13487-46-2Relevant articles and documents
Synthesis of lysophosphatidylethanolamine analogs that inhibit renin activity
Turcotte,Yu,Lee,Pavanaram,Sen,Smeby
, p. 1184 - 1190 (1975)
A series of lysophosphatidylethanolamine analogs containing saturated and methylene interrupted cis olefinic fatty chains was synthesized by phosphorylation and phosphonylation of respective fatty alcohols. Arachidonyl and linolenyl phosphoryl ethanolamines, arachidonyl (2 phthalimidoethyl)phosphonate and arachidonyl (2 aminoethyl)phosphonate were found to be effective inhibitors of the renin renin substrate reaction in vitro; lysophosphatidylethanolamine analogs of lesser unsaturation were either weakly active or inactive. In a preliminary study, intramuscular administration of 25 mg/kg/day of arachidonyl (2 aminoethyl)phosphonate to the hypertensive rat caused pronounced reduction (50 mm) in blood pressure within 3 days; upon continued dosage (15 mg/kg/day) for an additional 4 days, plasma renin activity was found to be 16 ng/0.1 ml/15 hr as compared with 69 ng/0.1 ml/15 hr before initial drug administration. Arachidonic acid, arachidonyl alcohol, and several corresponding tetraenoid ester, amide, mesylate, and glyceryl ether derivatives, that are not phosphate or phosphonates esters, were found to exhibit negligible or modest inhibition of renin activity in vitro.
Arachidonylsulfonyl derivatives as cannabinoid CB1 receptor and fatty acid amide hydrolase inhibitors
Segall, Yoffi,Quistad, Gary B.,Nomura, Daniel K.,Casida, John E.
, p. 3301 - 3303 (2003)
Arachidonylsulfonyl fluoride (3), reported here for the first time, is similar in potency to its known methyl arachidonylfluorophosphonate (2) analogue as an inhibitor of mouse brain fatty acid amide hydrolase activity (IC50 0.1 nM) and cannabinoid CB1 agonist [3H]CP 55,940 binding (IC50 304-530 nM). Interestingly, 3 is much more selective than 2 as an inhibitor for fatty acid amide hydrolase relative to acetylcholinesterase, butyrylcholinesterase and neuropathy target esterase. N-(2-Hydroxyethyl)arachidonylsulfonamide (4) is at least 2500-fold less potent than N-(2-hydroxyethyl)arachidonamide (anandamide) (1) at the CB1 agonist site.
FATTY ACID DERIVATIVES FOR TREATING NON-ALCOHOLIC STEATOHEPATITIS
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Page/Page column 82, (2019/06/23)
The present disclosure provides a compound for use in therapeutic and/or prophylactic treatment of non-alcoholic steatohepatitis (NASH) and/or alcoholic steatohepatitis (ASH). The compound for use according to the invention, is an unsaturated fatty acid with an oxygen incorporated in the β-position, and further comprising an α-substituent. More particularly, the invention provides a compound for use in treatment of NASH and/or ASH, and a method using this, wherein the compound is of Formula (II), wherein R1, R2, R3, X, and Y are as defined in the specification; and wherein this compound may be administered alone or in combination with an additional active agent.
METHODS FOR MODULATING IKS CHANNEL ACTIVITY
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Paragraph 00109, (2016/04/26)
Disclosed herein are methods of using polyunsaturated fatty acids and derivatives thereof ("PUFAs") to modulate Iks channels to treat conditions associated with a disruption in Iks channel activity, such as cardiac arrhythmias. In particular, disclosed herein are negatively charged PUFAs having decreased pKa values, which can activate (i.e., open) IKs channels, and positively charged PUFAs that can inhibit (i.e., close) IKS channels.
