Kymera Therapeutics Presents New Preclinical Data for its IRAKIMiD Degrader KT-413 Demonstrating Strong Antitumor Activity as Both Monotherapy and in Combination in MYD88-mutant Lymphoma Models
Kymera Therapeutics has announced promising preclinical data for its IRAKIMiD degrader KT-413, showcasing potent anti-tumor efficacy as both a monotherapy and in combination with other anticancer agents for treating MYD88-mutant DLBCL. Presented at the 16th ICML Meeting, KT-413 exhibited superior tumor regression compared to existing therapies in mouse models. The company aims to submit an IND application and start Phase 1 trials in the second half of 2021, marking a significant step forward in targeted therapy for B-cell lymphomas.
- KT-413 showed superior tumor regression compared to IRAK4 inhibitor CA-4948 and IMiD CC-220.
- Demonstrated strong tumor growth inhibition (up to 100%) in MYD88-mutant DLBCL models.
- Exhibited synergistic effects when combined with rituximab, BTK, or BCL-2 inhibitors.
- None.
Data presented at the 16th ICML Meeting demonstrate KT-413’s potent antitumor activity as a monotherapy compared to a clinically active IRAK4 kinase inhibitor or a latest generation IMiD in MYD88-mutant mouse xenograft model
KT-413 shows synergistic activity in driving deep tumor regressions in combination with other therapies in preclinical models, suggesting the potential for therapeutically relevant drug combinations in MYD88-mutant DLBCL
Kymera anticipates IND submission and, if cleared, initiation of Phase 1 trial of KT-413 in relapsed/refractory B cell lymphomas, including MYD88-mutant DLBCL, in 2H 2021
WATERTOWN, Mass., June 21, 2021 (GLOBE NEWSWIRE) -- Kymera Therapeutics, Inc. (NASDAQ: KYMR), a clinical-stage biopharmaceutical company advancing targeted protein degradation to deliver novel small molecule protein degrader medicines, today announced new preclinical data on its IRAKIMiD degrader KT-413’s potential as both a monotherapy and in combination with other anticancer agents. The data were featured in an oral presentation at the 16th Annual International Conference on Malignant Lymphoma (ICML) virtual meeting, taking place from June 18 - 22, 2021 (Abstract 013: KT-413, a novel IRAKIMiD degrader of IRAK4 and IMiD substrates, has a differentiated MOA that leads to single-agent and combination regressions in MYD88-mutant lymphoma models).
IRAKIMiDs are novel heterobifunctional degraders designed to degrade both IRAK4 and IMiD substrates, including Ikaros and Aiolos, with a single small molecule. IRAKIMiDs synergistically target both the MYD88-NFkB and IRF4-Type 1 interferon pathways to enhance and broaden antitumor activity in MYD88-mutant diffuse large B-cell lymphoma (DLBCL). KT-413 is being developed initially for the treatment of relapsed/refractory MYD88-mutant DLBCL, with the potential to expand into other MYD88-mutant indications and IL-1R/NFkB-driven malignancies. KT-413 is currently in preclinical development and Kymera plans to submit an Investigational New Drug Application (IND) to the U.S. Food and Drug Administration (FDA) in the second half of 2021 and, if cleared, initiate a Phase 1 clinical trial in patients thereafter.
“The combined MYD88 and IMiD pathway blockade with the KT-413 degrader drives single-agent tumor regressions in multiple models of MYD88-mutant DLBCL, including superior activity compared to IMiDs or IRAK4 kinase inhibitors,” said Jared Gollob, MD, Chief Medical Officer at Kymera Therapeutics. “The data demonstrate KT-413’s supra-additive activity in combination with rituximab, BTK inhibitors and BCL2 inhibitors, inducing deep and durable tumor regressions in vivo, and also support the broad clinical potential for KT-413 as a combination therapy in MYD88-mutant DLBCL and other MYD88-mutant B cell lymphomas.”
Data highlights include:
- In the OCI-Ly10 MYD88-mutant mouse xenograft model, intermittent dosing of KT-413 in vivo induced deep and sustained antitumor activity, including complete or partial regressions, that was superior to the clinically active IRAK4 kinase inhibitor CA-4948 or the latest generation IMiD CC-220.
- KT-413 showed strong tumor growth inhibition (
87% -100% ) in multiple MYD88-mutant DLBCL patient-derived xenograft in vivo models. - KT-413 showed strongly additive antitumor activity in combination with the anti-CD20 monoclonal antibody rituximab, the BTK inhibitor ibrutinib, or the BCL-2 inhibitor venetoclax, in MYD88-mutant OCI-Ly10 xenografts in vivo, suggesting the potential for therapeutically relevant drug combinations in MYD88-mutant DLBCL.
Presentation Details:
- Abstract: 013
- Title: KT-413, a novel IRAKIMiD degrader of IRAK4 and IMiD substrates, has a differentiated MOA that leads to single-agent and combination regressions in MYD88-mutant lymphoma models
- Session 1: New Therapeutics
- Session Time: 11:45 a.m. – 1:15 p.m. ET on Sunday, June 20, 2021
- Presenter: Duncan Walker, Ph.D.
A copy of the presentation is available for download at https://investors.kymeratx.com/events-and-presentations and https://www.kymeratx.com/scientific-resources/.
About Pegasus™
Pegasus™ is Kymera Therapeutics’ proprietary protein degradation platform, created by its team of experienced drug hunters to improve the effectiveness of targeted protein degradation and generate a pipeline of novel therapeutics for previously undruggable diseases. The platform consists of informatics-driven target identification, novel E3 ligases, proprietary ternary complex predictive modeling capabilities, and degradation tools.
About Kymera Therapeutics
Kymera Therapeutics (Nasdaq: KYMR) is a clinical-stage biopharmaceutical company founded with the mission to discover, develop, and commercialize transformative therapies while leading the evolution of targeted protein degradation, a transformative new approach to address previously intractable disease targets. Kymera’s Pegasus™ platform enables the discovery of novel small molecule degraders designed to harness the body’s natural protein recycling machinery to degrade disease-causing proteins, with a focus on undrugged nodes in validated pathways currently inaccessible with conventional therapeutics. Kymera’s initial programs are IRAK4, IRAKIMiD, and STAT3, each of which addresses high impact targets within the IL-1R/TLR or JAK/STAT pathways, providing the opportunity to treat a broad range of immune-inflammatory diseases, hematologic malignancies, and solid tumors. Kymera’s goal is to be a fully integrated biopharmaceutical company at the forefront of this new class of protein degrader medicines, with a pipeline of novel degrader medicines targeting disease-causing proteins that were previously intractable.
Founded in 2016, Kymera is headquartered in Watertown, Mass. Kymera has been named a “Fierce 15” biotechnology company by FierceBiotech and has been recognized by the Boston Business Journal as one of Boston’s “Best Places to Work.” For more information about our people, science, and pipeline, please visit www.kymeratx.com or follow us on Twitter or LinkedIn.
Cautionary Note Regarding Forward-Looking Statements
This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, including, without limitation, implied and express statements regarding its: PegasusTM platform; and plans and timelines for the clinical development of Kymera Therapeutics' product candidates, including the therapeutic potential and clinical benefits thereof. The words "may," “might,” "will," "could," "would," "should," "expect," "plan," "anticipate," "intend," "believe," “expect,” "estimate," “seek,” "predict," “future,” "project," "potential," "continue," "target" and similar words or expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Any forward-looking statements in this press release are based on management's current expectations and beliefs and are subject to a number of risks, uncertainties and important factors that may cause actual events or results to differ materially from those expressed or implied by any forward-looking statements contained in this press release, including, without limitation, risks associated with: the impact of COVID-19 on countries or regions in which we have operations or do business, as well as on the timing and anticipated results of Kymera Therapeutics’ current preclinical studies and future clinical trials, strategy and future operations; the delay of any current preclinical studies or future clinical trials or the development of Kymera Therapeutics' drug candidates; the risk that the results of current preclinical studies may not be predictive of future results in connection with future clinical trials; Kymera Therapeutics' ability to successfully demonstrate the safety and efficacy of its drug candidates; the timing and outcome of the Company’s planned interactions with regulatory authorities, including the resolution of the current partial clinical hold for KT-474; and obtaining, maintaining and protecting its intellectual property. These and other risks and uncertainties are described in greater detail in the section entitled "Risk Factors" in the Quarterly Report on Form 10-Q for the period ended March 31, 2021, filed on May 6, 2021, as well as discussions of potential risks, uncertainties, and other important factors in Kymera Therapeutics' subsequent filings with the Securities and Exchange Commission. In addition, any forward-looking statements represent Kymera Therapeutics' views only as of today and should not be relied upon as representing its views as of any subsequent date. Kymera Therapeutics explicitly disclaims any obligation to update any forward-looking statements. No representations or warranties (expressed or implied) are made about the accuracy of any such forward-looking statements.
Investor Contact:
Paul Cox
VP, Investor Relations and Communications
pcox@kymeratx.com
917-754-0207
Media Contact:
Lissette L. Steele
Verge Scientific Communications for Kymera Therapeutics
lsteele@vergescientific.com
202-930-4762
FAQ
What is the purpose of Kymera's KT-413 in clinical trials?
When will Kymera submit the IND application for KT-413?
What were the results of KT-413 in preclinical trials?
How does KT-413 work in combination therapy?
What are the implications of KT-413’s data for the stock symbol KYMR?
