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Peer Reviewed Papers, Books, Chapters

Year Title Citation Authors Review type Summary Keywords File filename File mime type
1. 2010 Continued exploration of the triazolopyridine scaffold as a platform for p38 MAP kinase inhibition Bioorg. Med. Chem. Lett., 2010, 20, 469-473
2. 2009 Discovery of N-substituted pyridinones as potent and selective inhibitors of p38 kinase. Bioorg. Med. Chem. Lett., 2009, 19, 5851-5856.
3. 2009 Advancement of structure-activity relationship of multidrug resistance-associated protein 2 interactions. AAPS J, 2009, 11, 406-413
4. 2009 Homo-timeric structural model of human microsomal prostaglandin E synthase-1 and characterization of its substrate/inhibitor binding interactions J. Comput. Aided. Mol. Des., 2009, 23, 13-24
5. 2009 Sulfoximine-substituted trifluoromethylpyrimidine analogs as inhibitors of proline-rich tyrosine kinase 2 (PYK2) show reduced hERG activity. Bioorg. Med. Chem. Lett., 2009, 19, 3253-3258
6. 2009 2-(6-phenyl-1H-indazol-3-yl)-1H-benzo[d]imidazoles: Design and synthesis of a potent and isoform selective PKC-ζ inhibitor Bioorg. Med. Chem. Lett., 2009, 19, 908-911.
7. 2007 Structure-activity relationships for interaction with multidrug resistance protein 2 (ABCC2/MRP2): The role of torsion angles for a series of biphenyl-substituted heterocycles Drug Metab. Dispos., 2007, 35, 937-945
8. 2004 Evaluation and application of multiple scoring functions for a virtual screening experiment J. Comput. Aided. Mol. Des., 2004, 18, 333-344
9. 2004 Influence of molecular flexibility and polar surface area metrics on oral bioavailability in rat J. Med. Chem., 2004, 47, 6104-6107.
10. 2003 Predicting pKa by molecular tree structured fingerprints and PLS J. Chem. Inf. Comput. Sci., 2003, 43, 870-879
11. 2002 Novel methods for the prediction of logP, pKa, and logD J. Chem. Inf. Comput. Sci., 2002, 42, 796-805
12. 1999 Comparison of estrogen receptor α and β subtypes based on comparative molecular field analysis (CoMFA). SAR QSAR Environ. Res. 1999, 10, 215-237
13. 1999 Comparative molecular field analysis as a tool to evaluate mode of action of chemical hybridization agents J. Agric. Food Chem. 1999, 47, 245-5251
14. 1998 Large internal structures of micelles of triblock copolymers with small insoluble molecules in their cores. Langmuir 1998, 14, 4074-4080
15. 1997 Strong solubilization of small molecules by triblock-copolymer micelles in selective solvents Macromolecules 1997, 30, 1711-1717.
16. 1997 QSAR models for binding of estrogenic compounds to estrogen receptor  and  subtypes Endocrinology 1997, 138, 4022-4025
17. 1997 Geometric properties of micelles formed by triblock copolymers and solubilizates in dilute solutions. Macromol Theory Simul. 1997, 6, 553-563
18. 1996 Atomistic simulations of self-assembled monolayers that contain azobenzene Langmuir 1996, 12, 3024-3030
19. 1995 Simulations of self-assembled monolayers with the same surface density, but different grafting patterns Langmuir 1995, 11, 2103-2108.
20. 1995 Designing packing of photo-responsive molecules to promote surface sensitivity Polym. Mater. Sci. Eng. 1995, 73, 400-401
21. Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Pubmed Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. (-)-Epigallocatechin-3-gallate (EGCG), a major polyphenol in green tea, is widely studied as a cancer chemopreventive agent with potential anti-cancer effects. The NF-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway is considered to mediate cellular resistance to EGCG. Metformin, a classical antidiabetic drug, has been shown to prevent cancer progression. Researchers have not reported whether metformin potentiates the anti-cancer efficacy of EGCG. In this study, metformin inhibited HO-1 expression and augmented the anti-tumor effect of EGCG. Metformin also enhanced ROS (reactive oxygen species) generation induced by EGCG (100 μM), subsequently resulting in apoptosis. Based on the results of the in vivo study, size of xenografts treated with the combination of metformin and EGCG was smaller than other groups. Mechanistically, metformin modulated the EGCG-activated Nrf2/HO-1 pathway through Sirtuin 1 (SIRT1)-dependent deacetylation of Nrf2. Moreover, metformin upregulated SIRT1 expression partially through the NF-kB pathway. Comparatively, the combination of EGCG and metformin showed little impact on normal lung epithelial BEAS-2B cells. Based on our findings, metformin sensitized NSCLC cells to the EGCG treatment by suppressing the Nrf2/HO-1 signaling pathway. 1-(diaminomethylidene)-3; 3-dimethylguanidine (metformin); NF-E2-related factor 2 (Nrf2); epigallocatechin-3-gallate (EGCG); heme oxygenase-1 (HO-1); non-small cell lung cancer (NSCLC)


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