88336-89-4

Upstream product

• 5581-75-9 6-phenylhexanic acid 
• 21389-46-8 6-phenylhexanoyl chloride 
• 88343-63-9 2-(6-phenyl-1-oxohexyl)thiophene 

Downstream Products

• 88336-90-7 2-[3(RS)-methyl-1-oxo-5-hydroxypentanoyl]-5-(6-phenylhexyl)thiophene 
• 90046-93-8 2-(3(R,S)-Methyl-1-oxo-4-carbomethoxybutyl)-5-(6-phenylhexyl)thiophene 
• 88336-91-8 2-(3(R,S)-Methyl-4-carboxybutyl)-5-(6-phenylhexyl)-thiophene 
• 104426-53-1 3,3-Dimethyl-5-[5-(6-phenyl-hexyl)-thiophen-2-yl]-pentanoic acid 
• 1027476-25-0 3,3-Dimethyl-1-morpholin-4-yl-5-[5-(6-phenyl-hexyl)-thiophen-2-yl]-pentan-1-one 
• 116754-80-4 15-Phenyl-3(R,S)-methylpentadecanoic Acid 
• 116754-87-1 15‐(4‐iodophenyl)‐3‐methylpentadecanoic acid 
• 88336-88-3 Methyl 15-Phenyl-3(R,S)-methylpentadecanoate 
• 88336-93-0 methyl 15-(p-iodophenyl)-3(RS)-methylpentadecanoate 

Relevant academic research and scientific papers

Amino derivatives of phenyl alkyl thiophene as inhibitors of bone resorption. Structure-activity relationship

Metabolism of arachidonic acid through the 5-lipoxygenase (LO) pathway generates compounds that stimulate osteoclastic bone resorption; since LO metabolites might play a role in bone loss due to excessive resorption it was tried to develop a series of antiresorptive agents starting from an already known LO inhibitor. Of the 35 compounds synthesized, 11 strongly inhibited (10 μmol/l) retinoic acid-induced bone resorption in cultured mouse calvariae; they were also tested for their effect on LO activity using rat peritoneal neutrophils, but no correlation could be drawn between inhibition of LO and bone resorption. Other pathways, still to be identified, must therefore be targeted by these compounds even though LO inhibition might contribute to their effects on bone. Two compounds selected for further studies were found active on parathyroid hormone-induced osteolysis, while they had no effect on basal resorption; they must, therefore, act at some key point in the process of activation of osteoclastic resorption. This series of compounds may represent a new way for the treatment of bone loss due to excessive resorption.

Synthesis and Evaluation of Radioiodinated Terminal p-Iodophenyl-Substituted α- and β-Methyl-Branched Fatty Acids

Methods have been developed for the preparation of terminal p-iodophenyl-substituted α- and β-methyl-branched long-chain fatty acids.The syntheses and physical properties of 14-(p-iodophenyl)-2(RS)-methyltetradecanoic acid and 15-(p-iodophenyl)-3(RS)-methylpentadecanoic acid are described.The radioiodinated agents are of interest as a result of the expected pronounced uptake and prolonged myocardial retention that may result from the inhibition of fatty acid metabolism.Tissue distribution studies in rats with 14-(p-iodophenyl)-2(RS)-methyltetradecanoic acidand 15-(p-iodophenyl)-3(RS)-methylpentadecanoic acid show significant heart uptake and prolonged retention accompanied by low in vivo deiodination and high blood levels.A comparison of the heart uptake of the radioiodinated methyl-branched fatty acids and their unbranched analogues has demonstrated a greater myocardial retention of the methyl-branched fatty acids than the unbranched analogues.These results suggest that the mechanism of myocardial retention results from steric or chemical inhibition of the metabolism of these fatty acids by the presence of the methyl group.