SR-3306 Inhibitor

Solid. Powder

98.00%

Store at -20 degree C for 3 years powder
-80 degree C for 2 years in solvent

490.56

DMSO: 125mg/mL (254.81mM) Need ultrasonic
(<1mg/ml refers to the product slightly soluble or insoluble)

C28H26N8O

Cc1ccc(cn1)-c1ncn(n1)-c1ccc(Nc2nccc(n2)-c2cccc(c2)N2CCOCC2)cc1

1128096-91-2

JNK

SR-3306 (10mg/kg/day (s.c.) for 14 days) decreases d-amphetamine-induced circling by 87% compared to 6-hydroxydopamine (6-OHDA)-lesioned animals given vehicle. Steady-state brain levels of SR-3306 at day 14 are 347nM, which is approximately 2-fold higher than the cell-based IC50 for this compound. SR-3306 (10mg/kg/day (s.c.) for 14 days) administration increases the number of tyrosine hydroxylase immunoreactive (TH+) neurons in the SNpc by 6-fold and reduces the loss of the TH+ terminals in the striatum relative to the corresponding side of 6-OHDA-lesioned rats that receive the only vehicle (p<0.05). Finally, immunohistochemical staining for phospho-c-jun (p-c-jun) reveals that SR-3306 (10mg/kg/day (s.c.) for 14 days) produces a 2.3-fold reduction of the number of immunoreactive neurons in the substantia nigra pars compacta (SNpc) relative to vehicle-treated rats. In lean mice, intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of SR-3306 reduces food intake and body weight. SR11935(i.p. and i.c.v.) treatment,exert similar anorectic effects as SR3306, which suggests JNK2 or JNK3 mediates aspect of the anorectic effect by pan-JNK inhibition. Furthermore, SR-3306 (daily i.p. injection, 7 days) prevents the increases in food intake and weight gain in lean mice upon high-fat diet feeding, and this injection paradigm reduced high-fat intake and obesity in diet-induced obese mice [1][3].

MAPK; JNK