2. Immunology/Inflammation NF-κB Metabolic Enzyme/Protease Apoptosis
  3. Reactive Oxygen Species (ROS) Apoptosis Mitochondrial Metabolism
  4. Mito-DHH chloride

Mito-DHH chloride is a mitochondria-targeted catechol-type diphenylhexatriene. Mito-DHH chloride rapidly accumulates in mitochondria and undergoes auto-oxidation in the alkaline mitochondrial matrix to generate ROS. Mito-DHH chloride triggers ROS-dependent reduction of ATP levels via dual inhibition of mitochondrial oxidative phosphorylation and glycolytic metabolism, and induces selective apoptosis in cancer cells. Mito-DHH chloride can be used in research related to lung cancer, liver cancer, malignant melanoma, and colon cancer.

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Mito-DHH chloride

Mito-DHH chloride Chemical Structure

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Mito-DHH chloride Related Antibodies

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Description

Mito-DHH chloride is a mitochondria-targeted catechol-type diphenylhexatriene. Mito-DHH chloride rapidly accumulates in mitochondria and undergoes auto-oxidation in the alkaline mitochondrial matrix to generate ROS. Mito-DHH chloride triggers ROS-dependent reduction of ATP levels via dual inhibition of mitochondrial oxidative phosphorylation and glycolytic metabolism, and induces selective apoptosis in cancer cells. Mito-DHH chloride can be used in research related to lung cancer, liver cancer, malignant melanoma, and colon cancer[1].

In Vitro

Mito-DHH (0.25-2.8 μM; 48 h) potently and selectively kills A549, HepG2, A375, and SW620 cancer cells over normal L02 cells, with the highest potency against A549 cells (IC50 = 0.25 μM) and a selectivity index of 11.2[1].
Mito-DHH (0.25-0.5 μM; 10 days) impairs long-term clonogenic survival of A549 cells at concentrations of 0.25 μM and 0.5 μM[1].
Mito-DHH (1 μM; 0.5-3 h) rapidly and selectively accumulates in the mitochondria of A549 cells within 0.5 h, with minimal enrichment in L02 cell mitochondria[1].
Mito-DHH (50 μM; 2 h) under alkaline conditions (pH 8 and 10) promotes auto-oxidation to generate reactive oxygen species, with more robust ROS production at higher pH[1].
Mito-DHH (1 μM; 2 h) preferentially induces mitochondrial superoxide anion generation in A549 cells over L02 cells after 2 h of treatment[1].
Mito-DHH (1 μM; 3 h) preferentially induces intracellular hydroxyl radical generation in A549 cells over L02 cells after 3 h of treatment[1].
Mito-DHH (1-2 μM; 6-12 h) induces a ROS-dependent reduction in ATP production in A549 cells after 6 and 12 h, with no effect on ATP levels in L02 cells at 10 μM[1].
Mito-DHH (2 μM; 5 h) inhibits both mitochondrial oxidative phosphorylation and cytoplasmic glycolysis in A549 cells after 5 h of treatment, inducing a dual-effect energy crisis[1].
Mito-DHH (1-2 μM; 18-24 h) preferentially disrupts mitochondrial membrane potential in A549 cells after 18 and 24 h of treatment, with no effect on L02 cells[1].
Mito-DHH (10 μM; 1-12 h) induces late-stage apoptosis in A549 cells, with detectable PI nuclear localization starting at 6 h and progressing over time[1].
Mito-DHH (1-2 μM; 48 h) preferentially induces apoptosis in A549 cells over L02 cells after 48 h of treatment[1].
Mito-DHH (1-2 μM; 24 h) preferentially induces G0/G1 cell cycle arrest in A549 cells over L02 cells after 24 h of treatment[1].

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

Mito-DHH chloride Related Antibodies

Cell Proliferation Assay[1]

Cell Line: human lung cancer A549 cells
Concentration: 0.25 μM; 0.5 μM
Incubation Time: 10 days, with medium replacement every 48 h
Result: Significantly suppressed clonogenic survival, with colony counts of 83.5 (0.25 μM) and 61 (0.5 μM), compared to 138.8 in the control group.

Immunofluorescence[1]

Cell Line: human lung cancer A549 cells, normal human liver L02 cells
Concentration: 1 μM
Incubation Time: 0.5 h; 3 h
Result: Showed strong overlap with MitoTracker Deep Red in A549 cells, with a Pearson's colocalization coefficient of 0.91 at 0.5 h, indicating full mitochondrial localization within 30 min.
Displayed limited mitochondrial enrichment in L02 cells.

Apoptosis Analysis[1]

Cell Line: human lung cancer A549 cells
Concentration: 10 μM
Incubation Time: 1 h, 6 h, 9 h, 12 h
Result: Showed no PI nuclear localization at 1 h; exhibited prominent red fluorescence (PI entry) in nuclei at 6 h, indicating late-stage apoptosis, with nearly complete PI nuclear localization after longer incubation.

Apoptosis Analysis[1]

Cell Line: human lung cancer A549 cells, normal human liver L02 cells
Concentration: 1 μM, 2 μM
Incubation Time: 48 h
Result: Induced significant apoptosis in A549 cells, with 14.5% early apoptosis and 49.0% late apoptosis at 2 μM.
Induced no significant apoptosis in L02 cells.

Cell Cycle Analysis[1]

Cell Line: human lung cancer A549 cells, normal human liver L02 cells
Concentration: 1 μM, 2 μM
Incubation Time: 24 h
Result: Arrested the cell cycle of A549 cells at the G0/G1 phase, with no significant effect on L02 cell cycle distribution.
Molecular Weight

633.15

Formula

C40H38ClO3P
SMILES

OC1=CC=C(/C=C/C=C/C=C/C2=CC=C(OCCCC[P+](C3=CC=CC=C3)(C4=CC=CC=C4)C5=CC=CC=C5)C=C2)C=C1O.[Cl-]
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Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
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Mito-DHH chloride Related Classifications

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  • Do most proteins show cross-species activity?

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Keywords:

Mito-DHHReactive Oxygen Species (ROS)ApoptosisMitochondrial Metabolismreactive oxygen speciesmalignant melanomaliver cancermitochondriaoxidative phosphorylationlung cancerglycolytic metabolismATP synthesisapoptosiscolon cancerInhibitorinhibitorinhibit

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