The goal of this clinical research study is to learn if the combination of brigatinib and either local consolidation therapy (such as radiotherapy or surgery) or chemotherapy (pemetrexed and carboplatin) can help to control the disease compared with brigatinib alone. The safety of these combinations will also be studied.

开始日期2025-12-01

申办/合作机构

The University of Texas MD Anderson Cancer Center

NCT06095986 / Suspended临床2期

A Proof of Concept, Prospective, Randomized, Placebo-controlled, Double-blind, Study to Evaluate the Safety, Tolerability, and Efficacy of Aramchol Meglumine in Patients With Primary Sclerosing Cholangitis

The objectives of this study is to Evaluate the Safety, Tolerability, and Efficacy of Aramchol Meglumine in Patients with Primary Sclerosing Cholangitis

开始日期2025-06-01

申办/合作机构

Galmed Pharmaceuticals Ltd.

[+1]

NCT06632327 / Not yet recruiting临床3期IIT

Perioperative Versus Adjuvant Systemic Therapy in Patients With Resectable Non-Small Cell Lung Cancer - PROSPECT LUNG

This phase III trial compares standard therapy given after surgery (adjuvant) to standard therapy given before and after surgery (perioperative) in treating patients with stage II-IIIB non-small cell lung cancer (NSCLC) that can be removed by surgery (resectable). The usual approach for patients with resectable NSCLC is chemotherapy and/or immunotherapy before surgery, after surgery, or both before and after surgery. This study is being done to find out which approach is better at treating patients with lung cancer. Treatment will be administered according to the current standard of care at the time of enrollment. Chemotherapy options may include cisplatin, carboplatin, pemetrexed, gemcitabine, docetaxel, and vinorelbine at standard doses according to the treating physician. Cisplatin is in a class of medications known as platinum-containing compounds. It works by killing, stopping or slowing the growth of tumor cells. Carboplatin is in a class of medications known as platinum-containing compounds. It works in a way similar to the anticancer drug cisplatin, but may be better tolerated than cisplatin. Carboplatin works by killing, stopping or slowing the growth of tumor cells. Pemetrexed is in a class of medications called antifolate antineoplastic agents. It works by stopping cells from using folic acid to make deoxyribonucleic acid (DNA) and may kill tumor cells. Gemcitabine is a chemotherapy drug that blocks the cells from making DNA and may kill tumor cells. Docetaxel is in a class of medications called taxanes. It stops tumor cells from growing and dividing and may kill them. Other chemotherapy drugs, such as vinorelbine, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading . Immunotherapy with monoclonal antibodies, such as nivolumab, pembrolizumab, and atezolizumab, may help the body's immune system attack the tumor, and may interfere with the ability of tumor cells to grow and spread. Starting treatment with chemotherapy and immunotherapy prior to surgery and continuing treatment after surgery may be a more effective treatment option than adjuvant therapy alone in patients with stage II-IIIB resectable NSCLC.

开始日期2025-05-30

申办/合作机构

Alliance for Clinical Trials in Oncology

[+1]

100 项与 Oxidoreductases 相关的临床结果

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100 项与 Oxidoreductases 相关的转化医学

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0 项与 Oxidoreductases 相关的专利（医药）

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444,210

项与 Oxidoreductases 相关的文献（医药）

2025-08-01·Neural Regeneration Research

AAV2-PDE6B restores retinal structure and function in the retinal degeneration 10 mouse model of retinitis pigmentosa by promoting phototransduction and inhibiting apoptosis

Article

作者: Zhang, Xiaoli ; Han, Jinfeng ; Liu, Jingyang ; Lei, Bo ; Wang, Weiping ; Qiu, Ruiqi ; Jin, Xiuxiu ; Yang, Mingzhu

JOURNAL/nrgr/04.03/01300535-202508000-00030/figure1/v/2024-09-30T120553Z/r/image-tiff Retinitis pigmentosa is a group of inherited diseases that lead to retinal degeneration and photoreceptor cell death. However, there is no effective treatment for retinitis pigmentosa caused by PDE6B mutation. Adeno-associated virus (AAV)-mediated gene therapy is a promising strategy for treating retinitis pigmentosa. The aim of this study was to explore the molecular mechanisms by which AAV2-PDE6B rescues retinal function. To do this, we injected retinal degeneration 10 (rd10) mice subretinally with AAV2-PDE6B and assessed the therapeutic effects on retinal function and structure using dark- and light-adapted electroretinogram, optical coherence tomography, and immunofluorescence. Data-independent acquisition-mass spectrometry-based proteomic analysis was conducted to investigate protein expression levels and pathway enrichment, and the results from this analysis were verified by real-time polymerase chain reaction and western blotting. AAV2-PDE6B injection significantly upregulated PDE6β expression, preserved electroretinogram responses, and preserved outer nuclear layer thickness in rd10 mice. Differentially expressed proteins between wild-type and rd10 mice were closely related to visual perception, and treating rd10 mice with AAV2-PDE6B restored differentially expressed protein expression to levels similar to those seen in wild-type mice. Kyoto Encyclopedia of Genes and Genome analysis showed that the differentially expressed proteins whose expression was most significantly altered by AAV2-PDE6B injection were enriched in phototransduction pathways. Furthermore, the phototransduction-related proteins Pde6α, Rom1, Rho, Aldh1a1, and Rbp1 exhibited opposite expression patterns in rd10 mice with or without AAV2-PDE6B treatment. Finally, Bax/Bcl-2, p-ERK/ERK, and p-c-Fos/c-Fos expression levels decreased in rd10 mice following AAV2-PDE6B treatment. Our data suggest that AAV2-PDE6B-mediated gene therapy promotes phototransduction and inhibits apoptosis by inhibiting the ERK signaling pathway and upregulating Bcl-2/Bax expression in retinitis pigmentosa.

2025-08-01·Neural Regeneration Research

Neuronal regulated cell death in aging-related neurodegenerative diseases: key pathways and therapeutic potentials

Article

作者: Yin, Shiyi ; Wu, Jiannan ; Yan, Junqiang ; Song, Run

Regulated cell death (such as apoptosis, necroptosis, pyroptosis, autophagy, cuproptosis, ferroptosis, disulfidptosis) involves complex signaling pathways and molecular effectors, and has been proven to be an important regulatory mechanism for regulating neuronal aging and death. However, excessive activation of regulated cell death may lead to the progression of aging-related diseases. This review summarizes recent advances in the understanding of seven forms of regulated cell death in age-related diseases. Notably, the newly identified ferroptosis and cuproptosis have been implicated in the risk of cognitive impairment and neurodegenerative diseases. These forms of cell death exacerbate disease progression by promoting inflammation, oxidative stress, and pathological protein aggregation. The review also provides an overview of key signaling pathways and crosstalk mechanisms among these regulated cell death forms, with a focus on ferroptosis, cuproptosis, and disulfidptosis. For instance, FDX1 directly induces cuproptosis by regulating copper ion valency and dihydrolipoamide S-acetyltransferase aggregation, while copper mediates glutathione peroxidase 4 degradation, enhancing ferroptosis sensitivity. Additionally, inhibiting the Xc- transport system to prevent ferroptosis can increase disulfide formation and shift the NADP+/NADPH ratio, transitioning ferroptosis to disulfidptosis. These insights help to uncover the potential connections among these novel regulated cell death forms and differentiate them from traditional regulated cell death mechanisms. In conclusion, identifying key targets and their crosstalk points among various regulated cell death pathways may aid in developing specific biomarkers to reverse the aging clock and treat age-related neurodegenerative conditions.

2025-05-01·Neural Regeneration Research

Tranylcypromine upregulates Sestrin 2 expression to ameliorate NLRP3-related noise-induced hearing loss

Article

作者: Yang, Shiming ; Xu, Liangwei ; Guo, Weiwei ; Chen, Xihang ; Yuan, Shuolong ; Shi, Xi ; Lin, Chang ; Li, Menghua ; Chen, Wei ; Chen, Zhifeng

JOURNAL/nrgr/04.03/01300535-202505000-00030/figure1/v/2024-07-28T173839Z/r/image-tiff Noise-induced hearing loss is the primary non-genetic factor contributing to auditory dysfunction. However, there are currently no effective pharmacological interventions for patients with noise-induced hearing loss. Here, we present evidence suggesting that the lysine-specific demethylase 1 inhibitor–tranylcypromine is an otoprotective agent that could be used to treat noise-induced hearing loss, and elucidate its underlying regulatory mechanisms. We established a mouse model of permanent threshold shift hearing loss by exposing the mice to white broadband noise at a sound pressure level of 120 dB for 4 hours. We found that tranylcypromine treatment led to the upregulation of Sestrin2 (SESN2) and activation of the autophagy markers light chain 3B and lysosome-associated membrane glycoprotein 1 in the cochleae of mice treated with tranylcypromine. The noise exposure group treated with tranylcypromine showed significantly lower average auditory brainstem response hearing thresholds at click, 4, 8, and 16 kHz frequencies compared with the noise exposure group treated with saline. These findings indicate that tranylcypromine treatment resulted in increased SESN2, light chain 3B, and lysosome-associated membrane glycoprotein 1 expression after noise exposure, leading to a reduction in levels of 4-hydroxynonenal and cleaved caspase-3, thereby reducing noise-induced hair cell loss. Additionally, immunoblot analysis demonstrated that treatment with tranylcypromine upregulated SESN2 expression via the autophagy pathway. Tranylcypromine treatment also reduced the production of NOD-like receptor family pyrin domain-containing 3 (NLRP3) production. In conclusion, our results showed that tranylcypromine treatment ameliorated cochlear inflammation by promoting the expression of SESN2, which induced autophagy, thereby restricting NLRP3-related inflammasome signaling, alleviating cochlear hair cell loss, and protecting hearing function. These findings suggest that inhibiting lysine-specific demethylase 1 is a potential therapeutic strategy for preventing hair cell loss and noise-induced hearing loss.

4,070

项与 Oxidoreductases 相关的新闻（医药）

2024-10-31

·PRNewswire

Immunic, Inc. to Announce Financial Results for the Third Quarter Ended September 30, 2024, and Provide Corporate Update

– Webcast to be Held at 8:00 am ET on November 7, 2024 – NEW YORK, Oct. 31, 2024 /PRNewswire/ -- Immunic, Inc. (Nasdaq: IMUX), a biotechnology company developing a clinical pipeline of orally administered, small molecule therapies for chronic inflammatory and autoimmune diseases, today announced that the company will release its financial results for the third quarter ended September 30, 2024, including a corporate update, on Thursday, November 7, 2024, before the opening of the U.S. financial markets. A webcast will follow at 8:00 am ET. To participate in the webcast, please register in advance at: or on the "Events and Presentations" section of Immunic's website at: ir.imux.com/events-and-presentations. Registrants will receive a confirmation email containing a link for online participation or a telephone number for dial in access. An archived replay of the webcast will be available approximately one hour after completion on Immunic's website at: ir.imux.com/events-and-presentations. About Immunic, Inc. Immunic, Inc. (Nasdaq: IMUX) is a biotechnology company developing a clinical pipeline of orally administered, small molecule therapies for chronic inflammatory and autoimmune diseases. The company's lead development program, vidofludimus calcium (IMU-838), is currently in phase 3 and phase 2 clinical trials for the treatment of relapsing and progressive multiple sclerosis, respectively, and has shown therapeutic activity in phase 2 clinical trials in patients suffering from relapsing-remitting multiple sclerosis, progressive multiple sclerosis and moderate-to-severe ulcerative colitis. Vidofludimus calcium combines neuroprotective effects, through its mechanism as a first-in-class nuclear receptor related 1 (Nurr1) activator, with additional anti-inflammatory and anti-viral effects, by selectively inhibiting the enzyme dihydroorotate dehydrogenase (DHODH). IMU-856, which targets the protein Sirtuin 6 (SIRT6), is intended to restore intestinal barrier function and regenerate bowel epithelium, which could potentially be applicable in numerous gastrointestinal diseases, such as celiac disease, for which it is currently in preparations for a phase 2 clinical trial. IMU-381, which currently is in preclinical testing, is a next generation molecule being developed to specifically address the needs of gastrointestinal diseases. For further information, please visit: . Cautionary Statement Regarding Forward-Looking Statements This press release contains "forward-looking statements" that involve substantial risks and uncertainties for purposes of the safe harbor provided by the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical facts, included in this press release regarding strategy, future operations, future financial position, future revenue, projected expenses, sufficiency of cash and cash runway, expected timing, development and results of clinical trials, prospects, plans and objectives of management are forward-looking statements. Examples of such statements include, but are not limited to, statements relating to Immunic's development programs and the targeted diseases; the potential for Immunic's development programs to safely and effectively target diseases; preclinical and clinical data for Immunic's development programs; the timing of current and future clinical trials and anticipated clinical milestones; the nature, strategy and focus of the company and further updates with respect thereto; the development and commercial potential of any product candidates of the company; and the company's expected cash runway. Immunic may not actually achieve the plans, carry out the intentions or meet the expectations or projections disclosed in the forward-looking statements and you should not place undue reliance on these forward-looking statements. Such statements are based on management's current expectations and involve substantial risks and uncertainties. Actual results and performance could differ materially from those projected in the forward-looking statements as a result of many factors, including, without limitation, the COVID-19 pandemic, increasing inflation, impacts of the Ukraine – Russia conflict and the conflict in the Middle East on planned and ongoing clinical trials, risks and uncertainties associated with the ability to project future cash utilization and reserves needed for contingent future liabilities and business operations, the availability of sufficient financial and other resources to meet business objectives and operational requirements, including the ability to satisfy the minimum average price and trading volume conditions required to receive funding in tranche 2 and 3 of the January 2024 private placement, the fact that the results of earlier preclinical studies and clinical trials may not be predictive of future clinical trial results, the protection and market exclusivity provided by Immunic's intellectual property, risks related to the drug development and the regulatory approval process and the impact of competitive products and technological changes. A further list and descriptions of these risks, uncertainties and other factors can be found in the section captioned "Risk Factors," in the company's Annual Report on Form 10-K for the fiscal year ended December 31, 2023, filed with the SEC on February 22, 2024, and in the company's subsequent filings with the Securities and Exchange Commission. Copies of these filings are available online at or ir.imux.com/sec-filings. Any forward-looking statement made in this release speaks only as of the date of this release. Immunic disclaims any intent or obligation to update these forward-looking statements to reflect events or circumstances that exist after the date on which they were made. Immunic expressly disclaims all liability in respect to actions taken or not taken based on any or all the contents of this press release. Contact Information Immunic, Inc. Jessica Breu Vice President Investor Relations and Communications +49 89 2080 477 09 [email protected] US IR Contact Rx Communications Group Paula Schwartz +1 917 633 7790 [email protected] US Media Contact KCSA Strategic Communications Caitlin Kasunich +1 212 896 1241 [email protected] SOURCE Immunic, Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

临床2期财报

2024-10-31

·生物探索

Immunity | 抑制性共受体Lag3通过限制Myc依赖的代谢程序调节Treg细胞功能

引言调节性T（Treg）细胞是免疫系统中的一种特殊T细胞亚群，负责维持免疫耐受性和防止自身免疫性疾病的发生。它们通过抑制过度的免疫反应，避免对自身组织发起攻击。Treg细胞特异性表达Foxp3转录因子，并通过分泌抑制性细胞因子（如IL-10和TGF-β）或直接与其他免疫细胞接触来抑制其活性【1】。Treg细胞在控制慢性炎症、预防自身免疫性疾病以及调节肿瘤微环境中都发挥着重要作用【2】。Treg细胞表达一系列表面受体，其中Lag3是一种类似于CD4的共受体，主要在活化的T细胞和Treg细胞中表达【3】。Lag3被认为是一种抑制性共受体，能够限制常规T细胞的增殖和IL-2的产生。有研究报道，Lag3缺陷的Treg细胞不能缓解自身免疫性脑脊髓炎，但是Lag3可能会限制自身免疫性糖尿病中Treg细胞的增殖和功能【4,5】。虽然Lag3对Treg细胞功能的调节已经被证实，但是Lag3调节Treg细胞的确切机制仍不清楚。近日，来自美国西北大学范伯格医学院的Booki Min课题组在Immunity上发表了研究论文Inhibitory co-receptor Lag3 supports Foxp3+ regulatory T cell function by restraining Myc-dependent metabolic programming。在本研究中，作者特异性突变Treg细胞的Lag3受体，揭示了Lag3通过PI3K-Akt通路抑制Myc的表达，从而支持Treg细胞免疫抑制功能的分子机制。为了探究Lag3在Treg细胞功能调节中具体作用，研究人员在Lag3基因位点引入了loxP位点，将Lag3基因的1-3号外显子进行flox处理，然后与Foxp3CreYFP小鼠进行交配，构建了在Treg细胞中特异性缺陷Lag3的突变（Treg△Lag3E1-3）小鼠。通过诱导实验性自身免疫性脑脊髓炎（EAE），研究发现相较于野生型小鼠，Treg△Lag3E1-3小鼠的疾病进展更快且症状更严重，表现为中枢神经系统（CNS）中Treg细胞和CD4 T细胞浸润增加，促炎细胞因子也显著增加。这些结果表明，Lag3缺失的Treg细胞功能异常，未能有效控制EAE的发展。同时，研究人员还进一步的验证了Lag3在免疫抑制和肿瘤生长调控中的作用。总的来说，Lag3在维持Treg细胞的抑制功能和调节免疫反应方面发挥重要作用，其缺失可能导致更严重的炎症反应和免疫失调。接下来，为了揭示Lag3调节Treg细胞功能的具体机制，研究人员先对CNS中分离的Treg细胞进行了RNA-seq分析。研究发现，代谢过程是Lag3缺失的Treg细胞中主要富集的途径。GSEA分析进一步确认，Lag3缺失的Treg细胞中上调的基因高度富集在细胞代谢途径中，包括Myc靶基因、氧化磷酸化、糖酵解和脂肪酸代谢途径。Myc是多种细胞代谢过程的关键调节因子，它直接激活几乎所有编码糖酵解酶的基因。在Lag3缺失的Treg细胞中，Myc表达高于对照组且与糖酵解相关的基因表达显著增加，与此相对应的是糖酵解活性增加。此外，在Lag3缺失的Treg细胞中敲低Myc的表达，糖酵解活性受到明显抑制，Treg细胞的免疫抑制功能得到恢复。研究人员还探究了Lag3抑制Myc表达的分子机制。他们发现Lag3胞质结构域缺失导致Myc及其代谢靶基因的过度表达，进而引发Treg细胞的代谢失调。这些结果表明，Lag3通过控制Myc的表达来调节Treg细胞的代谢和功能，Myc相关的代谢变化直接影响Treg细胞在体内的抑制功能。研究人员还探究了Lag3抑制Myc表达的分子机制。他们发现Lag3胞质结构域缺失导致Myc及其代谢靶基因的过度表达，进而引发Treg细胞的代谢失调。之前的研究表明，PI3K-Akt信号通路在调控Myc表达中起重要作用，并且Lag3缺失在其他T细胞中能增强Akt磷酸化。因此作者推测Lag3可能通过PI3K-Akt信号通路抑制了Treg细胞中Myc的表达。为了证实这个推测，研究人员分析了Lag3缺失的Treg细胞中PI3K信号的激活情况以及使用PI3K-Akt通路的相关抑制剂处理细胞。结果表明，Lag3突变导致的PTEN下调、Rictor上调和Akt的异常磷酸化共同作用，引发Treg细胞的代谢失调和抑制功能减弱。当抑制PI3K和Rictor可以有效降低Myc的表达，恢复Lag3缺失的Treg细胞正常代谢活动，并改善其免疫抑制功能。文章的最后，研究人员详细的分析了Lag3对Myc的调控是如何影响Treg细胞的代谢活动。前面介绍到Lag3的缺失会导致Treg细胞的糖酵解活性增强，一个显著特征是细胞外酸化率增加，而乳酸脱氢酶A（Ldha）是介导这种状况发生的关键基因，并且Ldha也是Myc的靶基因之一。因此，研究人员对Ldha的功能进行了分析。结果表明，Lag3缺失会导致Ldha的表达增加，这与Myc的表达升高相一致，乳酸分泌也随之增加。抑制Ldha的活性能够恢复Lag3缺失导致的Treg细胞功能障碍以及代谢异常，从而揭示了Myc-Ldha轴在Treg细胞功能中的关键作用。模式图（Credit: Immunity）总的来说，这篇文章揭示了Lag3共受体调节Treg细胞免疫抑制功能的具体机制，Lag3通过PI3K-Akt信号通路抑制Myc的表达，当Lag3缺失后Myc表达升高并激活下游代谢基因的表达，改写了Treg细胞的代谢进而影响了Treg细胞的抑制性功能。参考文献 1. Sakaguchi, S., Yamaguchi, T., Nomura, T., and Ono, M. (2008). Regulatory T cells and immune tolerance. Cell 133, 775–787. 2. Vignali, D.A.A., Collison, L.W., and Workman, C.J. (2008). How regulatory T cells work. Nat. Rev. Immunol. 8, 523–532. 3. Andrews, L.P., Marciscano, A.E., Drake, C.G., and Vignali, D.A.A. (2017). LAG3 (CD223) as a cancer immunotherapy target. Immunol. Rev. 276, 80–96. 4. Kim, D., Le, H.T., Nguyen, Q.T., Kim, S., Lee, J., and Min, B. (2019). Cutting Edge: IL-27 Attenuates Autoimmune Neuroinflammation via Regulatory T Cell/Lag3-Dependent but IL-10-Independent Mechanisms In Vivo. J. Immunol. 202, 1680–1685. 5. Zhang, Q., Chikina, M., Szymczak-Workman, A.L., Horne, W., Kolls, J.K., Vignali, K.M., Normolle, D., Bettini, M., Workman, C.J., and Vignali, D.A.A. (2017). LAG3 limits regulatory T cell proliferation and function in autoimmune diabetes. Sci. Immunol. 2, eaah4569. https://doi.org/10.1016/j.immuni.2024.08.008 责编|探索君排版|探索君来源|BioArt End 往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文 Cell | 是什么决定了细胞的大小？热文 Nature | 2024年值得关注的七项技术热文 Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文 CRISPR技术进化史 | 24年Cell综述

AACR会议临床结果临床1期免疫疗法临床终止

2024-10-31

·PipelineReview

BridgeBio Oncology Therapeutics (BBOT) Announces First Patient Dosed with First-in-Class BBO-10203, a RAS:PI3Kα Breaker, in the Phase 1 BREAKER-101 Trial for Advanced Solid Tumors

SOUTH SAN FRANCISCO, CA, USA I October 30, 2024 I TheRas, Inc. d/b/a BridgeBio Oncology Therapeutics (“BBOT” or the “Company”), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, has announced that the first patient has been dosed with BBO-10203 in the BREAKER-101 trial. BBO-10203 is a first-in-class orally bioavailable RAS:PI3Ka breaker that blocks the interaction between RAS and PI3Kα to inhibit PI3Kα-AKT signaling in tumors, without directly inhibiting the catalytic activity of PI3Kα. “I am thrilled to partner with BBOT to bring a potentially transformable new therapeutic to the clinic,” said Dr. Minal Barve, Chief Medical Officer and Principal Investigator at Mary Crowley Cancer Research, Dallas, TX. “BBO-10203 represents a first-in-class drug with potential to address high unmet medical needs and change the landscape of cancer care. We look forward to evaluating BBO-10203 in the BREAKER-101 trial.” BBO-10203 was designed to bind covalently and selectively to the RAS-binding domain (RBD) of PI3Kα. This selective inhibition is agnostic to the mutational status of PI3Kα and RAS, and in preclinical models, results in complete inhibition of RAS-driven pAKT signal at single digit nanomolar concentration. Additionally, no hyperglycemia was observed in preclinical species treated with BBO-10203. The discovery of BBO-10203 was the result of a collaboration between the RAS Initiative at Frederick National Laboratory, Lawrence Livermore National Laboratory, and BBOT. “BBO-10203 is a first-in-class program that inhibits the interaction of the two most mutated oncogenes in human cancer, and it will allow us to test, for the first time, the importance of RAS-coordinated activation of the MAPK and AKT signaling pathways,” said Pedro Beltran, PhD, Chief Scientific Officer of BBOT. “The discovery of BBO-10203 was made possible by the dedicated collaboration between academic, national laboratory, and industry experts that synergized to advance medicines for patients suffering from cancer.” The BREAKER-101 trial will enroll patients globally with locally advanced or metastatic HER2-positive breast cancer, HR-positive/HER2-negative breast cancer, KRAS mutant advanced colorectal cancer, and KRAS mutant advanced non-small cell lung cancer. “There is a tremendous opportunity to improve the standard of care in oncology by inhibiting oncogenic pAKT signaling without the metabolic side effects observed with kinase inhibitors, and the initiation of the Phase 1 study of BBO-10203 marks an important milestone in this regard,” said Yong (Ben) Ben, MD, Chief Medical and Development Officer of BBOT. “The second IND within six months of establishing BBOT clearly demonstrates our team’s capability in advancing our novel programs into the clinic. This novel mechanism and scientific rationale behind it will allow tremendous combination opportunities that optimally inhibit both pAKT and pERK – an approach we hope will bring unprecedented benefit to patients with RAS-driven cancers.” About TheRas, Inc. d/b/a BridgeBio Oncology Therapeutics (BBOT) BridgeBio Oncology Therapeutics (BBOT) is a clinical-stage biopharmaceutical company advancing a next generation pipeline of novel small molecule therapeutics targeting RAS and PI3K malignancies. Initially formed as a subsidiary of BridgeBio, BBOT completed a $200M private financing with external investors in 2024 with the goal of improving outcomes for patients with cancers driven by the two most prevalent oncogenes in human tumors. For more information visit bridgebiooncology.com . SOURCE: BridgeBio Oncology Therapeutics

临床1期