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KT-579 demonstrated consistent disease-modifying activity comparable or superior to approved and clinically active therapies in multiple preclinical lupus models
KT-579 在多种临床前狼疮模型中表现出一致的疾病修饰活性,其疗效与已获批且具有临床活性的疗法相当或更优。
KT-579 Phase 1 healthy volunteer trial ongoing, with data expected in 2H26
KT-579 一期健康志愿者试验正在进行中,数据预计将于2026年下半年公布
WATERTOWN, Mass., June 08, 2026 (GLOBE NEWSWIRE) --
马萨诸塞州沃特敦,2026年6月8日(环球新闻社)--
Kymera Therapeutics, Inc.
凯迈拉治疗公司
(NASDAQ: KYMR), a clinical-stage biopharmaceutical company advancing a new class of oral small molecule degrader medicines for immunological diseases, today announced the presentation of new preclinical data for KT-579, its potent, selective, oral IRF5 degrader, demonstrating disease-modifying activity in lupus models.
(纳斯达克股票代码:KYMR)是一家处于临床阶段的生物制药公司,致力于推进用于免疫性疾病治疗的新型口服小分子降解剂药物。该公司今日宣布公布其强效、选择性口服IRF5降解剂KT-579的最新临床前数据,数据显示该药物在狼疮模型中表现出疾病修饰活性。
The findings show that by selectively targeting and degrading IRF5, KT-579 offers a novel oral approach for complex, heterogeneous autoimmune diseases driven by multiple validated inflammatory pathways, including Type I interferons, pro-inflammatory cytokines and autoantibody responses. These data were presented at the European Alliance of Associations for Rheumatology (EULAR) Annual Meeting held June 3-6, 2026, in London, UK, and will be presented at the Federation of Clinical Immunology Societies (FOCIS) Annual Meeting being held June 9-12, 2026, in San Francisco, CA..
研究结果显示,通过选择性靶向并降解IRF5,KT-579为一种由多种已验证的炎症通路(包括I型干扰素、促炎细胞因子和自身抗体反应)驱动的复杂且异质性自身免疫性疾病提供了一种新颖的口服治疗方案。相关数据已在2026年6月3日至6日于英国伦敦举行的欧洲抗风湿病联盟(EULAR)年会上公布,并将在2026年6月9日至12日于加利福尼亚州旧金山举行的临床免疫学会联合会(FOCIS)年会上进行展示。
“Lupus remains a complex and heterogeneous autoimmune disease, with many patients continuing to experience inadequate disease control despite available therapies,” said Juliet Williams, PhD, Head of Research, Kymera Therapeutics. “The data presented at these key medical meetings reinforce KT-579’s potential as a novel oral approach to modulating multiple disease-driving pathways implicated in lupus, including Type I IFN, pro-inflammatory cytokine and B cell-driven responses.
“狼疮仍然是一种复杂且异质性强的自身免疫性疾病,尽管已有多种治疗方法,但许多患者的病情控制仍不理想。”Kymera Therapeutics研究主管Juliet Williams博士表示,“在这些关键医学会议上公布的数据进一步证实了KT-579作为一种新型口服疗法的潜力,它能够调节与狼疮相关的多种疾病驱动通路,包括I型干扰素、促炎细胞因子和B细胞驱动的免疫反应。”
The consistent activity observed across patient-derived cells and multiple preclinical lupus models provides strong support for IRF5 degradation as a promising strategy to broadly address the underlying disease biology with a convenient oral medicine.”.
在患者来源细胞和多种临床前狼疮模型中观察到的持续活性,为IRF5降解作为一种有前景的策略提供了有力支持,该策略可通过便捷的口服药物广泛应对疾病的根本生物学机制。
The Company previously reported data demonstrating KT-579’s compelling profile in preclinical studies using human primary cell systems, patient-derived cells and
该公司此前报告的数据表明,在使用人原代细胞系统和患者来源细胞的临床前研究中,KT-579 展现出令人瞩目的特性。
in vivo
体内
disease models of lupus, rheumatoid arthritis, and inflammatory bowel disease showing activity comparable or superior to existing standards of care.
狼疮、类风湿性关节炎和炎症性肠病的疾病模型,显示出与现有标准治疗相当或更优的活性。
New data presented at EULAR and FOCIS further validate KT-579’s broad and consistent activity across preclinical models of lupus. In healthy donor and lupus patient-derived human cells, with or without a common SLE-associated polymorphism, KT-579 selectively degraded IRF5, blocked TLR-induced IRF5 nuclear translocation, and reduced key downstream inflammatory mediators, including Type I IFN and pro-inflammatory cytokines, as well as plasmablast differentiation and IgG production.
在EULAR和FOCIS会议上公布的新数据进一步验证了KT-579在狼疮临床前模型中广泛且一致的活性。在来自健康供体和狼疮患者的人体细胞中(无论是否携带常见的SLE相关多态性),KT-579选择性降解IRF5,阻断TLR诱导的IRF5核转位,并减少关键的下游炎症介质(包括I型干扰素和促炎细胞因子),同时抑制浆母细胞分化和IgG产生。
.
。
In vivo
体内
, KT-579 demonstrated dose-dependent IRF5 degradation and inhibition of TLR7- and TLR9-induced cytokine release, including TNFα, IL-6, IL-12 and IFNβ. Across multiple lupus models spanning low to high Type I IFN signaling, KT-579 treatment led to reductions in disease-relevant biomarkers, including proteinuria, serum autoantibodies and kidney pathology, with activity comparable or superior to approved and clinically active agents tested.
KT-579 表现出剂量依赖性的 IRF5 降解作用,并抑制 TLR7 和 TLR9 诱导的细胞因子释放,包括 TNFα、IL-6、IL-12 和 IFNβ。在涵盖低到高 I 型干扰素信号的多种狼疮模型中,KT-579 治疗降低了疾病相关生物标志物水平,包括蛋白尿、血清自身抗体和肾脏病理损伤,其活性与所测试的已获批且具有临床活性的药物相当或更优。
Together, these findings demonstrate consistent modulation of pro-inflammatory, Type I IFN and B cell-driven pathways, supporting KT-579’s potential as a first-in-class, oral approach in lupus and other chronic autoimmune diseases..
这些发现共同表明,促炎通路、I型干扰素通路以及B细胞驱动通路受到了一致的调节,从而支持KT-579作为首创口服疗法在狼疮及其他慢性自身免疫性疾病中的潜力。
The KT-579 Phase 1 healthy volunteer trial is ongoing. The Phase 1 study is evaluating the safety, tolerability, pharmacokinetics and pharmacodynamics of single- and multiple-ascending doses of orally administered KT-579 compared to placebo. The key study aim is to show that KT-579 can robustly degrade IRF5 in blood at doses that are safe and well tolerated.
KT-579 的 I 期健康志愿者试验正在进行中。该 I 期研究旨在评估与安慰剂相比,单次和多次递增剂量口服给药 KT-579 的安全性、耐受性、药代动力学和药效学。研究的主要目标是证明 KT-579 在安全且耐受性良好的剂量下能够强效降解血液中的 IRF5。
The functional impact of IRF5 degradation on the induction of Type I interferons, pro-inflammatory cytokines, and inflammatory pathway gene transcripts will also be assessed with whole blood ex vivo stimulation assays. The Company expects to report data from the trial in the second half of 2026 and, following the healthy volunteer study, plans to initiate a patient proof-of-concept trial, likely in lupus..
还将通过全血离体刺激试验,评估IRF5降解对I型干扰素、促炎细胞因子和炎症通路基因转录本诱导的功能性影响。公司预计在2026年下半年公布该试验的数据,并在完成健康志愿者研究后,计划启动一项患者概念验证试验,可能针对狼疮。
European Alliance of Associations for Rheumatology (EULAR)
欧洲抗风湿病联盟(EULAR)
Title
标题
: First-in-class Oral IRF5 Degrader, KT-579, Demonstrates Selective and Potent In Vitro and In Vivo Activity in Human Cellular Assays and Mouse Models of Lupus
首创口服IRF5降解剂KT-579在人类细胞实验及狼疮小鼠模型中展现出选择性且强效的体外和体内活性
Presenter:
主持人:
Veronica Campbell, Senior Director, Immunology, Kymera Therapeutics
维罗妮卡·坎贝尔,凯麦拉治疗公司免疫学高级总监
Type/Session:
类型/会话:
Poster, Poster View VIII
海报,海报视图八
Date/Time:
日期/时间:
Saturday, June 6, 2026, at 10:15 AM BST
2026年6月6日,星期六,上午10:15(英国夏令时)
Federation of Clinical Immunology Societies (FOCIS)
临床免疫学会联合会(FOCIS)
Title
标题
: Potent and Selective First-in-Class Oral IRF5 Degrader, KT-579, Inhibits Endosomal TLR-Induced Responses in SLE Derived PBMCs and Significantly Reduces Disease Activity in the MRL.lpr Mouse Lupus Model
强效且选择性同类首创口服IRF5降解剂KT-579抑制系统性红斑狼疮患者外周血单个核细胞中内体TLR诱导的反应,并在MRL.lpr小鼠狼疮模型中显著降低疾病活动度
Presenter:
主持人:
Erik Corcoran, Principal Scientist, Kymera Therapeutics
埃里克·科科兰,首席科学家,Kymera Therapeutics
Type/Session:
类型/会话:
Poster, Autoimmune Diseases
海报,自身免疫性疾病
Date/Time:
日期/时间:
Thursday, June 11, 2026, at 7:00 PM PT
2026年6月11日,星期四,太平洋时间晚上7:00
Copies of the EULAR and FOCIS posters will be available in the
EULAR 和 FOCIS 的海报副本将在
Resource Library
资源库
section of Kymera's website.
Kymera 网站的一个部分。
About KT-579
关于 KT-579
KT-579 is an investigational, first-in-class, oral degrader of IRF5, a genetically validated transcription factor and master regulator of immunity, and currently in Phase 1 testing. By selectively degrading IRF5, KT-579 is designed to modulate multiple disease-driving pathways simultaneously, including Type I interferons, pro-inflammatory cytokines and autoantibody responses, offering the potential for biologics-like activity in a convenient oral medicine.
KT-579 是一种在研的首创类口服 IRF5 降解剂,目前正处于 I 期临床试验阶段。IRF5 是一种经遗传学验证的转录因子,也是免疫反应的关键调控因子。通过选择性降解 IRF5,KT-579 旨在同时调节多种疾病驱动通路,包括 I 型干扰素、促炎细胞因子和自身抗体反应,从而以便捷的口服药物形式提供媲美生物制剂的疗效潜力。
In preclinical studies, KT-579 degraded IRF5 across multiple preclinical species and in all disease-relevant tissues. In preclinical models of lupus, rheumatoid arthritis (RA), and inflammatory bowel disease (IBD), KT-579 activity was equal to or more efficacious than small molecule inhibitors and biologics currently marketed or in the clinic.
在临床前研究中,KT-579 在多种临床前物种及所有疾病相关组织中均能降解 IRF5。在狼疮、类风湿性关节炎(RA)和炎症性肠病(IBD)的临床前模型中,KT-579 的疗效等同于或优于目前上市或处于临床试验阶段的小分子抑制剂和生物制剂。
In preclinical safety studies, KT-579 did not show any adverse effects of any type at all doses tested. KT-579 has the potential to be the first novel mechanism with broad utility in diseases where effective and well tolerated oral therapies are needed, such as lupus, IBD, RA, Sjögren's and others..
在临床前安全性研究中,KT-579 在所有测试剂量下均未表现出任何类型的不良反应。KT-579 有望成为首个具有广泛适用性的新型作用机制药物,适用于需要有效且耐受性良好的口服疗法的疾病,如系统性红斑狼疮、炎症性肠病(IBD)、类风湿关节炎(RA)、干燥综合征等。
About Kymera Therapeutics
关于 Kymera Therapeutics
Kymera is a clinical-stage biotechnology company pioneering the field of targeted protein degradation (TPD) to develop medicines that address critical health problems and have the potential to dramatically improve patients’ lives. Kymera is deploying TPD to address disease targets and pathways inaccessible with conventional therapeutics.
Kymera 是一家处于临床阶段的生物技术公司,致力于开拓靶向蛋白降解(TPD)领域,开发旨在解决关键健康问题并有望显著改善患者生活的药物。Kymera 正利用 TPD 技术攻克传统疗法无法触及的疾病靶点和通路。
Having advanced the first degrader into the clinic for immunological diseases, Kymera is focused on building an industry-leading pipeline of oral small molecule degraders to provide a new generation of convenient, highly effective therapies for patients with these conditions. Founded in 2016, Kymera has been recognized as one of Boston’s top workplaces for the past several years.
随着首款降解剂进入免疫性疾病临床试验阶段,Kymera 正致力于构建行业领先的口服小分子降解剂研发管线,为患有这些疾病的患者提供新一代便捷、高效的治疗方案。Kymera 成立于 2016 年,在过去几年中多次被评为波士顿最佳雇主之一。
For more information about our science, pipeline and people, please visit .
如需了解更多关于我们的科学研发、产品管线及团队的信息,请访问。
www.kymeratx.com
www.kymeratx.com
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Cautionary Note Regarding Forward-Looking Statements
关于前瞻性陈述的警示说明
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 about our expectations regarding strategy, business plans and objectives on the development of our clinical and preclinical pipeline, including the therapeutic potential, clinical benefits and safety thereof, including for KT-579, the Phase 1 healthy volunteer data readout of KT-579 in the second half of 2026.
本新闻稿包含经修订的《1995年私人证券诉讼改革法》所定义的“前瞻性陈述”,包括但不限于关于我们对战略、业务计划以及临床和临床前管线开发目标的预期之明示或暗示陈述,涵盖其治疗潜力、临床获益及安全性,包括KT-579的相关情况,以及预计于2026年下半年公布的KT-579在健康志愿者中进行的I期临床试验数据读出结果。
The words 'may,' 'might,' 'will,' 'could,' 'would,' 'should,' 'expect,' 'plan,' 'anticipate,' 'intend,' 'believe,' 'expect,' 'estimate,' 'seek,' 'predict,' 'future,' 'project,' 'potential,' 'continue,' 'target,' “upcoming” and similar words or expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words.
“可能”、“也许”、“将”、“能够”、“会”、“应该”、“预期”、“计划”、“预计”、“打算”、“相信”、“期望”、“估计”、“寻求”、“预测”、“未来”、“规划”、“潜在”、“继续”、“目标”、“即将”以及类似词语或表述旨在识别前瞻性陈述,尽管并非所有前瞻性陈述都包含这些识别性词语。
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 any forward-looking statements contained in this press release, including, without limitation, risks associated with: uncertainties inherent in the initiation, timing and design of future clinical trials, the availability and timing of data from ongoing and future trials and the results of such trials, whether preclinical results will be indicative of the results of clinical trials, the ability to successfully demonstrate the safety and efficacy of drug candidates, the timing and outcome of planned interactions with regulatory authorities, the availability of funding sufficient for our operating expenses and capital expenditure requireme.
本新闻稿中的任何前瞻性陈述均基于管理层当前的预期和信念,并受多种风险、不确定性和重要因素的影响,这些因素可能导致实际事件或结果与本新闻稿中包含的任何前瞻性陈述存在重大差异,包括但不限于与以下方面相关的风险:未来临床试验的启动、时间安排和设计所固有的不确定性;正在进行及未来试验的数据可用性及时间安排,以及此类试验的结果;临床前结果是否能预示临床试验结果;能否成功证明候选药物的安全性和有效性;与监管机构计划互动的时间安排和结果;以及是否有足够资金满足我们的运营费用和资本支出需求。
Investor Contact:
投资者联系:
Justine Koenigsberg
贾斯汀·科尼格斯伯格
investors@kymeratx.com
investors@kymeratx.com
857-285-5300
857-285-5300
Media Contact:
媒体联系人:
Bridgette Chandhoke
布里奇特·钱多克
media@kymeratx.com
media@kymeratx.com
857-285-5300
857-285-5300