Introduction: Angiotensin 2 is a biologically active octapeptide known to bind with high affinity to two separate receptors, angiotensin type 1 receptor (AT1R) and angiotensin type 2 receptor (AT2R). The two receptors can be seen having opposite effects when activated. The effects of AT2R activation oppose the pathophysiological effects of AT1R and causes vasodilation, anti-inflammatory and anti-fibrotic effects. The first non-peptide selective AT2R agonist compound 21(C21) has as of recent entered phase two clinical trials for the indication idiopathic pulmonary fibrosis. Two novel newly synthesized non-peptide compounds MH280 and MH727 which exert AT2R selectivity have been evaluated. The data regarding these compounds is limited and the compounds are still being investigated. MH280 was tested as an antagonist to complement previous work, while MH727 was tested as an agonist and an antagonist on AT2R in mouse thoracic aortic vessels. Method: Isolated mouse thoracic aortic vessels was used to assess the functional cardiovascular effects of compounds MH280 and MH727 in vitro. The thoracic aortic vessel was used to determine whether the compound could contract the vessel indicating agonistic effect or blocking a vasorelaxant effect indicating antagonistic effect. Result: MH280 could not be seen abolishing the effects of C21-mediated vasorelaxation in mouse thoracic aortic vessels. MH727 evoked a concentration-dependent relaxation in mouse thoracic aortic vessels. MH727 caused a relaxation of 89.9% which was very similar to the relaxations by C21 which was 86.2 ± 8.6%. The compound could not be seen abolishing the effects of C21 when tested for antagonistic effects. Additionally, the concentration-dependent vasorelaxant effect of MH727 was abolished in the presence of the AT2R antagonist PD123319. Conclusion: Both MH280 and MH727 compounds seem to exert agonistic behavior which is believed to be caused by the stimulation of AT2R in isolated thoracic aortic vessels