ATP Synthesis-IN-4

ATP Synthesis-IN-4 (48 h) potently inhibits proliferation of malignant melanoma cell lines A375, SK-MEL-2, and A2058 with IC₅₀ values of 7.0 ± 0.41 μM, 8.0 ± 2.0 μM, and 16.8 ± 0.7 μM respectively, and shows low toxicity to noncancerous BJ skin fibroblasts (IC₅₀ >50 μM)^[1].
ATP Synthesis-IN-4 (1 μM; 20 min) is selectively localized to the mitochondria of live A375 cells, with no significant localization to the nucleus, lysosomes, or endoplasmic reticulum^[1].
ATP Synthesis-IN-4 (3.5-7 μM; 60 min) disrupts mitochondrial membrane potential in A375 cells in vitro in a concentration-dependent manner^[1].
ATP Synthesis-IN-4 (1 μM; 20 min) delivery to mitochondria in A375 cells is primarily dependent on mitochondrial membrane potential, as FCCP-induced MMP reduction inhibits its uptake, while CsA-mediated mPTP blockade does not^[1].
ATP Synthesis-IN-4 (5 μM; 1 min shaking, RT incubation) selectively binds to mtDNA G4 structures in vitro with high affinity (K_d 0.65−1.28 μM for top targets), showing far weaker binding to non-G4 DNA substrates^[1].
ATP Synthesis-IN-4 (3.5-7 μM; 48 h) downregulates expression of mitochondrial respiratory chain-related genes in A375 cells in a concentration-dependent manner (7 μM treatment reduces mRNA levels by ≥75% after 48 h) without affecting nuclear G4-associated genes KRAS and VEGF^[1].
ATP Synthesis-IN-4 (3.5-7 μM; 48 h) inhibits translation of key mitochondrial respiratory chain proteins (CYTB, ATP8, COX1, COX3, ND2) and downregulates OXPHOS complex expression in A375 cells, while activating AMPK phosphorylation^[1].
ATP Synthesis-IN-4 (3.5-7 μM; 2 h) impairs mitochondrial oxidative phosphorylation in A375 cells, reducing ATP production by ~83% (3.5 μM) and ~98% (7 μM) after 2 h treatment, while upregulating glycolysis in a concentration-dependent manner^[1].
ATP Synthesis-IN-4 (3.5-7 μM; 48 h) arrests A375 melanoma cells in the S phase of the cell cycle^[1].
ATP Synthesis-IN-4 (1.75 μM; 48 h) shows synergistic antiproliferative activity with 0.2 μM Vemurafenib against A375 cells (CI=0.67), reducing the IC₅₀ of ATP Synthesis-IN-4 to 0.63 ± 0.2 μM after 48 h treatment^[1].
ATP Synthesis-IN-4 (1.75 μM; 72 h), when combined with 0.2 μM Vemurafenib for 72 h, induces acute cellular senescence in A375 melanoma cells, as indicated by strong SA-β-galactosidase activity and enlarged cell morphology^[1].

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