EN
登录

EpiBiologics细胞外蛋白质降解剂显示出强大的临床前抗肿瘤活性和生存效益

EpiBiologics Extracellular Protein Degraders Demonstrate Robust Preclinical Anti-tumor Activity and Survival Benefit

BioSpace 等信源发布 2024-04-08 14:03

可切换为仅中文


Data presented at AACR 2024 show EpiTAC activity is greater than standard of care in multiple preclinical tumor models

AACR 2024上提供的数据显示,在多种临床前肿瘤模型中,EpiTAC活性高于标准治疗

EpiTACs drive EGFR degradation independent of EGFR mutational status and can overcome resistance mechanisms that arise with standard of care

EpiTAC驱动EGFR降解而不依赖于EGFR突变状态,并且可以克服标准护理产生的耐药机制

SAN MATEO, Calif.--(BUSINESS WIRE)-- EpiBiologics, a preclinical stage company advancing new bispecific antibody therapeutics for extracellular protein degradation, is presenting data today on its EpiTAC protein degraders in oncology demonstrating robust in vivo anti-tumor activity and survival benefit.

加利福尼亚州圣马特奥(商业新闻短讯)--EpiBiologics是一家临床前阶段公司,致力于开发用于细胞外蛋白降解的新型双特异性抗体疗法,今天正在提供其EpiTAC蛋白降解剂在肿瘤学中的数据,证明其强大的体内抗肿瘤活性和生存益处。

EpiTAC bispecific antibodies leverage cell-surface degrader receptors enriched in disease tissue to selectively degrade membrane and extracellular targets and address significant unmet needs..

EpiTAC双特异性抗体利用富含疾病组织的细胞表面降解受体选择性降解膜和细胞外靶标,并解决重大未满足的需求。。

These data are being presented this morning at the American Association for Cancer Research (AACR) Annual Meeting 2024 in poster presentation #1866, “Discovery of mutation-independent EGFR degrading bispecific antibodies that suppress tumor growth in preclinical tumor models' with Jon Sitrin, Ph.D., Head of Translational Science for EpiBiologics as lead author..

这些数据于今天上午在美国癌症研究协会(AACR)2024年年会上发布,海报介绍#1866,“发现突变非依赖性EGFR降解双特异性抗体,抑制临床前肿瘤模型中的肿瘤生长”,EpiBiologics转化科学负责人Jon Sitrin博士为主要作者。。

Current cancer treatments targeting EGFR often yield limited benefits due to target-related toxicities and reduced effectiveness in patients with acquired resistance. Recognizing the importance of improving therapeutic outcomes, EpiBiologics tested the efficacy of its novel EpiTACS on this oncogenic driver..

由于靶向相关毒性和获得性耐药患者的有效性降低,目前针对EGFR的癌症治疗通常产生有限的益处。认识到改善治疗结果的重要性,EpiBiologics测试了其新型EpiTAC对这种致癌驱动因子的功效。。

“Our proof-of-concept data demonstrate that EpiTAC activity is greater than standard of care in multiple preclinical tumor models. EpiTAC degradation of EGFR is mutation-independent and can overcome resistance mechanisms. These data motivate us to develop new and clinically meaningful therapies,” said Shyra Gardai, Ph.D., Chief Scientific Officer of EpiBiologics..

EpiBiologics首席科学官Shyra Gardai博士说:“我们的概念验证数据表明,在多种临床前肿瘤模型中,EpiTAC活性高于标准治疗。EGFR的EpiTAC降解与突变无关,可以克服耐药机制。这些数据激励我们开发新的临床有意义的疗法。”。。

Poster Presentation Highlights

海报展示亮点

EpiTACs are bispecific antibodies with a target binding arm and degrader binding arm that together localize degradation of extracellular and membrane targets to disease tissue, sparing normal tissue and increasing efficacy

EpiTAC是具有靶标结合臂和降解物结合臂的双特异性抗体,它们共同将细胞外和膜靶标的降解定位于疾病组织,从而保留了正常组织并提高了疗效

Novel EpiTACs were rapidly selected and tested using the EpiAtlas of 270+ tumor- and tissue-specific degraders, including transmembrane E3 ubiquitin ligases, chemokine/cytokine receptors and tissue-enriched internalizing receptors

使用270多种肿瘤和组织特异性降解物的EpiAtlas快速选择和测试了新型EpiTAC,包括跨膜E3泛素连接酶,趋化因子/细胞因子受体和组织富集的内化受体

EpiTACs drove robust in vitro tumoricidal activity in colorectal cancer (CRC) and non-small cell lung cancer (NSCLC) models, independent of KRAS or EGFR mutational status

EpiTACs在结直肠癌(CRC)和非小细胞肺癌(NSCLC)模型中具有强大的体外杀肿瘤活性,与KRAS或EGFR突变状态无关

In vivo tumor models demonstrated EpiTACs degraded mutant EGFR and disrupts downstream signaling, suppressing tumor growth and increasing survival beyond osimertinib standard of care

体内肿瘤模型显示,EpiTACs降解突变型EGFR,破坏下游信号传导,抑制肿瘤生长,提高生存率,超过osimertinib标准治疗

'We believe EpiTACs are a promising new modality, especially for difficult-to-drug targets,” said Ann Lee-Karlon, Ph.D., President and CEO of EpiBiologics. “Our modular bispecific antibodies coupled with our EpiAtlas allow us to rapidly screen and manufacture EpiTACs that drive deep anti-tumor responses.

EpiBiologics总裁兼首席执行官AnnLeeKarlon博士说:“我们认为EpiTACs是一种很有前景的新模式,特别是对于难以药物靶点。”。“我们的模块化双特异性抗体与EpiAtlas相结合,使我们能够快速筛选和制造驱动深度抗肿瘤反应的EpiTAC。

We’re committed to advancing EpiTACs for diverse targets in oncology and other disease areas as we move quickly toward the clinic.”.

随着我们迅速走向临床,我们致力于推进肿瘤和其他疾病领域不同目标的EPITAC。”。

About EpiBiologics

关于EpiBiologics

EpiBiologics is advancing a next-generation protein degradation pipeline and platform that targets membrane and extracellular proteins. EpiBiologics was founded on pioneering work from scientific founder Dr. Jim Wells of the University of California, San Francisco (UCSF). The Company’s proprietary EpiTAC platform is a modular bispecific antibody system that enables targeted degradation of disease-driving membrane and extracellular proteins in a tissue-specific manner.

EpiBiologics正在推进针对膜和细胞外蛋白质的下一代蛋白质降解管道和平台。EpiBiologics是在加州大学旧金山分校(UCSF)科学创始人吉姆·威尔斯博士的开创性工作基础上成立的。该公司专有的EpiTAC平台是一种模块化双特异性抗体系统,能够以组织特异性方式靶向降解疾病驱动膜和细胞外蛋白。

Preclinical anti-tumor data support the innovative EpiTAC approach to extracellular protein degradation as the company moves toward the clinic. Headquartered in the San Francisco Bay Area, EpiBiologics is backed by leading healthcare investors and aims to develop first-in-class and best-in-class targeted therapies across multiple therapeutic areas, including oncology, immunology, neurodegeneration and metabolism.

随着公司走向临床,临床前抗肿瘤数据支持创新的EpiTAC细胞外蛋白降解方法。EpiBiologics总部位于旧金山湾区,由领先的医疗保健投资者支持,旨在开发跨多个治疗领域的一流和一流的靶向治疗,包括肿瘤学,免疫学,神经退行性疾病和代谢。

For more information, please visit epibiologics.com and follow us on LinkedIn..

有关更多信息,请访问epibiologics.com并在LinkedIn上关注我们。。

View source version on businesswire.com: https://www.businesswire.com/news/home/20240408193004/en/

在businesswire.com上查看源版本:https://www.businesswire.com/news/home/20240408193004/en/

Contacts

联系人

Michelle Linn

米歇尔·林恩

Linnden Communications

林登通信公司

michelle@linndencom.com

michelle@linndencom.com

Source: EpiBiologics

来源:EpiBiologics

View this news release online at:

在线查看此新闻稿,网址为:

http://www.businesswire.com/news/home/20240408193004/en

http://www.businesswire.com/news/home/20240408193004/en