1. Metabolic Enzyme/Protease PI3K/Akt/mTOR Epigenetics Apoptosis Autophagy
  2. Mitochondrial Metabolism AMPK mTOR Apoptosis Autophagy
  3. Mitochondrial complex I-IN-1

Mitochondrial complex I-IN-1 is a Mitochondrial complex I inhibitor. Mitochondrial complex I-IN-1 activates the AMPK signaling pathway, inhibits the downstream mTOR/S6 axis, induces Apoptosis and triggers Autophagy. Mitochondrial complex I-IN-1 can be used for the research of non-small cell lung cancer.

For research use only. We do not sell to patients.

Mitochondrial complex I-IN-1

Mitochondrial complex I-IN-1 Chemical Structure

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Description

Mitochondrial complex I-IN-1 is a Mitochondrial complex I inhibitor. Mitochondrial complex I-IN-1 activates the AMPK signaling pathway, inhibits the downstream mTOR/S6 axis, induces Apoptosis and triggers Autophagy. Mitochondrial complex I-IN-1 can be used for the research of non-small cell lung cancer[1].

In Vitro

Mitochondrial complex I-IN-1 (Compound IV-16) (0.0001-10 μM; 72 h) potently inhibits the proliferation of non-small cell lung cancer A549 cells with an IC50 of 0.43 μM, while exhibits low cytotoxicity against non-small cell lung cancer H1299 cells and renal proximal tubular epithelial HK2 cells[1].
Mitochondrial complex I-IN-1 (3 μM; 2-72 h) potently inhibits the migration of A549 cells in a time-dependent manner[1].
Mitochondrial complex I-IN-1 (3 μM; 24 h) effectively induces apoptosis in A549 cells[1].
Mitochondrial complex I-IN-1 (3 μM; 8 h) strongly induces autophagy in A549 cells, and its response is more significant than that of the reference compound DBI-2[1].
Mitochondrial complex I-IN-1 (1-3 μM) activates the AMPK signaling pathway, inhibits the downstream mTOR/S6 axis, and enhances autophagy in A549 cells in a dose-dependent manner; at a concentration of 3 μM, it exhibits stronger potency than the reference compound DBI-2 (HY-162516)[1].
Mitochondrial complex I-IN-1 specifically inhibits mitochondrial complex I in A549 cells, and this is supported by evidence that succinate supplementation restores the suppressed OCR[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[1]

Cell Line: A549
Concentration: 1 μM, 3 μM
Incubation Time: Not specified
Result: Significantly altered the phosphor-
ylation status of mTOR pathway effectors and the conversion of auto-
phagy markers in a dose-dependent manner.
Markedly upregulated the p-AMPK/AMPK ratio.
Molecular Weight

514.61

Formula

C31H34N2O5

SMILES

O=C1C(C2=CC=C(OC3=CC=CC=C3)C=C2)=COC4=C1C=CC(OCCCCN5CCN(CCO)CC5)=C4

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Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Product Name:
Mitochondrial complex I-IN-1
Cat. No.:
HY-184282
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