Clinical and preclinical studies have shown that reduction in parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) can ameliorate anemia associated with chronic kidney disease (CKD). Additionally, clinical studies have demonstrated that salmon calcitonin (sCT) effectively reduces secondary hyperparathyroidism (SHPT) and FGF23. Thus, this study aimed to investigate the potential of sCT to improve renal anemia in a rat model. Male Wistar rats (N=24) were orally administered with adenine (100 mg/kg/day) for 28 days to induce renal anemia. Subsequently, subcutaneous administration of sCT (20 IU/kg/day) or recombinant human erythropoietin (rhEPO) (30 IU/kg/day) was carried out for 21 days. Hematological, biochemical parameters, and histopathological analysis were measured at the end of study (Day 50) with primary objective of investigating the effect of sCT on serum EPO levels. Adenine exposure resulted in reduced (EPO) serum levels, decreased total red blood cell (RBC) counts, hemoglobin (Hb), and hematocrit (Hct), accompanied by elevated serum levels of blood urea nitrogen (BUN), creatinine, PTH, and FGF23. In adenine-treated wistar rats, both sCT and rhEPO administrations successfully increased EPO serum levels, total RBC counts, Hb, and Hct, while decreasing serum BUN, creatinine, FGF23, and PTH levels. Histopathological analysis revealed characteristic kidney damage indicative of CKD in adenine-treated rats, which was notably absent in rats treated with sCT or rhEPO. The study concludes that sCT successfully mitigated renal anemia in rats suggesting its potential as a promising therapeutic strategy for CKD-related anemia. These findings support the translational potential of sCT for improving anemia in CKD patients.