产品
编 号：F225187
分子式：C19H14F2N4O2
分子量：368.34
分子式：C19H14F2N4O2
分子量：368.34
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
50mg
询价
询价
100mg
询价
询价
结构图
CAS No: 1808714-73-9
产品详情
生物活性：
EN6 is a small-molecule in vivo autophagy activator that covalently targets cysteine 277 in the ATP6V1A subunit of the lysosomal v-ATPase. EN6-mediated modification of ATP6V1A uncouples v-ATPase from Rag, leading to inhibition of mTORC1 signalling, increased lysosomal acidification, and activation of autophagy. EN6 also scavenges TDP-43 aggregates (causative agents of frontotemporal dementia) in a lysosome-dependent manner.
体内研究：
EN6 (50 mg/kg; i.p.; single) 在体内抑制 mTORC1 并激活自噬。Animal Model:Six-week-old male C57BL/6 mice.
Dosage:50 mg/kg
Administration:Intraperitoneal injection; single
Result:Significantly inhibited mTORC1 signaling in both skeletal muscle and heart, as demonstrated by reduced phosphorylation of S6, 4EBP1 and ULK1.Strongly activated autophagy as shown by heightened LC3BII levels and reduced p62 levels.
体外研究：
在 HEK293A 细胞中，EN6 (50 μM; 1, 4, 8 h) 增加 LC3BII 的水平，并以时间和剂量依赖的方式触发 LC3 斑点的形成。 EN6 导致 HEK293A 细胞中自噬体和自噬溶酶体数量显著增加。EN6 (25 μM；1 h) 阻断 HEK293A 细胞中的 mTORC1 溶酶体定位和激活。EN6 (50 μM；4 h) 激活 HEK293A 细胞中的 v-ATPase 和溶酶体酸化。EN6 (25 μM；7 h) 促进 IPTG 诱导的 GFP-TDP43 U2OS 骨肉瘤细胞系模型中蛋白质聚集体的自噬清除。
EN6 is a small-molecule in vivo autophagy activator that covalently targets cysteine 277 in the ATP6V1A subunit of the lysosomal v-ATPase. EN6-mediated modification of ATP6V1A uncouples v-ATPase from Rag, leading to inhibition of mTORC1 signalling, increased lysosomal acidification, and activation of autophagy. EN6 also scavenges TDP-43 aggregates (causative agents of frontotemporal dementia) in a lysosome-dependent manner.
体内研究：
EN6 (50 mg/kg; i.p.; single) 在体内抑制 mTORC1 并激活自噬。Animal Model:Six-week-old male C57BL/6 mice.
Dosage:50 mg/kg
Administration:Intraperitoneal injection; single
Result:Significantly inhibited mTORC1 signaling in both skeletal muscle and heart, as demonstrated by reduced phosphorylation of S6, 4EBP1 and ULK1.Strongly activated autophagy as shown by heightened LC3BII levels and reduced p62 levels.
体外研究：
在 HEK293A 细胞中，EN6 (50 μM; 1, 4, 8 h) 增加 LC3BII 的水平，并以时间和剂量依赖的方式触发 LC3 斑点的形成。 EN6 导致 HEK293A 细胞中自噬体和自噬溶酶体数量显著增加。EN6 (25 μM；1 h) 阻断 HEK293A 细胞中的 mTORC1 溶酶体定位和激活。EN6 (50 μM；4 h) 激活 HEK293A 细胞中的 v-ATPase 和溶酶体酸化。EN6 (25 μM；7 h) 促进 IPTG 诱导的 GFP-TDP43 U2OS 骨肉瘤细胞系模型中蛋白质聚集体的自噬清除。
产品资料
Copyright©2015-2024 沪ICP备2022026524号-1
沪公网安备