XAN-5
XAN-5 is a mitochondrial DNA G-quadruplex (mtG4) ligand with a Kd of 3.8 μM. XAN-5 selectively binds and stabilizes mtG4 structures, disrupting mitochondrial gene transcription and DNA replication. XAN-5 triggers mitochondrial dysfunction, ROS overproduction, G0 phase arrest and caspase-dependent apoptosis. XAN-5 inhibits autophagy and induces immunogenic cell death. XAN-5 inhibits tumor growth in a mouse liver cancer model while enhancing tumor-infiltrating CD4+ and CD8+ T cells. XAN-5 targets two cancer resistance mechanisms simultaneously. XAN-5 can be used for the research of liver cancer.
For research use only. We do not sell to patients.
- CAS No.: 3062796-70-4
- Formula: C29H28ClNO7S
- Molecular Weight:570.05
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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Caspase-8 |
Caspase-9 |
Caspase-3 |
Bax |
Bcl-2 |
bad |
XAN-5 (10 μM; 2 h) stabilizes the mtG4 model mt6363 with a ΔTm of 10 °C[1].
XAN-5 (5 μM; 30 min) accumulates selectively in the mitochondria of HepG2 cells[1].
XAN-5 (24 h) potently inhibits proliferation of liver cancer HepG2 cells (IC50 = 1.8 μM), while exhibiting reduced toxicity to normal liver and breast epithelial cells[1].
XAN-5 (1-4 μM; 24 h) significantly reduces transcription of OXPHOS genes ATP6, CYTB, and COX-1 in HepG2 cells[1].
XAN-5 (1-4 μM; 24 h) inhibits mtDNA replication in HepG2 cells in vitro in a dose-dependent manner, reducing D-Loop copy number by 80% at 4 μM[1].
XAN-5 (1-4 μM; 24 h) induces concentration-dependent reactive oxygen species overproduction, mitochondrial membrane potential dissipation and reduces cellular ATP levels in HepG2 cells[1].
XAN-5 (1-4 μM; 24 h) at 1 μM induces G0/G1 phase arrest in HepG2 cells, while 2 and 4 μM progressively increase the sub-G0 apoptotic cell population[1].
XAN-5 (1-4 μM; 24 h) induces dose-dependent apoptosis in HepG2 cells, with 30% Annexin V-positive cells at 4 μM[1].
XAN-5 (1-4 μM; 24 h) inhibits autophagy in HepG2 cells in vitro in a dose-dependent manner, as evidenced by reduced LC3B-II conversion, p62 accumulation, suppressed ATG gene expression, and diminished DAPGreen fluorescence, with this effect mediated by reactive oxygen species[1].
XAN-5 (1-4 μM; 24 h) induces immunogenic cell death in HepG2 cells, as demonstrated by upregulated calreticulin expression, increased cell surface calreticulin, and elevated extracellular ATP levels[1].
XAN-5 (0.25-4 μM; 0-7 days) significantly impairs HepG2 cell migration, colony formation and 3D tumors pheroid growtn in a concentration-dependentmanner[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HepG2 cells
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Concentration:1, 2, 4 μM
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Incubation Time:24 h
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Result:Reduced ATP synthase subunit 6 (ATP6), Cytochrome b (CYTB), and cytochrome c oxidase subunit 1 (COX-1) expression.
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Cell Line:HepG2 cells
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Concentration:1, 2, 4 μM
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Incubation Time:24 h
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Result:Induced G0/G1 phase arrest at 1 μM, increasing the proportion of cells in this phase from 57.9% to 60.9% while decreasing the G2/M phase population from 17.1% to 14.2%.
At 2 and 4 μM, progressively increased the sub-G0 phase (indicative of apoptotic cell death) from 8.9% to 12.2% and finally 30%, respectively.
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Cell Line:HepG2 cells
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Concentration:1, 2, 4 μM
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Incubation Time:24 h
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Result:Led to cytochrome c release from mitochondria, cleavage of caspase-9, caspase-3, and PARP, activation of caspase-8, and cleavage of BID into truncated BID (tBID), confirming activation of both intrinsic (mitochondrial) and extrinsic (death receptor) apoptotic pathways.
Reduced Bcl-2 and Bad levels and increased Bax levels.
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Cell Line:HepG2 cells
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Concentration:1, 2, 4 μM
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Incubation Time:24 h
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Result:Effectively downregulated the LC3B-II/LC3B-I ratio, caused accumulation of p62/SQSTM1, decreased expression of autophagy-related genes (ATG3, ATG5, ATG7, and ATG12), and reduced DAPGreen fluorescence intensity in a dose-dependent manner, indicating impaired autophagosome formation and autophagic flux inhibition.
Reversed by the ROS scavenger N-acetylcysteine, confirming ROS mediation.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 3062796-70-4
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Molecular Weight 570.05
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Formula C29H28ClNO7S
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SMILES
CCN(C1=CC2=[O+]C3=C(CCC/C3=C\C4=CC=CS4)C(C5=CC=CC=C5C(O)=O)=C2C=C1)CC.O=Cl(=O)([O-])=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
XAN-5 Related Classifications
Cat. No.: HY-181599
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- XAN-5
- 3062796-70-4
- XAN5
- XAN 5
- Mitochondrial Metabolism
- DNA/RNA Synthesis
- Reactive Oxygen Species (ROS)
- Apoptosis
- Autophagy
- Caspase
- Bcl-2 Family
- Atg8/LC3
- HepG2 cells
- mitochondrial dysfunction
- mouse liver cancer model
- mtG4
- CD4+ T cells
- reactive oxygen species
- mitochondrial DNA G-quadruplex
- autophagic flux
- CD8+ T cells
- caspase-dependent apoptosis
- Inhibitor
- inhibitor
- inhibit