MOLECULAR DOCKING STUDIES OF MONOMERIC WILDTYPE AND MUTANT (H81A, H49R) SOD1 WITH EDARAVONE AND RILUZOLE

Objective: Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder that causes progressive loss of the upper and lower neurons in brain spinal cord. SOD1 was first gene linked to ALS, which more than 150 mutations throughout sequence protein have been found be associated with ALS. Methods: The drugs can interact inhibit misfolding or revert misconformation useful treatment Monomer apo SOD1-WT MBR mutants (H81A, H49R) were docked only two FDA-approved for ALS are edaravone riluzole assess if patients carrying these particular aggregates will derive any therapeutic efficacy. Results: both wild-type mutant at different positions type interaction, degree interaction their binding energies determined. has hydrophobic interactions V103, H110, R115 hydrogen bond H110 edaravone. T54, F64 D52, T58 riluzole. Both its H46 residue drugs. SOD1-H49R F45 SOD1-H81A Conclusion: L42A Interaction may make it possible restore stability structure attenuate disease progression mutations.