PubMed · 579267
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J Wójcicki, J Pieczyl-Mróz, M Ilnicka-Madry, H Cwajda. 1977-10-01. [Cynarin and hyperlipidemia].. https://pubmed.ncbi.nlm.nih.gov/579267/
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A Pseudomonas putida S12 strain was constructed that is able to convert glucose to p-coumarate via the central metabolite L: -tyrosine. Efficient production was hampered by product degradation, limited cellular L: -tyrosine availability, and formation of the by-product cinnamate via L: -phenylalanine. The production host was optimized by inactivation of fcs, the gene encoding the first enzyme in the p-coumarate degradation pathway in P. putida, followed by construction of a phenylalanine-auxotrophic mutant. These steps resulted in a P. putida S12 strain that showed dramatically enhanced production characteristics with controlled L: -phenylalanine feeding. During fed-batch cultivation, 10 mM (1.7 g l(-1)) of p-coumarate was produced from glucose with a yield of 3.8 Cmol% and a molar ratio of p-coumarate to cinnamate of 85:1.
A group of tri and tetrasubstituted urea derivatives have been found to be hH(3)-antagonists. The most potent compounds were found in the class of (piperazine-1-yl)-(piperidine-1-yl)-methanones which in addition showed negligible hERG inhibition.
PPAR ligands with varied subtype selectivity have been synthesized using an achiral aminomethyl dihydrocinnamate template. Several compounds in this series have demonstrated potent plasma glucose and triglyceride lowering capability in rodent models of type 2 diabetes.