73354-08-2Relevant articles and documents
Synthesis and pharmacological characterisation of arctigenin analogues as antagonists of AMPA and kainate receptors
Butts, Craig P.,Collingridge, Graham L.,Jane, David E.,Mallah, Shahida,Molnár, Elek,Re?nik, Lisa-Maria,Thatcher, Robert J.,Willis, Christine L.
supporting information, p. 9154 - 9162 (2021/11/16)
(-)-Arctigenin and a series of new analogues have been synthesised and then tested for their potential as AMPA and kainate receptor antagonists of human homomeric GluA1 and GluK2 receptors expressed in HEK293 cells using a Ca2+ influx assay. In general, these compounds showed antagonist activity at both receptors with greater activity evident at AMPARs. Schild analysis indicates that a spirocyclic analogue 6c acts as a non-competitive antagonist. Molecular docking studies in which 6c was docked into the X-ray crystal structure of the GluA2 tetramer suggest that (-)-arctigenin and its analogues bind in the transmembrane domain in a similar manner to the known AMPA receptor non-competitive antagonists GYKI53655 and the antiepileptic drug perampanel. The arctigenin derivatives described herein may serve as novel leads for the development of drugs for the treatment of epilepsy. This journal is
Studies on differentiation inducers. VI. Lignan derivatives from arctium fructus. (2)
Umehara,Nakamura,Miyase,Kuroyanagi,Ueno
, p. 2300 - 2304 (2007/10/03)
In the previous paper, we reported the differentiation inducing activities of lignoids from Arctium Fructus (the fruits of Arctium lappa L., Compositae) against mouse myeloid leukemia cells (M1). We reinvestigated the active components of this extract and isolated three new dilignans. Furthermore, structure modifications were carried out using the most active lignan (arctigenin, 1) and its structure activity relationship was investigated. Its aliphatic esters were more effective in inducing the differentiation of M1 cells than its aromatic esters. Especially, n- decanoate, which was the most active derivative, induced more than half of the M1 cells into phagocytic cells at a concentration of 2 μM.