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As well as increasing H2AX levels, PHA665752 was shown to trigger H2AX tyrosine phosphorylation and its subsequent association with pro-apoptotic kinase JNK1 [56]

This orphan status has created a dichotomy in the scientific community: while empirical evidence from animal models and human clinical trials in the 1980s demonstrated significant therapeutic potential, particularly in addiction and stress management, the lack of a defined molecular pathway has stalled its development into a licensed pharmaceutical agent

It accelerates the process of neurogenesis and angiogenesis, which are critical for repairing brain damage and restoring function after a stroke

Rambeck B, Wolf P