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Chemical Structure| 371924-24-2 Chemical Structure| 371924-24-2

Structure of MCU-i4
CAS No.: 371924-24-2

Chemical Structure| 371924-24-2

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MCU i4 is a negative modulator of mitochondrial calcium (Ca2+) uniporter (MCU) complex, which binds to MICU1, a regulatory protein within MCU complex. MCU i4 reduces mitochondrial Ca2+ uptake in multiple cell lines including MEFs, MDA-MB,231 and HEK293T cells, and demonstrates a negative effect on mitochondrial membrane potential.

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Product Details of MCU-i4

CAS No. :371924-24-2
Formula : C23H27N3O2
M.W : 377.48
SMILES Code : O=C(C1=C(NC2=CC=C(N(CC)CC)C=C2)C3=CC(C)=CC=C3N=C1)OCC
MDL No. :MFCD02730422
InChI Key :RIWXBJCWHVMATR-UHFFFAOYSA-N
Pubchem ID :1568449

Safety of MCU-i4

GHS Pictogram:
Signal Word:Warning
Hazard Statements:H315-H319
Precautionary Statements:P264-P280-P302+P352-P305+P351+P338-P332+P313-P337+P313-P362

Isoform Comparison

Biological Activity

In Vitro:

Cell Line
Concentration Treated Time Description References
Mouse primary cortical neurons PCNs 2.5 µM 18 hours MCU-i4 prevented RSL3-induced neuronal network loss, indicating its protective role in neurons under ferroptotic conditions. Cell Death Dis. 2023 Nov 25;14(11):772
Human dopaminergic neurons LUHMES cells 1 µM 6 hours MCU-i4 prevented RSL3-induced neuronal network degeneration, demonstrating that negative modulation of MCU complex could prevent dopaminergic cell death in ferroptotic conditions. Cell Death Dis. 2023 Nov 25;14(11):772
HT22 cells 500 nM –5 µM MCU-i4 prevented RSL3-induced cell death in a concentration-dependent manner and reversed major ferroptotic cellular hallmarks. Cell Death Dis. 2023 Nov 25;14(11):772
mouse MII oocytes 2 μM 2 hours To evaluate the effect of MICU1 modulators on mitochondrial activity and developmental competence of MII oocytes. Results showed that MCU-i4 treatment significantly increased mitochondrial calcium concentration and ATP levels. Int J Mol Sci. 2022 Aug 3;23(15):8629
Breast cancer BT474 cells 3-30 μM 48 hours MCU-i4 induced apoptotic cell death, decreased mitochondrial Ca2+ concentration, increased cytosolic Ca2+ concentration, enhanced glycolysis and ATP production, and triggered a large production of reactive oxygen species (ROS) and mitochondrial membrane potential collapse Oncol Res. 2025 Jan 16;33(2):397-406

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