Senna occidentalis, synonym Cassia occidentalis, is a native American pantropical plant species previously classified under the genus Cassia. This study is for testing and to discover new potent phytochemicals from this plant as wound healing and anti-inflammatory agents. The Excision and Assay of Red Blood Cell (RBC) Membrane Stabilization for Anti-Inflammatory Activity Test Method was used to test how well extracts of S. occidentalis leaves from methanol, n-hexane, chloroform, and absolute alcohol helped wounds heal and stopped inflammation. In silico is another method for finding potent phytochemicals for both activities. These leaf extracts effectively cure wound areas and promote re-epithelialization. The methanol extract exhibited maximum wound healing (95.04%) and anti-inflammation (62.94%) activity compared to their other extracts, standard, and control groups. In silico molecular docking of Apigenin, Aloe-emodin with GSK-3B protein, and 1-Methoxynaphthalene, Quinine with COX-2 protein showed binding affinity in (kjJ/mol) of −8.4, −8.6, and −7.3, −7.7, for wound healing and anti-inflammatory activity, respectively, in their binding sites with stability. They support the "Lipinski Rule of Five." This plant leaf extract is recommended as a traditional medicine and an alternative, complementary treatment for its continued contribution to drug discovery and development.

Breast cancer remains a leading cause of mortality among women despite advances in early detection and targeted therapies, underscoring the need for safer and more effective treatment options. Drug repurposing offers a promising strategy by leveraging existing pharmacological agents with established safety profiles. Desloratadine, a second-generation H1-histamine receptor antagonist widely prescribed for allergic conditions, has attracted interest in oncology because histamine signaling influences proliferation, angiogenesis, and immune responses, yet its anticancer potential remains poorly understood. In this study, we investigated its effects in MCF-7 breast cancer cells, which harbor wild-type TP53. Desloratadine inhibited cell viability in a dose-dependent manner, with an IC₅₀ of 14.2 µg/mL. Mechanistic analyses revealed that growth inhibition was primarily mediated through apoptosis, confirmed by Hoechst 33342 staining, ROS generation, annexin V/PI staining, and caspase-dependent pathways. Gene expression profiling demonstrated upregulation of TP53, FAS, and BAX, alongside reduced PARP-1 and NF-κB expression, with no detectable STAT3 or BCL2 expression. Flow cytometry indicated accumulation of cells in the sub-G₁ phase and G₂/M arrest, consistent with apoptosis induction. Molecular docking further supported these findings, showing that Desloratadine binds with high affinity to p53 (−7.0 kcal/mol), FAS (−6.8 kcal/mol), and NF-κB (−6.5 kcal/mol), forming stabilizing hydrogen bonds and hydrophobic interactions aligned with the observed gene expression changes. To confirm the functional role of TP53, we generated CRISPR-Cas9 knockout MCF-7 cells. Compared with wild-type cells, these knockout cells displayed markedly reduced sensitivity to Desloratadine, with the IC₅₀ shifting from 14.2 µg/mL to 36.4 µg/mL, demonstrating that p53 is a key mediator of the drug’s cytotoxic effect. Collectively, these findings identify Desloratadine as a potential repurposed drug candidate for breast cancer therapy, acting at least in part through a p53-dependent apoptotic pathway.