L-2286 - CAS 684276-17-3
Catalog number: 684276-17-3
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
L-2286 is a novel PARP inhibitor. L-2286 exerted significant protective effect against ischemia-reperfusion-induced myocardial injury in both experimental models. More importantly, L-2286 facilitated the ischemia-reperfusion-induced activation of Akt, extracellular signal-regulated kinase, and p38-MAPK in both isolated hearts and in vivo cardiac injury.
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white solid powder
L-2286; L 2286; L2286.
1.Effect of L-2286, a poly(ADP-ribose)polymerase inhibitor and enalapril on myocardial remodeling and heart failure.
Bartha E1, Kiss GN, Kalman E, Kulcsár G, Kálai T, Hideg K, Habon T, Sumegi B, Toth K, Halmosi R. J Cardiovasc Pharmacol. 2008 Sep;52(3):253-61. doi: 10.1097/FJC.0b013e3181855cef.
Increased activation of poly(ADP-ribose) polymerase (PARP) enzyme has been implicated in the pathogenesis of acute and chronic myocardial dysfunction. We have demonstrated the protective effect of PARP inhibitors against postinfarction myocardial remodeling and heart failure. The primary aim of our recent work was to compare the effect and efficacy of a potent PARP-inhibitor (L-2286) to enalapril, a widely used angiotensin-converting enzyme (ACE) inhibitor. in experimental heart failure model. Both L-2286 and enalapril were tested in a rat model of chronic heart failure after isoproterenol-induced myocardial infarction. After a 12-week treatment period, echocardiography was performed, cardiac hypertrophy and interstitial collagen deposition were assessed, and the phosphorylation state of Akt-1/GSK-3beta pathway as well as the PKC and MAPK kinases were determined. Both PARP and ACE inhibition reduced the progression of postinfarction heart failure by attenuating cardiac hypertrophy and interstitial fibrosis.
2.A novel PARP inhibitor L-2286 in a rat model of impact acceleration head injury: an immunohistochemical and behavioral study.
Kövesdi E1, Bukovics P, Besson V, Nyirádi J, Lückl J, Pál J, Sümegi B, Dóczi T, Hernádi I, Büki A. Int J Mol Sci. 2010 Mar 26;11(4):1253-68. doi: 10.3390/ijms11041253.
We examined the neuro/axono-protective potential of a novel poly (ADP-ribose) polymerase (PARP) inhibitor L-2286 in a rat impact acceleration brain injury model. Male Wistar rats (n = 70) weighing 300-350 grams were used to determine the most effective intracerebroventricular (i.c.v.) dose of L-2286 administered 30 min after injury, and to test the neuroprotective effect at two time points (immediately, and 30 min after injury). The neuroprotective effect of L-2286 was tested using immunohistochemical (amyloid precursor protein and mid-sized mouse anti-neurofilament clone RMO-14.9 antibody) and behavioral tests (beam-balance, open-field and elevated plus maze). At both time-points, a 100 microg/rat dose of i.c.v. L-2286 significantly (p < 0.05) reduced the density of damaged axons in the corticospinal tract and medial longitudinal fascicle compared to controls. In the behavioral tests, treatment 30 min post-injury improved motor function, while the level of anxiety was reduced in both treatment protocols.
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CAS 684276-17-3 L-2286

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