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J Clin Invest 2004

The proposed therapeutic mechanism involves the down-regulation of c-Jun-N-terminal kinase (JNK) by inducing Gadd45-beta activity, which ultimately disrupts a mechanism of mitochondrial damage

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Additional studies tied the catalase-induced decrease in hydrogen peroxide with diminished activation of nuclear factor B (NFB) survival pathways that are necessary to counteract apoptotic signaling (240)

It is classified as a research chemical and is only available for scientific research

Rotate injection sites to prevent tissue irritation and induration