The frequency of cardiotoxicity is a worrying trend on a global scale. Currently, it is proposed that the causes of cardiotoxicity are oxidative stress, cardiac inflammation, and apoptosis. Numerous cardioprotective drugs have been developed to treat cardiotoxicity, but sadly, their potential side effects have made physicians seriously concerned about their use. We, therefore, intended to investigate the effect of α-phellandrene against cyclophosphamide (CP) in Wistar rats. Animals were divided into 6 groups: Normal control; Toxic (CP 200mg); α-phellandrene + CP [I]; α-phellandrene + CP [II]; α-phellandrene per se; Propranolol (PLN) +CP. Dosing was completed for 14 days laterally with a dose of CP once on the seventh day. After the final day of treatment, the weight of each animal was measured and animals were sacrificed on the 15th day, and after the serum had been separated using a homogenizer (3000 RPM) for 15 minutes. Various biochemical markers including Total Antioxidant Capacity (TAC), Creatinine Kinase- Myoglobin Binding (CK-MB), Lactate dehydrogenase (LDH) in blood, and other biochemical parameters such as Thiobarbituric acid reactive substances (TBARS), Reduced Glutathione (GSH), Catalase and superoxide dismutase (SOD) were also measured. When cyclophosphamide is given to rats, histology studies show that there are pathological changes, tissue damage, and an increase in relative heart weight, as well as an increase in serum marker enzymes, a substantial rise in the heart lipid concentrations, and a substantial drop in body weight at the end. The level of heart lipids, cardiac mitochondrial activity, and serum marker enzymes was all markedly normalized by the addition of α-phellandrene. In Conclusion, our research discovered that α-phellandrene had a strong cardioprotective impact against cardiotoxicity caused by cyclophosphamide.