1839150-63-8
1839150-63-8 結構式
基本信息
1,1'-(((乙烷-1,2-二基雙(氧基))雙(4,1-亞苯基))雙(亞甲基))雙(4-(二甲氨基)吡啶-1-鎓)溴化物
1,1'-(((乙烷-1,2-二基雙(氧基))雙(4,1-亞苯基))雙(亞甲基))雙(4-(二甲氨基)吡啶-1-鎓)溴化物
ChoK inhibitor EB-3D
物理化學性質
| 報價日期 | 產品編號 | 產品名稱 | CAS號 | 包裝 | 價格 |
| 2026/06/05 | HY-115463 | EB-3D EB-3D | 1839150-63-8 | 5mg | 1900元 |
| 2026/06/05 | HY-115463 | EB-3D EB-3D | 1839150-63-8 | 10mM * 1mLin DMSO | 2694元 |
| 2026/06/05 | HY-115463 | EB-3D EB-3D | 1839150-63-8 | 10mg | 3000元 |
常見問題列表
| Target | Value |
|
ChoKα1
(Cell-free assay) | 1 μM |
EB-3D displays (0-100 μM; 72 hours) excellent antiproliferative activity against a wide cohort of T-leukemic cell lines, with GI GI
50
s 13 values in the nanomolar range.
EB-3D (1.25-5μM; 24 hours) induced apoptosis in leukemia cell lines.
EB-3D (0.5-1 μM; 24 hours) induces a G0/G1 arrest that lead to apoptosis.
EB-3D (0.3 μM; 48 hours) shows a first spike of activation of AMPKα after 30 minutes and a later increase in the phosphorylation of T172.
EB-3D (1-40 μM; 48?hours) inhibits cell growth in HepG2 cells with a GI
50
of 14.55 μM.
EB-3D induces deregulation of the AMPK-mTOR pathway and apoptosis in leukemia T-cells.
Cell Proliferation Assay
| Cell Line: | JURKAT, CCRF-CEM, HSB-2, MOLT-16, DNA-41, LOUCY, PEER, ALL-SIL cells |
| Concentration: | 0.001, 0.01, 0.1, 1, 10, 100 μM |
| Incubation Time: | 72 hours |
| Result: | Inhibited JURKAT, CCRF-CEM, HSB-2, MOLT-16, DNA-41, LOUCY, PEER, and ALL-SIL cells growth with GI 50 s of 136.2, 478.8, 17.7, 0.9, 60.6, 200, 265, and 132 nM, respectively. |
Apoptosis Analysis
| Cell Line: | Jurkat, CCRF-CEM and HSB-2 cells |
| Concentration: | 1.25, 2.5, 5 μM |
| Incubation Time: | 24 hours |
| Result: | Induced apoptosis in leukemia cell lines. |
Cell Cycle Analysis
| Cell Line: | Jurkat, CCRF-CEM and HSB-2 cells |
| Concentration: | 0.5, 1 μM |
| Incubation Time: | 24 hours |
| Result: | Induces cell cycle arrest in G0/G1 phase. |
Western Blot Analysis
| Cell Line: | Jurkat cells |
| Concentration: | 0.3 μM |
| Incubation Time: | 48 hours |
| Result: | Showed a first spike of activation of AMPKα after 30 minutes of treatment and a later increase in the phosphorylation of T172. The increase in S79 phosphorylation of its main target ACC (acetyl-coenzyme A (CoA) carboxylase), followed the same pattern. This rapid activation of AMPK, in turn induced a consequent reduction in mTOR phosphorylation that is visible already at 30’ and that becomes amplified at longer time probably due to the interruption of feedback loops that are characteristic of mTOR connecting pathways. |
EB-3D (1 mg/kg; i.p.; every other day) impairs mammary tumor growth in syngeneic orthotopic E0771-C57BL/6 mouse model.
EB-3D (2.5 mg/kg; every other day for 4 weeks) shows a reduction of the number of spontaneous lung macro- and micrometastasis.
| Animal Model: | E0771-C57BL/6 mice |
| Dosage: | I.p.; every other day for 4 weeks |
| Administration: | 2.5 mg/kg |
| Result: | A reduction of the number of spontaneous lung macro- and micrometastasis. |