Authors
Jean A Boutin, Frederic Bouillaud, Elzbieta Janda, István Gacsalyi, Gerald Guillaumet, Etienne C Hirsch, Daniel A Kane, Françoise Nepveu, Karine Reybier, Philippe Dupuis, Marc Bertrand, Monivan Chhour, Thierry Le Diguarher, Mathias Antoine, Karen Brebner, Herve Da Costa, Pierre Ducrot, Adeline Giganti, Vishalgiri Goswami, Hala Guedouari, Patrick P Michel, Aakash Patel, Jerome Paysant, Johann Stojko, Marie-Claude Viaud-Massuard, Gilles Ferry
Publication date
2019/3/1
Journal
Molecular Pharmacology
Volume
95
Issue
3
Pages
269-285
Publisher
American Society for Pharmacology and Experimental Therapeutics
Description
Quinone reductase 2 (QR2, E.C. 1.10.5.1) is an enzyme with a feature that has attracted attention for several decades: in standard conditions, instead of recognizing NAD(P)H as an electron donor, it recognizes putative metabolites of NADH, such as N-methyl- and N-ribosyl-dihydronicotinamide. QR2 has been particularly associated with reactive oxygen species and memory, strongly suggesting a link among QR2 (as a possible key element in pro-oxidation), autophagy, and neurodegeneration. In molecular and cellular pharmacology, understanding physiopathological associations can be difficult because of a lack of specific and powerful tools. Here, we present a thorough description of the potent, nanomolar inhibitor [2-(2-methoxy-5H-1,4b,9-triaza(indeno[2,1-a]inden-10-yl)ethyl]-2-furamide (S29434 or NMDPEF; IC50 = 5–16 nM) of QR2 at different organizational levels. We provide full detailed syntheses …
Scholar articles
JA Boutin, F Bouillaud, E Janda, I Gacsalyi… - Molecular Pharmacology, 2019