GNE-140 racemate

GNE-140 (200-300 μM) racemate inhibits intracellular LDH activity in pII ER- breast cancer cells^[1].
GNE-140 (200-300 μM) racemate reduces extracellular lactate levels in ER⁻ breast cancer cells^[1].
GNE-140 (0.001-100 μM; 6 h) racemate inhibits LDHA activity in MIA PaCa-2 human pancreatic cancer cells, reducing lactate levels with an IC₅₀ of 0.67 μM and increasing pyruvate levels after 6 hours of treatment^[3].
GNE-140 (2 μM; 24 h) racemate alters global metabolism in MIA PaCa-2 human pancreatic cancer cells treated with 2 μM for 24 hours, increasing levels of glycolytic and pentose phosphate pathway metabolites without substantially affecting oxidative phosphorylation-associated metabolites^[3].
GNE-140 (0.001-100 μM; 6 h) racemate reduces glucose uptake in MIA PaCa-2 human pancreatic cancer cells with an IC₅₀ of 0.47 μM after 6 hours of treatment^[3].
GNE-140 (2 μM; 6 h) racemate redirects glucose carbon flux away from lactate production and toward pyruvate, alanine, and pentose phosphate pathway metabolites in MIA PaCa-2 human pancreatic cancer cells treated with 2 μM for 6 hours, without increasing glutamine-dependent TCA cycle flux^[3].
GNE-140 (72 h) racemate synergizes with AMPK inhibitor, S6K inhibitor, and Phenformin (HY-16397) to reduce viability and shift metabolism away from oxidative phosphorylation in MIA PaCa-2 human pancreatic cancer cells^[3].
GNE-140 (200-300 μM; 4 days) inhibits proliferation of pII ER⁻ breast cancer cells after 4 days of incubation at concentrations of 200 μM and 300 μM, with no effect seen after 1 day of incubation^[1].
GNE-140 (200-300 μM; 24 h) racemate inhibits motility of pII ER- breast cancer cells after 24 h of incubation at concentrations of 200 μM and 300 μM^[1].
GNE-140 (200-300 μM; 48 h) racemate inhibits invasion of pII ER- breast cancer cells after 48 h of incubation at concentrations of 200 μM and 300 μM^[1].
GNE-140 (100-300 μM; 4 days) racemate inhibits proliferation of YS1.2 ER⁺ breast cancer cells after 4 days of incubation at concentrations of 100 μM, 200 μM, and 300 μM, with no effect seen after 1 day of incubation^[1].
GNE-140 (200-300 μM; 24 h) racemate inhibits motility of YS1.2 ER⁺ breast cancer cells after 24 h of incubation at concentrations of 200 μM and 300 μM^[1].
GNE-140 (200 μM; 30 min pre-incubation prior to 30 min EGF stimulation) racemate reduces EGF-induced phosphorylation of p38 MAPK and AKT, and lowers total p38 MAPK levels, in pII ER- breast cancer cells without altering EGF-induced phosphorylation of ERK1/2, Src, or NF-κB^[1].
GNE-140 (0.001-100 μM) racemate inhibits proliferation of MIA PaCa-2 human pancreatic cancer cells with an IC₅₀ of 0.43 μM, with potency dependent on cellular LDHA expression levels^[3].
GNE-140 (72 h) racemate inhibits proliferation of 13% (4/30) of tested human pancreatic cancer cell lines with IC₅₀ values below 5 μM, with sensitive lines relying more on glycolysis (lower baseline OCR) than resistant lines that rely on oxidative phosphorylation^[3].
GNE-140 (200-300 μM; 4 days) racemate inhibits proliferation of MCF10A normal breast epithelial cells after 4 days of incubation at concentrations of 200 μM and 300 μM^[1].
GNE-140 (1 μM; 72 h) racemate increases the extracellular pH of cultured IB3-1 CF lung epithelial cells^[2].
GNE-140 racemate potently inhibits purified human LDHA, LDHB, and LDHC enzymes with nanomolar potency, shows no appreciable inhibition of MDH-1/MDH-2, and is highly selective against a broad panel of kinases^[3].
GNE-140 (2 μM; 1-5 days) racemate induces caspase-3 activation starting at 1-2 days and cell death starting at 3 days in MIA PaCa-2 human pancreatic cancer cells treated with 2 μM, and sustained inhibition for more than 2 days is required to drive irreversible cell death^[3].
GNE-140 (10 μM; 0-48 h) racemate increases reactive oxygen species levels in a time-dependent manner in MIA PaCa-2 human pancreatic cancer cells treated with 10 μM^[3].

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