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Abstract Pulmonary arterial hypertension (PAH) is a fatal cardiovascular disorder characterized by vascular obstruction and elevated pulmonary arterial pressure. A key contributor to PAH pathogenesis is endothelial dysfunction, which leads to vascular remodelling, excessive cell proliferation, increased vascular resistance, chronic inflammation, vasoconstriction, and reduced vascular compliance. Histopathological features include arteriolar intimal proliferation, medial hypertrophy, adventitial thickening, laminar sclerosis, and plexiform lesions. Heritable PAH is commonly associated with BMPR2 mutations, part of the TGFβ superfamily, which plays a critical role in vascular homeostasis. This study aims to investigate the molecular mechanisms underlying TGF-β and BMP signalling pathways in PAH and identify potential therapeutic interventions. A reporter assay was employed in HEK293T cells to screen compounds of interest and assess their effects on these pathways. Selected compounds were further evaluated using RT-PCR, qPCR, and western blot analyses. An MTT assay was performed to assess the rate of cell proliferation of pulmonary arterial smooth muscle cells (PASMCs). Preliminary results indicate that some compounds inhibit the TGF-β pathway, whilst others promote BMP signalling, or have no detectable effect. Further analysis and confirmatory assays are being performed on selected compounds. As a conclusion, this study determines compounds that modulate TGFβ and BMP signaling pathways, providing potential therapeutic interventions for PAH via targeting key mechanisms of vascular remodeling and dysfunctions. Taken together, these agents may have broader therapeutic implications for TGFβ-BMP-associated disorders.