KT-579 demonstrated activity comparable or superior to approved and clinically active therapies in preclinical IBD models

KT-579在临床前IBD模型中表现出与已批准和临床活跃疗法相当或更优的活性。

KT-579 Phase 1 healthy volunteer trial ongoing, with data expected in 2H26

KT-579 第一阶段健康志愿者试验正在进行中，预计2026年下半年获得数据。

WATERTOWN, Mass., May 05, 2026 (GLOBE NEWSWIRE) --

马萨诸塞州沃特敦，2026年5月5日（环球新闻社）--

Kymera Therapeutics, Inc.

奇美拉治疗公司

(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 an inflammatory bowel disease (IBD) model.

(NASDAQ: KYMR)是一家临床阶段的生物制药公司，致力于开发一类新型的口服小分子降解药物，用于治疗免疫性疾病。该公司今日宣布了其强效、选择性口服IRF5降解剂KT-579的新临床前数据展示，证明了其在炎症性肠病（IBD）模型中的疾病修饰活性。

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 Digestive Disease Week (DDW) being held May 2-5, 2026, in Chicago, IL..

研究结果显示，通过选择性靶向并降解IRF5，KT-579为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、异质性自身免疫疾病提供了一种新颖的口服治疗途径。这些数据在2026年5月2日至5日于伊利诺伊州芝加哥举行的消化疾病周（DDW）上发布。

“Despite advances, many patients with chronic inflammatory diseases like IBD still cycle through therapies or remain inadequately controlled, in part because existing treatments don’t fully address the complexity of their disease or the realities of long-term management,” said Juliet Williams, PhD, Head of Research, Kymera Therapeutics.

“尽管取得了进展，但许多患有慢性炎症性疾病（如IBD）的患者仍然在不同疗法之间循环，或仍然控制不佳，部分原因是现有治疗未能完全解决其疾病的复杂性或长期管理的现实情况，”Kymera Therapeutics研究主管Juliet Williams博士说道。

“KT-579 has the potential to deliver a novel oral mechanism that can modulate multiple disease-driving pathways simultaneously. The consistent activity we’ve observed across these pathways in preclinical models provides strong validation of this approach and its opportunity to more fully address disease biology.

“KT-579 有潜力提供一种新型的口服机制，可以同时调节多种疾病驱动通路。我们在临床前模型中观察到的这些通路的一致活性，为这种方法及其更全面解决疾病生物学的机会提供了有力验证。”

We believe this could translate into a meaningful new option for millions of patients in need of effective, safe, and convenient oral therapies.”.

我们相信，这可以为数百万需要有效、安全和便捷的口服疗法的患者提供一个有意义的新选择。"

The Company previously reported data demonstrating KT-579’s compelling profile in preclinical studies using human primary cell systems, patient-derived cells and

公司此前报告的数据表明，在使用人体原代细胞系统和患者来源的细胞进行的临床前研究中，KT-579展现出了令人信服的特性。

in vivo

体内

disease models of lupus and rheumatoid arthritis, showing activity comparable or superior to existing standards of care. The new data presented at DDW further demonstrate KT-579’s consistent modulation of pro-inflammatory pathways. KT-579 showed impact on myeloid cell effector function, including potent inhibition of cytokines known to amplify inflammatory responses and promote Th1 and Th17 T cell activity in IBD..

在狼疮和类风湿性关节炎的疾病模型中，显示出与现有护理标准相当或更优的活性。在DDW上展示的新数据进一步证明了KT-579对促炎通路的一致调节作用。KT-579显示出对髓系细胞效应功能的影响，包括有效抑制已知会放大炎症反应并促进IBD中Th1和Th17 T细胞活性的细胞因子。

In the TNBS model of IBD, KT-579 demonstrated activity comparable or superior to clinically relevant comparators, including a JAK inhibitor and biologic agents targeting integrins and TNF. Prophylactic dosing of KT-579 led to a significant reduction in disease activity score, including protection from body weight loss and maintenance of colon density.

在IBD的TNBS模型中，KT-579表现出与临床相关比较物相当或更优的活性，这些比较物包括JAK抑制剂和针对整合素及TNF的生物制剂。预防性给药KT-579显著降低了疾病活动评分，包括防止体重减轻和维持结肠密度。

KT-579 demonstrated complete inhibition of key colon inflammatory cytokines, including TNFα, IL-1β and IL-6, and reduced pathological findings, including fewer inflammatory infiltrates, improved crypt structure integrity and absence of crypt abscesses. Transcriptomic analysis further demonstrated broad normalization of inflammatory, myeloid, and fibrosis-associated pathways, showing effects comparable to an anti-TNF agent.

KT-579完全抑制了关键的结肠炎症细胞因子，包括TNFα、IL-1β和IL-6，并减少了病理学表现，包括减少炎症浸润、改善隐窝结构完整性以及无隐窝脓肿。转录组学分析进一步表明，炎症、髓系和纤维化相关通路广泛恢复正常，显示出与抗TNF药物相当的效果。

Collectively, these findings position KT-579 as a novel oral approach capable of broadly modulating pathogenic pathways in IBD and other complex autoimmune diseases, where current treatment options remain limited..

这些发现共同表明，KT-579 作为一种新型口服疗法，能够广泛调节 IBD 和其他复杂自身免疫疾病中的致病途径，而目前的治疗选择仍然有限。

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第一阶段健康志愿者试验正在进行中。第一阶段研究正在评估口服KT-579与安慰剂相比，单次和多次递增剂量的安全性、耐受性、药代动力学和药效学。该研究的主要目标是证明KT-579能够在安全且耐受良好的剂量下，有效降解血液中的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..

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影响也将通过全血离体刺激试验进行评估。公司预计将在2026年下半年报告该试验的数据。

Digestive Disease Week (DDW) 2026

消化疾病周（DDW）2026

Title

标题

: Potent and Selective Oral IRF5 Degrader, KT-579, Demonstrates Robust Anti-inflammatory Activity and Disease Modulation in Preclinical In Vivo Models of Inflammatory Bowel Disease

强效且选择性口服IRF5降解剂KT-579在炎症性肠病的临床前体内模型中显示出强大的抗炎活性和疾病调节作用

Presenter:

主持人：

Ryan Camire, PhD, Scientist, Immunology, Kymera Therapeutics

瑞安·卡米尔，博士，科学家，免疫学，凯米拉治疗公司

Type/Session:

类型/会话：

Poster, Mechanisms of IBD Therapeutics

海报，《IBD治疗机制》

Date/Time:

日期/时间：

Tuesday, May 5, 2026, at 12:30pm CT

2026年5月5日星期二，中部时间下午12点30分

A copy of the poster is available in the

海报的副本可在

Resource Library

资源库

section of Kymera's website.

Kymera网站的部分内容。

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 是一种研究性、首创的口服 IRF5 降解剂，IRF5 是一种经过基因验证的转录因子和免疫主调控因子，目前处于第一阶段测试。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，为便捷的口服药物提供类似生物制剂的活性潜力。

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 在多个临床前物种和所有与疾病相关的组织中降解了 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 的活性等于或优于目前市场上或临床中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显示任何类型的不良反应。KT-579有潜力成为首个具有广泛用途的新机制药物，适用于需要有效且耐受性良好的口服疗法的疾病，如狼疮、IBD、RA、干燥综合征等。

About Kymera Therapeutics

关于凯米拉治疗学

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，率先在靶向蛋白质降解（TPD）领域开展工作，致力于开发解决关键健康问题并有潜力显著改善患者生活的药物。Kymera正在利用TPD来应对传统治疗方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.

Kymera已将首个降解剂推进至免疫疾病领域的临床阶段，目前专注于构建行业领先的口服小分子降解剂管线，旨在为这些疾病的患者提供新一代便捷且高效的治疗方案。Kymera成立于2016年，近年来多次被评为波士顿最佳工作场所之一。

For more information about our science, pipeline and people, please visit .

有关我们的科学、研发管线和人员的更多信息，请访问。

www.kymeratx.com

www.kymeratx.com

or follow us on

或关注我们

X

X

or

或

LinkedIn

领英

.

。

Cautionary Note Regarding Forward-Looking Statements

关于前瞻性陈述的谨慎声明

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1995年《私人证券诉讼改革法案》（经修订）所指的前瞻性声明，包括但不限于关于我们对战略、业务计划及开发临床和临床前管线的目标的隐含和明确声明，包括其治疗潜力、临床益处和安全性，特别是关于KT-579，以及预计在2026年下半年公布KT-579一期健康志愿者数据。

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”、“预期”、“打算”、“相信”、“估计”、“寻求”、“预测”、“未来”、“项目”、“潜力”、“继续”、“目标”、“即将”等词语或类似表达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词。

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的当前预期和信念，并受到许多风险、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：与以下事项相关的风险：未来临床试验的启动、时间和设计所固有的不确定性，正在进行和未来试验的数据的可用性和时间以及此类试验的结果，临床前结果是否预示临床试验结果，成功证明药物候选物安全性和有效性的能力，与监管机构计划互动的时间和结果，以及是否有足够的资金满足我们的运营费用和资本支出需求。

Investor Contact:

投资者联系方式：

Justine Koenigsberg

朱斯汀·科尼格斯伯格

investors@kymeratx.com

投资者@凯米拉公司. com

857-285-5300

857-285-5300

Media Contact:

媒体联系人：

Bridgette Chandhoke

布丽奇特·钱德霍克

bchandhoke@kymeratx.com

bchandhoke@kymeratx.com

857-285-5300

857-285-5300