Delving into the Latest Updates on ZeCardio Therapeutics with Synapse

概览

疾病领域	数量

肿瘤	5

排名前五的药物类型	数量

小分子化药	5

关联

5

项与 ZeCardio Therapeutics 相关的药物

ZC-003

靶点-

作用机制-

在研机构

ZeCardio Therapeutics

原研机构

ZeCardio Therapeutics

在研适应症

肿瘤

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期-

ZC-002

靶点-

作用机制-

在研机构

ZeCardio Therapeutics

原研机构

ZeCardio Therapeutics

在研适应症

肿瘤

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期-

ZC-004

靶点-

作用机制-

在研机构

ZeCardio Therapeutics

原研机构

ZeCardio Therapeutics

在研适应症

肿瘤

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期-

100 项与 ZeCardio Therapeutics 相关的临床结果

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0 项与 ZeCardio Therapeutics 相关的专利（医药）

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2

项与 ZeCardio Therapeutics 相关的文献（医药）

Phenotypic impact of individual conserved neuronal microexons and their master regulators in zebrafish

作者: Mackensen, Tahnee ; Cuadrado, Myriam ; de Polavieja, Gonzalo G ; Irimia, Manuel ; Fernandez-Albert, Jordi ; Permanyer, Jon ; Bustelo, Xosé R ; Iñiguez, Luis P ; Kita, Elizabeth M ; Mantica, Federica ; Rodríguez-Marin, Cristina ; Romero-Ferrero, Francisco ; Lopez-Blanch, Laura ; Codina-Tobias, Mireia

Microexons exhibit striking evolutionary conservation and are subject to precise, switch-like regulation in neurons, orchestrated by the splicing factors Srrm3 and Srrm4 . Disruption of these regulators in mice leads to severe neurological phenotypes, and their misregulation is linked to human disease. However, the specific microexons involved in these phenotypes and the effects of individual microexon deletions on neurodevelopment, physiology, and behavior remain poorly understood. To explore this, we generated zebrafish lines with deletions of 18 individual microexons, alongside srrm3 and srrm4 mutant lines, and conducted comprehensive phenotypic analyses. We discovered that while loss of srrm3 , alone or together with srrm4 , resulted in significant alterations in neuritogenesis, locomotion, and social behavior, individual microexon deletions typically produced mild or no noticeable effects. Nonetheless, we identified specific microexons associated with defects in neuritogenesis ( evi5b , vav2 , itsn1 , src ) and social behavior ( vti1a , kif1b ). Additionally, microexon deletions triggered coordinated transcriptomic changes in neural pathways, suggesting the presence of molecular compensatory mechanisms. Our findings suggest that the severe phenotypes caused by Srrm3/4 depletion arise from the combined effects of multiple subtle disruptions across various cellular pathways, which are individually well-tolerated.

Phenotypic impact of individual conserved neuronal microexons and their master regulators in zebrafish

作者: Mackensen, Tahnee ; Cuadrado, Myriam ; de Polavieja, Gonzalo G ; Irimia, Manuel ; Fernandez-Albert, Jordi ; Permanyer, Jon ; Bustelo, Xosé R ; Iñiguez, Luis P ; Kita, Elizabeth M ; Mantica, Federica ; Rodríguez-Marin, Cristina ; Romero-Ferrero, Francisco ; Lopez-Blanch, Laura ; Codina-Tobias, Mireia

Microexons exhibit striking evolutionary conservation and are subject to precise, switch-like regulation in neurons, orchestrated by the splicing factors Srrm3 and Srrm4 . Disruption of these regulators in mice leads to severe neurological phenotypes, and their misregulation is linked to human disease. However, the specific microexons involved in these phenotypes and the effects of individual microexon deletions on neurodevelopment, physiology, and behavior remain poorly understood. To explore this, we generated zebrafish lines with deletions of 18 individual microexons, alongside srrm3 and srrm4 mutant lines, and conducted comprehensive phenotypic analyses. We discovered that while loss of srrm3 , alone or together with srrm4 , resulted in significant alterations in neuritogenesis, locomotion, and social behavior, individual microexon deletions typically produced mild or no noticeable effects. Nonetheless, we identified specific microexons associated with defects in neuritogenesis ( evi5b , vav2 , itsn1 , src ) and social behavior ( vti1a , kif1b ). Additionally, microexon deletions triggered coordinated transcriptomic changes in neural pathways, suggesting the presence of molecular compensatory mechanisms. Our findings suggest that the severe phenotypes caused by Srrm3/4 depletion arise from the combined effects of multiple subtle disruptions across various cellular pathways, which are individually well-tolerated.

100 项与 ZeCardio Therapeutics 相关的药物交易

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100 项与 ZeCardio Therapeutics 相关的转化医学

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管线布局

2025年05月31日管线快照

管线布局中药物为当前组织机构及其子机构作为药物机构进行统计，早期临床1期并入临床1期，临床1/2期并入临床2期，临床2/3期并入临床3期

药物发现

5

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当前项目

药物(靶点)	适应症	全球最高研发状态

ZC-001	肿瘤更多	药物发现
ZC-003	肿瘤更多	药物发现
ZC-002	肿瘤更多	药物发现
ZC-005	肿瘤更多	药物发现
ZC-004	肿瘤更多	药物发现