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, MA, USA I June 21, 2021 I 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.
SOURCE: Kymera Therapeutics
Post Views: 209
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, MA, USA I June 21, 2021 I 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.
SOURCE: Kymera Therapeutics
Post Views: 209
