Gold nanoparticles are extensively used across various industries, particularly in biomedical fields, due to their high biocompatibility, stability, and low toxicity. The rising use of gold nanoparticles in biomedical applications has increased the demand for more sustainable synthesis methods that reduce costs and environmental impacts compared to traditional chemical processes. This study presents a green synthesis approach utilizing leaf extracts from Pterospermum canescens and Vernonia elaeagnifolia. The synthesized nanoparticles were characterized using UV‐VIS, XRD, HRTEM‐SAED, FESEM‐EDX, XPS, and FTIR analyses. These characterizations confirmed the formation, size, shape, and morphological features of the nanoparticles, as well as the involvement of secondary plant metabolites in their synthesis. The nanoparticles were found to be less than 50 nm in size, with P.C AuNPs averaging 27.48 nm and V.E AuNPs averaging 14.79 nm. The particles predominantly exhibited spherical or distorted spherical shapes. In cytotoxicity assays using C6 rat glioma cells, both types of nanoparticles demonstrated significant effects. V.E AuNPs induced apoptosis in 78 % of the cells, while P.C AuNPs induced apoptosis in 50 %, confirming their cytotoxic efficacy. Gene expression studies further revealed that V.E AuNPs significantly upregulated caspase‐3 and downregulated BCL‐2, indicating a potent apoptotic response, while P.C AuNPs showed a similar but less pronounced effect. Additionally, in collagen‐induced platelet aggregation studies, V.E AuNPs exhibited substantial anti‐platelet activity with increasing dosages, reducing platelet aggregation to less than 10 % at a concentration of 30 μg/ml, compared to minimal inhibition by P.C AuNPs. Overall, the study demonstrates that gold nanoparticles synthesized from Vernonia elaeagnifolia and Pterospermum canescens are effective and offer promising applications in biomedicine. The results confirm the potential of these green‐synthesized nanoparticles for use in cancer treatment and sustainable anti‐platelet drug development