This review covers published data (mostly from 2019 to 2025) on the synthesis and biological activity of azolo[a]quinoxalines, including pyrazolo-, imidazo- and triazolo-annelated systems. We highlight that most research efforts are directed toward the design of anticancer agents, with additional applications as Toll-like receptor antagonists, monoamine oxidase inhibitors, opioid receptor modulators, PI3Kα inhibitors, tubulin polymerization inhibitors, GABAᴀ receptor modulators, VEGFR-2 kinase inhibitors, BRD9 binders, and anti-inflammatory, antimicrobial, and antifungal agents. Recent synthetic strategies include Cu-catalyzed oxidative annulations, I2-mediated C-H functionalization, metal-free cascade cyclization, and multicomponent reactions, often employing eco-friendly catalysts and reductants. A growing number of studies integrate virtual screening, molecular docking, and pharmacophore-based in silico approaches to guide lead discovery and optimization. Innovative drug delivery systems, such as nanogels and hybrid molecules combining azoloquinoxalines with pharmacophores like thalidomide, have also been explored. This review emphasizes both the medicinal chemistry aspects of azolo[a]quinoxalines and the synthetic methodologies for their preparation from the perspective of drug development and discovery.

In this study, a pH-responsive chondroitin sulfate-methotrexate (MTX) polymeric prodrug was synthesized through Schiff base formation between oxidized chondroitin sulfate and MTX. The resulting amphiphilic conjugate exhibited a conjugation degree of 184 mg MTX per g conjugate and spontaneously self-assembled into stable nanoparticles (CSMXPs) with a mean diameter of 120 ± 10 nm, a polydispersity index of 0.24, and a critical aggregation concentration of 4.7 × 10-4 mg mL-1. Drug release studies demonstrated a marked pH-dependent behavior, with complete MTX release after 24 h at pH 5.0 and a sustained release profile under physiological conditions. The release mechanism followed reversible first-order kinetics and was accelerated by acid-catalyzed hydrolysis of the imine linkage. Biological evaluation revealed enhanced therapeutic selectivity of CSMXPs compared with free MTX. At 36 μM MTX-equivalent concentration, CSMXPs reduced HeLa cell viability to 37%, while maintaining MCF-10A viability above 88%, whereas free MTX decreased viability in both cell lines (51% and 65%, respectively). Fluorescence confocal microscopy confirmed efficient nanoparticle uptake by cancer cells. These findings demonstrate that CSMXPs represent a promising self-assembling nanoprodrug platform for selective and targeted cancer therapy.

Estrogen receptor-positive breast cancer remains difficult to treat, driving the search for new therapeutic agents. Juncus effusus L., a medicinal plant rich in bioactive constituents, has shown preliminary anticancer activity, yet its efficacy in hormone-responsive tumor models in vivo has not been established. We evaluated the antitumor effects of the ethyl acetate sub-extract of J. effusus L. subsp. effusus in an N-methyl-N-nitrosourea (NMU)-induced rat mammary tumor model, assessing tumor burden, histopathology, and molecular markers. Thirty-six Sprague-Dawley rats were divided into six groups (n = 6): sham, control, reference, and three groups receiving the sub-extract at 100, 200, or 400 mg/kg. After NMU induction (50 mg/kg), treatment began once tumor volumes reached approximately 2000 mm3 and continued for eight weeks. The 200 mg/kg dose markedly reduced tumor volume relative to control (p < 0.0001) and lowered both ERα and PCNA expression (p < 0.001 and p < 0.0001). The 100 and 200 mg/kg groups also showed lower p53 and ERα mRNA levels than the other treatment groups. HIF-1α, though elevated in control tumors, declined only modestly and without statistical significance after treatment. These results indicate that J. effusus subsp. effusus, particularly at 200 mg/kg, suppresses proliferation and modulates ERα- and p53 expression, supporting its potential for further preclinical investigation.

Background: Pituranthos scoparius (Apiaceae), commonly known in Algeria as "Kozah", is a medicinal plant traditionally used for various therapeutic purposes. However, its potential as a source of antiproliferative agents and its underlying molecular mechanisms remain poorly characterized. Purpose: This study aimed to investigate the antiproliferative potential of P. scoparius through an integrated strategy combining phytochemical profiling, in vitro evaluation, and computational approaches, with particular emphasis on its activity against key cancer-related pathways. Study Design: An integrated experimental-computational study was performed to explore the multitarget antiproliferative profile of P. scoparius extracts. Methods: Phytochemical characterization was carried out using LC-MS/MS and GC-MS/MS to identify the major bioactive constituents. Antiproliferative activity was assessed in vitro against human colorectal (HT-29) and hepatocellular carcinoma (HepG2) cell lines using the MTT assay. Molecular docking studies were conducted on selected major metabolites against relevant oncogenic targets, including PI3Kα, mTOR, COX-2, and BCL-2, to investigate potential mechanisms of action. Machine learning approaches were further employed to support the prediction of multitarget antiproliferative activity. Results: Chlorogenic acid and trans-ferulic acid were identified as the predominant phenolic compounds, while α-pinene was the major constituent of the essential oil. Both preparations exhibited significant dose- and time-dependent antiproliferative effects, with the essential oil showing enhanced cytotoxicity (IC50 up to 35.4 µg/mL). In silico analyses revealed strong binding affinities of key metabolites toward critical oncogenic proteins, particularly within the PI3Kα/mTOR signaling pathway. Machine learning predictions further supported a multitarget antiproliferative profile. Conclusions: P. scoparius represents a promising source of natural compounds with multitarget antiproliferative potential. The combined experimental and computational findings provide mechanistic insights into its activity and support its relevance within the context of natural product-based cancer therapy, highlighting its potential for further preclinical development.

While anti-tumor drugs markedly improve patient survival, dose-limiting toxicities remain major constraints on clinical efficacy and quality of life. Conventional management strategies lack timeliness and precision. Traditional Chinese medicine (TCM) and its active ingredients offer unique potential for mitigating anti-tumor drug toxicities through multi-component and multi-target regulation. However, the transformation of TCM is hampered by poor bioavailability and targeting. This review summarizes and evaluates an integrated strategy combining TCM with nanotechnology to develop novel nanomedicines. It elucidates the distinct toxicity mechanisms of chemotherapy drugs, targeted drugs, and immunotherapy drugs, revealing toxicopathological transitions from non-specific killing to microenvironment disruption and immune imbalance. Subsequently, it discusses the intervention mechanisms and research progress of TCM and its active ingredients targeting different categories of anti-tumor drug toxicity. To overcome delivery challenges, this review explores construction strategies for diverse nanodelivery systems, including carrier-free self-assembled nanomedicines, physically loaded nanomedicines, and chemically coupled nanomedicines, highlighting their value in organ-specific accumulation and controlled release. Finally, it objectively analyzes challenges in the clinical translation of these nanomedicines, encompassing safety and industrialization, while prospecting future trends, aiming to contribute to a new therapeutic paradigm focused on "toxicity attenuation and efficacy potentiation" and steer cancer treatment toward greater precision and intelligence.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent worldwide and represents the hepatic manifestation of a systemic cardiometabolic-inflammatory syndrome rather than an isolated organ disease. In parallel, anticancer therapies carry a well-recognised burden of cancer therapy-related cardiovascular toxicity (CTR-CVT). Evidence suggests that the metabolic-inflammatory cascade driving steatosis → steatohepatitis → fibrosis may also contribute to endothelial dysfunction, myocardial remodelling and cardiomyocyte vulnerability to chemotherapy-induced oxidative stress. This narrative review proposes a unifying conceptual framework in which MASLD may act as a potential amplifier of cardiotoxicity in oncology patients and examines whether lifestyle and dietary interventions could mitigate this cumulative risk. Methods: A structured literature search of PubMed, Scopus and Web of Science was performed, prioritising systematic reviews, meta-analyses, randomised controlled trials, large cohort studies and recent international guidelines on MASLD, cardio-oncology and nutritional interventions. Results: Four converging molecular axes were identified as plausible links between MASLD and cardiomyocyte susceptibility to anticancer therapy: mitochondrial dysfunction with reactive oxygen species overproduction, NLRP3 inflammasome activation and metaflammation, endothelial nitric oxide impairment, and pro-fibrotic TGF-β/hepatic stellate cell signalling. Mediterranean-style dietary patterns, selected micronutrients and emerging metabolic therapies modulate the same network and may offer translational opportunities. Conclusions: Reframing MASLD as a potentially modifiable amplifier of CTR-CVT supports the integration of hepatic phenotyping into baseline cardio-oncology risk stratification and the use of personalised nutrition as a precision tool acting on shared mitochondrial, inflammatory, endothelial and fibrotic pathways. Multidisciplinary framework and prospective interventional studies, adopting composite hepato-cardio-oncological endpoints, are warranted.

Wood-inhabiting fungi constitute a valuable source of biologically active compounds with significant therapeutic potential. Particular attention is paid to species known for their high content of polysaccharides, triterpenoids, phenolic compounds, and other secondary metabolites exhibiting cytotoxic and immunomodulatory activities. The results indicate that extracts obtained from these fungi may inhibit tumor growth, induce apoptosis, and support the immune response of the organism. Although further clinical studies are required, wood-inhabiting medicinal fungi represent a promising direction in the development of natural anticancer therapies and complementary treatment strategies.

Background: Chemotherapy-induced intestinal mucositis (CIM) is a common gastrointestinal complication of anticancer therapy, and 5-fluorouracil (5-FU) is among the agents most frequently implicated. Betulin (BE), a lupane-type pentacyclic triterpenoid with anti-inflammatory and cytoprotective activities, has not been systematically evaluated in 5-FU-induced CIM. Purpose: This study evaluated the therapeutic effects of BE in a mouse model of 5-FU-induced CIM and examined associated histopathological, apoptotic, inflammatory, and gut microbiota changes. Methods: BALB/c mice received intraperitoneal 5-FU (30 mg/kg/day) for four consecutive days, followed by oral BE at 0, 50, 100, 200, or 400 mg/kg/day for another four days. Clinical manifestations, colon morphometry, blinded descriptive histopathological assessment, apoptosis- and inflammation-related markers, and gut microbiota were assessed. Results: BE treatment alleviated body weight loss, diarrhea, and reduced food intake and was associated with improved colon morphometry and less severe histological injury. At 200 mg/kg, BE treatment was associated with lower Tnf and Nos2 mRNA expression, lower Bax and total caspase-3 protein abundance, higher Bcl-2 protein abundance, and lower iNOS protein abundance. Microbiota analysis of the 200 mg/kg group showed treatment-associated differences in microbial diversity and community composition; these findings were considered exploratory because of the small sample size. Conclusions: BE showed therapeutic potential in 5-FU-induced intestinal mucositis. The molecular and microbiota findings obtained at 200 mg/kg support associations with apoptosis-, inflammation-, and microbiota-related changes but do not establish a definitive mechanism.

Triple-negative breast cancer (TNBC) remains a highly aggressive malignancy with limited therapeutic options and frequent resistance to platinum-based chemotherapy. Rosmarinic acid (RA), a naturally occurring polyphenol, has attracted considerable interest as a potential chemosensitising agent. This study investigated the anticancer activity and the underlying mechanisms of RA combined with cisplatin (CDDP) in 4T1 breast cancer cells while assessing the cytotoxic responses of non-cancerous HaCaT keratinocytes as a preliminary indicator of differential treatment sensitivity. Cytotoxicity was assessed using the MTT assay, followed by calculation of the Combination Index (CI), Drug Reduction Index (DRI), and Selectivity Index (SI). The generation of intracellular reactive oxygen species (ROS) was evaluated by DCFH-DA fluorescence imaging, and the functional contribution of oxidative stress was examined using N-acetyl-L-cysteine (NAC) rescue experiments. Apoptosis was analysed by Annexin V/PI flow cytometry, NucBlue nuclear staining, and Calcein-AM/propidium iodide (PI) Live/Dead fluorescence imaging. Three-dimensional (3D) tumour spheroids were used to assess treatment-induced alterations in spheroid morphology, morphometric parameters, viability based on adenosine triphosphate (ATP), and Live/Dead staining. The expression of genes related to apoptosis was determined by RT-qPCR, and potential molecular mechanisms were explored using the construction of protein-protein interaction (PPI) networks together with Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment analyses. The combination of RA + CDDP exhibited strong synergistic cytotoxicity in 4T1 cells while demonstrating comparatively lower toxicity toward HaCaT keratinocytes. Combination treatment markedly increased intracellular ROS generation, whereas NAC significantly reduced ROS accumulation and partially restored cell viability, indicating that oxidative stress is a major but not exclusive mediator of cytotoxicity. Combined treatment significantly enhanced apoptotic cell death, increased chromatin condensation and membrane damage, upregulated the expression of Bax, Casp9, Cycs, and Trp53, and downregulated Bcl2, consistent with transcriptional regulation of intrinsic apoptotic signalling. In 3D tumour spheroids, the combination markedly reduced spheroid size, disrupted structural integrity, decreased ATP-based viability, and substantially increased tumour cell death compared to monotherapy. Bioinformatic analyses identified central genes related to apoptosis and cell survival and predicted significant enrichment of PI3K/Akt, p53, MAPK, and apoptosis signalling pathways. RA significantly potentiates the antitumor efficacy of CDDP through synergistic induction of ROS-associated apoptotic signalling while showing a more favourable cytotoxic response in 4T1 breast cancer cells than in non-cancerous HaCaT keratinocytes. The integrated findings from two-dimensional (2D) and 3D models, NAC rescue experiments, molecular analyses, and bioinformatics collectively support the potential of RA as a promising chemosensitising adjuvant for CDDP-based breast cancer therapy and warrant further validation in preclinical in vivo models.

Glioblastoma multiforme (GBM) remains one of the most aggressive and treatment-resistant brain tumors, characterized by rapid proliferation and poor patient prognosis. Novel therapeutic strategies are urgently needed to improve clinical outcomes. In this study, we investigated the cytotoxic and pro-apoptotic effects of bortezomib (BORT), a proteasome inhibitor, and graphene oxide (GO), a nanomaterial with known anticancer potential, on human glioblastoma cell lines. Treatment with BORT and GO, both individually and in combination, significantly reduced cell viability in a dose-dependent manner, as determined by MTT. In this study, we observed enhanced apoptotic cell death, accompanied by increased activation of both caspase-8 and caspase-9, indicating simultaneous engagement of extrinsic and intrinsic apoptotic pathways. Western blot analysis demonstrated downregulation of anti-apoptotic proteins Bcl-2 and upregulation of pro-apoptotic markers (NOXA, cleaved PARP). A central finding of this work is the pronounced increase in intracellular reactive oxygen species (ROS) levels following BORT-GO treatment. The elevated ROS levels observed in BORT-GO-treated cells compared with free bortezomib therefore suggest that GO-mediated oxidative stress may amplify proteasome inhibition-induced apoptosis, which is particularly visible in the A172 and LN229 cell lines. Notably, the combination of BORT and GO may suggest a potential cooperative mechanism through proteasome inhibition and oxidative stress induction. These findings indicate that graphene oxide may modulate the antitumor efficacy of bortezomib in a cell line-dependent manner and support further investigation of this combination as a promising therapeutic approach for glioblastoma.

Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer with limited therapeutic options for patients at high risk of disease recurrence and metastasis. The cyclic nucleotide-degrading enzyme, phosphodiesterase 10A (PDE10), that hydrolyzes both cAMP and cGMP has been previously reported to be expressed in multiple cancers and regulates key cellular signaling pathways involved in cancer cell proliferation, survival, and maintenance of stem cell-like properties. We found that PDE10 overexpression was associated with poor relapse-free survival of TNBC patients and identified its potential as a therapeutic target for TNBC using a novel inhibitor, ADT-030. Our results showed that ADT-030 inhibited the growth of TNBC cells, reduced colony-forming efficiency and enhanced the therapeutic efficacy of paclitaxel. A TNBC mouse model demonstrated that oral administration of ADT-030 significantly suppressed syngeneic tumor growth and enhanced the antitumor efficacy of paclitaxel. ADT-030 treatment altered differentially expressed genes (DEGs), signaling pathways, and cellular processes. Overall, our findings suggest that ADT-030, as a monotherapy or in combination with standard-of-care chemotherapy, may be an effective therapeutic approach for TNBC. Further studies are warranted to better understand the oncogenic role of PDE10 in TNBC and the mechanisms by which ADT-030 modulates the tumor microenvironment (TME) and enhances chemotherapy response.

Free radicals with reactive chemical properties can combat tumors without inducing drug resistance. Reactive oxygen species (ROS) have been widely applied in tumor therapy; however, the prevalent hypoxic conditions within tumors severely hinder the generation of ROS, leading to suboptimal antitumor efficacy. Herein, we designed an endogenous H2O2-triggered chlorine radical nanogenerator (Cl•) and hydroxyl radicals(•OH), which have better kinetic advantages and higher catalytic activity in catalyzing the H2O2 reaction. In vitro cytotoxicity tests revealed that the nano-urchins induced marked cancer cell death (up to ∼80% at the highest tested concentration) in a concentration-dependent manner, attributable to the chlorine radical-mediated oxidative stress. Moreover, the H2O2-specific activation strategy reduces toxic side effects on normal tissues, thereby enhancing the safety of tumor therapy. Finally, compared with conventional Cu2O nanocatalysts that solely generate •OH, our designed nano-urchins exhibit enhanced therapeutic efficacy, which is mainly attributed to the synergistic therapeutic effect. Therefore, our nano-urchins can serve as a novel nanocatalyst for tumor therapy.

Patients with unresectable pancreatic ductal adenocarcinoma (PDAC) frequently experience impaired treatment continuity, and many cannot reach second-line treatment. We evaluated whether pretreatment geriatric nutritional risk index (GNRI) could identify patients at risk of impaired treatment continuity, treatment-related adverse events, and shorter survival.

The genus Hedera L. has long been recognized as a valuable source of anticancer agents, such as triterpenoid saponins. In contrast, Hedera pastuchovii Woronow remains largely unexplored. This study investigates the cytotoxic profiles and genoprotective potential of H. pastuchovii leaf extracts. Leaves were extracted with ethanol and fractionated into n-hexane (Hex-F), ethyl acetate (Eth-F), and methanolic (Met-F) fractions using vacuum liquid chromatography. Phenolic, flavonoid, and saponin contents were quantified. Cytotoxicity was evaluated against four human cancer cell lines: A549 (lung), MCF-7 (breast), HeLa (cervical), and SKOV3 (ovarian), using the MTT assay. Apoptosis was assessed by Annexin V/PI flow cytometry, and genotoxicity or genoprotective effects were measured by the micronucleus assay in human lymphocytes. Phytochemical analysis revealed a total saponin yield of 29.95%. The Met-F fraction exhibited the highest concentrations of total phenolics (77.93 mg GAE/g) and triterpenoids (138.62 mg UAE/g), as well as the most pronounced cytotoxic activity, significantly reducing cell viability across all tested cancer lines in a concentration-dependent manner. The IC50 values were 108.23, 150.70, 213.77, and 781.07 µg/mL for SKOV3, MCF-7, HeLa, and A549 cell lines, respectively. In comparison, the Hex-F and Eth-F demonstrated weak cytotoxicity (IC50 > 1000 µg/mL). Flow cytometry suggested apoptosis as the predominant mode of cell death induced by Met-F. The micronucleus assay showed that Met-F reduced cisplatin-induced micronuclei formation in lymphocytes in a dose-dependent manner, indicating measurable genoprotective activity. These findings provide preliminary evidence that H. pastuchovii leaf fractions, particularly Met-F, possess in vitro cytotoxic and genoprotective properties that warrant further investigation.

In the present work a novel series of 11H-indeno[1,2-b]quinoxaline derivatives were rationally designed and synthesised, with the aim of exploring their potential anticancer properties.The novel compounds were studied by IR, 1H NMR, 13C NMR, 31P NMR, mass spectrometry, and single-crystal analysis. The anticancer efficacy of compounds 8a and 8b against the MCF-7 cell line demonstrated promising activity with IC50 values of 18.9 and 33.0 µg/mL, respectively. On the other hand, the antitumor efficacy of compounds 12 and 14 against the HCT116 cell line demonstrated encouraging results, with IC50 values of 47.3 and 21.4 µg/mL, respectively. Furthermore, in silico methodologies including ADME, BOILED-Egg, and bioactivity radar were employed to assess the oral bioavailability of the synthesized hybrids. Molecular docking was conducted to determine the docking poses and binding interactions of the derivatives with proteins bearing PDB: 6vj3 and 6GUE.

In this study, we engineered pH/glutathione dual-responsive nanoparticles (LP/CC-Cu-Cur NPs) based on a poly-γ-glutamic acid (γ-PGA)/chitosan (CS) core-shell architecture for synergistic chemo/chemodynamic therapy of glioma. The nanoparticles feature a core of CC-Cu-Cur NPs, formed via Cu2+-coordinated self-assembly of caffeic acid-grafted CS and curcumin (Cur), encapsulated within a phenylboronic acid-conjugated γ-PGA shell through pH-sensitive borate ester bonds. Surface modification with lactoferrin conferred brain-penetrating and glioma-targeting capabilities. The resulting spherical nanoparticles had a uniform size of 235.89 nm, a zeta potential of -22.66 mV, and high Cur loading (6.02%) and encapsulation efficiency (83.09%). Upon exposure to the acidic tumor microenvironment, the nanoparticle shell detaches, reversing surface charge from negative to positive, thereby enhancing cellular uptake and mitochondrial targeting. Intracellular glutathione then triggers core degradation, releasing Cur and Cu2+. Cur induces mitochondrial apoptosis, while Cu2+ catalyzes a Fenton-like reaction, converting endogenous hydrogen peroxide into highly cytotoxic reactive oxygen species. In vitro, the nanoparticles showed enhanced blood-brain barrier penetration, efficient lysosomal escape, and potent cytotoxicity against GL-261 cells (IC50 = 18.34 μg/mL) via a synergistic action of Cu2+ and Cur (CI = 0.28). In vivo, LP/CC-Cu-Cur NPs achieved superior brain accumulation and antitumor efficacy, highlighting their potential as a promising strategy for glioma therapy.

A man in his 70s with lung adenocarcinoma (cStage IVA) received POSEIDON-based therapy with durvalumab, tremelimumab and chemotherapy. After six cycles, progressive disease prompted a switch to carboplatin plus nab-paclitaxel. Nineteen weeks after the final immune checkpoint inhibitor (ICI) administration, he developed fatigue and anorexia. Adrenocorticotropic hormone (ACTH) and cortisol were below assay detection limits, and a corticotropin-releasing hormone stimulation test showed no ACTH response, consistent with ICI-related isolated ACTH deficiency. Symptoms improved with hydrocortisone replacement. Five weeks later, he developed diabetic ketoacidosis, with a glucose level of 30.4 mmol/L (reference range, 3.9-6.1 mmol/L) and a ketone level of 6.3 mmol/L (<0.6 mmol/L). HbA1c and urinary C-peptide excretion were 6.9% (4.6%-6.2%) and 1.8 nmol/day (7.5-51.4 nmol/day) respectively. These findings supported a diagnosis of fulminant type 1 diabetes mellitus, considered ICI-related. This case highlights the need for continued vigilance, as immune-related adverse events may develop sequentially even after ICI therapy has ended.

Glioblastoma (GBM) remains a lethal primary brain tumor, in part because therapeutic efficacy is limited by the blood-brain barrier (BBB) and the complex tumor microenvironment (TME). Sonodynamic therapy (SDT), i.e., use of ultrasound to activate chemical sensitizers and generate cytotoxic stress, offers a non-invasive strategy for treating deep-seated intracranial disease, but progress is constrained by the scarcity of validated sonosensitizers and the inefficiency of conventional in vitro screening methods. Here, we introduce a New Approach Methodology (NAM) that couples a neural network-based positive-unlabeled (PU) learning framework with a high-throughput, magnetic field-guided 3D bioprinting platform to accelerate identification and experimental validation of SDT-sensitizing agents. Using curated drug and small-molecule data and RDKit-derived molecular descriptors, the PU classifier identifies candidate ultrasound-responsive compounds without requiring reliable negative labels. We then validate the AI-based predictions in physiologically relevant U-87 MG glioblastoma spheroids that reproduce key TME features, including spatial heterogeneity and a hypoxic core. The NAM identifies two FDA-approved drugs, carboplatin (advanced ovarian cancer) and memantine hydrochloride (Alzheimer's disease), as effective ultrasound-responsive agents. In 3D spheroids, combining low-intensity pulsed ultrasound with either drug significantly reduces viability compared with drug-only controls, and both combinations outperform temozolomide (TMZ), the current standard chemotherapeutic. Time-resolved responses reveal distinct kinetics: memantine produces strong early cytotoxicity (24 h) enhanced by ultrasound, whereas carboplatin shows delayed but pronounced cytotoxicity (72 h), also improved by ultrasound. Together, these results establish an integrated computational-experimental NAM that enables rapid repurposing of approved drugs as SDT sensitizers and provides a scalable framework for advancing GBM therapeutic discovery while reducing reliance on animal studies.

Poor aqueous solubility and low permeability limit the oral bioavailability of Nilotinib, a second-generation tyrosine kinase inhibitor used in chronic myeloid leukemia. Nanosponges prepared using cyclodextrin derivatives offer a scalable and efficient platform for enhancing solubility, controlling release, and improving bioavailability. Therefore, this study aimed to formulate Nilotinib-loaded hydroxypropyl β-cyclodextrin nanosponges to enhance oral absorption.

Breast cancer remains one of the leading causes of cancer-related mortality among women worldwide. Tumor angiogenesis plays a crucial role in breast cancer progression, making angiogenesis-associated pathways attractive therapeutic targets. Computational drug discovery approaches, including virtual high-throughput screening (VHTS), molecular docking, molecular dynamics simulations, and binding free energy calculations, have emerged as valuable tools for identifying and optimizing anticancer compounds. This review evaluates the application of these computational techniques in the discovery of antiangiogenic therapeutic candidates for breast cancer.