Coumarin derivatives constitute a versatile small-molecule chemotype with broad anticancer potential. This narrative review synthesizes recent in vitro and in vivo evidence on coumarin-based scaffolds, emphasizing breast cancer and covering lung, prostate, and colorectal models. We summarize major mechanisms of action—including induction of apoptosis (caspase activation and BAX/BCL-2 balance), modulation of PI3K/Akt/mTOR signaling, inhibition of angiogenesis (VEGFR-2), interference with estrogen biosynthesis (aromatase/ER axis), chaperone targeting (Hsp90), and attenuation of multidrug resistance (efflux pumps/autophagy)—and highlight representative chemotypes (e.g., benzimidazole, triazole, furocoumarins, topoisomerase- and CDK-oriented hybrids). Where available, we contrast potency and selectivity across models (e.g., MCF-7 vs. MDA-MB-231; A549; PC-3; colon lines) and discuss structure–activity trends linking substituent patterns (heteroaryl linkers, judicious halogenation, polar handles) to pathway engagement. We also delineate translational gaps limiting clinical progress—selectivity versus non-malignant cells, incomplete pharmacokinetic and safety characterization, and limited validation beyond xenografts. Finally, we outline priorities for preclinical optimization: biology-aligned target selection with biomarkers, resistance-aware combinations (e.g., PI3K/mTOR ± autophagy modulation; MDR mitigation), and early integration of ADME/tox and PK/PD to confirm on-target exposure. Collectively, the evidence supports coumarins as adaptable, multi-target anticancer leads, particularly promising in hormone-dependent breast cancer while remaining relevant to other tumor types.

Pyrazole derivatives have emerged as an important class of heterocyclic compounds in anticancer research due to their structural versatility and broad spectrum of biological activities. This review provides a concise overview of recent advances in the development of pyrazole-based anticancer agents, with emphasis on synthetic strategies, structure–activity relationships, and molecular mechanisms of action. Common synthetic approaches, particularly condensation and cyclization reactions, have enabled the preparation of structurally diverse pyrazole derivatives for biological evaluation. Available evidence indicates that the type and position of substituents within the pyrazole scaffold markedly influence anticancer potency, selectivity, and target affinity. Reported compounds act through multiple mechanisms, including inhibition of cancer-related targets such as tubulin, epidermal growth factor receptor (EGFR), cyclin-dependent kinases (CDKs), Bruton tyrosine kinase (BTK), and deoxyribonucleic acid (DNA)-associated pathways, as well as induction of apoptosis and disruption of cell-cycle progression. Several pyrazole derivatives have shown promising activity in in vitro and in vivo models. Overall, the findings summarized in this review identify the pyrazole scaffold as a valuable platform for the design and optimization of novel anticancer agents and support its continued exploration in medicinal chemistry.

Systemic glucocorticoids are effective in rheumatoid arthritis, but long-term exposure carries dose-dependent risks. We developed a “nano-in-micro” platform in which cellulose nanocrystals (CNCs; <100 nm) are embedded within polymeric microspheres (about 100–400 μm) to modulate dexamethasone release while preserving drug identity and matrix integrity. Microsphere formulations varying in CNC and chitosan content were prepared and characterized at a fixed drug load. FT-IR and UV–Vis spectroscopy confirmed drug identity and assay linearity. Optical microscopy and SEM assessed particle size and morphology; CNCs were examined by TEM. Process yield, encapsulation efficiency (EE), equilibrium swelling, and cumulative drug release over 10 h were measured. Release data were fitted to zero-order, first-order, Higuchi, Hixson–Crowell, and Korsmeyer–Peppas models. Microspheres (predominantly 100–150 μm within a 100–400 μm design space) were produced with high process yields (approximately 85–89%) and moderate encapsulation efficiency (approximately 52–63%). Increasing cellulose nanocrystal (CNC) content reduced equilibrium swelling (from about 180% to about 150%) and slowed dexamethasone release over 10 h (from approximately 100% for chitosan-only to approximately 87% at the highest CNC loading). UV–Vis quantitation was highly linear (R² = 0.9876). Diffusion-based models best described release profiles (Higuchi, Korsmeyer–Peppas; R² ≥ 0.97), whereas first-order kinetics were comparatively stronger in the fastest-releasing, chitosan-rich formulations. Embedding CNCs within polymeric microspheres provides a controllable lever to tune swelling and diffusional pathways, enabling short-to-medium dexamethasone release profiles without compromising analytical identity or process robustness. The platform’s reproducible yields and predictable CNC-dependent slowing of release support further optimization (e.g., cross-link density, medium conditions) and in vivo evaluation toward dosing concepts that minimize systemic glucocorticoid exposure. Clinical applicability has not yet been established; in vivo biocompatibility, pharmacokinetic, and efficacy studies—aligned with medicinal‑product guidance—are required before any translational claims can be made.

Glycogen synthase kinase-3 beta (GSK-3β) is a multifunctional serine/threonine kinase mediating multiple cellular functions, such as differentiation, apoptosis, and cell proliferation. Because of their ability to alter carcinogenic pathways, GSK-3β inhibitors are being explored for the development of anticancer molecules. In the present study, we synthesized and evaluated the cytotoxic properties of a series of twenty indole–triazole-linked pyrazolone derivatives, 10Aa–Ed. All derivatives were characterized by FTIR, ¹H/¹³C NMR, and high-resolution mass spectrometry (HRMS) methods. All compounds and standards, sunitinib and 5-Fluorouracil (5-FU), were screened against four adherent cell lines, including pancreatic adenocarcinoma (Capan-1), colorectal carcinoma (HCT-116), glioblastoma(LN229), and lung carcinoma (NCI-4460), and four non-adherent cell lines, including acute myeloid leukemia (HL-60), chronic myeloid leukemia (K562), T lymphoblast (MOLT4), and non-Hodgkin lymphoma (Z138). Among the screened derivatives, molecule 10Aa showed cytotoxicity against MOLT 4, Z138, and HL60 with CC₅₀ values of 14.45 μM, 15.34 μM, and 17.56 μM, respectively. GSK-3β kinase inhibition was evaluated with the 10Aa, which is capable of inhibiting GSK-3β in a dose-dependent manner. Additionally, molecular docking was performed to estimate the correlation between invitro data and GSK-3β binding affinity. The outcomes of the invitro experiments demonstrated strong concordance with the insilico data. The discovery yielded compounds 10Aa and 10Cd, which can be modified to create effective anticancer agents that target GSK-3β.

This study retrospectively evaluates agreement between target-level molecular-modeling rankings from a previously published coumarin–pyrimidine library and an available cellular dataset for 14 experimentally evaluated compounds with documented structure assignments. Laboratory-reported MDA-MB-231 and MCF-10A IC₅₀ values from multi-concentration MTT testing were compared with published AutoDock Vina scores using rank-based analyses. Compound 5e had the lowest laboratory-reported MDA-MB-231 IC₅₀ (12.4 ± 0.2 µM; n = 2) and the largest descriptive selectivity index (7.75); this ratio is specific to the MDA-MB-231/MCF-10A comparison and is not interpreted as evidence of general tumor selectivity. Docking rankings showed weak correspondence with cellular potency, and no docking–phenotype association remained statistically significant after Benjamini–Hochberg adjustment. No basic 2D descriptor showed a compelling adjusted association. Complete ¹H/¹³C NMR and validated HRMS documentation, quantitative purity measurements, and the complete full-series MTT raw export are not available; structure-dependent and potency claims are therefore interpreted cautiously. Overall, the analysis demonstrates limited cross-endpoint transferability between target-level docking rankings and whole-cell activity in the MDA-MB-231/MCF-10A dataset, without establishing a validated structure–activity relationship, generalized TNBC activity, apoptosis induction, a BCL-2 mechanism, or translational efficacy.