| CAS |
No.371924-24-2 |
| 英文名称 |
MCU-i4 |
| 分子式 |
C23H27N3O2 |
| 分子量 |
377.48 |
| 溶解性 |
Soluble in DMSO ≥1mg/mL(Need ultrasonic) |
| 纯度 |
≥98% |
| 外观(性状) |
White to yellow Solid |
| 储存条件 |
Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year |
| 运输条件 |
冷藏运输 |
| MDL |
MFCD02730422 |
| SMILES |
CCN(CC)C1=CC=C(C=C1)NC2=C3C=C(C=CC3=NC=C2C(=O)OCC)C |
| InChIKey |
RIWXBJCWHVMATR-UHFFFAOYSA-N |
| InChI |
InChI=1S/C23H27N3O2/c1-5-26(6-2)18-11-9-17(10-12-18)25-22-19-14-16(4)8-13-21(19)24-15-20(22)23(27)28-7-3/h8-15H,5-7H2,1-4H3,(H,24,25) |
| PubChem CID |
1568449 |
| 靶点 |
Calcium Channel |
| 通路 |
Membrane Transporter&Ion Channel;Neuronal Signaling |
| 背景说明 |
MCU-i4阻断IP3 依赖的线粒体 Ca2+ 的摄取,维持靶点的“管家”角色。 |
| 生物活性 |
MCU-i4 blocks the IP3-dependent mitochondrial Ca2+-uptake， maintaining the gatekeeping role of their target[1][2]. |
| In Vitro |
Here， we screen a library of 44，000 non-proprietary compounds for their ability to modulate mitochondrial CA2+ uptake. Two of them， named MCU-i4 and MCU-i11， are confirmed to reliably decrease mitochondrial CA2+ influx. Docking simulations reveal that these molecules directly bind a specific cleft in MICU1， a key element of the MCU complex that controls channel gating. Accordingly， in MICU1-silenced or deleted cells， the inhibitory effect of the two compounds is lost. Moreover， MCU-i4 and MCU-i11 fail to inhibit mitochondrial CA2+ uptake in cells expressing a MICU1 mutated in the critical Amino acids that forge the predicted binding cleft.[1]。Cell Differentiation Assay[1]：Cell Line:Growing medium of 90% confluent C2C12 myoblasts.Concentration:10 μM.Incubation Time: 24 h.Result:Decreased myotube width. |
| 数据来源文献 |
[1]. Giulia Di Marco， et al. A High-Throughput Screening Identifies MICU1 Targeting Compounds. Cell Rep. 2020 Feb 18;30(7):2321-2331.e6.
[2]. Alessandro Rimessi， et al. Update on Calcium Signaling in Cystic Fibrosis Lung Disease. Front Pharmacol. 2021 Mar 11;12:581645. |
| 规格 |
5mg 10mg 25mg 50mg 100mg |
| 单位 |
瓶 |
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