-in-class oral IRAK4 degrader, KT-474 is progressing in two Phase 2 trials in hidradenitis suppurativa and atopic dermatitis. These trials are being conducted by Sanofi under our collaboration, and we expect to be in a position to share top line data in the first-half of 2025. Recall that Sanofi moved this program into Phase 2 studies based on the early clinical data we generated in HS and AD patients in Phase 1 trial. In that study, not only did we achieve our study objectives in terms of PK, PD, and safety, but we also delivered encouraging signs of clinical activity that we will also evaluate over a longer dosing period in the Phase 2 trials.
These randomized placebo-controlled trials represent an opportunity to demonstrate the potential for IRAK4 degradation generally, and KT-474 specifically to transform the treatment of complex inflammatory diseases and to offer HS and AD patients well-tolerated, effective, and convenient oral medicine. So, switching gears now to oncology, I'll start by noting that we recently presented scientific data on our oncology pipeline in both the late-breaking poster session and during the major symposium at the AACR Annual Meeting. As we shared in the past, our preclinical and early clinical findings, highlighted last month at the meeting, support the advantages of degraders over other existing technologies and agents, and further validate our differentiated molecular design, target selection, and translational strategies to advance a new generation of medicines for patients.
KT-253, our highly potent degrader of MDM2 E3 ligase that modulates the most common tumor suppressor p53, is currently in development for the treatment of liquid and solid tumors. Preliminary data from the Phase 1 clinical trial showed evidence of target engagement and in p53 pathway activation, along with initial signs of anti-tumor activity with out dose-liming toxicity, including typical hematological toxicity. These findings support our therapeutic hypothesis for MDM2 degraders, and the potential to improve the therapeutic index compared to MDM2 small-molecule inhibitors. As we finish dose escalation of the Phase 1 trial this year, we hope to see anti-tumor activity in a variety of tumor types. And coupled with our biomarker selection strategy, we plan to assess these data collectively to inform next steps.
Finally, on MDM2, we are announcing today that we've had an abstract accepted for a poster presentation at ASCO, in June, where we will provide a clinical data update. Once the trial is completed, we expect to present the full dataset at a medical meeting later in the year. KT-333, our highly selective degrader of STAT3, a traditionally undrugged transcription factor recognized as a key component of the JAK/STAT signaling pathway with both tumor cell intrinsic and tumor cell extrinsic effects on the tumor microenvironment is currently in development for the treatment of multiple STAT3-dependent pathologies, including hematological malignancies and solid tumors. Preliminary data from the Phase 1 trial demonstrated early signs of anti-tumor activity at doses that were generally well tolerated and associated with substantial STAT3 knockdown in blood and tumor.
Our preclinical to clinical translation showed some early but encouraging responses in both CTCL and Hodgkin's lymphoma. We also demonstrated stimulation of an inherent gamma response in tumor and blood, which is encouraging given the correlation between interferon gamma and how tumors respond to anti-PD-1 drugs. Dose escalation in the KT-333 Phase 1 study is ongoing, with the goal to further assess safety and anti-tumor activity in both liquid and solid tumors. We expect to complete the study this year, and deliver additional proof of concept data to define KT-333's path for late-stage development. We are also announcing that we've had an abstract accepted for presentation at the European Hematology Association, or EHA meeting, in June, where we will present a clinical update.
We plan to present the full dataset at a medical meeting later in the year. Now, I'll hand the call over to Bruce to share financials for the quarter. Bruce?
Bruce Jacobs: Thanks, Jared. I'll quickly review our first quarter 2024 financial highlights, and you can certainly reference the tables down in today's press release. Revenue in the first quarter of 2024 was $10.3 million. All of that was attributable to our Sanofi collaboration. And just a quick reminder, we had received or have received $55 million in total milestones as a result of the start of the two Phase 2 studies in the fourth quarter of last year. With respect to operating expenses, R&D for the quarter was $48.8 million, about $6.1 million of that represented non-cash stock-based comp, resulting in an adjusted cash R&D spend of $42.7 million, a 10% decrease from the comparable amount in the fourth quarter of 2023. On the G&A side, our spending for the quarter was $14.4 million, of which $5.9 million was non-cash stock-based comp.
The adjusted cash G&A spend of $8.5 million, again excluding the stock-based comp, reflects a 1% decrease from the comparable sequential quarter. Our cash balance at the end of the first quarter was $745 million. In January, as we mentioned, we realized approximately $300 million in net proceeds from our equity offering. And our cash balance is expected to provide a runway into the first quarter of 2027, and that will enable us to execute on multiple -- or I should say, the first-half of '27. That will enable us to execute on multiple data readouts including oncology proof of concept results in 2024, KT-474 Phase 2 data expected in the first-half of 2025, and several clinical inflection points for our STAT6 and TYK2 programs, also in 2025. So, this concludes our prepared remarks.
We'd be happy to take your questions. Operator, if you could open the line for questions? Thank you.
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