Aim:Our study focuses on neural tube defects (NTDs), which are central nervous system malformations resulting from incomplete neural tube closure in embryos. We aimed to evaluate tenoxicam’s effects on embryonic neural tube formation to identify potential teratogenicity and determine the underlying mechanisms leading to NTD. This study enhances our understanding of embryonic neural tube development and the risks of tenoxicam exposure during pregnancy.Material and Methods:This study was conducted at our University’s Neuro-embryology Laboratory. A total of 100 fertile chicken eggs were opened using the windowing method after 24 hours of incubation. The embryo cultures were divided into four groups based on tenoxicam dosage: 0.01, 0.02, 0.10 g, and control group (0.9% SF was administered). The tenoxicam groups were administered 20 µL volume sub-blastodermally. The eggs were incubated for another 24 hours after being covered with sterile draping. All the eggs were opened at the 48th hour, and the embryos were evaluated. Results:Each group consisted of 25 chicken embryos. Normal neural tube development was observed in Group 1 (0.01g) with 23 out of 25 embryos, Group 2 (0.02g) with 20 out of 25 embryos, Group 3 (0.10g) with 16 out of 25 embryos, and Group 4 (control group) with 24 out of 25 embryos. Additionally, the absence of development rate was 8%, 8%, 12%, and 4% in Groups 1, 2, and 3 and the control group, respectively.Conclusion:We observed that tenoxicam use caused midline closure defects in early chicken embryos in a dose-dependent manner. Further studies are required to determine the mechanisms underlying the embryonic damage and teratogenic effects due to genetic and environmental factors and minimize the development of congenital defects.