<rss version='2.0' >

                    <channel>

                    <title><![CDATA[Current Pharmacogenomics and Personalized Medicine (Volume 23 - Issue 1)]]></title>

                    <link>https://www.benthamscience.com/journal/104</link>

                    <description>

                    RSS Feed for Journals <![CDATA[Current Pharmacogenomics and Personalized Medicine]]> | BenthamScience

                    </description>

                    <generator>EurekaSelect (+https://www.benthamscience.com)</generator>

                    <pubDate>2026-05-18</pubDate>

                    <image>

                    <title><![CDATA[Current Pharmacogenomics and Personalized Medicine (Volume 23 - Issue 1)]]></title>

                    <url></url>

                    <link>https://www.benthamscience.com/journal/104</link>

                    </image><item><title><![CDATA[Role of Artificial Intelligence in Transforming Diagnosis, Treatment, and Patient Care: A Review]]></title><link>https://www.benthamscience.com/article/151584</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Artificial intelligence has recently begun to expand the capabilities of precision medicine in diverse fields of medicine. Artificial intelligence-based solutions like deep learning, machine learning, predictive analytics, etc., have transformed disease detection, treatment planning, and patient care horizons. In oncology, artificial intelligence assists in early cancer diagnosis and personalized treatment protocols. In cardiology, predictive models help diagnose diseases and prevent serious events. Artificial intelligence applications in seizure prediction and neurodegenerative disease progression analysis enhance neurology diagnostic and therapeutic methods. Pharmacogenomics applies artificial intelligence in customizing drug remedies according to genetic profiling to increase therapeutic efficiency and avoid unfavourable responses. Artificial intelligence also helps manage neurodegenerative disorders through early diagnosis and intervention strategies. It contributes to more precise diagnostics, better therapy efficiency, and improved prognosis of the patients. Other significant benefits of integrating AI into clinical practice are health administration, the analysis of medical records, and processing massive datasets in medical research. To fully benefit from artificial intelligence, there is a need to overcome the obstacles, including model interpretability, data privacy issues, and regulatory compliance requirements. In this study, we examine the use of AI in precision medicine, emphasizing developments in necessary medical fields and noteworthy results. Artificial intelligence is transforming contemporary healthcare and building a more effective and efficient medical system through automated decision-making, personalized treatment, and early diagnosis. </p>]]></description> </item><item><title><![CDATA[Tracking the Evolution of Artificial Intelligence in Pharmacogenomics: A Bibliometric Approach to Personalized Healthcare]]></title><link>https://www.benthamscience.com/article/151349</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> The application of artificial intelligence (AI) techniques like machine learning (ML) and deep learning (DL) has gained significant momentum in pharmacogenomics (PGx). AI models can identify promising drug candidates likely to interact with particular genetic profiles. The research works and bibliographic details regarding the use of artificial intelligence in pharmacogenomics were obtained from PubMed between 1st January 2004 and 1st April 2025. The relative growth rate (RGR) analysis shows a decline in recent years, but the increasing doubling time might reflect the complex nature of research in this field. Out of 282 publications, most articles were published in 2024, reflecting the growing adoption of AI tools within this area. Multiple researchers authored many studies. India ranks fifth, contributing 11 (3.9%) articles. The findings underscore the swift expansion, collaborative efforts, and international scope of research in AI-driven pharmacogenomics. </p>]]></description> </item><item><title><![CDATA[A Roadmap to the Scientific Society of the Future]]></title><link>https://www.benthamscience.com/article/151585</link><pubDate>2026-05-18</pubDate><description><![CDATA[]]></description> </item><item><title><![CDATA[Exploring Medicine and Health Data Security: Key Insights and Best Practices]]></title><link>https://www.benthamscience.com/article/150981</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: With the exponential growth of digital health information systems, ensuring secure health data analytics has become critical for enhancing healthcare delivery, protecting patient privacy, and fostering innovation. The rise in privacy breaches and unauthorized data access has amplified the need for robust data security mechanisms during the health data analytics process. </p> <p> Methods: This study employed a qualitative research methodology, incorporating multiple case studies from various healthcare organizations. Through in-depth interviews and document analysis, the study explored real-world challenges and strategies implemented to secure health data during analytics. </p> <p> Results: Key findings revealed that while organizations face common challenges such as data integration, privacy concerns, and compliance with regulatory standards, the successful implementation of security practices like end-to-end encryption, strict access control, anonymization techniques and employee training can significantly mitigate risks. The comparative analysis across institutions highlighted recurring themes and effective practices that enhance data protection. </p> <p> Discussion: The case studies demonstrate that secure health data analytics is achievable through a proactive, multi-layered approach. Integration of advanced cybersecurity protocols with existing health information systems not only prevents breaches but also builds public trust. Limitations of the study include the small sample size and organizational diversity, which may limit generalizability. </p> <p> Conclusion: By synthesizing lessons learned and outlining best practices, this study provides a valuable reference for healthcare professionals, researchers, and policymakers. Adopting these measures enables stakeholders to securely leverage health data for insightful analytics, thereby advancing healthcare outcomes while maintaining patient confidentiality. </p>]]></description> </item><item><title><![CDATA[An Updated Mini-review: Newer Quinazoline Based EGFR Inhibitors as Anticancer Agents]]></title><link>https://www.benthamscience.com/article/150745</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: Cancer remains one of the most prevalent and deadly illnesses, even with notable advancements in novel treatment alternatives. One important strategy for targeted cancer therapy is the EGFR (epidermal growth factor receptor) signaling pathway. Cancer treatment has greatly improved when the EGFR-driven pathway is inhibited by targeting the tyrosine kinase domain of EGFR. Several small compounds, particularly quinazoline-containing derivatives, have been developed using simulation studies to determine EGFR tyrosine kinase inhibitors (TKIs). The design process also assessed the appearance of epigenetic alterations and resistance issues, which limited the effectiveness of medications over time and clarified the necessity for additional research in this area. In recent decades, extensive research has investigated the genetic alterations occurring in the EGFR tyrosine kinase domain. These alterations have paved the way for the development and production of highly potent and efficacious inhibitors. </p> <p> Methods: This review highlights the structure-activity relationship (SAR) and biological activity of different quinazoline derivatives that have been reported to have EGFR-TK inhibitory antiproliferative activity. We searched Embase, Cochrane, and PubMed for literature on quinazoline derivatives showing EGFR inhibition as anticancer agents. </p> <p> Results: We confirmed that quinazoline derivatives with different substitutions are useful pharmacophores as EGFR TK inhibitors for achieving strong anticancer activity after a thorough review of the literature. </p> <p> Discussion: This review offers insights into the latest advancements in developing novel and potent quinazoline derivatives as potential EGFR tyrosine kinase inhibitors, which could be further optimized to develop new EGFR inhibitors in the future. </p> <p> Conclusion: Quinazoline-based scaffolds remain promising leads for developing nextgeneration EGFR tyrosine kinase inhibitors with enhanced anticancer efficacy. </p>]]></description> </item><item><title><![CDATA[Chemotherapy Drug-induced Neurotoxicity: A Pharmacogenomic Perspective]]></title><link>https://www.benthamscience.com/article/151151</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Chemotherapy remains the cornerstone of cancer treatment, and has significantly improved patient survival. However, it is often accompanied by adverse effects that negatively impact quality of life, with neurotoxicity being one of the most debilitating yet often overlooked complications. This study aims to explore the influence of genetic variations on chemotherapy-induced neurotoxicity. Utilizing the PharmGKB database, we identified genetic variants associated with neurotoxic responses and assessed their Level of Evidence (LOE). Our findings highlight several genes, <i>BCL2, OPRM1, SOX10, TRPV1, CYP3A4*22, GSK3β, DPYD,</i> and <i>ADORA2A</i>, that are involved in neurotoxicity induced by chemotherapeutic agents, such as platinum/taxane, vincristine, fluorouracil, and methotrexate. These genetic factors modulate individual susceptibility to neurotoxic side effects. Understanding these associations supports the development of genotypeguided therapeutic strategies to reduce toxicity and improve quality of life in cancer patients receiving chemotherapy. </p>]]></description> </item><item><title><![CDATA[Advanced Cancer Drug Development through Reverse Pharmacology: Integrating Traditional Knowledge and Herbal Therapies]]></title><link>https://www.benthamscience.com/article/153048</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> The global rise in cancer incidence, together with limitations of conventional therapies, including drug resistance, adverse effects, and high costs, underscores the need for innovative and multi-target treatment strategies. Reverse Pharmacology (RP) offers a translational framework that integrates traditional medical knowledge, particularly from Ayurveda, into modern oncology. Unlike conventional drug discovery, RP begins with clinically documented traditional remedies and progresses through experimental validation, mechanistic elucidation, and formulation standardization. This strategy may be advantageous for complex diseases like cancer, which often require multimodal therapeutic interventions. Medicinal plants such as <i>Curcuma longa, Withania somnifera</i>, and <i>Tinospora cordifolia</i> show notable anticancer potential by modulating key molecular targets, including NF-κB, PI3K/Akt, STAT3, and p53. Their key phytoconstituents, such as curcumin, withaferin A, and berberine, exhibit anti-proliferative, pro-apoptotic, antiangiogenic, and anti-metastatic properties in diverse cancer models. Additionally, these botanicals are generally considered safe, supported by centuries of traditional use and increasing preclinical validation. RP may facilitate the development of plant-based therapeutics and promote evidence-based, patient-centric approaches in cancer care. This review highlights how RP bridges ethnomedical knowledge and scientific research, thereby encouraging the integration of bioactive plant compounds into modern oncological practice to deliver cost-effective, accessible, and personalized treatment solutions. </p>]]></description> </item><item><title><![CDATA[Pharmacogenomics and Toxicogenomics in Personalized Public Health: Integrating Genetic Insights, Emerging Technologies, and Global Regulatory Perspectives to Prevent Drug-induced Toxicity and Enhance Therapeutic Outcomes]]></title><link>https://www.benthamscience.com/article/152342</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: Patient drug response, therapeutic outcomes, and the prevention of adverse reactions rely on pharmacogenomics and toxicogenomics, which study genetic variations influencing drug metabolism and toxicity. Integrating pharmacogenomics with toxicogenomics enhances patient safety by identifying individuals at risk of drug-induced toxicity and enables clinicians to make precise dose adjustments. </p> <p> Objectives: This research explores the implementation of pharmacogenomics and toxicogenomics in personalized medicine to assess their safety benefits, improvements in disease treatment, and potential to reduce healthcare costs. It also evaluates emerging technologies and discusses challenges associated with deploying these methodologies. </p> <p> Methods: A comprehensive analysis of genetic studies involving drug-metabolizing enzymes, receptors, and transport proteins was conducted. The evaluation focused on biomedical technologies, bioinformatics, and computational modeling to determine their ability to detect genomic indicators of drug toxicity. Additionally, this study examined how artificial intelligence (AI), machine learning (ML), and gene-editing technologies contribute to the advancement of personalized medical treatments. </p> <p> Results and Discussion: Technological advancements have facilitated the discovery of genomic markers, improving drug toxicity prediction, regulatory assessment, and public health strategies. Integrating pharmacogenomic and toxicogenomic data into electronic medical records supports enhanced clinical decision-making and strengthens drug safety monitoring. However, widespread adoption remains limited due to ongoing ethical concerns, accessibility barriers, and regulatory inconsistencies. </p> <p> Conclusion: Collaboration among researchers, clinicians, industry stakeholders, and policymakers is essential to overcome implementation barriers to pharmacogenomic integration. The successful incorporation of pharmacogenomic and toxicogenomic data depends on expanding research foundations, enacting policy reforms, and developing educational initiatives to enhance patient safety and global healthcare outcomes. </p>]]></description> </item><item><title><![CDATA[Evolutionary Study on the Y Chromosome: A Comprehensive Review]]></title><link>https://www.benthamscience.com/article/152830</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: The Y chromosome, essential for male sex determination and reproduction, has undergone significant evolutionary shrinkage, losing most of its genetic content. This review explores the biological and historical significance of the Y chromosome, its role in male-specific traits, spermatogenesis, and secondary sexual characteristics. It also examines the implications of its shrinking for male infertility, cancer risk, and aging-related diseases, along with potential pharmacological and genetic solutions. </p> <p> Methods: A comprehensive review of existing literature, cross-species studies, and recent advancements in genetics and medical research was conducted. Based on mechanisms of Y chromosome degeneration, its impact on health, and possible therapeutic interventions, including hormone replacement therapies, assisted reproductive technologies, and gene-editing techniques like CRISPR. </p> <p> Results: Despite reducing from 1,400 to 55 active genes, the Y chromosome retains key functions in testosterone production and sperm maturation through genes like <i>SRY, DAZ</i>, and <i>TSPY</i>. Studies suggest alternative mechanisms for male traits in the absence of the Y chromosome, raising questions about its future in humans. </p> <p> Discussion: The shrinkage is linked to infertility, increased cancer risk, and aging-related disorders. Potential pharmacological approaches involve hormone replacement therapies, assisted reproductive technologies, and gene-editing techniques like CRISPR. </p> <p> Conclusion: The shrinking Y chromosome poses challenges to male health, but scientific advancements offer hope for mitigating its effects. Integrating genetic research, evolutionary studies, and medical innovations is crucial for addressing Y-linked disorders and guiding the future of male health and reproduction. </p>]]></description> </item><item><title><![CDATA[Computational Investigation of Harmful Single-nucleotide Polymorphisms in the ABCB4 Gene and their Potential Links to Liver Disease]]></title><link>https://www.benthamscience.com/article/153040</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: Single-Nucleotide Polymorphisms (SNPs) are one of the common genetic variants that can affect disease risk and other phenotypes. ABCB4 encodes a phosphatidylcholine translocator important for liver function, and ABCB4 mutations can be linked to both liver disorders and breast cancer. </p> <p> Objective: This study aims to identify the deleterious SNPs within the ABCB4 gene using <i>in silico</i> methodologies. </p> <p> Methods: The ABCB4 amino acid sequence was acquired from the UniProt database, and gene interactions were examined by GeneMANIA. A summary of the 135 SNP IDs of the ABCB4 gene was gathered from the UCSC genome browser. Deleterious SNPs were screened by SIFT and PolyPhen and validated by PROVEAN, SNAP, PhD-SNP, and SNPs and GO. Effects on protein stability were assessed using I-Mutant, MuPRO, and DynaMut. </p> <p> Results and Discussion: Out of 135 SNPs, 4 non-synonymous SNPs, which are C433W, K435E, R788P, and R788Q, were predicted as deleterious. We showed that these variants decrease protein stability and may profoundly impact ABCB4 activity. Three SNPs (rs8187801, rs20129202, and rs201168284) were identified as high-confidence candidates with likely pathogenic clinical relevance. </p> <p> Conclusion: This work identifies putative liver disease- and cancer-predisposing nsSNPs in the ABCB4 gene with functional importance. These associations have only limited direct medical application at the moment, apart from risk prediction and genetic counseling, but will be a major driver for the identification of targeted therapeutic strategies. </p>]]></description> </item><item><title><![CDATA[Pharmacogenomic Alterations in High-Risk Triple-Negative Breast Cancer and Its Adverse Drug Reactions: A Cross-Sectional and Observational Study]]></title><link>https://www.benthamscience.com/article/152794</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer, with a significant prevalence in India, potentially due to distinct etiological factors. Genetic mutations are closely associated with an increased risk of TNBC. While chemotherapy remains the primary treatment, it is associated with a high risk of adverse drug reactions (ADRs). This study aims to investigate genetic mutations and their association with TNBC in the Mizo geo-ethnic population, which has a high incidence of TNBC. </p> <p> Methods: A cross-sectional study including 27 participants, comprising TNBC patients and healthy controls, was conducted, and ADR events were monitored in patients. Wholeexome sequencing was performed using blood genomic DNA. The sequence data were evaluated, and the pathogenicity of variants was predicted using <i>in-silico</i> tools. Associations and correlations of the variants with ADRs were analyzed using statistical methods. </p> <p> Results: Genetic variants were observed in BRCA1, BRCA2, ABCB1, ALKBH3, CYP4F2, DPYD, MTHFR, and SLC22A10. Pathogenic variants in pharmacogenes, including DPYD (rs1801265), CYP2C9 (T620C), SLC22A16 (rs201574154), SLCO1B1 (rs201722521), RYR1 (rs777680485), AHR (C1282A), and NUDT15 (rs116855232), were identified in association with ADRs. Patients carrying variants in UGT1A1 (rs4148323) and CYP2B6 (rs8192709) experienced ADRs following chemotherapy treatment regimens. </p> <p> Discussion: In addition to known BRCA1 mutations, novel gene associations were identified, including CYP4F2, DPYD, and ABCB1. Some variants were associated with side effects such as hair loss, fatigue, and cardiac complications. G6PD variants may also contribute to drug resistance. </p> <p> Conclusion: This study identified certain gene variants linked to a higher risk of TNBC and ADRs during chemotherapy. Alongside established BRCA1 mutations, associations were observed in CYP4F2, DPYD, and ABCB1. Some variants were linked to side effects including hair loss, fatigue, and heart-related issues. As a pilot study with a small sample size, it was underpowered to detect small or medium effects, and its primary purpose is to estimate variability and effect sizes to inform the design of a larger study. </p>]]></description> </item><item><title><![CDATA[Wearable Devices in Electrogenetics: Bridging Real-time Monitoring and Genetic Modulation]]></title><link>https://www.benthamscience.com/article/150865</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: Wearable technologies are revolutionizing personalized medicine by integrating biosensing and therapeutic capabilities into compact, user-friendly formats. Electrogenetics, a novel discipline that employs electrical stimuli to regulate gene expression, offers promising applications for dynamic disease management. This review explores the intersection of wearable devices and electrogenetics, focusing on their potential to enable real-time monitoring and precise genetic modulation in clinical and research settings. </p> <p> Methods: A comprehensive literature search was conducted across databases such as PubMed, Scopus, and IEEE Xplore using keywords like “wearable bioelectronics,” “electrogenetics,” “gene modulation,” and “real-time biosensors.” Studies from 2015 to 2025 were screened, emphasizing devices capable of both sensing and electrical stimulation for genetic control. Design principles, materials, power systems, and biocompatibility were critically reviewed. </p> <p> Results: Recent advances demonstrate the development of wearable platforms integrating flexible electrodes, wireless communication, and biosensors with synthetic gene circuits. These systems detect physiological cues (<i>e.g.</i>, pH, glucose, inflammation) and respond by triggering gene expression <i>via</i> localized electrical pulses. For instance, closed-loop systems for glucose regulation in diabetes or inflammation-responsive gene switches in wound healing have shown promising preclinical outcomes. </p> <p> Discussion: Wearable electrogenetic devices offer a paradigm shift toward autonomous, precision-based therapeutic interventions. However, challenges remain in ensuring longterm stability, minimizing immune responses, and integrating complex genetic circuits with miniaturized hardware. Ethical and regulatory considerations also require careful navigation. </p> <p> Conclusion: The convergence of wearable electronics and electrogenetics holds transformative potential for personalized therapy. Continued interdisciplinary research is essential to translate these innovations from bench to bedside, enabling real-time, responsive, and genetically targeted healthcare solutions. </p>]]></description> </item><item><title><![CDATA[The Future of Biotics: Individualized Probiotic, Prebiotic, and Postbiotic Solutions]]></title><link>https://www.benthamscience.com/article/151152</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: The gut microbiome plays a critical role in health and disease, influencing metabolic, gastrointestinal, and immune functions. With growing evidence supporting the role of microbiome-targeted therapies, personalized biotics, probiotics, prebiotics, and postbiotics tailored to individual microbial profiles are emerging as a novel approach in precision medicine. </p> <p> Methods: A narrative review was conducted using studies published between January 2019 and January 2024 from databases including PubMed, Scopus, Web of Science, and Google Scholar. Inclusion criteria focused on clinical trials, systematic reviews, or meta-analyses involving personalized biotic interventions in humans. Data extraction included intervention types, populations, outcomes, and study design. </p> <p> Results: Thirty-four studies met the inclusion criteria. Personalized probiotics showed up to a 30% reduction in inflammatory symptoms in IBD patients and improvements in metabolic and mental health markers. Selective prebiotics demonstrated a 25% decrease in obesity-related biomarkers and supported microbial diversity. Postbiotics exhibited stable immunomodulatory effects with better safety and storage profiles. However, challenges include high costs, methodological heterogeneity, and lack of standardization. </p> <p> Discussion: Personalized biotics show promising therapeutic potential across diverse health conditions, particularly were microbiome variability impacts treatment response. Emerging technologies such as metagenomics and biomarker profiling support the feasibility of individualized approaches. </p> <p> Conclusion: Personalized biotics represent a transformative step in gut health and precision medicine. Ongoing clinical validation and standardization are essential to translating this approach into routine healthcare. </p>]]></description> </item><item><title><![CDATA[AI-Augmented Cytogenetics in Hematologic Malignancies: A Diagnostic Paradigm Shift]]></title><link>https://www.benthamscience.com/article/153940</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Cytogenetic testing plays a critical role in the diagnosis and risk stratification of hematologic malignancies. However, conventional techniques are inherently constrained by technical limitations, including low resolution, labor-intensive workflows, and inter-observer variability. Recent advances in artificial intelligence, particularly deep learning-based approaches, have shown promise in addressing these limitations by enhancing image analysis, automating interpretation, and standardizing complex workflows. Many studies have demonstrated that AI-integrated platforms significantly reduce diagnostic turnaround time, detect cryptic or subclonal chromosomal aberrations, and improve interpretive concordance across laboratories. Despite these advantages, barriers, such as limited model interpretability, data heterogeneity, and regulatory challenges, remain. Rather than replacing human expertise, AI is emerging as a powerful adjunct that strengthens the accuracy and reproducibility of genomic assessments and promotes timely, individualized therapeutic decision-making. As the technology matures, AI is expected to become an integral component of cytogenetic diagnostics, driving a shift toward more efficient, scalable, and precision-guided clinical workflows in hematologic oncology. </p>]]></description> </item><item><title><![CDATA[Shaping the Future of Pharmacogenomics: Integrating Genomic Insights into Personalized Therapeutics]]></title><link>https://www.benthamscience.com/article/153862</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Advances in genomic science, molecular diagnostics, and precision drug development are changing the landscape of healthcare. Pharmacogenomics, a once small scientific area, is quickly becoming a pillar of personalized medicine. This editorial addresses contemporary trends, translational challenges, and potential future directions to optimally harness genomic insights towards the clinic. It emphasises the importance of multidisciplinary approaches, global equity, and ethical principles to facilitate pharmacogenomics implementation, and looks ahead to artificial intelligence, multi-omics integration, and real-world evidence as the next major drivers of change. </p>]]></description> </item><item><title><![CDATA[Pharmacokinetics and Pharmacodynamics of Natural Products in Oncology: Bridging the Gap between Promise and Clinical Reality]]></title><link>https://www.benthamscience.com/article/153468</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: Natural products have historically contributed to cancer therapeutics, leading to agents like paclitaxel and vincristine. Recently, compounds such as curcumin, resveratrol, quercetin, and berberine have gained attention due to their multitargeted mechanisms and favorable safety profiles. However, their clinical application remains limited owing to significant pharmacokinetic (PK) and pharmacodynamic (PD) challenges. This review aims to highlight these limitations and explore emerging strategies to enhance their oncotherapeutic potential. </p> <p> Methods: A comprehensive literature review was conducted using peer-reviewed articles and clinical trial reports from databases including PubMed, Scopus, and Web of Science. Key PK/PD limitations and advanced formulation approaches were identified and critically analyzed. </p> <p> Results: Major PK barriers include poor oral bioavailability, low solubility, rapid metabolism, and short half-life. PD challenges involve multi-target effects, inconsistent dose-response relationships, and a lack of validated biomarkers. Examples include curcumin’s poor bioavailability and resveratrol’s rapid metabolism. Emerging strategies such as nanotechnology-based delivery systems, prodrug development, structural modifications, and co-administration with bioavailability enhancers, such as piperine, have shown promise. Success stories such as Abraxane® (albumin-bound paclitaxel) and topotecan (a camptothecin derivative) illustrate effective translational approaches. </p> <p> Discussion: Overcoming PK/PD limitations is essential for translating natural compounds into effective oncotherapeutics. Integrating nanomedicine, chemical modifications, and bioenhancers improves pharmacological profiles. </p> <p> Conclusion: Future directions should combine pharmacogenomics, nanotechnology, and AI-driven drug discovery to enhance the clinical relevance of natural anticancer agents. For example, AI-guided structural optimization of camptothecin analogs (e.g., topotecan) and nanoparticle-based formulations such as Abraxane® demonstrate how computational and translational innovations can successfully advance natural products into clinical oncology. </p>]]></description> </item><item><title><![CDATA[The Role of 3D-printed Medicines in Pharmacogenomics and Personalized Prescriptions]]></title><link>https://www.benthamscience.com/article/153500</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Pharmacogenomics, the study of how genetic variability influences individual responses to drugs, has opened new frontiers in the era of personalized medicine. The integration of 3D printing into pharmaceutical sciences further advances this paradigm by enabling customized drug dosing, combinations, and release profiles tailored to an individual’s genetic makeup. This study examines the role of 3D-printed medicines in pharmacogenomics, the technological advancements supporting personalized prescriptions, regulatory challenges, and the potential for integrating genomic data with additive manufacturing technologies to enable individualized drug therapy. </p>]]></description> </item><item><title><![CDATA[Targeting Drug Metabolism in Psychiatry: Pharmacogenetic Insights into <i>CYP2D6</i> and <i>CYP2C19</i>]]></title><link>https://www.benthamscience.com/article/153586</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Introduction: Pharmacogenetics is revolutionising psychiatric care by providing insights into how genetic variants, particularly in <i>CYP2D6</i> and <i>CYP2C19</i>, affect drug metabolism, efficacy, and side effects. These insights help clinicians tailor treatment for drugs such as SSRIs, tricyclic antidepressants, and antipsychotics, reducing trial-and-error prescribing and improving patient outcomes. This study aims to investigate the influence of genetic variations, particularly in <i>CYP2D6</i> and <i>CYP2C19</i>, on drug metabolism, therapeutic effectiveness, and adverse effects in psychiatric treatment. </p> <p> Methods: This systematic review integrates information from PharmGKB and the Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines, as well as data from PubMed, Medline, Scopus, Web of Science, Google Scholar, and reputable health organisations using keywords related to the study topic. Inclusion criteria encompassed peerreviewed articles, studies in English, and research published within the last 10 years. Exclusion criteria included non-relevant or duplicate studies. The selection process followed PRISMA guidelines, with data extraction focusing on study design, outcomes, and reliability to ensure transparency and credibility. The review also examines new findings, such as polygenic risk scores and expanded multigene testing platforms, and highlights clinically relevant gene–drug interactions, including the effect of <i>CYP2D6</i> polymorphisms on risperidone metabolism. </p> <p> Results: This study emphasises the significant role of pharmacogenetics in psychiatric treatment, specifically regarding genetic variants in <i>CYP2D6</i> and <i>CYP2C19</i>. These genetic factors influence treatment with SSRIs, tricyclic antidepressants, and antipsychotics by altering medication metabolism, effectiveness, and adverse effects. The study examines key gene–drug interactions and emerging technologies such as polygenic risk scores, utilising data from PharmGKB, CPIC recommendations, and major medical databases. </p> <p> Discussion: Despite its promise, widespread implementation faces challenges such as cost, accessibility, and the need for clinician education. Addressing these obstacles through improved insurance coverage and integration of electronic health records can advance precision medicine, thereby enhancing patient outcomes and reducing adverse effects. The gap can be narrowed by employing strategies such as increasing insurance coverage for testing and incorporating genetic decision-support tools into electronic health records. </p> <p> Conclusion: Integrating pharmacogenetics into psychiatric care can improve treatment safety and precision. For broad adoption, challenges such as cost, test accessibility, and physician education must be addressed. This review supports a future in which pharmacogenetic insights guide psychiatric care to improve treatment outcomes and reduce adverse drug reactions. </p>]]></description> </item><item><title><![CDATA[Advancements in Pharmaceutical Approaches for Psoriasis Management: A Comprehensive Review]]></title><link>https://www.benthamscience.com/article/153585</link><pubDate>2026-05-18</pubDate><description><![CDATA[<p> Chronic inflammatory skin conditions like psoriasis have a major negative impact on quality of life. In recent years, there have been remarkable advancements in pharmaceutical approaches to managing psoriasis, including the evaluation of biologics, treatments using tiny molecules, and innovative topical treatments. Biologics, such as IL- 17, IL-23, and TNF-α inhibitors, have changed the way that treatment is administered, offering targeted and efficient options for psoriasis that is moderate to severe. Small molecule therapies, including PDE4 and JAK inhibitors, provide additional therapeutic options, especially for patients with mild to moderate disease or those unresponsive to biologics. Nanotechnology-based treatments, microneedles, and gene editing are emerging as potential innovations to enhance drug delivery and address the underlying genetic mechanisms of the disease. Personalized medicine, driven by biomarker research, is increasingly recognized as a crucial strategy to maximize the results of treatment and minimize adverse effects. Furthermore, the rise of biosimilars offers cost-effective alternatives to traditional biologics, making advanced therapies more accessible. Despite these advancements, challenges such as drug resistance, long-term safety concerns, and limited access to innovative treatments remain. Continued research and development in these areas hold promise for improving long-term psoriasis management and patient outcomes. </p>]]></description> </item></channel></rss>