Azepino[4,5-b]indoles have been identified as potent agonists of the farnesoid X receptor (FXR). In vitro and in vivo optimization has led to the discovery of 6m (XL335, WAY-362450) as a potent, selective, and orally bioavailable FXR agonist (EC(50) = 4 nM, Eff = 149%). Oral administration of 6m to LDLR(-/-) mice results in lowering of cholesterol and triglycerides. Chronic administration in an atherosclerosis model results in significant reduction in aortic arch lesions.

2-Amino-2-methyl-1-propanol (AMP) and the blends of AMP with other amines appear to be commercially attractive solvents for postcombustion CO 2 capture by absorption/stripping. Oxidative degradation experiments involving AMP aqueous solutions were performed in a 200 mL glass batch reactor with initial AMP concentrations of 5 mol•kg −1 , oxygen partial pressures of 250−350 kPa, and at temperatures of 100−140 °C in order to elucidate the degradation mechanistic pathways. The amine loss was determined by cation ion chromatography (IC), while the degradation compounds were identified and quantified by gas chromatography−mass spectrometry (GC−MS) and anion IC. The possible chemical pathways of AMP oxidative degradation are proposed on the basis of the identified and quantified products and the context of the current amine degradation schemes. The role of O 2 in the proposed pathways is much more explicit than the previously proposed MEA oxidation mechanisms.

Acidovorax citrulli is a seed-borne pathogen causing bacterial fruit blotch of cucurbits including melon and watermelon. We investigated the roles of quorum sensing in the wild-type group II strain Aac-5 of A. citrulli by generating aacR and aacI knockout mutants and their complementation strains. We found that twitching motility and virulence were reduced, but biofilm formation and seed attachment were increased significantly in the two mutants as compared to the wild type strain. Deletion of aacR and aacI, however, had no effect on swimming motility and polar flagella formation of Aac-5. Furthermore, deletion of aacR resulted in reduced gene expression of hrpE, hrcN and pilT, while deletion of aacI affected only the expression of hrpE and pilT, not hrcN.