Muscular dystrophy (MD) is a group of rare genetic disorder that weakens the muscles that helps in the body movement. Although all MD are genetic disorders, the types of inheritance vary, and Duchenne muscular dystrophy arises from new mutations. The gene for DMD, found on the X chromosome, encodes a large protein—dystrophin. HDAC also define a common target for independent pharmacological interventions in the treatment of Duchenne muscular dystrophy. Dystrophin protein is modeled using the Modeller9v1 and the modeled protein is simulated for molecular dynamics studies using GROMACS. Trichostatin A is an example of a HDAC inhibitor which is being studied as a breast cancer therapy drug and has been studied in both the mdx mouse model (Duchenne) and sarcoglycan deficient mouse model (LGMD). From the binding database 175 hits were found for the HDAC1 inhibitor. These 175 compounds are then screened for the best activity against dystrophin. The detailed docking analysis of the complex structures and on their interaction energies derived by the docking study before and after the simulation at 310.15 K provided a reasonable basis for the inhibition potency of the inhibitors against dystrophin. By macro molecular interaction it is found that Benzamidine have higher affinity value compared to the commercial available drug TrichostatinA.