Methionine restriction (MR) has shown significant promise in cancer therapy because it targets the unique methionine dependency of many tumors. However, despite extensive research on MR, a clear synthesis of preclinical findings and their translation into clinical settings is lacking. This review aims to address this gap by consolidating existing evidence, identifying challenges, and highlighting opportunities for advancing MR as a viable cancer treatment strategy. Preclinical studies have revealed that MR effectively hinders cancer cell proliferation, triggers cell cycle arrest, and enhances the effectiveness of standard treatments, including chemotherapy and radiotherapy. Mechanistically, MR disrupts critical cancer pathways by influencing epigenetic regulation, redox balance, and autophagy. Moreover, animal models have demonstrated notable tumor suppression and extended survival, underscoring the therapeutic potential of MR. Early-phase clinical trials are now examining MR in combination with established therapies, reporting positive preliminary results regarding safety and tolerability, and investigating biomarkers for predicting patient responsiveness. These findings suggest the utility of MR as a complementary treatment strategy, particularly for tumors resistant to conventional therapies. The outcomes of this study underscore the importance of further research to refine MR protocols, understand long-term effects, and identify optimal patient groups. Furthermore, combining MR with immunotherapies, targeted treatments, and advanced modalities such as chimeric antigen receptor (CAR)-T cell therapy may offer new therapeutic pathways. Additionally, the development of MR-mimetic drugs and targeted supplements can improve patient compliance and broaden the therapeutic applicability of MR. Large-scale clinical trials are essential to evaluate the efficacy of MR across diverse cancer types, focusing on sustainability and safety over extended periods. If successful, MR can transform cancer therapy by exploiting metabolic vulnerabilities in cancer cells, providing a novel and less toxic treatment option for challenging malignancies.

Marine-derived compounds have emerged as a promising frontier in cancer research due to their remarkable structural diversity and broad-spectrum bioactivities. The marine environment, encompassing diverse organisms (e.g., sponges, algae, tunicates, mollusks, and marine microbes), is a prolific source of novel bioactive molecules with potent anti-cancer properties. Key classes of these compounds include alkaloids, polysaccharides, peptides, terpenoids, and polyketides, which exert anti-tumor effects through diverse mechanisms, including the induction of apoptosis, inhibition of angiogenesis, modulation of immune responses, interference with cell cycle progression, and targeting of critical signaling pathways involved in tumorigenesis and metastasis. Notably, marine-derived drugs such as trabectedin, eribulin, and plitidepsin have received regulatory approval for the treatment of various malignancies, demonstrating the translational potential of these natural compounds. Ongoing clinical and preclinical investigations are exploring a wide range of marine metabolites for their cytotoxic, anti-proliferative, and chemosensitizing properties. Advances in marine biotechnology, including genome mining, synthetic biology, and fermentation technologies, have significantly facilitated the discovery, sustainable production, and structural optimization of marine natural products. However, challenges such as low yield, structural complexity, limited water solubility, and poor bioavailability hinder their broader clinical application. The integration of novel drug delivery systems, such as nanoparticles, liposomes, and conjugates, offers a viable solution to overcome these limitations and improve pharmacokinetic profiles. This review provides a comprehensive overview of the mechanisms of action, therapeutic applications, and clinical development of marine-derived anti-cancer compounds. It also emphasizes the need for deeper insights into their molecular targets and the potential for synergistic use with existing chemotherapeutic agents. Future directions should focus on exploring untapped marine biodiversity, developing eco-friendly harvesting strategies, and developing innovative delivery platforms to fully harness the therapeutic promise of the marine pharmacopeia in oncology.

Background Alzheimer disease (AD) is a progressive dementia affecting a large proportion of the aging population. There is evidence that brain tissue in patients with AD is exposed to oxidative stress during the course of the disease. Conessine is a natural steroidal glycoside, which has been reported to exert various biological activities such as antioxidant and anti-inflammatory effect. Aim The present study aimed to investigate the effects of Conessine on neurobehavioral activity and superoxide dismutase (SOD), glutathione reductase (GRx) and catalase (CAT) enzymes activity, malondialdehyde (MDA) levels in hippocampal area of rats in an experimental model of AD. Methods The AD was induced in animals by intracerebroventricular injection of STZ (icv-STZ) unilaterally. Animals were treated with the Conessine (20 mg/kg body weight), then after three successive weeks, recognition memory was examined (passive avoidance test and novel object recognition test) and antioxidant parameters were evaluated. Results In our study behavioural testes showed improvement on memory retrieval and recognition memory consolidation. Furthermore the Conessine increased the activity of antioxidant enzymes SOD, glutathione GRx and CAT levels and decreased MDA in the hippocampal area. Conclusion These results suggested that Conessine may inhibit STZ-induced oxidative stress, and that it may possess therapeutic potential for the treatment of AD.

Alzheimer’s disease (AD) represents an escalating global neuropharmacological crisis, with prevalence in high-growth demographic regions such as India projected to exceed 14 million by 2040. This study addresses the urgent need for high-potency, dual-site acetylcholinesterase (AChE) inhibitors through an integrated computational pipeline. We address the failure of mono-target paradigms by designing scaffolds capable of simultaneously anchoring the Catalytic Active Site (CAS) and the Peripheral Anionic Site (PAS). A robust GA-MLR QSAR model was developed from 115 quinoline analogs using 11,135 descriptors. Lead candidates were prioritized via cavity directed molecular docking (7XN1) and 100 ns molecular dynamics (MD) simulations. The five-descriptor model (R² = 0.7569, $Q_{LOO}^2$ = 0.7244) was validated by an external set of 8 experimental compounds ($R_{ext}^2$ = 0.8620). Lead Compound 19 emerged as a superior candidate (ΔG = −11.1 kcal/mol), exhibiting a stable MD trajectory (PL-RMSD ≈ 2.4 Å) and preserving essential Gly121-His447 catalytic anti-correlations. This study provides a statistically validated scaffold and computational mechanistic foundation for future in vitro experimental validation, advancing the high throughput screening of neuroprotective agents on a global scale.

Daclatasvir is a direct-acting antiviral agent against hepatitis C virus (HCV) used for the treatment of chronic HCV genotype infections of 1 and 3. Hepatitis C is an infectious liver disease caused by infection with hepatitis C virus (HCV). There are no reports found to be daclatasvir in ionic liquid-based extraction. A simple vortex assisted an environmental eco-friendly ionic liquid dispersive liquid–liquid microextraction method for determination of daclatasvir form rat serum. For the sample extraction, various green solvents, like ionic liquids, were used. The repercussion of various dispersive solvents, extractant, and disperser ratios was evaluated; non-identical ionic liquids assess the salt concentration on sample recoveries and enrichment factors were examined. Amid all the ionic liquids that were scrutinized, 1-butyl-3-methylimidazolium hexafluorophosphate was selected as the most effective ionic liquid. The present bioassay recoveries were found to be more than 99.4% at an extractant and disperser ratio of 0.43 with an addition of 5.0% NaCl (sodium chloride) that was selected as an effective salt concentration for present extraction. Compared to protein precipitation, the enhanced detection and quantification limits attained were 0.015 μg/mL and 0.045 μg/mL, respectively. A linear relationship in the range of 0.05–10.0 μg/mL respectively with a correlation coefficient of (r2) 0.9996 was observed. The developed method was successfully applied to study the pharmacokinetics of daclatasvir in rat serum according to the bioanalytical method validation guidelines.

Background: Phytotherapy is considered a complementary approach for preventing and treating many diseases. Plants are rich source of bioactive secondary metabolites of a wide variety such as saponins, tannins, terpenoids, alkaloids, and flavonoids. Sapindus laurifolia (fam: Sapindaceae), well known as soapnuts, are used medicinally as an expectorant, emetic, contraceptive, and for treatment of excessive salivation, epilepsy, chlorosis, and migraines. Objective: To isolation of fractions, estimation of total flavonoid content, in vitro antioxidant and in vivo neuroprotective activity of S. laurifolia fruit kernel. Materials and Methods: In this study, in vitro antioxidant activity is estimated by 2,2-diphenyl-1-picrylhydrazyl assay method. Neuroprotective activity is estimated by scopolamine-induced dementia method. In neuroprotective method, behavioral parameters were checked by escape latency (EL) time (s) by using the Morris water maze, active avoidance testing using elevated plus maze, and neurochemicals such as glutathione, catalase (CAT), superoxide dismutase (SOD), and Cholinesterase were estimated. Results: In scopolamine-induced dementia, increased EL time, active avoidance and neurochemicals such as glutathione, CAT, SOD and cholinesterase decreased. Whereas standard and Fraction S-treated animals decreased in EL time, active avoidance and increased locomotor activity, neurochemicals such as glutathione, CAT, SOD, and cholinesterase also increased. Conclusion: The present study clearly demonstrates that methanolic extract of S. laurifolia Fraction A (50 and 100 mg/kg) kernel significantly attenuate scopolamine-induced dementia by improving the learning, memory, antioxidant potentiality, and anti-acetyl cholinesterase activity. Therefore, this Fraction A can be a potential novel therapeutic strategy for controlling neurodegenerative dementia especially Alzheimer's disease. Yet, advance studies are needed to characterize the active compound(s) and expose the possible mechanism of action.