OTX-2002是一种通过脂质纳米颗粒(LNPs)递送的mRNA疗法,旨在通过表观遗传学调控从转录前下调MYC的表达,同时有可能克服MYC的自动调节。 OTX-2002目前正作为单药和与标准治疗--TKI或PD-(L)1抑制剂联合使用,在1/2期MYCHELANGELO I试验(NCT05497453)中对复发或难治性HCC和其他已知与MYC癌基因有关的实体瘤类型患者进...
2022年11月2日,Omega Therapeutics宣布FDA授予旗下OTX-2002孤儿药称号,OTX-2002是一类首个表观基因组控制药物,用于治疗肝细胞癌(HCC)患者。 OTX-2002是一种通过脂质纳米颗粒给予患者的mRNA治疗。该因子通过表观遗传调节在转录前下调MYC表达,同时克服MYC的自动调节。MYC是调节细胞增殖、分化和凋亡的主要转录因子。此外,...
6.肝癌mRNA疗法OTX-2002临床结果积极 9月27日,Omega Therapeutics公布其正在进行的1/2期MYCHELANGELO I试验的初步积极结果。该试验评估其在研mRNA疗法OTX-2002在肝细胞癌(HCC)和其他带有与MYC基因相关实体瘤...
Treatment with OTX-2002 led to controlled downregulation of MYC gene expression and resulted in significant inhibition of tumor growth as a monotherapy and in combination with standard of care agents in preclinical models of HCC Proof-of-concept data for OTX-2002 support potential of epigenomic contr...
基本信息 药品名称 OTX-2002 药品类别 创新药; 生物; 基因疗法; CGT; 难成药靶点; 表观遗传编辑疗法 靶点 c-Myc 作用机制 表观遗传编辑疗法 药品简介 -- 研发机构 Omega Therapeutics 最高研发阶段 全球: I/II期临床 中国: 临床前 审评审批类型 -- 外置链接 -- 了解药物更多情报 登录查看 ...
The publication, titled “Targeted Transcriptional Downregulation of MYC Using Epigenomic Controllers Demonstrates Antitumor Activity in Hepatocellular Carcinoma Models,”describes OTX-2002 and its effects on tumor growth in cellular and animal models of HCC. Treatment with OTX-2002 resulted in the following...
OTX-2002, an Omega Epigenomic Controller (OEC), is designed to downregulate c-Myc (MYC) expression pre-transcriptionally through epigenetic modulation while potentially overcoming MYC autoregulation. “We are thrilled to o...
About OTX-2002 OTX-2002 is an mRNA therapeutic delivered via lipid nanoparticles (LNPs) designed to downregulate MYC expression pre-transcriptionally through epigenetic modulation while potentially overcoming MYC autoregulation. MYC is a master transcription factor that ...
OTX2 expression contributes to proliferation and progression in Myc-amplified medulloblastoma Am. J. Cancer Res., 7 (2017), pp. 647-656 Google Scholar 41 H.M. Itkonen, M. Loda, I.G. Mills O-GlcNAc Transferase - An Auxiliary Factor or a Full-blown Oncogene? Mol. Cancer Res., 19 (202...
dramatically impaired liver regeneration and delayed cell cycle progression. However, the MDIG-deleted liver was eventually restored over a long latency. RNA-seq analysis revealed Myc as a crucial effector downstream of MDIG. However, ATAC-seq identified the reduced chromatin accessibility of OTX2 ...