2003234-63-5
Chemical Structure
(R)-GNE-140
- CAS No.: 2003234-63-5
- Formula:C25H23ClN2O3S2
- Molecular Weight:499.04
IUPAC Name: (R)-3-((2-chlorophenyl)thio)-4-hydroxy-6-(4-morpholinophenyl)-6-(thiophen-3-yl)-5,6-dihydropyridin-2(1H)-one
InChIKey: SUFXXEIVBZJOAP-RUZDIDTESA-N
SMILES: O=C1N[C@@](C2=CSC=C2)(C3=CC=C(N4CCOCC4)C=C3)CC(O)=C1SC5=CC=CC=C5Cl
Biological Activity: (R)-GNE-140 is a potent inhibitor of lactate dehydrogenase (LDH) A, B and C, with IC50 values of 3, 5 and 5 nM against LDHA, LDHB, LDHC, respectively. (R)-GNE-140 blocks the conversion of pyruvate to lactate, reduces lactate production and histone lysine lactylation, and inhibits glycolysis. (R)-GNE-140 attenuates cardiac hypertrophy, alleviates PM2.5-induced pulmonary inflammation and fibrosis, blocks MRSA-induced Arg1 expression. (R)-GNE-140 is applicable to research related to pathological cardiac hypertrophy, pulmonary fibrosis, MRSA infection and pancreatic cancer[1][2][3][4].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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(R)-GNE-140 | 99.73% | (R)-GNE-140 is a potent inhibitor of lactate dehydrogenase (LDH) A, B and C, with IC50 values of 3, 5 and 5 nM against LDHA, LDHB, LDHC, respectively. (R)-GNE-140 blocks the conversion of pyruvate to lactate, reduces lactate production and histone lysine lactylation, and inhibits glycolysis. (R)-GNE-140 attenuates cardiac hypertrophy, alleviates PM2.5-induced pulmonary inflammation and fibrosis, blocks MRSA-induced Arg1 expression. (R)-GNE-140 is applicable to research related to pathological cardiac hypertrophy, pulmonary fibrosis, MRSA infection and pancreatic cancer. | ||||||||||||||||||||
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(R)-GNE-140 (Standard) | ≥98% | (R)-GNE-140 (Standard) is the analytical standard of (R)-GNE-140 (HY-100742A). This product is intended for research and analytical applications. (R)-GNE-140 is a potent inhibitor of lactate dehydrogenase (LDH) A, B and C, with IC50 values of 3, 5 and 5 nM against LDHA, LDHB, LDHC, respectively. (R)-GNE-140 blocks the conversion of pyruvate to lactate, reduces lactate production and histone lysine lactylation, and inhibits glycolysis. (R)-GNE-140 attenuates cardiac hypertrophy, alleviates PM2.5-induced pulmonary inflammation and fibrosis, blocks MRSA-induced Arg1 expression. (R)-GNE-140 is applicable to research related to pathological cardiac hypertrophy, pulmonary fibrosis, MRSA infection and pancreatic cancer. | ||||||||||||||||||||
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References
- [1]. Zhao SS, et al. Lactate regulates pathological cardiac hypertrophy via histone lactylation modification. J Cell Mol Med. 2024;28(16):e70022. [Content Brief]
- [2]. Li J, et al. Urban airborne PM2.5 induces pulmonary fibrosis through triggering glycolysis and subsequent modification of histone lactylation in macrophages. Ecotoxicol Environ Saf. 2024;273:116162. [Content Brief]
- [3]. Ma W, et al. Methylsulfonylmethane protects against lethal dose MRSA-induced sepsis through promoting M2 macrophage polarization. Mol Immunol. 2022;146:69-77. [Content Brief]
- [4]. Purkey HE, et al. Cell Active Hydroxylactam Inhibitors of Human Lactate Dehydrogenase with Oral Bioavailability in Mice. ACS Med Chem Lett. 2016 Aug 26;7(10):896-901. [Content Brief]
