A Phase 1b Study to Evaluate the Safety, Pharmacokinetics, and Anti-Tumour Activity of the Myc Inhibitor OMO-103 Administered Intravenously in Patients With Advanced Solid Tumours

This study is an open-label, multicentre, Phase 1b trial designed to determine the safety, tolerability, efficacy, PK, pharmacodynamics (PD) and proof-of-concept of OMO-103 in combination with the standard regimen gemcitabine/nab-paclitaxel in patients with metastatic pancreatic cancer who are treatment-naïve in the advanced disease setting.

开始日期2023-08-31

申办/合作机构

Peptomyc SL初创企业

NCT04808362 / Terminated临床1/2期

A Phase 1/2 Study to Evaluate the Safety, Pharmacokinetics, and Anti-Tumour Activity of the MYC Inhibitor OMO-103 Administered Intravenously in Patients With Advanced Solid Tumours

This study is an open label, two-part, First in Human (FIH) Phase 1/2 dose-finding study designed to determine the safety, tolerability, Pharmacokinetics (PK), Pharmacodynamics (PD) and proof-of-concept (POC) of OMO-103 in patients with advanced solid tumours.

开始日期2021-04-28

申办/合作机构

Peptomyc SL初创企业

100 项与 Omomyc 相关的临床结果

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100 项与 Omomyc 相关的转化医学

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100 项与 Omomyc 相关的专利（医药）

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项与 Omomyc 相关的文献（医药）

2024-01-24·Current cancer drug targets

Bromodomain Protein-directed Agents and MYC in Small Cell Lung Cancer

Article

作者: Hamilton, Gerhard ; Rath, Barbara ; Stickler, Sandra

Abstract:::

Small cell lung cancer (SCLC) has a dismal prognosis. In addition to the inactivation of the tumor suppressors TP53 and RB1, tumor-promoting MYC and paralogs are frequently overexpressed in this neuroendocrine carcinoma. SCLC exhibits high resistance to second-line chemotherapy and all attempts of novel drugs and targeted therapy have failed so far to achieve superior survival. MYC and paralogs have key roles in the oncogenic process, orchestrating proliferation, apoptosis, differentiation, and metabolism. In SCLC, MYC-L and MYC regulate the neuroendocrine dedifferentiation of SCLC cells from Type A (ASCL1 expression) to the other SCLC subtypes. Targeting MYC to suppress tumor growth is difficult due to the lack of suitable binding pockets and the most advanced miniprotein inhibitor Omomyc exhibits limited efficacy. MYC may be targeted indirectly via the bromodomain (BET) protein BRD4, which activates MYC transcription, by specific BET inhibitors that reduce the expression of this oncogenic driver. Here, novel BET-directed Proteolysis Targeting Chimeras (PROTACs) are discussed that show high antiproliferative activity in SCLC. Particularly ARV825, targeting specifically BRD4, exhibits superior cytotoxic effects on SCLC cell lines and may become a valuable adjunct to SCLC combination chemotherapy

2023-09-01·Computers in biology and medicine

Inhibition of cMYC-MAX transcription factors hetero-dimerization with structurally engineered omoMYC to downregulate oncogenic pathways in renal carcinoma.

Article

作者: Bano, Farah ; Khan, Abbas ; Xu, Bin ; Wei, Dong-Qing ; Alshammari, Abdulrahman ; Wang, Yanjing ; Li, Wenfeng

In the current study, we employed, structural informatics, and molecular simulation-based methods to engineer OmoMyc, a c-Myc dominant negative protein, to design novel mutants that could abrogate the c-MYC-MAX complex in Renal Carcinoma (RC). Among the total 472 mutations, only six mutations A61Q, Q64E, Q64K, N77R, Q64E-N77R, and Q64K-N77R were reported to increase the binding affinity and subjected to subsequent analysis such as protein-protein docking. The docking results revealed that the predicted mutants improve the functionality of the OmoMyc by not only increasing the binding affinity but also vdW and electrostatic energy in each complex that consequently increase the binding of the engineered OmoMyc by establishing extra hydrogen bonds, salt-bridges, and non-bonded contacts. Molecular simulation revealed a more stable behavior by the mutant complexes in contrast to the native OmoMyc however structural perturbations were reported in the regions, DBD (DNA-binding domain), loop region, and minor deviations at CTD (C terminal domain). Moreover, the hydrogen bonding and binding free energy results further validated the promising activity of our predicted mutants of OmoMyc. The results for TBE (total binding energy) revealed that the for each complex the TBE was calculated to be -87.88 ± 0.16 kcal/mol (WT OmoMyc-MAX), -91.89 ± 0.21 kcal/mol (A61Q OmoMyc-MAX), -91.55 ± 0.20 kcal/mol (Q64E OmoMyc-MAX), -95.17 ± 0.24 kcal/mol (Q64K OmoMyc-MAX), -96.49 ± 0.22 kcal/mol (N77R OmoMyc-MAX), -97.76 ± 0.22 kcal/mol (Q64E-N77R OmoMyc-MAX), and -95.31 ± 0.20 kcal/mol (Q64K-N77R OmoMyc-MAX) respectively. The results for TBE revealed promising results that allow the mutants to competitively inhibit the c-Myc-MAX complex more swiftly. Additionally, the internal motion and energy landscape were altered. These findings provide important insights into the potential of the mutants of OmoMyc as a therapeutic candidate for cancer treatment, particularly renal carcinoma, and could pave the way for the development of more effective clinical versions of OmoMyc.

2023-05-01·Biotechnology and bioengineering

Bacterial delivery of therapeutic proteins to the nuclei of cancer cells

Article

作者: Forbes, Neil S. ; Bloom, Shoshana M. K. ; O'Hare, Nicholas

Abstract:

Targeting nucleic targets with therapeutic proteins would enhance the treatment of hard‐to‐treat cancers. However, exogenous proteins are excluded from the nucleus by both the cellular and nuclear membranes. We have recently developed Salmonella that deliver active proteins into the cytoplasm of cancer cells. Here, we hypothesized that bacterially delivered proteins accumulate within nuclei, nuclear localization sequences (NLSs) increase delivery, and bacterially delivered proteins kill cancer cells. To test this hypothesis, we developed intranuclear delivering (IND) Salmonella and quantified the delivery of three model proteins. IND Salmonella delivered both ovalbumin and green fluorescent protein to nuclei of MCF7 cancer cells. The amount of protein in nuclei was linearly dependent on the amount delivered to the cytoplasm. The addition of a NLSs increased both the amount of protein in each nucleus and the number of nuclei that received protein. Delivery of Omomyc, a protein inhibitor of the nuclear transcript factor, Myc, altered cell physiology, and significantly induced cell death. These results show that IND Salmonella deliver functional proteins to the nucleus of cancerous cells. Extending this method to other transcription factors will increase the number of accessible targets for cancer therapy.

项与 Omomyc 相关的新闻（医药）

2024-04-21

·精准药物

【Nature Medicine】首款MYC抑制剂完成临床I期试验

肿瘤药理学研究交流群在人类癌症中，MYC 是一种经常失调的癌基因，也是癌症治疗中“理想中”的靶点。它作为一种多效性转录因子，协调涉及细胞增殖、细胞生长、代谢、凋亡和免疫抑制的转录程序。在生理条件下，这些活动通常是短暂的并且与组织再生程序相关。然而，在癌症中，MYC 及其所有功能不断受到上游致癌信号的影响，从而持续允许癌症的发生和/或维持。有人提出，在这些异常条件下，MYC 可以充当全局放大器，增加所有活性启动子的输出，导致癌细胞中的超转录。所有这些因素都表明 MYC 是一个极好的治疗靶点，但一些技术困难，特别是蛋白质本质上无序的性质，迄今为止阻碍了临床上可行的 MYC 抑制剂的开发。OMO-103 是一种基于 Omomyc 的药物，由 91 个氨基酸的小蛋白组成，Omomyc 可导致 MYC 显性失活，最初设计并发表于 1998 年，作为研究 MYC 扰动的实验室工具，后来用于模拟 MYC 抑制及其在不同疾病中的显着治疗潜力。小鼠癌症模型，它还显示出安全性和耐受性。Omomyc 干扰 MYC 与其专性伴侣MAX 的二聚化，并抑制它们与共有 DNA 结合位点（E-box序列）的相互作用。Omomyc 将 MYC 隔离在无法结合 DNA 的蛋白质二聚体中，同时还与 MAX 形成同二聚体和异二聚体，MAX 占据具有转录非活性蛋白质复合物的 E-box，从而阻止 MYC 靶标的转录。最近发现纯化的 Omomyc微型蛋白具有意想不到的细胞穿透特性，促使其发展成为一种药理学工具，在体外和小鼠非小细胞肺癌 (NSCLC) 和三阴性乳腺癌模型中均显示出治疗功效，并为其临床开发开辟了道路。在这些情况下，Omomyc 在鼻内和静脉内给药以及诱导 MYC 转录程序关闭和肿瘤微环境重新编程时均显示出安全性和有效性，概括了 Omomyc 转基因表达的几个关键特征都有治疗作用。在这些临床前模型中，对Omomyc 的反应程度仅与其表达水平相关，而与 MYC 水平无关。在此，报告了一项首次人体 1 期临床试验的结果，该试验旨在评估 OMO-103（一种首创的抗 MYC 微型蛋白）的安全性、药代动力学 (PK) 和初步活性迹象。首先，该研究旨在检查安全性和耐受性作为主要结果，药代动力学、推荐的 2 期剂量和初步活性迹象作为次要结果。采用经典的 3 + 3 设计，以 21 天为周期，每周静脉注射单药 OMO-103 剂量递增，涵盖六个剂量水平 (DL)。共有 22 名患者入组，治疗持续至疾病进展。其次，最常见的不良事件是 1 级输注相关反应，发生在 10 名患者中。DL5 时发生一种剂量限制性毒性。再次，药代动力学表现出非线性，在 DL5 时出现组织饱和迹象，血清中的终末半衰期为 40 小时。最后，在可评估反应的 19 名患者中，有 12 名达到了药物抗肿瘤活性评估的预定 9 周时间点，其中 8 名患者通过计算机断层扫描显示疾病稳定。一名根据实体瘤反应评估标准被定义为疾病稳定的患者显示，在最佳反应下，总肿瘤体积减少了 49%。转录组分析支持肿瘤活检中的靶点参与。此外，还确定了一系列可溶性因子，临床上受益于 OMO-103 的患者表现出MIP-1β、IL-8、CD62E 和 GM-CSF较低的水平，它们是潜在的药效学和预测反应标记物。根据所有这些数据，推荐的2期剂量确定为DL5（6.48mg·kg−1 ）。Peptomyc (www.peptomyc.com) 是 VHIO（Vall d’Hebron 肿瘤研究所，西班牙）和 ICREA（加泰罗尼亚研究与高级研究所）的合创公司，于 2014 年 12 月在西班牙巴塞罗那成立。该公司专注于开发针对 Myc 癌蛋白的创新细胞穿透肽 (CPP)，用于癌症治疗，并基于 Soucek 博士过去二十年对 Omomyc（迄今为止已知的最好的直接 Myc 抑制剂）的科学研究。它是第一家成功完成 MYC 抑制剂 1 期临床试验的公司。参考Garralda, E., Beaulieu, ME., Moreno, V. et al. MYC targeting by OMO-103 in solid tumors: a phase 1 trial. Nat Med 30, 762–771 (2024).声明：发表/转载本文仅仅是出于传播信息的需要，并不意味着代表本公众号观点或证实其内容的真实性。据此内容作出的任何判断，后果自负。若有侵权，告知必删！长按关注本公众号粉丝群/投稿/授权/广告等请联系公众号助手觉得本文好看，请点这里↓

临床1期临床2期临床结果AACR会议

2024-02-08

·生物探索

Nat Med | 挑战'不可药物化'：OMO-103在晚期实体瘤治疗中的突破性研究

引言癌症治疗领域长期以来一直寻找能够靶向并调控肿瘤发展和维护关键转录程序的策略。在众多的致癌基因中，MYC基因无疑是治疗研究中的“头号目标”。它不仅调控着肿瘤发展所需的核心转录程序，还在维持肿瘤生长中扮演着不可或缺的角色。然而，MYC因其蛋白质结构的特殊性和功能上的复杂性，长期被视为一个难以直接靶向的挑战。2月6日发表于Nature Medicine （IF 82.9）上的研究“MYC targeting by OMO-103 in solid tumors: a phase 1 trial”聚焦于OMO-103，它作为一种创新的MYC抑制剂，通过一种由91个氨基酸组成的小蛋白质来实现其作用，该研究旨在探索OMO-103在晚期实体肿瘤治疗中的应用前景。该研究基于对癌症治疗领域中一个关键而又难以靶向的蛋白质—MYC的深入研究。MYC是一种在许多类型的癌症中频繁失调的致癌基因(oncogene)，它通过协调细胞增殖(cell proliferation)、生长(cell growth)、代谢(metabolism)、凋亡(apoptosis)和免疫抑制(immune suppression)等关键的转录程序(transcriptional programs)在肿瘤发展(tumor development)和维护(tumor maintenance)中发挥着核心作用。尽管MYC的这些功能使其成为癌症治疗的理想靶点，但由于MYC蛋白的内在无序性(intrinsically disordered nature)，长期以来一直被认为是"不可药物化的"(undruggable)。OMO-103是一种基于Omomyc小蛋白设计的首创性MYC抑制剂，该小蛋白最初被设计和公布用于实验室研究MYC的扰动。Omomyc通过干扰MYC与其必需伴侣MAX的二聚化(dimerization)和它们与共识DNA结合位点(E-box sequence)的相互作用来发挥作用，有效地阻断了MYC的转录活性(transcriptional activity)。此外，Omomyc还展示了意想不到的细胞穿透(cell-penetrating)属性，这为其作为药物开发的可能性打开了大门。这种小蛋白在体外(in vitro)和小鼠模型(mouse models)中展示了治疗效果，尤其是在非小细胞肺癌(non-small cell lung cancer, NSCLC)和三阴性乳腺癌(triple-negative breast cancer)的模型中，显示出安全性和有效性。该研究旨在通过临床试验(phase 1 clinical trial)评估OMO-103在晚期实体肿瘤(advanced solid tumors)中的安全性、耐受性、药代动力学(pharmacokinetics)和初步的治疗活性(preliminary signs of activity)。该研究的目的是确定OMO-103的推荐二期剂量(recommended phase 2 dose)，并探索其对MYC作为癌症治疗靶点的潜力。通过这项研究，科研人员希望为癌症治疗提供新的策略，尤其是针对那些目前缺乏有效治疗手段的癌症类型。Strategies临床试验设计（Clinical Trial Design）：研究采用了经典的3+3剂量递增设计（dose-escalation design）进行，这是评估新药安全性和确定最大耐受剂量（Maximum Tolerated Dose, MTD）的常用方法。通过每周静脉给药（intravenous administration），在21天的周期内评估不同剂量水平（Dose Levels, DLs）的OMO-103。患者入选（Patient Enrollment）：选取了具有晚期实体瘤且对标准治疗（Standard of Care, SoC）无效或不耐受的患者参与本研究。安全性和耐受性评估（Safety and Tolerability Assessment）：监测和记录不良事件（Adverse Events, AEs）、严重不良事件（Serious Adverse Events, SAEs）和实验室异常等，根据通用不良事件术语标准（Common Terminology Criteria for Adverse Events, CTCAE）进行分级。药代动力学（PK）分析：通过测量OMO-103在血清中的浓度来评估其吸收、分布、代谢和排泄特性。使用特定的生物标志物（Biomarkers）评估药物的动态过程。初步疗效评估（Preliminary Efficacy Evaluation）：利用实体瘤响应评价标准（Response Evaluation Criteria in Solid Tumors, RECIST）和计算机断层扫描（Computed Tomography, CT）评估OMO-103的抗肿瘤活性。转录组和蛋白质组学分析（Transcriptomic and Proteomic Analysis）：通过从患者肿瘤组织样本中提取RNA和蛋白进行深入分析，评估OMO-103对MYC目标的影响及其转录活性的抑制。生物标志物研究（Biomarker Studies）：研究血清中可溶性因子的变化，寻找治疗响应的预测指标和药效学（Pharmacodynamics, PD）标志物。Main Findings安全性和耐受性（Safety and Tolerability）：OMO-103在治疗中表现出良好的安全性和耐受性。大多数不良事件（Adverse Events, AEs）为1级，主要是与输液相关的反应（infusion-related reactions），这些反应可通过常规预防和管理措施得到控制。研究未达到最大耐受剂量（Maximum Tolerated Dose, MTD）。药代动力学（Pharmacokinetics, PK）：OMO-103展示了非线性的药代动力学特性，其中在第五剂量水平（Dose Level 5, DL5）出现组织饱和迹象，且血清中的终末半衰期（terminal half-life）约为40小时。这些发现提示OMO-103在体内具有持久的药效和较长的作用时间。初步疗效（Preliminary Efficacy）：虽然根据实体瘤响应评价标准（Response Evaluation Criteria in Solid Tumors, RECIST）未观察到明确的肿瘤缩小（objective response），但有一部分患者在治疗后表现出疾病稳定（Stable Disease, SD）。特别是，有一个患者在治疗过程中总肿瘤体积（total tumor volume）减少了49%，显示出OMO-103在某些病例中可能具有抗肿瘤活性。靶向作用验证（Target Engagement）：通过转录组分析（transcriptomic analysis）和蛋白质组学研究（proteomic studies），证实了OMO-103能够有效靶向MYC，并抑制其在肿瘤中的转录活性。这表明OMO-103作为MYC抑制剂的机制得到了实验支持。生物标志物发现（Biomarker Discovery）：研究发现了潜在的生物标志物，这些标志物可能预测治疗响应或作为药效学（Pharmacodynamics, PD）指标。这些发现为未来个体化治疗和治疗监测提供了新的工具和策略。所以，OMO-103在晚期实体瘤的治疗中显示出安全性和初步的治疗活性，特别是在某些患者中观察到疾病稳定的现象。OMO-103的药代动力学特性和对MYC的靶向作用为其在未来癌症治疗中的应用提供了科学依据。此外，识别的生物标志物为OMO-103的进一步开发和临床应用提供了重要的参考信息。所有队列中肿瘤反应的评估以及一名患有胰腺导管腺癌（PDAC）患者的时间依赖性疾病评估（Credit: Nature Medicine）Highlights首次人类应用（First-in-Human Application）：这是首次将OMO-103，一种基于Omomyc小蛋白的MYC抑制剂，在人类中进行测试，标志着一个关键的里程碑，即将长期被认为是"不可药物化"（undruggable）的MYC作为潜在的癌症治疗靶标进行临床评估。良好的安全性和耐受性（Good Safety and Tolerability）：OMO-103在治疗晚期实体瘤的患者中表现出良好的安全性和耐受性，大多数不良事件为低等级，这为后续的临床开发提供了积极的安全依据。非线性药代动力学（Non-linear Pharmacokinetics）：OMO-103展示了非线性的药代动力学特性，特别是在更高剂量水平观察到组织饱和现象，这些发现对于理解OMO-103在体内的药效和优化剂量策略具有重要意义。初步疗效迹象（Preliminary Signs of Efficacy）：虽然未达到传统的响应评价标准（Response Evaluation Criteria），但观察到部分患者疾病稳定（Stable Disease, SD），包括一个病例中总肿瘤体积显著减少，表明OMO-103可能对某些癌症患者具有治疗潜力。明确的靶向作用验证（Clear Target Engagement）：通过转录组和蛋白质组学分析验证了OMO-103对MYC的靶向抑制作用，为其作为MYC抑制剂的机制提供了直接的科学支持。潜在生物标志物的发现（Discovery of Potential Biomarkers）：研究中识别出的生物标志物不仅有助于预测对OMO-103治疗的响应，也为监测药物的药效学效果提供了工具，为个性化医疗（Precision Medicine）和治疗决策提供了新的策略。Prospects剂量-效应关系：OMO-103的最佳治疗剂量是多少？是否存在更高效的剂量水平，同时保持良好的安全性和耐受性？长期疗效：OMO-103长期治疗的效果如何？患者在持续治疗后的总体生存期（Overall Survival, OS）和无进展生存期（Progression-Free Survival, PFS）表现如何？治疗反应生物标志物：哪些生物标志物可以准确预测患者对OMO-103治疗的响应？这些生物标志物的应用是否可以帮助个性化治疗方案的制定？机制性抵抗：治疗过程中是否会出现对OMO-103的抵抗机制？如果存在，这些抵抗机制是什么，如何克服？特定癌症类型的疗效：OMO-103在不同类型的实体瘤中的疗效是否存在差异？哪些癌症类型最有可能从OMO-103治疗中获益？与其他治疗方案的组合：OMO-103与现有的治疗方法（如化疗、靶向治疗、免疫治疗）组合使用时的疗效和安全性如何？是否可以通过组合治疗提高疗效？患者生活质量：OMO-103治疗对患者生活质量的影响如何？是否能在控制疾病的同时，保持或提高患者的生活质量？原文链接https://www-nature-com.libproxy1.nus.edu.sg/articles/s41591-024-02805-1Garralda E, Beaulieu ME, Moreno V, Casacuberta-Serra S, Martínez-Martín S, Foradada L, Alonso G, Massó-Vallés D, López-Estévez S, Jauset T, Corral de la Fuente E, Doger B, Hernández T, Perez-Lopez R, Arqués O, Castillo Cano V, Morales J, Whitfield JR, Niewel M, Soucek L, Calvo E. MYC targeting by OMO-103 in solid tumors: a phase 1 trial. Nat Med. 2024 Feb 6. doi: 10.1038/s41591-024-02805-1. Epub ahead of print. PMID: 38321218.责编|探索君排版|探索君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Science最新发布：全世界最前沿的125个科学问题热文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Nature | 癌症与神经系统的致命舞蹈

临床结果临床2期临床1期AACR会议

2023-07-27

·BioSpace

Peptomyc Announces the Approval of Its Phase 1b Trial Testing OMO-103 in Combination With Standard of Care in PDAC Patients

OMO-103 in Phase 1b clinical trial BARCELONA, SPAIN / ACCESSWIRE / July 27, 2023 / Peptomyc S.L., a biotech company specialized in the development of protein therapeutics for cancer treatment, announces that it has received full study approval for its new Phase 1b clinical trial, which will evaluate the combination of the first-in-class MYC inhibitor, OMO103, together with the standard of care (SoC) regimen Gemcitabine and Nab-Paclitaxel in metastatic Pancreatic Ductal Adenocarcinoma (PDAC) patients in first line. PDAC is the most common form of pancreatic cancer. Currently, it is the fourth highest cause of cancer mortality worldwide and its incidence is rising steeply. Current therapies offer limited chance of a lasting cure and the five-year survival rate is one of the lowest among the most commonly occurring cancers. Peptomyc logo Peptomyc logo MYC is an oncoprotein deregulated in most -if not all- types of cancers. It is activated in many PDAC cases, where it contributes to aggressiveness of the disease and resistance to treatments. The company recently completed a FIH Phase 1 study of OMO103 in all-comers solid tumor patients, demonstrating excellent safety and promising anti-tumor activity. Manuela Niewel, MD, PhD, Chief Medical Officer of the company, leading Peptomyc's clinical development, regulatory and medical affairs activities, says: "I am excited to be able to start our new Phase 1b study in PDAC patients. With OMO-103, we hope to address this devastating disease and one of the highest unmet medical needs in the oncology field". This Phase 1b combination study will be conducted in four sites in Spain. The lead PI will be Dr. Teresa Macarulla at the Vall d'Hebron Institute of Oncology in Barcelona, and she will collaborate with Dr. Andres Muñoz at the Hospital Gregorio Marañon in Madrid, Dr. Mariona Calvo at the ICO-Hospitalet in Barcelona, and Dr. Roberto Pazo at the Hospital Miguel Servet in Zaragoza. The study is planned to start in Q3/2023. About Peptomyc Peptomyc ( ) is a spin-off from VHIO - the Vall d'Hebron Institute of Oncology - and ICREA - the Catalan Institute of Research and Advanced Studies - founded in December 2014 in Barcelona, Spain. The company is focused on the development of innovative cell penetrating peptides (CPPs) targeting the Myc oncoprotein for cancer treatment and based on Dr. Soucek's scientific research in Omomyc (the best direct Myc inhibitor known to date) over the last twenty years. It is the first company to have successfully completed a Phase I clinical trial with a direct MYC inhibitor. Contact Information Laura Soucek CEO lsoucek@peptomyc.com +34695207869 SOURCE: Peptomyc SL View source version on accesswire.com:

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适应症	最高研发状态	国家/地区	公司	日期
晚期恶性实体瘤	临床2期	西班牙	Peptomyc SL初创企业	2021-04-28
结直肠癌	临床2期	西班牙	Peptomyc SL初创企业	2021-04-28
胰腺癌	临床2期	西班牙	Peptomyc SL初创企业	2021-04-28
胰腺导管腺癌	临床1期	西班牙	Peptomyc SL初创企业	2023-08-31
胰腺继发性恶性肿瘤	临床1期	西班牙	Peptomyc SL初创企业	2023-08-31

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04808362 (CTgov)	临床1/2期	胰腺癌 \| 晚期恶性实体瘤 \| 结直肠癌	22	OMO-103	製願鑰艱願鏇製膚鏇廠(遞築願觸鹹製顧構構淵) = 製夢鏇鹹積鏇簾遞觸選淵觸積積窪衊衊膚壓餘 (膚積範憲鏇餘構遞觸鏇, 淵醖範夢製繭淵製衊簾 ~ 襯積觸憲顧衊範鹹顧鹹) 更多	-	2024-04-25
NCT04808362 (OMO-103, Pubmed)	临床1期	实体瘤 MYC	22	OMO-103	積鑰積積蓋積繭襯築範(觸齋糧壓製襯糧觸獵蓋) = 膚艱鹽觸齋觸觸艱壓製鬱鹽衊觸築廠顧繭齋鬱 (糧淵醖廠觸衊鏇淵觸繭 ) 更多	积极	2024-03-01
NCT04808362 (ENA2022) 人工标引	临床1期	实体瘤	22	OMO-103	獵獵衊膚膚鬱廠鑰膚齋(鹽膚鹹壓繭構構觸淵製) = 顧艱簾壓夢獵醖餘蓋衊網蓋鑰獵願淵鏇獵鑰鏇 (鏇艱獵選壓蓋積繭顧鹽 ) 更多	积极	2022-11-01