Background: With an estimated global population of 2.2 million, most of whom are in their twenties or thirties, patients with MS suffer from demyelinating diseases of the brain and spinal cord. Multiple sclerosis is thought to be caused by an overproduction of reactive oxygen species (ROS) and a deficiency in iron metabolism (MS). Regulatory ROS generation is primarily fueled by NADPH oxidases, which are enzymes that break down NADPH into NADPH phosphate. Seven catalytic homologues of the NADPH oxidase (NOX) family, NOX1–5, and two dual oxidases make up the NOX family. Endothelial failure and inflammation are linked to NOX1 and NOX5, but NOX4 is protective of vascular function. Serum endothelial NOXs (NOX5 and NOX 4) and their link to iron metabolism biomarkers in relapsing-remitting MS patients is the primary goal of this research. Also, it is probable that NOXs (NOX5 and NOX 4) and iron metabolism biomarkers have a correlate with disease severity. The following are the steps we took and the results we got: Study participants were divided into two groups: those with RRMS and those who did not have the disease. All of the research individuals had their levels of serum NOX4,5, ferritin, iron, and iron binding capacity, as well as C-reactive protein (CRP), complete blood count (CBC), and erythrocyte sedimentation rate (ESR). Medical history, neurological examination, and the Expanded Disability Status Scale were completed for all subjects (EDSS). Researchers discovered significantly higher levels of NOX5, CRP, and ferritin in patients, as well as significantly lower levels of NOX4 and iron in controls (all p 0.0001). Patients' NOXs, CRP, WBCs, ESR, and iron metabolism indicators were not associated with each other. MS patients may be more susceptible to oxidative stress-related vascular alterations and BBB breakdown because of increased NOX5 expression and reduced NOX4 levels. We also found that RRMS patients had reduced iron and TIBC concentrations. Serum iron levels in MS patients should be regularly monitored due to iron's role in myelination and oligodendrocyte activity.