ZLN005

• CAT Number: I003738
• CAS Number: 49671-76-3
• Molecular Formula: C17H18N2
• Molecular Weight: 250.34
• Purity: ≥95%
• Synonyms: 2-(4-tert-butylphenyl)-1H-benzimidazole
• Target: PGC-1α
• Solubility: DMSO: ≥ 47 mg/mL
• Storage: -20°C
• InChI: InChI=1S/C17H18N2/c1-17(2,3)13-10-8-12(9-11-13)16-18-14-6-4-5-7-15(14)19-16/h4-11H,1-3H3,(H,18,19)
• InChIKey: LQUNNCQSFFKSSK-UHFFFAOYSA-N
• SMILES: CC(C)(C)C1=CC=C(C=C1)C2=NC3=CC=CC=C3N2

ZLN005（Cat No.:I003738）is a small-molecule activator of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), a key regulator of mitochondrial biogenesis and energy metabolism. By enhancing PGC-1α activity, ZLN005 promotes mitochondrial function and fatty acid oxidation, making it a promising compound in metabolic research, particularly for conditions like obesity, type 2 diabetes, and neurodegenerative diseases where energy metabolism is impaired. Its ability to stimulate mitochondrial activity without significant toxicity offers potential therapeutic benefits in improving metabolic health and protecting against diseases linked to mitochondrial dysfunction, highlighting its value in therapeutic development.

Reference

1:Exp Cell Res. 2016 Jul 1;345(1):25-36. doi: 10.1016/j.yexcr.2016.05.012. Epub 2016 May 18. ZLN005 protects cardiomyocytes against high glucose-induced cytotoxicity by promoting SIRT1 expression and autophagy.Li W,Li X,Wang B,Chen Y,Xiao A,Zeng D,Ou D,Yan S,Li W,Zheng Q, PMID: 27208585 DOI: 10.1016/j.yexcr.2016.05.012 Abstract: Diabetic cardiomyopathy increases the risk for the development of heart failure independent of coronary artery disease and hypertension. Either type 1 or type 2 diabetes is often accompanied by varying degrees of hyperglycemia, which has been proven to induce myocardial apoptosis in animal models. Recently, a novel small molecule, ZLN005, has been reported to show antidiabetic efficacy in a mouse model, possibly by induction of PGC-1α expression. In this study, we investigated whether ZLN005 protects cardiomyocytes against high glucose-induced cytotoxicity and the mechanisms involved. Neonatal mouse cardiomyocytes were incubated with media containing 5.5 or 33mM glucose for 24h in the presence or absence of ZLN005. ZLN005 treatment led to ameliorated cardiomyocyte oxidative injury, enhanced cell viability, and reduced apoptosis in the high glucose environment. Western blot analysis revealed that high glucose suppressed cardiomyocyte autophagy, whereas ZLN005 increased the expression of autophagy marker proteins ATG5, beclin1, and LC3 II/LC3 I; this increase was accompanied by increased expression of SIRT1. Furthermore, EX527, a SIRT1-specific inhibitor, weakened the protective effects of ZLN005 on cardiomyocytes subjected to high glucose. Taken together, these results suggest that ZLN005 suppresses high glucose-induced cardiomyocyte injury by promoting SIRT1 expression and autophagy. Copyright © 2016 Elsevier Inc. All rights reserved.