Duchenne muscular dystrophy (DMD) is an incurable disease, characterized by the muscle inflammation and progressive deterioration of muscle function.

We discuss and review the role of arachidonic acid (AA) metabolites in DMD in muscle fiber degeneration and regeneration and new opportunities for developing new drugs by targeting the AA pathway, providing evidence that the AA pathway could represent an efficacious strategy to ameliorate the treatment of DMD patients. Currently a series of DMD care recommendations regarding management of rehabilitation, orthopedic, respiratory, cardiovascular, gastroenterology exist and the therapy is restricted to corticosteroids for muscle dysfunction with serious side effects. Nowadays there are still no effective cures for the disease. The alternative pharmacological strategies targeting the AA metabolites may yield favorable outcomes in DMD. 5-LOX inhibition might be important for the survival of myofibers. Moreover H-PGDS inhibitors, cyclooxygenase (COX)-inhibiting NO donors (CINODs), inhibitors of Ca2+-independent PLA_2, are some of the different pathways which can bring to further development of new drugs.