1057394-06-5

AL 8697 is a selective and potent p38α inibitor and has potential use as antiinflammatory agents against diseases such as arthritis.

al8697 is a selective p38 mapk(mitogen-activated protein kinase) inhibitor, which is also named p38 α inhibitor. it has the function of inhibiting the activity of p38 mapk.[1]mitogen activated protein kinases (mapk) are a group of signaling molecules that appear to play important roles in inflammatory processes. the p38 mapk is one of the best described mapk cascades. the p38 mapk plays a key role in both the synthesis and the signalling of pro-inflammatory cytokines such as tnfa and il-6 by monocyte/macrophages. the p38 mapk are involved in the up-regulation of tnf production by murine macrophages.it has high activity in cardiovascular cells under a variety of cellular stresses. in cardiovascular disease, the p38 mapk signaling pathways are activated.[2,3]al8697 function by the inhibition of p38 mapk. it regulates a variety of cell activities related with p38 mapk.in a rat adjuvant-induced arthritis model, al8697 exhibited a good anti-inflammatory effect and induced leukocytosis and increased total plasma cholesterol, these properties were evidently at 10 mg/kg. in addition, al8697 partially restored the platelet count. the complex profile for al8697 in rat aia (adjuvant-induced arthritis) is not observed in human ra (rheumatoid arthritis).[1]

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[1]. balagué c, pont m, prats n, godessart n. profiling of dihydroorotate dehydrogenase, p38 and jak inhibitors in the rat adjuvant-induced arthritis model: a translational study. br j pharmacol. 2012 jun;166(4):1320-32
[2]. ajizian sj, english bk, meals ea.specific inhibitors of p38 and extracellular signal-regulated kinase mitogen-activated protein kinase pathways block inducible nitric oxide synthase and tumor necrosis factor accumulation in murine macrophages stimulated with lipopolysaccharide and interferon-gamma. j infect dis. 1999 apr;179(4):939-44.
[3]. bao w, behm dj, nerurkar ss, ao z, et al. effects of p38 mapk inhibitor on angiotensin ii-dependent hypertension, organ damage, and superoxide anion production. j cardiovasc pharmacol. 2007 jun;49(6):362-8.