XAN-5 

XAN-5 is a mitochondrial DNA G-quadruplex (mtG4) ligand with a K_d 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^[1].

XAN-5 (10 μM; 2 h) stabilizes the mtG4 model mt6363 with a ΔT_m 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.

XAN-5 (10 mg/kg; every 48 h for 6 days) induces a 59% reduction in tumor volume in a BALB/c mouse H22 liver cancer model, inhibits tumor cell proliferation, enhances tumor-infiltrating and splenic CD4⁺ and CD8⁺ T cell frequencies, and exhibits no observable systemic toxicity at the tested dose^[1].

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

570.05

C₂₉H₂₈ClNO₇S

3062796-70-4

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

Room temperature in continental US; may vary elsewhere.

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

• [1]. Wang R, et al. Novel Tetrahydroxanthylium-Based Ligands Targeting Mitochondrial DNA G-Quadruplex Structures for Concurrent Induction of Apoptosis and Inhibition of Autophagy in Liver Cancer. J Med Chem. 2026;69(3):2685-2702.  [Content Brief]