1802977-61-2
Chemical Structure
GNE-140 racemate
- CAS No.: 1802977-61-2
- Formula:C25H23ClN2O3S2
- Molecular Weight:499.04
IUPAC Name: 3-((2-chlorophenyl)thio)-6-(4-morpholinophenyl)-6-(thiophen-3-yl)piperidine-2,4-dione
InChIKey: GLDDJXYFHWRGPI-UHFFFAOYSA-N
SMILES: O=C(C1SC2=CC=CC=C2Cl)NC(C3=CSC=C3)(C4=CC=C(N5CCOCC5)C=C4)CC1=O
Biological Activity: GNE-140 racemate is a racemic mixture of (R)-GNE-140 (HY-100742A) and (S)-GNE-140 (HY-100742B), and also a tautomer of GNE-140 (HY-118241). GNE-140 racemate is an orally active lactate dehydrogenase inhibitor, with an IC50 of 3 nM against human LDHA and an IC50 of 5 nM against LDHB. GNE-140 racemate reduces the phosphorylation level and total protein expression of p38 MAPK, and inhibits EGF-induced AKT phosphorylation. GNE-140 racemate decreases lactate production, regulates glycolysis, the pentose phosphate pathway and nucleotide biosynthesis, increases extracellular pH, inhibits cell proliferation, migration and invasion, and induces caspase-3 activation and ROS accumulation. GNE-140 racemate can be used in research related to breast cancer, cystic fibrosis and pancreatic cancer[1][2][3][4].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
GNE-140 racemate | 99.25% | GNE-140 racemate is a racemic mixture of (R)-GNE-140 (HY-100742A) and (S)-GNE-140 (HY-100742B), and also a tautomer of GNE-140 (HY-118241). GNE-140 racemate is an orally active lactate dehydrogenase inhibitor, with an IC50 of 3 nM against human LDHA and an IC50 of 5 nM against LDHB. GNE-140 racemate reduces the phosphorylation level and total protein expression of p38 MAPK, and inhibits EGF-induced AKT phosphorylation. GNE-140 racemate decreases lactate production, regulates glycolysis, the pentose phosphate pathway and nucleotide biosynthesis, increases extracellular pH, inhibits cell proliferation, migration and invasion, and induces caspase-3 activation and ROS accumulation. GNE-140 racemate can be used in research related to breast cancer, cystic fibrosis and pancreatic cancer. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
|
|
GNE-140 racemate (Standard) | ≥98% | GNE-140 racemate (Standard) is the analytical standard of GNE-140 racemate (HY-100742). This product is intended for research and analytical applications. GNE-140 racemate is a racemic mixture of (R)-GNE-140 (HY-100742A) and (S)-GNE-140 (HY-100742B), and also a tautomer of GNE-140 (HY-118241). GNE-140 racemate is an orally active lactate dehydrogenase inhibitor, with an IC50 of 3 nM against human LDHA and an IC50 of 5 nM against LDHB. GNE-140 racemate reduces the phosphorylation level and total protein expression of p38 MAPK, and inhibits EGF-induced AKT phosphorylation. GNE-140 racemate decreases lactate production, regulates glycolysis, the pentose phosphate pathway and nucleotide biosynthesis, increases extracellular pH, inhibits cell proliferation, migration and invasion, and induces caspase-3 activation and ROS accumulation. GNE-140 racemate can be used in research related to breast cancer, cystic fibrosis and pancreatic cancer. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
- [1]. Khajah MA, et al. The effect of lactate dehydrogenase inhibitors on proliferation, motility and invasion of breast cancer cells highlights a new role for lactate. Molecular medicine reports. 2024 Jan;29(1):12.
- [2]. Valdivieso ÁG, et al. Impairment of CFTR activity in cultured epithelial cells upregulates the expression and activity of LDH resulting in lactic acid hypersecretion. Cellular and molecular life sciences : CMLS. 2019 Apr;76(8):1579-1593. [Content Brief]
- [3]. Boudreau A, et al. Metabolic plasticity underpins innate and acquired resistance to LDHA inhibition. Nature chemical biology. 2016 Oct;12(10):779-86. [Content Brief]
- [4]. Ji JJ, et al. Kallistatin/Serpina3c inhibits cardiac fibrosis after myocardial infarction by regulating glycolysis via Nr4a1 activation. Biochimica et biophysica acta. Molecular basis of disease. 2022 Sep 01;1868(9):166441.
