Pub Date : 2025-11-29DOI: 10.1016/j.drudis.2025.104565
Mengqiao Chen , Xiangyu Fu , Huiping Wang , Xinyi Qi , Leilei Fu
Autophagy is an intracellular degradation and recycling mechanism, crucial for maintaining cellular homeostasis. In recent years, the dual role of protein kinases in autophagy has gradually been elucidated. Designing small-molecule compounds to regulate these targets can actively or passively intervene in cell-protective autophagy or autophagy-related cell death. This approach could provide new clues for modern targeted cancer therapies. In this review, we focus on summarizing the regulatory roles of key protein kinases in autophagy, including positive regulation, negative regulation and bidirectional regulation of autophagy. Moreover, we explore the anticancer potential of small-molecule compounds targeting these kinases in cancer therapy, providing new clues for precise treatment by regulating autophagy pathways.
{"title":"Decoding protein kinases in autophagy with small-molecule modulators for cancer therapy","authors":"Mengqiao Chen , Xiangyu Fu , Huiping Wang , Xinyi Qi , Leilei Fu","doi":"10.1016/j.drudis.2025.104565","DOIUrl":"10.1016/j.drudis.2025.104565","url":null,"abstract":"<div><div>Autophagy is an intracellular degradation and recycling mechanism, crucial for maintaining cellular homeostasis. In recent years, the dual role of protein kinases in autophagy has gradually been elucidated. Designing small-molecule compounds to regulate these targets can actively or passively intervene in cell-protective autophagy or autophagy-related cell death. This approach could provide new clues for modern targeted cancer therapies. In this review, we focus on summarizing the regulatory roles of key protein kinases in autophagy, including positive regulation, negative regulation and bidirectional regulation of autophagy. Moreover, we explore the anticancer potential of small-molecule compounds targeting these kinases in cancer therapy, providing new clues for precise treatment by regulating autophagy pathways.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104565"},"PeriodicalIF":7.5,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145652931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-27DOI: 10.1016/j.drudis.2025.104562
Ka-Shi Nozomi Choi, Wei-Bo Liu
Japan has long been positioned as a global leader in regenerative medicine, and a critical moment occurred in 2025 when the world’s first regulatory submission for an induced pluripotent stem (iPS)-cell-based therapy was filed. In this article, we detail the Japanese government’s strategic investment in regenerative medicine since the early 2000s, and elucidate the advancement of regulatory guidelines tailored to the unique characteristics of regenerative medical products (RMPs) and designed to ensure safety while accelerating commercialization. We also provide an extensive summary of the latest clinical studies using iPS-cell-based therapies conducted by Japanese companies and academic institutions, as well as the current landscape of corporate involvement in this field. In addition, we address the challenges facing the development of RMPs by discussing the withdrawal cases that occurred in Japan last year.
{"title":"Driving the future of iPS-cell-based therapy in Japan: government strategies, regulatory review and clinical development","authors":"Ka-Shi Nozomi Choi, Wei-Bo Liu","doi":"10.1016/j.drudis.2025.104562","DOIUrl":"10.1016/j.drudis.2025.104562","url":null,"abstract":"<div><div>Japan has long been positioned as a global leader in regenerative medicine, and a critical moment occurred in 2025 when the world’s first regulatory submission for an induced pluripotent stem (iPS)-cell-based therapy was filed. In this article, we detail the Japanese government’s strategic investment in regenerative medicine since the early 2000s, and elucidate the advancement of regulatory guidelines tailored to the unique characteristics of regenerative medical products (RMPs) and designed to ensure safety while accelerating commercialization. We also provide an extensive summary of the latest clinical studies using iPS-cell-based therapies conducted by Japanese companies and academic institutions, as well as the current landscape of corporate involvement in this field. In addition, we address the challenges facing the development of RMPs by discussing the withdrawal cases that occurred in Japan last year.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104562"},"PeriodicalIF":7.5,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-27DOI: 10.1016/j.drudis.2025.104563
Chieh-Te Lin , Ya-Ping Shiau , Chu-Chung Lin
Targeted protein degradation (TPD) allows catalytic removal of disease-associated proteins by exploiting the ubiquitin–proteasome system (UPS). Proteolysis-targeting chimeras (PROTACs) and molecular glues represent two complementary TPD modalities, yet their rational design remains hindered by challenges in ternary complex formation, ligand discovery, and pharmacokinetic optimization. Recent machine learning (ML) advances address these barriers through predictive modeling, virtual screening, and generative design of degrader candidates. In this review, we summarize how ML is integrated across PROTACs and molecular glue development, including ternary complex prediction, linker and fragment design, degradation efficiency modeling, and absorption, distribution, metabolism, excretion, and toxicity (ADMET) optimization. We also highlight emerging artificial intelligence (AI)-driven strategies for de novo glue discovery. Together, these innovations demonstrate how ML is accelerating degrader design and expanding the landscape of druggable targets.
{"title":"Machine learning in targeted protein degradation drug design: a technical review of PROTACs and molecular glues","authors":"Chieh-Te Lin , Ya-Ping Shiau , Chu-Chung Lin","doi":"10.1016/j.drudis.2025.104563","DOIUrl":"10.1016/j.drudis.2025.104563","url":null,"abstract":"<div><div>Targeted protein degradation (TPD) allows catalytic removal of disease-associated proteins by exploiting the ubiquitin–proteasome system (UPS). Proteolysis-targeting chimeras (PROTACs) and molecular glues represent two complementary TPD modalities, yet their rational design remains hindered by challenges in ternary complex formation, ligand discovery, and pharmacokinetic optimization. Recent machine learning (ML) advances address these barriers through predictive modeling, virtual screening, and generative design of degrader candidates. In this review, we summarize how ML is integrated across PROTACs and molecular glue development, including ternary complex prediction, linker and fragment design, degradation efficiency modeling, and absorption, distribution, metabolism, excretion, and toxicity (ADMET) optimization. We also highlight emerging artificial intelligence (AI)-driven strategies for <em>de novo</em> glue discovery. Together, these innovations demonstrate how ML is accelerating degrader design and expanding the landscape of druggable targets.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104563"},"PeriodicalIF":7.5,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-26DOI: 10.1016/j.drudis.2025.104560
J C J Loggers, M E J Reinders, T van Gelder, V M van der Horst, K M S L Bischoff, H J Guchelaar
Effective collaboration between university medical centres and biotechnology companies is increasingly crucial for driving translational innovation in the health and life sciences. In particular, collaboration is strongly encouraged within biotechnology and life sciences clusters where there is physical and institutional proximity between academia and industry. However, collaboration in such clusters is dependent on many different interacting actors. This review examines the triple helix model, the university-enterprise collaboration model, and the Lewinian approach, and identifies barriers and facilitators of academic-industry collaboration. Despite mutual interest, barriers such as intellectual property issues, regulatory complexity, divergent visions, and institutional rigidity arise. Conversely, shared infrastructure, effective intermediary structures, and trust-based relationships facilitate collaboration. Based on the literature, several actionable strategies are proposed to enhance partnerships between academia and industry.
{"title":"Academic-industry collaboration in biomedical innovation: A multi-model review of barriers and facilitators.","authors":"J C J Loggers, M E J Reinders, T van Gelder, V M van der Horst, K M S L Bischoff, H J Guchelaar","doi":"10.1016/j.drudis.2025.104560","DOIUrl":"10.1016/j.drudis.2025.104560","url":null,"abstract":"<p><p>Effective collaboration between university medical centres and biotechnology companies is increasingly crucial for driving translational innovation in the health and life sciences. In particular, collaboration is strongly encouraged within biotechnology and life sciences clusters where there is physical and institutional proximity between academia and industry. However, collaboration in such clusters is dependent on many different interacting actors. This review examines the triple helix model, the university-enterprise collaboration model, and the Lewinian approach, and identifies barriers and facilitators of academic-industry collaboration. Despite mutual interest, barriers such as intellectual property issues, regulatory complexity, divergent visions, and institutional rigidity arise. Conversely, shared infrastructure, effective intermediary structures, and trust-based relationships facilitate collaboration. Based on the literature, several actionable strategies are proposed to enhance partnerships between academia and industry.</p>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":" ","pages":"104560"},"PeriodicalIF":7.5,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145626977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-26DOI: 10.1016/j.drudis.2025.104561
Saroj Verma , Vaishali M. Patil , Uma Agarwal
Tuberculosis (TB) drug resistance poses a major global health challenge. The first-line antitubercular prodrug isoniazid (INH) is metabolized by N-acetyltransferase 2 (NAT2) and activated by catalase peroxidase (KatG) to inhibit enoyl-acyl carrier protein reductase (InhA) in the mycolic acid biosynthesis pathway. Genetic variations in NAT2 are associated with the formation of slow and fast acetylators, influencing drug efficacy and toxicity. Despite significant advances that have clarified key aspects of NAT2-mediated isoniazid metabolism, the complete spectrum of mechanisms governing isoniazid deactivation and their broader implications for treatment efficacy and resistance evolution remain to be fully elucidated. In this review, we discuss the pharmacokinetics (PK), pharmacodynamics (PD), dosing regimens, and pharmacogenomics of isoniazid, along with the role of artificial intelligence (AI)/machine learning (ML) in its personalized use. In addition, we analyze NAT2 mutations and their impact on acetylation rates using bioinformatics. These insights collectively advance our understanding of genotype-driven variability in isoniazid response, aiding the development of personalized therapy.
{"title":"Pharmacogenomics and mutation informatics: correlation of NAT2 mutations and isoniazid acetylation rate","authors":"Saroj Verma , Vaishali M. Patil , Uma Agarwal","doi":"10.1016/j.drudis.2025.104561","DOIUrl":"10.1016/j.drudis.2025.104561","url":null,"abstract":"<div><div>Tuberculosis (TB) drug resistance poses a major global health challenge. The first-line antitubercular prodrug isoniazid (INH) is metabolized by <em>N</em>-acetyltransferase 2 (NAT2) and activated by catalase peroxidase (KatG) to inhibit enoyl-acyl carrier protein reductase (InhA) in the mycolic acid biosynthesis pathway. Genetic variations in NAT2 are associated with the formation of slow and fast acetylators, influencing drug efficacy and toxicity. Despite significant advances that have clarified key aspects of NAT2-mediated isoniazid metabolism, the complete spectrum of mechanisms governing isoniazid deactivation and their broader implications for treatment efficacy and resistance evolution remain to be fully elucidated. In this review, we discuss the pharmacokinetics (PK), pharmacodynamics (PD), dosing regimens, and pharmacogenomics of isoniazid, along with the role of artificial intelligence (AI)/machine learning (ML) in its personalized use. In addition, we analyze NAT2 mutations and their impact on acetylation rates using bioinformatics. These insights collectively advance our understanding of genotype-driven variability in isoniazid response, aiding the development of personalized therapy.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104561"},"PeriodicalIF":7.5,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pharmaceuticals are essential for health but are increasingly impacting the environment, affecting ecosystems and human health, and contributing to biodiversity loss, antimicrobial resistance, and climate change. Active pharmaceutical ingredients designed for stability and biological activity, along with excipients and packaging materials, contaminate air, soil, and water globally. To address the issue of pharmaceutical pollution, the establishment of a sustainable pharmacy framework is required, beginning with drug development and the education of future professionals. In this article, we present a critical overview of initiatives already implemented and those emerging that aim to achieve a more sustainable pharmacy. We followed a cradle-to-grave life-cycle approach to identify the role of pharmacy professionals, including drug developers, in enabling mitigation measures for pharmaceutical pollution. Some of the emerging initiatives for reducing pharmaceutical pollution that were identified include a benign-by-design approach for drug development, the adoption of a One Health approach in healthcare systems, and advancing regulatory frameworks and education of healthcare professionals.
{"title":"Promoting sustainable pharmacy for tackling environmental pharmaceutical pollution","authors":"Iker Egaña , Vladimir Akhrimenko , Mirari Ayerbe , Eider Abasolo , Unax Lertxundi , Gorka Orive","doi":"10.1016/j.drudis.2025.104559","DOIUrl":"10.1016/j.drudis.2025.104559","url":null,"abstract":"<div><div>Pharmaceuticals are essential for health but are increasingly impacting the environment, affecting ecosystems and human health, and contributing to biodiversity loss, antimicrobial resistance, and climate change. Active pharmaceutical ingredients designed for stability and biological activity, along with excipients and packaging materials, contaminate air, soil, and water globally. To address the issue of pharmaceutical pollution, the establishment of a sustainable pharmacy framework is required, beginning with drug development and the education of future professionals. In this article, we present a critical overview of initiatives already implemented and those emerging that aim to achieve a more sustainable pharmacy. We followed a cradle-to-grave life-cycle approach to identify the role of pharmacy professionals, including drug developers, in enabling mitigation measures for pharmaceutical pollution. Some of the emerging initiatives for reducing pharmaceutical pollution that were identified include a benign-by-design approach for drug development, the adoption of a One Health approach in healthcare systems, and advancing regulatory frameworks and education of healthcare professionals.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104559"},"PeriodicalIF":7.5,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-24DOI: 10.1016/j.drudis.2025.104558
Sébastien Reig , Christel Becker
Medical affairs (MA) has transformed to become a strategic pillar in the pharmaceutical ecosystem. This article highlights the expanding role of MA across the drug lifecycle, from patient access to clinical adoption and evidence generation. By exploring the shift from ‘patient centricity’ to ‘patient as partner’, we emphasize how MA can bridge innovation with real healthcare needs. Case studies illustrate how MA actions impact patient outcomes beyond the treatment provided. As expectations from stakeholders rise, MA must lead with patient partnering as a strategic priority. Patient focus is no longer optional; it is a core driver of value for patients and industry.
{"title":"Reimagining medical affairs through strategic leadership in patient partnering healthcare","authors":"Sébastien Reig , Christel Becker","doi":"10.1016/j.drudis.2025.104558","DOIUrl":"10.1016/j.drudis.2025.104558","url":null,"abstract":"<div><div>Medical affairs (MA) has transformed to become a strategic pillar in the pharmaceutical ecosystem. This article highlights the expanding role of MA across the drug lifecycle, from patient access to clinical adoption and evidence generation. By exploring the shift from ‘patient centricity’ to ‘patient as partner’, we emphasize how MA can bridge innovation with real healthcare needs. Case studies illustrate how MA actions impact patient outcomes beyond the treatment provided. As expectations from stakeholders rise, MA must lead with patient partnering as a strategic priority. Patient focus is no longer optional; it is a core driver of value for patients and industry.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104558"},"PeriodicalIF":7.5,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-23DOI: 10.1016/j.drudis.2025.104557
Vaishnavi Kalmegh , Lahanya Guha , Deep Rohan Chatterjee , Hemant Kumar , Amit Shard
The glycolytic enzyme pyruvate kinase M2 (PKM2) is emerging as a crucial modulator of cancer cell proliferation and pain signaling. Pathological lactate accumulation causes tissue acidification, sensitizing pain pathways, in which PKM2 plays a central role. Evidence links PKM2 to both nociceptive and neuropathic pain via molecular cascades involving cyclooxygenase (COX)-1/2, interleukin (IL)-1β, and extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) activation. Phosphorylated PKM2 enhances NFκB, STAT3, and ERK pathways, promoting inflammatory and neuronal sensitization. By integrating metabolic reprogramming with pain signaling, PKM2 represents a pivotal bridge between inflammation, neuronal excitation, and energy metabolism, offering promising therapeutic potential for managing complex pain-linked conditions.
{"title":"Pyruvate kinase M2 – linked metabolic pathways in pain modulation","authors":"Vaishnavi Kalmegh , Lahanya Guha , Deep Rohan Chatterjee , Hemant Kumar , Amit Shard","doi":"10.1016/j.drudis.2025.104557","DOIUrl":"10.1016/j.drudis.2025.104557","url":null,"abstract":"<div><div>The glycolytic enzyme pyruvate kinase M2 (PKM2) is emerging as a crucial modulator of cancer cell proliferation and pain signaling. Pathological lactate accumulation causes tissue acidification, sensitizing pain pathways, in which PKM2 plays a central role. Evidence links PKM2 to both nociceptive and neuropathic pain via molecular cascades involving cyclooxygenase (COX)-1/2, interleukin (IL)-1β, and extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) activation. Phosphorylated PKM2 enhances NFκB, STAT3, and ERK pathways, promoting inflammatory and neuronal sensitization. By integrating metabolic reprogramming with pain signaling, PKM2 represents a pivotal bridge between inflammation, neuronal excitation, and energy metabolism, offering promising therapeutic potential for managing complex pain-linked conditions.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104557"},"PeriodicalIF":7.5,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145601687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hepatocellular carcinoma (HCC) microenvironments (MEs) are composed of immune and non-immune components that drive tumor progression and treatment resistance. This narrative review summarizes recent progress in systemic therapies combined with liver-directed approaches as a new frontier in metastatic HCC treatment. Immune checkpoint inhibitors (tremelimumab and durvalumab) in combination with small- molecule agents (lenvatinib and cabozantinib) enhance T-cell activation and improve progression-free survival in HCC. Epigenetic inhibitors and RNA-based therapeutics target the HCC ME and increase the efficacy of immunotherapy. Additionally, cellular therapy targeting agents like glypican-3 (GPC3) for chimeric antigen receptor T (CAR-T) cells have shown promising results. HCC ME has distinct immune subtypes exhibiting different responses to treatments, which complicates biomarker selection and treatment timing. Personalized therapy based on ME is the future path in HCC management.
{"title":"Integrated therapies for targeting the microenvironment of hepatocellular carcinoma","authors":"Shriraam Karunakaran , Mohan Krishna Ghanta , Anusha Lakshmi Cheetiyar , LVKS Bhaskar , Ganji Purnachandra Nagaraju","doi":"10.1016/j.drudis.2025.104556","DOIUrl":"10.1016/j.drudis.2025.104556","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) microenvironments (MEs) are composed of immune and non-immune components that drive tumor progression and treatment resistance. This narrative review summarizes recent progress in systemic therapies combined with liver-directed approaches as a new frontier in metastatic HCC treatment. Immune checkpoint inhibitors (tremelimumab and durvalumab) in combination with small- molecule agents (lenvatinib and cabozantinib) enhance T-cell activation and improve progression-free survival in HCC. Epigenetic inhibitors and RNA-based therapeutics target the HCC ME and increase the efficacy of immunotherapy. Additionally, cellular therapy targeting agents like glypican-3 (GPC3) for chimeric antigen receptor T (CAR-T) cells have shown promising results. HCC ME has distinct immune subtypes exhibiting different responses to treatments, which complicates biomarker selection and treatment timing. Personalized therapy based on ME is the future path in HCC management.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104556"},"PeriodicalIF":7.5,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145601697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The global reliance on herbal medicines underscores the urgent need for sustainable utilization and conservation of medicinal plants. Herbgenomics, merging omics technologies with traditional knowledge, explores plant genetics, diversity, and bioactive compound production. Advances in genomics research, combined with consortia of omics tools like transcriptomics, metabolomics, and proteomics, reveal pathways and enzymes involved in secondary metabolite biosynthesis. These insights uncover complex regulatory networks and enable our understanding of medicinal plant biology. Integrating multi-omics approaches supports precision breeding, metabolic engineering, and drug discovery, laying a strong foundation for optimizing herbal resources and accelerating the development of plant-based therapeutics.
{"title":"Integrating herbgenomics with systems biology approaches for sustainable utilization of medicinal plant resources","authors":"Tanvi Gupta , Jyoti Upadhyay , Sudesh Kumar Yadav , Rohit Joshi","doi":"10.1016/j.drudis.2025.104555","DOIUrl":"10.1016/j.drudis.2025.104555","url":null,"abstract":"<div><div>The global reliance on herbal medicines underscores the urgent need for sustainable utilization and conservation of medicinal plants. Herbgenomics, merging omics technologies with traditional knowledge, explores plant genetics, diversity, and bioactive compound production. Advances in genomics research, combined with consortia of omics tools like transcriptomics, metabolomics, and proteomics, reveal pathways and enzymes involved in secondary metabolite biosynthesis. These insights uncover complex regulatory networks and enable our understanding of medicinal plant biology. Integrating multi-omics approaches supports precision breeding, metabolic engineering, and drug discovery, laying a strong foundation for optimizing herbal resources and accelerating the development of plant-based therapeutics.</div></div>","PeriodicalId":301,"journal":{"name":"Drug Discovery Today","volume":"31 1","pages":"Article 104555"},"PeriodicalIF":7.5,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145581544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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