KH176m

KH176m (1 μM; 24 h) selectively reduces elevated levels of PGE₂, PGE₁, and PGA₂ in primary human dermal fibroblasts from patients with mitochondrial complex I deficiency, without altering levels of PGD₂ or PGF₂α^[1].
KH176m (72 h) dose-dependently reduces PGE₂ levels in primary human skin fibroblasts from patients with mitochondrial complex I deficiency, with an IC₅₀ of 85.3 nM^[1].
KH176m (24 h) dose-dependently and selectively inhibits LPS (HY-D1056)-induced PGE₂ production in primary human dermal fibroblasts from healthy donors and RAW264.7 cells, with IC₅₀ values of 92.9 nM and 0.56 nM, respectively, without altering PGD₂ levels^[1].
KH176m (24 h) dose-dependently and selectively inhibits IL-1β-induced PGE₂ production in primary dermal fibroblasts from healthy humans, with an IC₅₀ of 0.28 μM after 24 h of incubation, without altering the level of PGD₂^[1].
KH176m (15 min) inhibits the enzymatic activity of mPGES-1 in lipopolysaccharide (LPS)-stimulated mouse macrophage-like RAW264.7 cells and microsomes of healthy primary human dermal fibroblasts, with IC₅₀ values of 0.16 μM and 1.51 μM, respectively^[1].
KH176m (1-10 μM; 6-24 h) dose-dependently inhibits the expression of mPGES-1 protein and mRNA in LPS- and IL-1β-induced mouse macrophage-like RAW264.7 cells, without altering the expression of COX-2, mPGES-2, cPGES or COX-1^[1].
KH176m (0.62-5 µM; 2 min injection, 4 min dissociation) binds directly to purified recombinant human Prdx2 with a K_D value of 0.305 µM, whereas KH176 shows no dose-dependent binding to Prdx2^[3].
KH176m (1-10 μM; 24 h) dose-dependently reduces the expression of constitutive mPGES-1 protein in two-dimensionally cultured DU145 human prostate cancer cells and induces a decrease in spheroid size^[2].
KH176m (0.3-3 μM; 7 days) dose-dependently reduces the sphere size and mPGES-1 mRNA expression of CD44⁺ CD24⁻ cancer stem cells isolated from DU145 human prostate cancer cells cultured in Matrigel or ultra-low attachment plates for 7 days^[2].
KH176m (0.3-3 μM; 7 days) reduces the proportion of CD44⁺ CD24⁻ cancer stem cells in Matrigel-cultured human prostate cancer DU145 spheroids in a dose-dependent manner^[2].
KH176m (3.2-88 nM; 24 h) potently protects complex I-deficient P4 primary human skin fibroblasts and a variety of other oxidative phosphorylation (OXPHOS)-deficient primary human skin fibroblasts against BSO (HY-106376)-induced death, with an EC₅₀ value as low as 3.2 nM^[3].
KH176m (255 nM; 24 h) potently reduces ROS levels in complex I-deficient P4 primary human skin fibroblasts, with an IC₅₀ of 255 nM^[3].
KH176m (3 µM) effectively scavenges hydrogen peroxide and superoxide anion in complex I-deficient P4 primary human skin fibroblasts^[3].
KH176m (24 h) potently reduces the basal cytoplasmic superoxide level in complex I-deficient P4 primary human skin fibroblasts, with an EC₅₀ of 1.7 µM^[3].
KH176m (30 min) potently inhibits cumene hydroperoxide-induced lipid peroxidation in complex I-deficient P4 primary human skin fibroblasts, with an IC₅₀ of 0.71 µM^[3].
KH176m (30 min) potently reduces mitochondrial superoxide levels in complex I-deficient P4 primary human skin fibroblasts, with an IC₅₀ of 14 µM^[3].

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