Developing cost-effective, eco-friendly, efficient, stable, and unique catalytic systems remains a crucial issue in catalysis. Due to their superior physicochemical and electrochemical properties, exceptional structural characteristics, environmental friendliness, economic productivity, minimal energy demand, and abundant supply, a significant amount of research has been devoted to the development of various doped carbon materials as efficient catalysts. In addition, carbon-based materials (CBMs) with specified doping have lately become significant members of the carbon group, showing promise for a broad range of uses (e.g., catalysis, environmental remediation, critical chemical production, and energy conversion and storage). This study will, therefore, pay attention to the function of heteroatom-based doped and undoped CBMs for catalytical applications and discuss the underlying chemistries of catalysis. According to the findings, doping CBMs may greatly improve their catalytic activity, and heteroatom-doped CBMs may be a promising option for further metal doping to attach them to an appropriate place. This paper also covers the potential applications of both doped and undoped CBMs in the future.

In the modern world, cancer is now one of the most significant causes of death. Nuclear factor-kappa B (NF-κB) is critical for inflammation and immune responses. Still, its abnormal activation or dysfunction can promote tumor cell proliferation and inhibit apoptosis, thereby initiating cancer progression. The objectives of this study are to discover the potential lead molecules with anti-cancer activity against NF-κB complexed with DNA (PDB ID: 1A3Q) through virtual screening based on the NPACT and containing 1574 anti-cancer natural compounds. All compounds were docked against 1A3Q using PyRx, and the first three molecules from the docking results were selected for further ADMET analysis using ADMETlab3.0 and Protox 3.0. The top three natural compounds were stable against NF-κB, had high GI absorption and low toxicity, and exhibited high binding affinities. One of these molecules (PubChem ID: 21600009) is drug-like for cancer, with a binding affinity of − 8.7 kcal/mol, which is why it was considered more significant than the other two compounds. Then, the best compound obtained from those calculations was included in GROMACS 2022.4 to evaluate its dynamic properties and interactions with the receptor. A simulation was carried out using the CHARMM36 force field and TIP3P water model. The electronic properties of the compound have also been calculated to confirm its drug-likeness using DFT at the B3LYP/6-31G(d,p) level in Gaussian 09. These comparative studies therefore indicate the potential of a cancer drug candidate that requires further experimental testing to verify its stability and biological efficacy.

Cancer remains a global health challenge, driving the search for more effective therapeutic agents due to the limitations of existing treatments. We evaluated the anticancer potential of Eltrombopag olamine on MCF-7 (breast adenocarcinoma) and SMMC-7721 (hepatocellular carcinoma) cell lines. Eltrombopag olamine demonstrated dose-dependent antiproliferative effects, with IC₅₀ values of 31, 154, and 127 µg/ml for MCF-7, SMMC-7721, and non-cancer HEK293T cell lines, respectively. Apoptosis induction in MCF-7 and SMMC-7721 cell lines was confirmed through Hoechst 33342 staining-assisted detection of condensed nuclei. FITC-annexin V/PI staining showed a significant increase in late apoptosis in both MCF-7 and SMMC-7721 cells, as well as necrosis in SMMC-7721 cells. The cell cycle analysis revealed S-phase arrest in both MCF-7 and SMMC-7721 cell lines and a remarkable increase of sub-G1 phase in SMMC-7721 cells. Caspase-dependent apoptosis was evidenced by reduced cell death in the presence of Caspase-3/7, -8, and − 9 inhibitors. In MCF-7 cells, FAS, TP53, BAX, TNFα, and cytochrome-C were upregulated, while ERK expression was downregulated. In SMMC-7721 cells, TP53, BAX, and TNFα were similarly upregulated, whereas ERK, STAT3, MAPK, NOTCH, PARP1, and EGFR expression levels were reduced. The results show the involvement of mitochondrial (intrinsic), EGFR-MAPK-ERK, WNT1, and death receptor signaling pathways in the apoptosis process. Interactions of Eltrombopag with EGFR, FAS, p53, and TNFα proteins were detected through molecular docking simulations. These findings highlight the potential of Eltrombopag olamine as a repurposed, multi-targeted therapeutic candidate for the treatment of breast and liver cancer.

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.

Geodoram densiflorum or pink nodding orchid grows in wet habitats in Bangladesh. Rural people traditionally use this orchid’s pseudobulbs to treat skin inflammation, tumors and carbuncles. Though a protein from these bulbs previously showed antitumor activity against Ehrlich ascites carcinoma (EAC) cells in vitro, this study focused on proving this effect in vivo in a mice model and against a human cancer cell line. GDL exhibited around 45% growth inhibition against A549 cells at a concentration of 64 µg/mL implicating a caspase-dependent pathway modulated by caspase-3, -8, and -9 inhibitors. The condensed nuclei and morphological changes of GDL-treated cells indicating apoptosis also became evident by Hoechst 33342 and FITC-annexin V/PI staining. GDL up-regulated CASP9 and p53 while down-regulating PARP, MAPK, and STAT3 gene expression, suggesting the involvement of death receptor and intrinsic mitochondrial pathways. Flow cytometry analysis revealed GDL-induced G₀/G₁ phase cell cycle arrest. In vivo, GDL inhibited EAC cell proliferation by 48%, extending EAC-bearing mice lifespan by 37.05%, and improved hematological parameters, notably increasing red blood cell counts and hemoglobin levels to 2.41 × 10⁹ RBC/mL and 10.27 g/dL, respectively. These findings underscore the therapeutic potential of GDL, setting the stage for further in-depth research.