There is growing evidence that cancer DNA (called circulating tumour DNA - ctDNA) in the blood is often an early sign that the cancer is likely to return. The aim of this study is to investigate whether treating women who have detectable ctDNA in their blood with a drug called Capivasertib can help control ctDNA levels and prevent developing metastatic or secondary breast cancer.
A recruitment of 20 women with oestrogen receptor (ER) positive breast cancer (who are already on standard of care hormone therapy who are being treated with curative intent) is aimed for; which means that the disease has not yet spread to distant parts of the body. Each subject will be dosed with 400mg of Capivasertib twice a day for a maximum period of two years.

开始日期2024-11-01

申办/合作机构

Imperial College London

[+3]

CTR20242809 / Recruiting临床3期

一项Capivasertib+氟维司群治疗HR+/HER2-经1-2L内分泌治疗后疾病进展的晚期乳腺癌中国IIIb期研究（CAPItrue）

评价Capivasertib+氟维司群治疗接受内分泌治疗期间发生疾病进展或在完成辅助治疗后12个月内发生疾病复发的激素受体阳性（HR+）/HER2-局部晚期（不可手术）或转移性乳腺癌患者中的疗效和安全性

开始日期2024-09-26

申办/合作机构

AstraZeneca AB

[+1]

100 项与 Akt-3 x Akt-1 x Akt-2 相关的临床结果

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100 项与 Akt-3 x Akt-1 x Akt-2 相关的转化医学

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0 项与 Akt-3 x Akt-1 x Akt-2 相关的专利（医药）

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项与 Akt-3 x Akt-1 x Akt-2 相关的文献（医药）

2024-12-01·Annals of Pharmacotherapy

Capivasertib: A Novel AKT Inhibitor Approved for Hormone-Receptor-Positive, HER-2-Negative Metastatic Breast Cancer

Review

作者: DeRemer, David L. ; Luboff, Alexa J.

Objective: To review the pharmacology, efficacy, and safety of capivasertib for the treatment of adults with hormone receptor-positive, HER2-negative (HR+/HER2–) locally advanced or metastatic breast cancer with 1 or more PIK3CA/AKT1/PTEN alterations. Data sources: A literature search was conducted using PubMed and MEDLINE databases, published abstracts, and studies from ClinicalTrials.gov between 2003 and February 2024. Keywords included capivasertib, AZD5363, PI3K/AKT/mTOR pathway, and breast cancer. Data extraction: All applicable publications, package inserts, meeting abstracts, and clinical trials with capivasertib were reviewed. Data synthesis: Capivasertib is a first-in-class inhibitor of 3 isoforms of AKT (AKT-1, AKT-2, and AKT-3) which is an essential component in the PI3K/AKT/mTOR signaling pathway involved in oncogenesis. In the phase III CAPItello-291 trial, capivasertib in combination with fulvestrant (C+F) demonstrated improved progression-free survival (PFS) (7.3 vs 3.1 months) compared with placebo-fulvestrant (P+F) cohort in AKT-altered pathway patients who had progressed through prior aromatase inhibitor. The most common adverse reactions of any grade reported in the C+F group were diarrhea, cutaneous skin reactions, nausea, fatigue, and vomiting. Relevance to patient care and clinical practice in comparison with existing drugs: HR+/HER2– advanced breast cancer patients experience progression following endocrine therapies and cyclin-dependent kinase (CDK) 4/6 inhibitors. Capivasertib is a viable treatment option for patients with PIK3CA/AKT1/PTEN activating mutations following progression on endocrine-based regimens in the metastatic setting or recurrence within 12 months of completing adjuvant therapy. Conclusion: Integration of capivasertib into clinical practice is ongoing; intermittent dosing and favorable toxicity are attractive for future novel combination prospective trials.

2024-03-11·PPAR Research

PPARG and the PTEN-PI3K/AKT Signaling Axis May Cofunction in Promoting Chemosensitivity in Hypopharyngeal Squamous Cell Carcinoma

Article

作者: Han, Boxuan ; Hou, Lizhen ; Chen, Shaoshi ; Fang, Jugao ; Chen, Jiaming ; Lian, Meng ; Shen, Xixi

It has been demonstrated that PPARG may interact with the PTEN-PI3K/AKT pathway, contributing to its involvement in the chemotherapy treatment of hypopharyngeal squamous cell carcinoma (HSCC). However, the underlying mechanism remains largely unknown. In this study, gene expression profiles of 17 HSCC patients, comprising 8 chemotherapy-sensitive patients (CSP) and 9 chemotherapy-nonsensitive patients (CNSP), were collected and analyzed to investigate expression patterns, correlations, influencing factors of the PPARG-PTEN-PI3K/AKT pathway, and its role in regulating chemosensitivity. The results revealed significantly increased expression (

p < 0.04

) of AKT1, AKT2, AKT3, PIK3CA, PPARG, and PTEN in the CSP group compared to the CNSP group. Specifically, AKT2 exhibited significant overexpression in tumor tissue (

p = 0.01

), while AKT2, AKT3, PPARG, and PTEN displayed significant increases in normal tissue (

p \leq 0.04

). Positive correlations (

R \in [0.43, 0.71]

p < 0.014

) were observed between PIK3CA, AKT1, AKT2, AKT3, and PTEN, with AKT2, AKT3, and PTEN also showing significant correlations with PPARG (

R \in [0.35, 0.47]

p < 0.04

). Age, gender, and disease stage had no influence on PPARG, PIK3CA, and PTEN expression, but they may affect AKT expressions. Pathway analysis revealed that PPARG may interact with the PTEN-PI3K/AKT signaling pathway, playing a crucial role in regulating chemosensitivity in the normal tissue microenvironment. Our results suggest that AKT1 and PIK3CA may be associated with chemosensitivity in HSCC tumor cells, while PPARG and PTEN might exhibit a correlation with a specific segment of the PI3K/AKT pathway, potentially influencing chemosensitivity in the normal tissue microenvironment of HSCC patients.

2024-01-01·Burns & Trauma

Exosomal miR-4645-5p from hypoxic bone marrow mesenchymal stem cells facilitates diabetic wound healing by restoring keratinocyte autophagy

Article

作者: Xu, Kui ; Yang, Ronghua ; Li, Jun ; Wang, Zhengguang ; Shi, Yan ; Liu, Dewu ; Zhu, Yihan ; Li, Furong ; Wang, Shang ; Wen, Huicai

AbstractBackgroundRefractory diabetic wounds are a common occurrence in patients with diabetes and epidermis-specific macroautophagy/autophagy impairment has been implicated in their pathogenesis. Therefore, identifying and developing treatment strategies capable of normalizing epidermis-specific macroautophagy/autophagy could facilitate diabetic wound healing. The study aims to investigate the potential of bone marrow mesenchymal stem cell-derived exosomes (BMSC-exos) from hypoxic conditions as a treatment to normalize epidermis-specific autophagy for diabetic wound healing.MethodsWe compared the effects of bone marrow mesenchymal stem cell (BMSC)-sourced exosomes (BMSC-Exos) from hypoxic conditions to those of BMSC in normoxic conditions (noBMSC-Exos). Our studies involved morphometric assessment of the exosomes, identification of the microRNA (miRNA) responsible for the effects, evaluation of keratinocyte functions and examination of effects of the exosomes on several molecules involved in the autophagy pathway such as microtubule-associated protein 1 light chain 3 beta, beclin 1, sequestosome 1, autophagy-related 5 and autophagy-related 5. The experiments used human BMSCs from the American Type Culture Collection, an in vivo mouse model of diabetes (db/db) to assess wound healing, as well as the human keratinocyte HaCaT cell line. In the methodology, the authors utilized an array of approaches that included electron microscopy, small interfering RNA (siRNA) studies, RNA in situ hybridization, quantitative real-time reverse transcription PCR (qRT-PCR), the isolation, sequencing and differential expression of miRNAs, as well as the use of miR-4645-5p-specific knockdown with an inhibitor.ResultsHypoxia affected the release of exosomes from hypoxic BMSCs (hy-BMSCs) and influenced the size and morphology of the exosomes. Moreover, hyBMSC-Exo treatment markedly improved keratinocyte function, including keratinocyte autophagy, proliferation and migration. miRNA microarray and bioinformatics analysis showed that the target genes of the differentially expressed miRNAs were mainly enriched in ‘autophagy’ and ‘process utilizing autophagic mechanism’ in the ‘biological process’ category and miR-4645-5p as a major contributor to the pro-autophagy effect of hyBMSC-Exos. Moreover, mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2) was identified as a potential target of exosomal miR-4645-5p; this was confirmed using a dual luciferase assay. Exosomal miR-4645-5p mediates the inactivation of the MAPKAPK2-induced AKT kinase group (comprising AKT1, AKT2, and AKT3), which in turn suppresses AKT-mTORC1 signaling, thereby facilitating miR-4645-5p-mediated autophagy.ConclusionsOverall, the results of this study showed that hyBMSC-Exo-mediated transfer of miR-4645-5p inactivated MAPKAPK2-induced AKT-mTORC1 signaling in keratinocytes, which activated keratinocyte autophagy, proliferation and migration, resulting in diabetic wound healing in mice. Collectively, the findings could aid in the development of a novel therapeutic strategy for diabetic wounds.

项与 Akt-3 x Akt-1 x Akt-2 相关的新闻（医药）

2024-10-23

·PipelineReview

Atavistik Bio Presents Preclinical Data on Precision Oncology Development Candidate, ATV-1601, a Selective Allosteric AKT1 E17K Small Molecule Inhibitor, at EORTC-NCI-AACR Symposium

CAMBRIDGE, MA, USA I October 23, 2024 I Atavistik Bio, a biotechnology company discovering the next generation of precision allosteric therapeutics inspired by the body’s natural regulators, today presented preclinical data at the 36 th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics Meeting 2024 in Barcelona for ATV-1601, the company’s orally bioavailable selective allosteric small molecule inhibitor for AKT1 E17K-driven cancers. The preclinical data demonstrated that as a selective allosteric AKT1 E17K inhibitor, ATV-1601 provides enhanced target inhibition, superior efficacy and improved tolerability compared to pan-AKT inhibitors in preclinical models. Atavistik Bio anticipates initiating a first-in-human study with ATV-1601 in patients with AKT1 E17K mutant tumors in early 2025. AKT1 E17K is a clinically validated oncogene that impacts greater than 40,000 cancer patients per year in the United States, with the highest prevalence in breast, endometrial, and prostate cancers. In addition, early evidence indicates that the AKT1 E17K mutation appears to be an emerging mechanism of resistance to PI3Kα-targeted cancer therapies. The only approved AKT-targeted therapy is a pan-AKT inhibitor that blocks all three isoforms of AKT (AKT1, AKT2, and AKT3). Pan-AKT inhibitors offer limited efficacy for patients with AKT1 E17K-driven mutant tumors due to insufficient inhibition of the AKT1 E17K mutation. Additionally, pan-AKT inhibitors can cause significant adverse events, such as AKT2-driven hyperglycemia, rash, and diarrhea, which lead to treatment discontinuation or dose reductions in a considerable subset of patients. Data presented in today’s poster entitled, “ATV-1601 is a Potent and Selective Allosteric Inhibitor of AKT1 E17K and Shows Profound and Durable Regressions in AKT1 E17K-Driven Patient-Derived Xenograft Models,” demonstrates that the selectivity profile of ATV-1601 enables greater than 90% target engagement without inducing hyperglycemia in preclinical models. As a result of this potent target engagement and selectivity, ATV-1601 demonstrated profound and durable tumor regression in multiple AKT1 E17K driven patient-derived breast and endometrial tumor models and was well tolerated. “We are pleased to share these exciting preclinical data for our ATV-1601 program with the oncology community,” said Marion Dorsch, Ph.D., President and Chief Scientific Officer, Atavistik Bio. “As a selective allosteric AKT1 E17K inhibitor, ATV-1601 has the potential to be a transformative precision therapy against the validated AKT1 E17K oncogenic driver. The patient populations impacted by the AKT1 E17K mutation have a significant unmet need, which we are working with urgency to address. We look forward to transitioning into the clinic in our planned first-in-human study.” About Atavistik Bio Atavistik Bio is a biotechnology company accelerating the discovery and development of transformative precision allosteric therapeutics to address serious unmet patient needs, with a focus on oncology. Atavistik Bio is led by an experienced team of drug hunters with a proven track record of developing marketed small molecule therapies and supported by top-tier investors, including The Column Group, Nextech Invest, and Lux Capital. To learn more, visit us at atavistikbio.com and follow us on LinkedIn . SOURCE: Atavistik Bio

AACR会议

2024-10-21

·药渡Daily

下一代减肥药新星，BD预期打满

GLP-1减肥药市场已步入更为紧张刺激的下半场：一边是礼来与诺和诺德两大巨头，在临床试验、产能扩张及商业化上展开了全方位的激烈比拼；另一边，中国药企也在纷纷加速研发步伐，通过提高药物疗效和差异化设计突围。与此同时，新型减肥药正悄然崛起成为新的蓝海。其中，ActRII靶向药物凭借既减重又增肌的独特疗效脱颖而出。近日更是喜报频传：礼来启动了Bimagrumab联合替尔泊肽增肌减脂的Ⅱ期临床试验；来凯医药的LAE102临床试验也取得重大进展，且公司股价因此暴涨近40%。来凯医药，这个看似边缘的Biotech，正以其不俗实力，吸引着市场的高度关注和期待。 01 下一代减肥药崛起 GLP-1靶点的减肥药是这两年最火爆的赛道之一，两大巨头礼来、诺和诺德均实现业绩、股价双双“暴增”。更重要的是，下一代全球“药王”有望在GLP-1减肥药赛道诞生。 2024年上半年，诺和诺德的司美格鲁肽销售额高达129亿美元，同比增长43%，紧逼现任全球“药王”K药（142亿美元，同比增长21%）；同期，礼来的替尔泊肽销售额达66.56亿美元，同比增长329%。按减重适应症看，司美格鲁肽减重版注射制剂Wegovy销售额为30.8亿美元，同比增长74%；替尔泊肽减重版Zepbound销售额为17.6亿美元。不过，GLP-1减肥药并非完美，在减去脂肪的同时也使得肌肉流失，出现市场热议的“司美格鲁肽脸”（面部凹陷、皮肤松弛）。在此背景下，减脂增肌靶点成为了新的竞技场，包括ActRII、艾帕素（Apelin）、HIF2等。其中，ActRII是在脂肪和肌肉细胞中都表达的激活素受体，通过阻断ActRII通路可促进肌肉再生和减少脂肪。由此，具备减重增肌效果的ActRII单抗应运而生，再加上减肥药市场拥有巨大潜力，市场将ActRII誉为继GLP-1后又一个减重靶点“金矿”，吸引着资本市场的目光。 10月16日，来凯医药宣布其自研、全球首创的ActRIIA单抗LAE102，针对超重/肥胖在中国开展的I期临床试验取得重大进展：单次剂量递增研究的皮下注射部分已启动。消息一出，踩在风口上的来凯医药，在短短3个交易日股价暴涨近40%，足见市场对“下一代减肥药新星”的高度期待。股价暴涨背后的另一推动因素，还得益于礼来宣布启动Bimagrumab联合替尔泊肽增肌减脂的II期临床试验。尤其是，目前全球进入临床阶段的ActRII靶向药物（针对超重/肥胖）仅有少数几款，显著推升了来凯医药的内在价值。 02 三箭齐发，抢占先机在ActRII靶向药物研发这条道路上，礼来与来凯医药走在了前头。其中，礼来在2023年7月以近20亿美元重金收购Versanis，拿下其主要资产Bimagrumab（ActRIIA/B单抗）；来凯医药则一口气布局了3款ActRII靶向药物，包括LAE102（ActRIIA单抗）、LAE103（ActRIIB单抗）和LAE123（ActRIIA/B单抗），这一前瞻性的策略，为其在未来的市场竞争中赢得了先机。从临床进度看，礼来的Bimagrumab进展更快，目前正在进行临床IIb期BELIEVE研究，旨在评估其单药或联合司美格鲁肽治疗48周后在超重或肥胖的成年人中的效果。根据此前披露的II期试验数据显示：接受Bimagrumab治疗48周后，患者的的全身脂肪量减少了20.5%，肌肉量增加了3.6%，代谢指标也得到改善。与GLP-1药物联用，发挥更大的疗效，使得ActRII靶向药成为GLP-1最佳“减重伴侣”药物之一。目前，礼来正在进行联用策略的临床验证，期待后续数据读出。 ActRII赛道仍处于蓝海阶段，来凯医药正在打造差异化的竞争优势。首发管线LAE102，目前均已在中国和美国获批开展针对肥胖适应症的I期临床试验。此前已在临床前研究显示出增加肌肉并减少脂肪的效果。另外，鉴于ActRII具有治疗肌肉疾病、肥胖、糖尿病以及癌症的潜力，来凯医药计划探索LAE102用于更多适应症。其中，LAE102用于治疗患者数量庞大的非小细胞肺癌（NSCLC），已于2023年5月获FDA批准开展临床试验。就减重适应症而言，来凯医药正在开展的I期临床系一项随机、双盲、安慰剂对照、单次和多次给药剂量递增研究，旨在通过静脉输注和皮下注射两种给药方式，评价LAE102注射液在健康成年受试者及超重/肥胖受试者中的安全性、耐受性及药代动力学。截至2024年9月30日，已有过半数的静脉输注队列完成了给药，并在低剂量组中就观察到靶点结合的早期迹象和预期的PD生物标志物变化。近日，来凯医药宣布启动单次剂量递增研究的皮下注射部分，2024年底前有望完成该项研究。来凯医药董事长兼CEO吕向阳博士表示，“与静脉注射给药相比，皮下给药对慢性病患者长期使用更有优势，也更易与GLP-1受体激动剂联合用药。”LAE102与GLP-1受体激动剂联用，可进一步减少脂肪，并显著降低GLP-1受体激动剂导致的肌肉流失。目前，越来越多Biotech达成license out、实现出海，来凯医药LAE102从一开始便瞄准国际市场、向美国FDA提交临床试验申请，或许也是为了给后续BD交易铺路。 03 BD预期打满实际上，来凯医药不只有ActRII靶向药物这些管线，也不仅仅布局纤维化、代谢疾病领域，更值得关注的重头戏还有针对癌症的丰富管线。截至目前，来凯医药已在癌症领域布局了10个管线，其中小分子药物和大分子药物各5个，涵盖AKT、CYP17A/CYP11B2、PI3Ka、PARP1等各种前沿靶点，进度最快的是LAE002和LAE001。来凯医药的研发管线图片来源：公司官网 LAE002（Afuresertib）是一种AKT强效抑制剂，抑制所有三种AKT亚型（AKT1、AKT2及AKT3），也是全球仅有的2种处于晚期临床开发阶段的针对乳腺癌及前列腺癌的AKT抑制剂之一。 AKT抑制剂是极具潜力的蓝海赛道，目前全球仅有阿斯利康的Capivasertib获批上市，科睿唯安预测该药到2031年将在七国集团市场实现销售额超10亿美元，也有海外分析师预测该药的销售峰值可达38亿美元。目前，来凯医药正在开展LAE002针对乳腺癌、前列腺癌、卵巢癌及PD-1/PD-L1耐药实体瘤的多项临床试验，其中已有3项研究处于临床后期阶段。根据公开数据，与其他AKT抑制剂相比，LAE002具有疗效更高、药效更好、肿瘤抑制暴露更显著、安全性更佳等多项优势，具备BIC潜质。根据弗若斯特沙利文的资料，全球及中国的乳腺癌发病人数预计到2030年将达到266.64万人及37.24万人。估计中国60%以上的乳腺癌患者存在HR+/HER2-分子特征，针对这类疾病的一线及/或二线疗法是内分泌/抗雌激素疗法联合CDK4/6抑制剂。然而，15%至20%的患者对治疗产生原发性耐药，而另外30%至40%的患者会随时间对治疗产生耐药性。CDK4/6抑制剂及内分泌治疗后的HR+/HER2-乳腺癌仍是一个巨大的未满足医疗需求，具有数十亿美元的市场潜力。今年5月，来凯医药在中国启动了LAE002联合氟维司群治疗PIK3CA/AKT1/PTEN改变的HR+/HER2-局部晚期或转移性乳腺癌III期临床试验AFFIRM-205。值得关注的管线还有LAE001，作为全球首款CYP17A1/CYP11B2双靶点抑制剂，具备比CYP17A1抑制剂阿比特龙更优的有效性和安全性。今年5月，FDA批准了LAE002联合LAE001治疗转移性去势抵抗性前列腺癌（mCRPC）患者的III期临床试验。此前，该组合疗法展现出了惊艳的疗效。据II期临床数据显示：截至2023年11月21日，40名在接受1-3线标准治疗（包括至少接受过1线阿比特龙或第二代AR拮抗剂治疗）后病情进展的患者已加入推荐的II期剂量组，中位rPFS为8.1个月。与过去接受标准治疗的mCRPC患者2到4个月的中位rPFS相比，是一个显著的改善。可以说，LAE002和LAE001都具备磅礴的BD预期。实际上，来凯医药也正在寻求战略合作伙伴，加速两者的开发和商业化。 04 结语尽管作为小型Biotech，来凯医药却展现出了显著的内在价值，手握两款全球前二的潜力管线。这些管线的临床进展与满满的BD预期相互呼应，有望为来凯医药闯出一番天地。参考资料 1.各家公司的财报、公告、官微 2.《减脂又增肌！礼来正式启动Bima+替尔泊肽增肌减脂2期临床》，GLP1减重宝典 3.中邮证券、华创证券研报

临床2期并购申请上市

2024-10-15

·GlobeNewswire-Health Care

Atavistik Bio Announces Nomination of Precision Oncology Development Candidate, ATV-1601, a Selective Allosteric AKT1 E17K Small Molecule Inhibitor

AKT1 E17K mutation is a clinically validated oncogene that impacts greater than 40,000 cancer patients per year in the United States, with the highest prevalence in breast, endometrial, and prostate cancersAs a selective allosteric AKT1 E17K inhibitor, ATV-1601 has the potential to provide enhanced target inhibition, superior efficacy and improved tolerability compared to pan-AKT inhibitorsAtavistik Bio anticipates initiating a first-in-human study with ATV-1601 in patients with AKT1 E17K mutant tumors in early 2025Preclinical data on ATV-1601 to be presented at the EORTC-NCI-AACR Symposium on October 23, 2024The company continues to leverage the AMPS™ platform to bring forward additional high-value precision oncology programs CAMBRIDGE, Mass., Oct. 15, 2024 (GLOBE NEWSWIRE) -- Atavistik Bio, a biotechnology company discovering the next generation of precision allosteric therapeutics inspired by the body’s natural regulators, today announced its precision oncology development candidate ATV-1601, an orally bioavailable selective allosteric small molecule inhibitor for AKT1 E17K-driven cancers. ATV-1601 was developed leveraging the company’s AMPS™ technology, which is seamlessly integrated with its AI-enabled drug discovery engine to rapidly advance programs from discovery into development. “ATV-1601’s nomination as our first oncology development candidate is a major milestone for the company, validating the capabilities of our proprietary platform to rapidly discover and advance novel precision allosteric therapeutics for targets that have historically been hard to drug. We anticipate significant progress in our portfolio in the upcoming year for high value oncology targets that address the unmet needs of large patient populations,” said Bryan Stuart, Chief Executive Officer, Atavistik Bio. “We are working to quickly advance ATV-1601 to the clinic and to achieve early clinical proof of concept for this program. We believe our precision allosteric small molecule offers several advantages to target the difficult-to-drug AKT1 E17K mutation, with the potential to improve the lives of many cancer patients.” AKT1 E17K mutation is a clinically validated oncogene that impacts greater than 40,000 cancer patients per year in the United States, with the highest prevalence in breast, endometrial, and prostate cancers. In addition, early evidence indicates that the AKT1 E17K mutation appears to be an emerging mechanism of resistance to PI3Kα-targeted cancer therapies. A selective allosteric AKT1 E17K inhibitor has the potential to be a transformative therapy against the validated AKT1 E17K oncogenic driver as well as resistance mutations emerging from PI3Kα-targeted therapies. The only approved AKT-targeted therapy is a pan-AKT inhibitor that blocks all three isoforms of AKT (AKT1, AKT2, and AKT3). Pan-AKT inhibitors offer limited efficacy for patients with AKT1 E17K-driven mutant tumors due to insufficient inhibition of the AKT1 E17K mutation. Additionally, pan-AKT inhibitors can cause significant adverse events, such as AKT2-driven hyperglycemia, rash, and diarrhea, which leads to treatment discontinuation or dose-reductions in a considerable subset of patients. ATV-1601, a selective allosteric AKT1 E17K inhibitor, has the potential to provide enhanced target inhibition, superior efficacy and improved tolerability compared to pan-AKT inhibitors for AKT1 E17K-driven cancers. Atavistik Bio anticipates initiating a first-in-human study with ATV-1601 in patients with AKT1 E17K-mutant tumors in early 2025. “Behind ATV-1601, we have a robust pipeline of precision oncology programs derived from our AMPS platform, said Marion Dorsch, Ph.D., President and Chief Scientific Officer, Atavistik Bio. “We look forward to advancing our internal pipeline with urgency while also broadening the reach of our platform through partnerships to discover important new allosteric therapeutics across other diseases.” Atavistik Bio EORTC-NCI-AACR Symposium Data Presentation Details Date:Wed., October 23, 2024Time:12.00 – 19.00 CETPoster Session:New DrugsPoster Title:ATV-1601 is a Potent and Selective Allosteric Inhibitor of AKT1 E17K and Shows Profound and Durable Regressions in AKT1 E17K-Driven Patient-Derived Xenograft ModelsPoster #:PB128 About Atavistik Bio Atavistik Bio is a biotechnology company accelerating the discovery and development of transformative precision allosteric therapeutics to address serious unmet patient needs, with a focus on oncology. Atavistik Bio is led by an experienced team of drug hunters with a proven track record of developing marketed small molecule therapies and supported by top-tier investors, including The Column Group, Nextech Invest, and Lux Capital. To learn more, visit us at atavistikbio.com and follow us on LinkedIn. Media Contact: Liz MeloneMelone Communications, LLCliz@melonecomm.com

临床研究AACR会议