Transition metal complexes are considered a significant treatment for cancer diseases because of their efficacy toward cancer cells. However, most of these compounds have limited potential toward cancer cells due to their organic backbone structure. Here, the synthesis and anticancer screening of three different ligand structures of salen copper(II) complexes are reported: [Cu ^II (salophen)(H ₂ O) ₂ ] ( 1 ), [Cu ^II (salen)(H ₂ O) ₂ ] ( 2 ), and [Cu ^II (etho‐salen)(H ₂ O) ₂ ] ( 3 ). Using density functional theory‐optimized structures, docking active site interactions are evaluated to predict the activity of salen‐type ligands and their copper(II) complexes against cyclin‐dependent kinase 5 (Cdk5 ) and aromatase cytochrome (P450) proteins. The molecular docking study reveals that among all studied ligands and complexes, [Cu ^II (salen)(H ₂ O) ₂ ] ( 2 ) has the best docking score value, S = −8.79 and −7.73, with the lowest root mean square deviation (RMSD = 1.02 and 1.09) against proteins Cdk5 and P450, respectively. Anticancer activity against MCF‐7 and HCT‐116 cell lines reveals that [Cu ^II (salen)(H ₂ O) ₂ ] ( 2 ) shows favorable behavior with IC ₅₀ values of 212.5 and 98.9 μ m , respectively. Its parent ligand 2 shows lower potency, with IC ₅₀ values of 404.7 μ m in MCF‐7 and 305.2 μ m in HCT‐116. Notably, copper(II) complexes display reduced toxicity rather than cisplatin toward normal HFF‐1 fibroblasts, indicating a more favorable therapeutic window.

Medicinal plants provide a wide range of active compounds that can be exploited to create novel medicines with minimal side effects. The current study aimed to identify the anticancer properties of Juniperus procera (J. procera) leaves. Here, we demonstrate that J. procera leaves’ methanolic extract suppresses cancer cells in colon (HCT₁₁₆), liver (HepG2), breast (MCF-7), and erythroid (JK-1) cell lines. By applying GC/MS, we were able to determine the components of the J. procera extract that might contribute to cytotoxicity. Molecular docking modules were created that used active components against cyclin-dependent kinase 5 (Cdk5) in colon cancer, aromatase cytochrome P450 in the breast cancer receptor protein, the -N terminal domain in the erythroid cancer receptor of the erythroid spectrin, and topoisomerase in liver cancer. The results demonstrate that, out of the 12 bioactive compounds generated by GC/MS analysis, the active ingredient 2-imino-6-nitro-2H-1-benzopyran-3-carbothiamide proved to be the best-docked chemical with the chosen proteins impacted by DNA conformational changes, cell membrane integrity, and proliferation in molecular docking studies. Notably, we uncovered the capacity of J. procera to induce apoptosis and inhibit cell growth in the HCT₁₁₆ cell line. Collectively, our data propose that J. procera leaves’ methanolic extract has an anticancer role with the potential to guide future mechanistic studies.

6-Mercaptopurine (6-MP) is a chemotherapeutic agent with inadequate efficacy due to its poor aqueous solubility and limited bioavailability. Turmeric oil is a naturally occurring bioactive substance obtained from the rhizomes of Curcuma longa Linn that has well-known antiproliferative activities. The aim of this study was to develop a 6-MP-loaded turmeric oil-based self-nanoemulsifying drug delivery system (SNEDDS) to improve the anticancer activity of 6-MP. Turmeric oil was extracted and used in a range of 15–25% to develop SNEDDS formulations utilizing tween 80 and dimethyl sulfoxide as the surfactant and cosurfactant, respectively. The size, charge, and effect of the formulations on the viability against HepG2 and MCF-7 cell models, as well as the apoptosis and cell cycle, were analyzed. The prepared SNEDDS formulations were in the size range of 425.7 ± 7.4–303.6 ± 19.3 nm, using a polydispersity index of 0.429–0.692 and electronegative surface charges. Moreover, 6-MP-loaded SNEDDS with 15% turmeric oil content (F1) showed smaller particle sizes and a noticeable antiproliferative activity against both cell line models. Also, F1 showed a higher rate of late apoptosis than the pure drug and the corresponding non-medicated formulation. A morphological study revealed significant changes in the HepG2 cells compared to untreated cells. More cells halted in the S phase, and a marked decrease in the proportions of cells in the G1/G0 phase was observed when using SNEDDS formulation compared to pure drug. Thus, SNEDDS formulation is a promising drug delivery system for improving the antiproliferative activity of 6-MP, especially when turmeric oil is incorporated.