SR-3306

SR-3306 is a selective, potent, highly brain penetrant JNK inhibitor. In Vitro The effect of SR-3306 or Tat-Sab on cell viability in response to oxidative stress is measured by an MTT assay. H9c2 cells treated with 100 μM H 2 O 2 /FeSO 4 are ~40% viable, whereas the addition of 500 nM SR-3306 or 500 nM SR3562 to cells treated with 100 μM H 2 O 2 /FeSO 4 increases viability to ~90%, and the addition of 10 μM Tat-Sab peptide to cells treated with 100 μM H 2 O 2 /FeSO 4 increases viability to ~70% compared with 98% viability in untreated cells. Similar results are found for primary human cardiomyocytes. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Administration of SR-3306 [10 mg/kg/day (s.c.) for 14 days] 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 only vehicle (p Cell Assay H9c2 cells and primary human cardiomyocytes are grown under normal cell culture conditions (37 °C and 5% CO 2 ) in DMEM supplemented with 10% fetal bovine serum and penicillin/streptomycin. To assure that the cells are actively growing, only cells at ~80% confluency and between passages 5 and 15 are used in our experiments. H9c2 cells and primary human cardiomyocytes are exposed to 500 nM SR-3306 , 500 nM SR-3562, 0.01% DMSO vehicle control, 10 μM Tat-Sab KIM1 , and 10 μM Tat-scramble for 30 min prior to the addition of stress. To induce oxidative stress and mitochondrial dysfunction in H9c2 cells and primary human cardiomyocytes, 100 μM hydrogen peroxide (H 2 O 2 )/FeSO 4 or 100 μM hydrogen peroxide (H 2 O 2 )/FeSO 4 is added directly to the media of the cells. The cells are exposed to H 2 O 2 /FeSO 4 for the times indicated in the experiments. MCE has not independently confirmed the accuracy of these methods. They are for reference only. IC50& Target:JNK

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