Previous
Age-related neurological disorders such as ALS (Lou Gehrig’s disease), Parkinson’s disease, and Alzheimer’s disease have few truly effective treatment options. At best, these may slow the inexorable disease progression without providing a cure. Part of the problem with therapeutic approaches may arise due to the stage at which these diseases are detected, particularly the sporadic forms. In most cases, early signs and symptoms may be insidious, thus hiding the significant damage done to the areas of the nervous system impacted prior to any firm clinical diagnosis. This situation appears to necessitate the development of earlier detection methods for “biomarkers” that might allow for much earlier phase disease state treatments that might serve to significantly slow or even halt disease progression. Currently, most biomarkers in use serve primarily as aids to disease diagnosis, at which point there are no successful treatment options. In contrast, a search for more effective early treatment options would need to identify characteristic and specific molecular signatures of disease onset and progression using methods that are simple, such as blood-based analytical assays, relatively cheap, and crucially minimally invasive.
Age-related neurological disorders such as ALS (Lou Gehrig’s disease), Parkinson’s disease, and Alzheimer’s disease have few truly effective treatment options. At best, these may slow the inexorable disease progression without providing a cure. Part of the problem with therapeutic approaches may arise due to the stage at which these diseases are detected, particularly the sporadic forms. In most cases, early signs and symptoms may be insidious, thus hiding the significant damage done to the areas of the nervous system impacted prior to any firm clinical diagnosis. This situation appears to necessitate the development of earlier detection methods for “biomarkers” that might allow for much earlier phase disease state treatments that might serve to significantly slow or even halt disease progression. Currently, most biomarkers in use serve primarily as aids to disease diagnosis, at which point there are no successful treatment options. In contrast, a search for more effective early treatment options would need to identify characteristic and specific molecular signatures of disease onset and progression using methods that are simple, such as blood-based analytical assays, relatively cheap, and crucially minimally invasive.
DOI: https://doi.org/10.37349/ent.2025.1004133
Gut microbiota is critical for human immunity, metabolism, and overall well-being. Dysbiosis has been associated with a variety of diseases, including metabolic syndrome, inflammatory diseases, and neurodevelopmental issues. Kefir, a traditional fermented beverage produced with dairy or non-dairy substrates and kefir grains, contains probiotics and bioactive substances that may improve gut microbial composition. Current research indicates that kefir increases beneficial taxa such as Lactobacillus spp., Bifidobacterium spp., and Akkermansia spp., whereas decreasing pro-inflammatory microbes such as Enterobacteriaceae spp. and Clostridium spp. via antimicrobial metabolite production, competitive exclusion, prebiotic exopolysaccharides, short-chain fatty acid enhancement, immune modulation, and improved gut-barrier integrity. Furthermore, traditional kefir fermented with grains has higher microbial diversity and probiotic potential than kefir fermented with starting cultures. Despite these encouraging results, interpretation is constrained by variations in kefir production, dosage, intervention duration, and microbiota analysis methods; therefore, this review aims to evaluate how kefir modulates gut microbiota composition in human and animal models.
Gut microbiota is critical for human immunity, metabolism, and overall well-being. Dysbiosis has been associated with a variety of diseases, including metabolic syndrome, inflammatory diseases, and neurodevelopmental issues. Kefir, a traditional fermented beverage produced with dairy or non-dairy substrates and kefir grains, contains probiotics and bioactive substances that may improve gut microbial composition. Current research indicates that kefir increases beneficial taxa such as Lactobacillus spp., Bifidobacterium spp., and Akkermansia spp., whereas decreasing pro-inflammatory microbes such as Enterobacteriaceae spp. and Clostridium spp. via antimicrobial metabolite production, competitive exclusion, prebiotic exopolysaccharides, short-chain fatty acid enhancement, immune modulation, and improved gut-barrier integrity. Furthermore, traditional kefir fermented with grains has higher microbial diversity and probiotic potential than kefir fermented with starting cultures. Despite these encouraging results, interpretation is constrained by variations in kefir production, dosage, intervention duration, and microbiota analysis methods; therefore, this review aims to evaluate how kefir modulates gut microbiota composition in human and animal models.
DOI: https://doi.org/10.37349/eff.2025.1010107
Aim:
Parkinson’s disease (PD) and Alzheimer’s disease (AD) represent critical neurological disorders that have emerged as significant health concerns in the 21st century. The pharmacological interventions currently employed to manage these diseases demonstrate limited efficacy and some adverse side effects. Historically, natural products have been used to develop therapeutic agents targeting neurodegenerative disorders. This study aimed to apply in silico techniques to investigate the pharmacological mechanisms of capsaicin as a possible alternative treatment or coadjutant phytotherapy for PD and AD.
Methods:
We obtained target genes for capsaicin, PD, and AD from the HERB database, the Swiss Target Prediction database, the Comparative Toxicogenomics Database, and the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, and matched them. Subsequently, we constructed a protein-protein interaction network and performed enrichment analysis of the common targets. Then, the interactions of capsaicin with the proteins with the highest degree were tested using molecular docking. The stability of the complexes was verified using molecular dynamics techniques.
Results:
A total of 25 targets were found in common from the databases for capsaicin, AD, and PD. The enrichment analysis revealed that proteins from these targets influenced integrin activity in the IGF1-IGF1R complex, cholinesterase activity, and dopamine neurotransmitter receptor activity, all of which are coupled via protein Gi/Go, among other cellular processes. From the protein-protein interaction network, we identified the hub proteins IL6, GSK3B, CASP, BCL2, ESR1, SIRT1, NGF, IGF1, and HMOX1. Furthermore, molecular docking studies between hub proteins and capsaicin showed strong binding affinity. Finally, molecular dynamics simulations support a stable interaction between capsaicin and SIRT1, ESR1, HMOX1, and NGF.
Conclusions:
This work contributes to understanding the neuroprotective activity of capsaicin in PD and AD. However, these bioinformatic predictions require further experimental validation.
Aim:
Parkinson’s disease (PD) and Alzheimer’s disease (AD) represent critical neurological disorders that have emerged as significant health concerns in the 21st century. The pharmacological interventions currently employed to manage these diseases demonstrate limited efficacy and some adverse side effects. Historically, natural products have been used to develop therapeutic agents targeting neurodegenerative disorders. This study aimed to apply in silico techniques to investigate the pharmacological mechanisms of capsaicin as a possible alternative treatment or coadjutant phytotherapy for PD and AD.
Methods:
We obtained target genes for capsaicin, PD, and AD from the HERB database, the Swiss Target Prediction database, the Comparative Toxicogenomics Database, and the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, and matched them. Subsequently, we constructed a protein-protein interaction network and performed enrichment analysis of the common targets. Then, the interactions of capsaicin with the proteins with the highest degree were tested using molecular docking. The stability of the complexes was verified using molecular dynamics techniques.
Results:
A total of 25 targets were found in common from the databases for capsaicin, AD, and PD. The enrichment analysis revealed that proteins from these targets influenced integrin activity in the IGF1-IGF1R complex, cholinesterase activity, and dopamine neurotransmitter receptor activity, all of which are coupled via protein Gi/Go, among other cellular processes. From the protein-protein interaction network, we identified the hub proteins IL6, GSK3B, CASP, BCL2, ESR1, SIRT1, NGF, IGF1, and HMOX1. Furthermore, molecular docking studies between hub proteins and capsaicin showed strong binding affinity. Finally, molecular dynamics simulations support a stable interaction between capsaicin and SIRT1, ESR1, HMOX1, and NGF.
Conclusions:
This work contributes to understanding the neuroprotective activity of capsaicin in PD and AD. However, these bioinformatic predictions require further experimental validation.
DOI: https://doi.org/10.37349/ent.2025.1004132
This article belongs to the special issue Natural Products in Neurotherapeutic Applications
Diverticulitis is one of the most common gastrointestinal causes of hospitalization in Western society. While previously characterized as a disease of older patients, new literature highlights an increasing incidence among the younger population. Over the past few decades, the understanding of etiology and management of diverticulitis has changed drastically. New data refute past beliefs while promoting other novel recommendations to mitigate incidence and subsequent complications. Data now confirms the safety and possible protective benefit of particulate food, while highlighting evidence-based approaches for the use of diagnostic imaging and antibiotics. We recognize modifiable and non-modifiable risk factors that are commonly seen throughout the literature and play a significant role in the management and prevention of diverticulitis. Emerging evidence also links chronic inflammation with subsequent microbial dysbiosis and alterations in the neuroendocrine system, leading to visceral hypersensitivity and perturbation of the gut-brain axis. This review provides a comprehensive update on acute uncomplicated diverticulitis according to the most recent evidence-based literature, encompassing the risks, diagnostic modalities, and management treatment regimens.
Diverticulitis is one of the most common gastrointestinal causes of hospitalization in Western society. While previously characterized as a disease of older patients, new literature highlights an increasing incidence among the younger population. Over the past few decades, the understanding of etiology and management of diverticulitis has changed drastically. New data refute past beliefs while promoting other novel recommendations to mitigate incidence and subsequent complications. Data now confirms the safety and possible protective benefit of particulate food, while highlighting evidence-based approaches for the use of diagnostic imaging and antibiotics. We recognize modifiable and non-modifiable risk factors that are commonly seen throughout the literature and play a significant role in the management and prevention of diverticulitis. Emerging evidence also links chronic inflammation with subsequent microbial dysbiosis and alterations in the neuroendocrine system, leading to visceral hypersensitivity and perturbation of the gut-brain axis. This review provides a comprehensive update on acute uncomplicated diverticulitis according to the most recent evidence-based literature, encompassing the risks, diagnostic modalities, and management treatment regimens.
DOI: https://doi.org/10.37349/edd.2025.1005107
This article belongs to the special issue Diverticulitis: Pathomechanism, Diagnosis and Treatment
The ketogenic diet (KD) is increasingly recognized for its therapeutic benefits in managing metabolic disorders, including obesity, type 2 diabetes, and epilepsy. However, adherence to KD can elevate the body’s acid load through ketone body production, potentially leading to metabolic acidosis. Alkalinizing salts, such as sodium bicarbonate, potassium citrate, magnesium, and calcium, play a crucial role in maintaining acid-base balance and mitigating complications associated with this dietary regimen. Evidence from studies published between 2000 and 2024 highlights that these interventions can reduce acidosis-related complications, including bone demineralization, muscle cramps, and fatigue, while improving mineral balance and metabolic stability. These findings suggest that incorporating alkalinizing strategies may enhance the safety and effectiveness of KDs. Further research is needed to define optimal dosing, assess long-term safety, and develop practical clinical guidelines, particularly for vulnerable populations.
The ketogenic diet (KD) is increasingly recognized for its therapeutic benefits in managing metabolic disorders, including obesity, type 2 diabetes, and epilepsy. However, adherence to KD can elevate the body’s acid load through ketone body production, potentially leading to metabolic acidosis. Alkalinizing salts, such as sodium bicarbonate, potassium citrate, magnesium, and calcium, play a crucial role in maintaining acid-base balance and mitigating complications associated with this dietary regimen. Evidence from studies published between 2000 and 2024 highlights that these interventions can reduce acidosis-related complications, including bone demineralization, muscle cramps, and fatigue, while improving mineral balance and metabolic stability. These findings suggest that incorporating alkalinizing strategies may enhance the safety and effectiveness of KDs. Further research is needed to define optimal dosing, assess long-term safety, and develop practical clinical guidelines, particularly for vulnerable populations.
DOI: https://doi.org/10.37349/eff.2025.1010106
The most common clinical manifestation of hyperlipidemia is the formation of xanthomas, which are most often localized subcutaneously, sometimes involving tendons and ligaments, and are usually asymptomatic. A fairly rare manifestation of hyperlipidemia is hypercholesterolemic arthritis caused by cholesterol crystals. In this article, we present a case of atypical xanthoma formation in a patient in the area of the first metatarsophalangeal joint, which resembled a gouty tophus. Taking into account the presence of hyperuricemia in the blood and the “classic” lesion of the first metatarsophalangeal joint, gout was primarily suspected in the patient. The diagnosis of arthritis associated with cholesterol crystals was confirmed using the “gold standard” diagnosis of microcrystalline arthritis—crystal detection using polarization microscopy. This case gives a clear idea of how important it is not to rely solely on the clinical picture when diagnosing gout.
The most common clinical manifestation of hyperlipidemia is the formation of xanthomas, which are most often localized subcutaneously, sometimes involving tendons and ligaments, and are usually asymptomatic. A fairly rare manifestation of hyperlipidemia is hypercholesterolemic arthritis caused by cholesterol crystals. In this article, we present a case of atypical xanthoma formation in a patient in the area of the first metatarsophalangeal joint, which resembled a gouty tophus. Taking into account the presence of hyperuricemia in the blood and the “classic” lesion of the first metatarsophalangeal joint, gout was primarily suspected in the patient. The diagnosis of arthritis associated with cholesterol crystals was confirmed using the “gold standard” diagnosis of microcrystalline arthritis—crystal detection using polarization microscopy. This case gives a clear idea of how important it is not to rely solely on the clinical picture when diagnosing gout.
DOI: https://doi.org/10.37349/emd.2025.1007113
This article belongs to the special issue Evaluation and Outcomes in the Management of Gout
Inflammatory bowel disease (IBD), consisting of Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition of the gastrointestinal tract with significant clinical impact, leading to debilitating symptoms, impaired quality of life, and an increased risk of complications such as colorectal cancer. This review provides a comprehensive overview of current and emerging therapeutic strategies for IBD. We conducted a narrative review to explore therapeutic advances in IBD treatment, focusing on mechanisms of action, clinical development, and current therapeutic challenges. We analyzed existing knowledge on clinical drug development for IBD, up to July 2025. Our search encompassed databases including PubMed, ClinicalTrials.gov, and Google Scholar, using keywords such as “Inflammatory bowel disease”, “Crohn’s disease”, “Ulcerative colitis”, “therapeutics”, and relevant drug names. We delve into key progress in approved drugs in recent years, including biologic and targeted small molecule therapies, which have advanced the treatment paradigms by offering more precise targeting of inflammatory pathways. This review also covers investigational drugs in clinical development, including biologics and small molecules against novel molecular targets, cell and gene therapies, precision medicine approaches, and microbiome-based interventions. Those novel therapies could potentially address unmet medical needs by achieving deeper and more durable responses, inducing remission, preventing disease progression, and ultimately improving long-term patient outcomes. This review summarizes the latest progress in IBD treatment, outlines the advantages, pitfalls, and research prospects of various drugs and therapies, aiming to provide a foundational understanding for both clinical decision-making and future IBD research.
Inflammatory bowel disease (IBD), consisting of Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition of the gastrointestinal tract with significant clinical impact, leading to debilitating symptoms, impaired quality of life, and an increased risk of complications such as colorectal cancer. This review provides a comprehensive overview of current and emerging therapeutic strategies for IBD. We conducted a narrative review to explore therapeutic advances in IBD treatment, focusing on mechanisms of action, clinical development, and current therapeutic challenges. We analyzed existing knowledge on clinical drug development for IBD, up to July 2025. Our search encompassed databases including PubMed, ClinicalTrials.gov, and Google Scholar, using keywords such as “Inflammatory bowel disease”, “Crohn’s disease”, “Ulcerative colitis”, “therapeutics”, and relevant drug names. We delve into key progress in approved drugs in recent years, including biologic and targeted small molecule therapies, which have advanced the treatment paradigms by offering more precise targeting of inflammatory pathways. This review also covers investigational drugs in clinical development, including biologics and small molecules against novel molecular targets, cell and gene therapies, precision medicine approaches, and microbiome-based interventions. Those novel therapies could potentially address unmet medical needs by achieving deeper and more durable responses, inducing remission, preventing disease progression, and ultimately improving long-term patient outcomes. This review summarizes the latest progress in IBD treatment, outlines the advantages, pitfalls, and research prospects of various drugs and therapies, aiming to provide a foundational understanding for both clinical decision-making and future IBD research.
DOI: https://doi.org/10.37349/ei.2025.1003232
This article belongs to the special issue Advances in Cellular and Molecular Treatment of Autoimmune Diseases
Neurogenetic disorders remain genetically uncharacterized in many populations, including Libya. We report three Libyan patients from two consanguineous families with pathogenic variants in sodium channel genes. Two adult sisters (Patients 1 & 2) presented with global developmental delay and progressive spastic paraparesis without epilepsy. Whole exome sequencing identified the same heterozygous SCN8A variant (c.142G>A; p.Asp48Asn) in both sisters, classified as a variant of uncertain significance (VUS). Its occurrence in two affected siblings with a consistent phenotype and the absence of other explanatory variants provide supporting evidence for its potential pathogenicity. These cases represent the first documented instances of a suspected SCN8A-related disorder in Libya. A third, unrelated 10-year-old boy (Patient 3) with a phenotype consistent with Dravet syndrome, including refractory seizures and neurodevelopmental regression, was found to harbor a likely pathogenic heterozygous SCN1A variant (c.2113del; p.Glu705Lysfs*10). This report expands the genetic and phenotypic spectrum of neurological disorders in Libya and underscores the critical role of genetic testing, while also highlighting the need for segregation studies to achieve a definitive molecular diagnosis.
Neurogenetic disorders remain genetically uncharacterized in many populations, including Libya. We report three Libyan patients from two consanguineous families with pathogenic variants in sodium channel genes. Two adult sisters (Patients 1 & 2) presented with global developmental delay and progressive spastic paraparesis without epilepsy. Whole exome sequencing identified the same heterozygous SCN8A variant (c.142G>A; p.Asp48Asn) in both sisters, classified as a variant of uncertain significance (VUS). Its occurrence in two affected siblings with a consistent phenotype and the absence of other explanatory variants provide supporting evidence for its potential pathogenicity. These cases represent the first documented instances of a suspected SCN8A-related disorder in Libya. A third, unrelated 10-year-old boy (Patient 3) with a phenotype consistent with Dravet syndrome, including refractory seizures and neurodevelopmental regression, was found to harbor a likely pathogenic heterozygous SCN1A variant (c.2113del; p.Glu705Lysfs*10). This report expands the genetic and phenotypic spectrum of neurological disorders in Libya and underscores the critical role of genetic testing, while also highlighting the need for segregation studies to achieve a definitive molecular diagnosis.
DOI: https://doi.org/10.37349/en.2025.1006120
This article belongs to the special issue Advances in Epilepsy Research
Luminescent markers have been widely used in medicine, biology, agrotechnology, and for marking nuclear wastes and consumer goods. The high sensitivity and selectivity of the markers/labels allow the detection of various substances and the obtaining of valuable information about the distribution of constituents in specific media. This review describes the state of the art in luminescent marking/labeling of various cellulose forms, including nanosized ones, cellulose derivatives, and cellulose-containing materials. The importance of this consideration is explained by the role of cellulose and its derivatives in human life and their overall impact on mankind’s development. The structure and luminescence properties of cellulose and other related materials and cellulose derivatives are discussed from the viewpoint of cellulose luminescent “self-labeling”. It is shown that dyes, organic molecules, and organic-inorganic complexes, as well as inorganic dielectric and semiconductor micro/nanoparticles, can be effectively applied for the purposes of cellulose luminescent marking/labeling. This review discusses various application examples and explains the performance and mechanisms of various systems labeling (e.g., dye-cellulose, quantum dot-cellulose complex) in these applications. The review not only comprehensively summarizes existing approaches to luminescent labeling of cellulose-containing materials. It also highlights problematic issues that arise for developers of new luminescent markers (quenching of luminescence in an aqueous environment, the need to functionalize the luminescent marker material, etc.). At the same time, this work demonstrates the prospects for luminescent labeling data in modern digital technologies, particularly in the Internet of Things (IoT).
Luminescent markers have been widely used in medicine, biology, agrotechnology, and for marking nuclear wastes and consumer goods. The high sensitivity and selectivity of the markers/labels allow the detection of various substances and the obtaining of valuable information about the distribution of constituents in specific media. This review describes the state of the art in luminescent marking/labeling of various cellulose forms, including nanosized ones, cellulose derivatives, and cellulose-containing materials. The importance of this consideration is explained by the role of cellulose and its derivatives in human life and their overall impact on mankind’s development. The structure and luminescence properties of cellulose and other related materials and cellulose derivatives are discussed from the viewpoint of cellulose luminescent “self-labeling”. It is shown that dyes, organic molecules, and organic-inorganic complexes, as well as inorganic dielectric and semiconductor micro/nanoparticles, can be effectively applied for the purposes of cellulose luminescent marking/labeling. This review discusses various application examples and explains the performance and mechanisms of various systems labeling (e.g., dye-cellulose, quantum dot-cellulose complex) in these applications. The review not only comprehensively summarizes existing approaches to luminescent labeling of cellulose-containing materials. It also highlights problematic issues that arise for developers of new luminescent markers (quenching of luminescence in an aqueous environment, the need to functionalize the luminescent marker material, etc.). At the same time, this work demonstrates the prospects for luminescent labeling data in modern digital technologies, particularly in the Internet of Things (IoT).
DOI: https://doi.org/10.37349/ebmx.2025.101353
This article belongs to the special issue Nature-Based Biomaterials for Biomedical Applications
Aim:
Community-acquired pneumonia (CAP) is a leading cause of global morbidity and mortality, and it is often treated with fluoroquinolone antibiotics. Misuse of fluoroquinolones is a known driver of antimicrobial resistance, and de-escalation of antibiotics is not only effective for patient outcomes but also reduces resistance. The aim of this study was to assess the association of fluoroquinolone de-escalation with length of stay (LOS), mortality, and other microbiological culture results in hospitalized adults with CAP.
Methods:
A retrospective cohort investigation took place with adult patients suspected of CAP in a tertiary care center in Jordan. The study examined outcomes for fluoroquinolone de-escalation that included hospital LOS, mortality, and examined the relationship between the results of microbial cultures and the outcome of de-escalation.
Results:
The study sample consisted of 125 patients with a median age of 73 years [interquartile range (IQR) = 24]. Around 65% (n = 81) of the patients were male, and 35% (n = 44) were female. The fluoroquinolone therapy was mostly levofloxacin (99.2%, n = 124). Fluoroquinolone de-escalation was medically justified in 32.8% (n = 41) of patients. When comparing the rate of successful de-escalation between those with positive and negative cultures (after the exclusion of 3 patients), positive cultures were statistically more likely to de-escalate than negative cultures, 61.5% (16/26) to 26.0% (25/96) (p = 0.002). Patients in the successful de-escalation had a statistically shorter length of hospital stay; 12 days (IQR = 8) against the failed/inappropriate group, 18 days (IQR = 11) (p = 0.004). There was no significant difference in mortality; 70.1% (n = 29) survived in the de-escalated group and 76.5% (n = 62) in the failed/inappropriate group (p = 0.514).
Conclusions:
In CAP, fluoroquinolone de-escalation may result in shorter hospital stays but does not alter mortality rates. However, limitations in establishing appropriateness for de-escalation imply the need for further studies to validate the findings.
Aim:
Community-acquired pneumonia (CAP) is a leading cause of global morbidity and mortality, and it is often treated with fluoroquinolone antibiotics. Misuse of fluoroquinolones is a known driver of antimicrobial resistance, and de-escalation of antibiotics is not only effective for patient outcomes but also reduces resistance. The aim of this study was to assess the association of fluoroquinolone de-escalation with length of stay (LOS), mortality, and other microbiological culture results in hospitalized adults with CAP.
Methods:
A retrospective cohort investigation took place with adult patients suspected of CAP in a tertiary care center in Jordan. The study examined outcomes for fluoroquinolone de-escalation that included hospital LOS, mortality, and examined the relationship between the results of microbial cultures and the outcome of de-escalation.
Results:
The study sample consisted of 125 patients with a median age of 73 years [interquartile range (IQR) = 24]. Around 65% (n = 81) of the patients were male, and 35% (n = 44) were female. The fluoroquinolone therapy was mostly levofloxacin (99.2%, n = 124). Fluoroquinolone de-escalation was medically justified in 32.8% (n = 41) of patients. When comparing the rate of successful de-escalation between those with positive and negative cultures (after the exclusion of 3 patients), positive cultures were statistically more likely to de-escalate than negative cultures, 61.5% (16/26) to 26.0% (25/96) (p = 0.002). Patients in the successful de-escalation had a statistically shorter length of hospital stay; 12 days (IQR = 8) against the failed/inappropriate group, 18 days (IQR = 11) (p = 0.004). There was no significant difference in mortality; 70.1% (n = 29) survived in the de-escalated group and 76.5% (n = 62) in the failed/inappropriate group (p = 0.514).
Conclusions:
In CAP, fluoroquinolone de-escalation may result in shorter hospital stays but does not alter mortality rates. However, limitations in establishing appropriateness for de-escalation imply the need for further studies to validate the findings.
DOI: https://doi.org/10.37349/emed.2025.1001379
DOI: https://doi.org/10.37349/ebmx.2025.101354
This article belongs to the special issue Bioinspired Material for Regenerative Medicine
Aim:
Osimertinib’s clinical application is limited by poor aqueous solubility and systemic toxicity. Nano-niosomal formulations can address these challenges by providing controlled release and enhancing delivery. To develop and systematically evaluate nano-niosomal formulations of osimertinib using different surfactants, focusing on physicochemical characteristics, release kinetics, and cytotoxic activity.
Methods:
Four niosomal formulations were prepared using Span 60, Tween 60, Pluronic F-127, and Brij 52 (each at a 1:1 cholesterol-to-surfactant ratio). Particle size, zeta potential, and entrapment efficiency were measured. In vitro drug release was analyzed using Franz diffusion cells and fitted to standard kinetic models. Cytotoxicity was assessed by MTT assay in KAIMRC-2, MDA-MB231, and HCT-116 cell lines. Vesicle morphology was visualized by transmission electron microscopy.
Results:
All nano-niosomal formulations showed nanoscale particle sizes (47–292 nm), negative zeta potentials (−18.7 to −26.5 mV), and high entrapment efficiencies (69.8%–76.2%). Release studies indicated Span 60, Tween 60, and Pluronic F-127 followed diffusion-controlled kinetics (Higuchi/Korsmeyer–Peppas model, R2 up to 0.97), while Brij 52 provided a sustained zero-order release (R2 = 0.98). Compared to free osimertinib, all niosomal systems significantly prolonged release. Cytotoxicity studies demonstrated that all formulations enhanced anti-cancer effects, with Span 60-based niosomes exhibiting the greatest potency across cell lines.
Conclusions:
Optimized nano-niosomal encapsulation of osimertinib enables sustained and controlled drug release, improved cellular uptake, and enhanced cytotoxicity in vitro. Differences in surfactant composition critically influence formulation performance, supporting the further development of niosomal osimertinib as a promising strategy for oncological drug delivery applications.
Aim:
Osimertinib’s clinical application is limited by poor aqueous solubility and systemic toxicity. Nano-niosomal formulations can address these challenges by providing controlled release and enhancing delivery. To develop and systematically evaluate nano-niosomal formulations of osimertinib using different surfactants, focusing on physicochemical characteristics, release kinetics, and cytotoxic activity.
Methods:
Four niosomal formulations were prepared using Span 60, Tween 60, Pluronic F-127, and Brij 52 (each at a 1:1 cholesterol-to-surfactant ratio). Particle size, zeta potential, and entrapment efficiency were measured. In vitro drug release was analyzed using Franz diffusion cells and fitted to standard kinetic models. Cytotoxicity was assessed by MTT assay in KAIMRC-2, MDA-MB231, and HCT-116 cell lines. Vesicle morphology was visualized by transmission electron microscopy.
Results:
All nano-niosomal formulations showed nanoscale particle sizes (47–292 nm), negative zeta potentials (−18.7 to −26.5 mV), and high entrapment efficiencies (69.8%–76.2%). Release studies indicated Span 60, Tween 60, and Pluronic F-127 followed diffusion-controlled kinetics (Higuchi/Korsmeyer–Peppas model, R2 up to 0.97), while Brij 52 provided a sustained zero-order release (R2 = 0.98). Compared to free osimertinib, all niosomal systems significantly prolonged release. Cytotoxicity studies demonstrated that all formulations enhanced anti-cancer effects, with Span 60-based niosomes exhibiting the greatest potency across cell lines.
Conclusions:
Optimized nano-niosomal encapsulation of osimertinib enables sustained and controlled drug release, improved cellular uptake, and enhanced cytotoxicity in vitro. Differences in surfactant composition critically influence formulation performance, supporting the further development of niosomal osimertinib as a promising strategy for oncological drug delivery applications.
DOI: https://doi.org/10.37349/ebmx.2025.101355
Background:
The diversity of physiological actions and pharmacological effects of glucocorticoids (GCs) allows their use in a large group of diseases and pathological conditions. However, this treatment can be accompanied by a multitude of more or less severe side effects. As the mainstay of treatment for asthma and chronic obstructive pulmonary disease (COPD), inhaled corticosteroids (ICS) dramatically reduce morbidity and mortality. This research aims to examine the safety considerations associated with glucocorticoid therapy in patients with COPD and asthma.
Methods:
The search was performed in PubMed, EBSCO, UpToDate, Medline, and Google Scholar for pertinent English-language articles published between 1990 and 2025, using the following keywords: glucocorticoids, asthma, COPD, management, and side effects.
Results:
GCs stand out as one of the most widely prescribed classes of drugs globally, with well-established effectiveness in addressing acute or chronic inflammation, allergic conditions, and acute pathological situations. The undeniable efficacy of GCs, however, comes with a range of reported side effects. These include but are not limited to immunosuppression, cardiovascular issues, manifestation of Cushingoid features, development of diabetes, osteoporosis, suppression of the hypothalamic-pituitary-adrenal (HPA) axis, and adverse effects on the gastrointestinal and dermatologic systems. However, the majority of these events are associated with systemic drug administration, which is less commonly indicated in the treatment of COPD and asthma. There are several factors and specific considerations when deciding on GC treatment in COPD. In the context of corticosteroid treatment for asthma, the overarching impact involves the suppression of inflammatory genes, leading to reduced transcription of genes responsible for cytokines, chemokines, adhesion molecules, inflammatory enzymes, and receptors.
Discussion:
GCs are associated with fewer side effects in both COPD and asthma treatment. It’s crucial to take into account factors such as the patient’s overall health, the severity of symptoms, the presence of comorbidities, and the responsiveness of specific features to GCs therapy.
Background:
The diversity of physiological actions and pharmacological effects of glucocorticoids (GCs) allows their use in a large group of diseases and pathological conditions. However, this treatment can be accompanied by a multitude of more or less severe side effects. As the mainstay of treatment for asthma and chronic obstructive pulmonary disease (COPD), inhaled corticosteroids (ICS) dramatically reduce morbidity and mortality. This research aims to examine the safety considerations associated with glucocorticoid therapy in patients with COPD and asthma.
Methods:
The search was performed in PubMed, EBSCO, UpToDate, Medline, and Google Scholar for pertinent English-language articles published between 1990 and 2025, using the following keywords: glucocorticoids, asthma, COPD, management, and side effects.
Results:
GCs stand out as one of the most widely prescribed classes of drugs globally, with well-established effectiveness in addressing acute or chronic inflammation, allergic conditions, and acute pathological situations. The undeniable efficacy of GCs, however, comes with a range of reported side effects. These include but are not limited to immunosuppression, cardiovascular issues, manifestation of Cushingoid features, development of diabetes, osteoporosis, suppression of the hypothalamic-pituitary-adrenal (HPA) axis, and adverse effects on the gastrointestinal and dermatologic systems. However, the majority of these events are associated with systemic drug administration, which is less commonly indicated in the treatment of COPD and asthma. There are several factors and specific considerations when deciding on GC treatment in COPD. In the context of corticosteroid treatment for asthma, the overarching impact involves the suppression of inflammatory genes, leading to reduced transcription of genes responsible for cytokines, chemokines, adhesion molecules, inflammatory enzymes, and receptors.
Discussion:
GCs are associated with fewer side effects in both COPD and asthma treatment. It’s crucial to take into account factors such as the patient’s overall health, the severity of symptoms, the presence of comorbidities, and the responsiveness of specific features to GCs therapy.
DOI: https://doi.org/10.37349/eaa.2025.1009104
This article belongs to the special issue The Era of Biologics in Allergy
The oral microbiome has been increasingly implicated in the development and progression of neurological disorders. This narrative review synthesizes contemporary literature on alterations of oral microbial communities in Alzheimer’s disease, Parkinson’s disease, and migraine and evaluates their potential contribution to neuroinflammation and neurodegeneration. We first outline the core oral taxa that maintain microbial homeostasis and summarize evidence that patients with these neurological conditions exhibit dysbiosis characterized by reduced diversity and enrichment of periodontal pathogens. Proposed mechanisms include hematogenous or neural translocation of oral bacteria and their virulence factors, amplification of systemic inflammation, disruption of the blood-brain barrier, altered production of neuroactive metabolites, and bidirectional signaling along the ‘oral-gut-brain’ axis. On this mechanistic basis, microbiome-targeted strategies, particularly probiotics and fecal microbiota transplantation, have been explored as adjunctive approaches to restore microbial balance and potentially improve neurological outcomes, although available clinical data remain preliminary and heterogeneous. Current evidence is further limited by small samples, methodological variability in microbiome profiling, and a paucity of longitudinal and interventional studies, which hampers causal inference. Future research should adopt standardized sampling and multi-omic approaches and prioritize well-designed clinical trials to determine whether modulation of the oral microbiome can be translated into preventive or therapeutic strategies for neurological diseases.
The oral microbiome has been increasingly implicated in the development and progression of neurological disorders. This narrative review synthesizes contemporary literature on alterations of oral microbial communities in Alzheimer’s disease, Parkinson’s disease, and migraine and evaluates their potential contribution to neuroinflammation and neurodegeneration. We first outline the core oral taxa that maintain microbial homeostasis and summarize evidence that patients with these neurological conditions exhibit dysbiosis characterized by reduced diversity and enrichment of periodontal pathogens. Proposed mechanisms include hematogenous or neural translocation of oral bacteria and their virulence factors, amplification of systemic inflammation, disruption of the blood-brain barrier, altered production of neuroactive metabolites, and bidirectional signaling along the ‘oral-gut-brain’ axis. On this mechanistic basis, microbiome-targeted strategies, particularly probiotics and fecal microbiota transplantation, have been explored as adjunctive approaches to restore microbial balance and potentially improve neurological outcomes, although available clinical data remain preliminary and heterogeneous. Current evidence is further limited by small samples, methodological variability in microbiome profiling, and a paucity of longitudinal and interventional studies, which hampers causal inference. Future research should adopt standardized sampling and multi-omic approaches and prioritize well-designed clinical trials to determine whether modulation of the oral microbiome can be translated into preventive or therapeutic strategies for neurological diseases.
DOI: https://doi.org/10.37349/ent.2025.1004131
This article belongs to the special issue Role of Microbiota in Neurological Diseases
Aim:
Foodborne non-typhoidal Salmonella (NTS) infections are a major global health issue, frequently linked to animal source foods. However, there is limited data on NTS prevalence, distribution, and serotype diversity in common animal products and related food in Ghana. This study investigated the prevalence and serotype diversity of NTS in animal source foods, ready-to-eat (RTE) food, and animal fecal samples across six districts in the Greater Accra Region of Ghana.
Methods:
A total of 696 samples were randomly collected from selected markets across the districts. These included unprocessed animal products: beef (16), chicken (21), eggs (185), and raw cow milk (40). Additionally, 50 samples of RTE street foods and 36 samples of locally produced soft cheese (“wagashie”) were obtained from vendors. Fecal samples consisted of chicken droppings (70) and pig feces (138), which were purposively collected from 11 poultry farms and two pig slaughter facilities in the region. Furthermore, 140 pork samples were purposively collected from the slaughter facilities. Standard microbiological methods, including pre-enrichment, selective enrichment, and plating on selective media, were used for Salmonella species isolation, with identification confirmed by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Serotyping followed the White-Kauffman Le-Minor classification scheme.
Results:
Overall, 26 Salmonella isolates were recovered (3.7%). Prevalence was significantly higher in animal source foods (5.71%; 25/438) compared to fecal samples (0.4%; 1/208) (p = 0.0026). Salmonella contamination was highest in raw pork (13.6%), followed by “wagashie” (5.5%) and raw milk (5%). Nine distinct serotypes were identified. Among them, Salmonella Typhimurium was the most prevalent, accounting for 40.9%, followed by Salmonella Kaapstad at 13.6%. Additionally, pork samples contained seven of these serotypes.
Conclusions:
These findings highlight a potential risk posed by NTS in commonly consumed animal source foods in Greater Accra and emphasize the need for targeted interventions to control contamination, particularly in pork products.
Aim:
Foodborne non-typhoidal Salmonella (NTS) infections are a major global health issue, frequently linked to animal source foods. However, there is limited data on NTS prevalence, distribution, and serotype diversity in common animal products and related food in Ghana. This study investigated the prevalence and serotype diversity of NTS in animal source foods, ready-to-eat (RTE) food, and animal fecal samples across six districts in the Greater Accra Region of Ghana.
Methods:
A total of 696 samples were randomly collected from selected markets across the districts. These included unprocessed animal products: beef (16), chicken (21), eggs (185), and raw cow milk (40). Additionally, 50 samples of RTE street foods and 36 samples of locally produced soft cheese (“wagashie”) were obtained from vendors. Fecal samples consisted of chicken droppings (70) and pig feces (138), which were purposively collected from 11 poultry farms and two pig slaughter facilities in the region. Furthermore, 140 pork samples were purposively collected from the slaughter facilities. Standard microbiological methods, including pre-enrichment, selective enrichment, and plating on selective media, were used for Salmonella species isolation, with identification confirmed by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Serotyping followed the White-Kauffman Le-Minor classification scheme.
Results:
Overall, 26 Salmonella isolates were recovered (3.7%). Prevalence was significantly higher in animal source foods (5.71%; 25/438) compared to fecal samples (0.4%; 1/208) (p = 0.0026). Salmonella contamination was highest in raw pork (13.6%), followed by “wagashie” (5.5%) and raw milk (5%). Nine distinct serotypes were identified. Among them, Salmonella Typhimurium was the most prevalent, accounting for 40.9%, followed by Salmonella Kaapstad at 13.6%. Additionally, pork samples contained seven of these serotypes.
Conclusions:
These findings highlight a potential risk posed by NTS in commonly consumed animal source foods in Greater Accra and emphasize the need for targeted interventions to control contamination, particularly in pork products.
DOI: https://doi.org/10.37349/eff.2025.1010105
Immune checkpoint inhibitor (ICI) therapy has revolutionized metastatic melanoma treatment, yet only a subset of patients respond effectively, and the treatment can induce a variety of immune-related adverse events (irAEs), including colitis. The gut microbiome plays a critical role in determining patient responses to immunotherapy, prompting exploration of gut-modifying strategies such as prebiotics, probiotics, and fecal microbiota transplantation (FMT) to overcome both primary and acquired resistance and improve treatment outcomes. Prebiotics, defined as dietary substrates that selectively support the growth and/or activity of beneficial gut microorganisms, represent a feasible and safe strategy for microbiome reshaping. Plant-derived prebiotics like castalagin, inulin, fructooligosaccharides, galactooligosaccharides, mushroom extract, kale extract, and konjac glucomannan offer unique advantages over synthetic or animal-derived alternatives due to their natural fiber content alongside their ability to enhance gut microbial diversity. Prebiotics are known to achieve health benefits by selectively stimulating beneficial gut bacteria, producing short-chain fatty acids (SCFAs) that modulate the host immune system, suppressing pathogenic microbes, enhancing mucin production, and modulating systemic and gut-associated immune responses. SCFAs generated through prebiotic fermentation influence host innate and adaptive immunity and regulate metabolic activity via inhibition of histone deacetylases (HDACs), influencing mTOR/MAPK signaling and cytokine production. They also act as ligands for G-protein-coupled receptors (GPCRs), altering intracellular calcium and cAMP to modulate immune cell gene expression. However, the specific mechanisms by which individual prebiotics interact with host genetics, beneficial gut bacteria, and their metabolites are not very well understood. This is crucial to optimize their therapeutic potential in cancer immunotherapy. This review synthesizes current evidence on plant-derived prebiotics, highlighting the impact of beneficial gut bacteria and their metabolites. Given their established safety for human consumption, prebiotics represent a promising, low-risk option to improve gut microbiome composition and potentially enhance immunotherapy and clinical outcomes in cancer.
Immune checkpoint inhibitor (ICI) therapy has revolutionized metastatic melanoma treatment, yet only a subset of patients respond effectively, and the treatment can induce a variety of immune-related adverse events (irAEs), including colitis. The gut microbiome plays a critical role in determining patient responses to immunotherapy, prompting exploration of gut-modifying strategies such as prebiotics, probiotics, and fecal microbiota transplantation (FMT) to overcome both primary and acquired resistance and improve treatment outcomes. Prebiotics, defined as dietary substrates that selectively support the growth and/or activity of beneficial gut microorganisms, represent a feasible and safe strategy for microbiome reshaping. Plant-derived prebiotics like castalagin, inulin, fructooligosaccharides, galactooligosaccharides, mushroom extract, kale extract, and konjac glucomannan offer unique advantages over synthetic or animal-derived alternatives due to their natural fiber content alongside their ability to enhance gut microbial diversity. Prebiotics are known to achieve health benefits by selectively stimulating beneficial gut bacteria, producing short-chain fatty acids (SCFAs) that modulate the host immune system, suppressing pathogenic microbes, enhancing mucin production, and modulating systemic and gut-associated immune responses. SCFAs generated through prebiotic fermentation influence host innate and adaptive immunity and regulate metabolic activity via inhibition of histone deacetylases (HDACs), influencing mTOR/MAPK signaling and cytokine production. They also act as ligands for G-protein-coupled receptors (GPCRs), altering intracellular calcium and cAMP to modulate immune cell gene expression. However, the specific mechanisms by which individual prebiotics interact with host genetics, beneficial gut bacteria, and their metabolites are not very well understood. This is crucial to optimize their therapeutic potential in cancer immunotherapy. This review synthesizes current evidence on plant-derived prebiotics, highlighting the impact of beneficial gut bacteria and their metabolites. Given their established safety for human consumption, prebiotics represent a promising, low-risk option to improve gut microbiome composition and potentially enhance immunotherapy and clinical outcomes in cancer.
DOI: https://doi.org/10.37349/etat.2025.1002354
Glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1RAs) and dual incretin agonists have demonstrated significant potential in improving adipose tissue function beyond their established effects on appetite suppression and weight loss. These agents not only reduce overall fat mass but also induce favorable changes in fat distribution and adipose tissue quality. Notably, they enhance brown adipose tissue (BAT) activity and promote the browning of white adipose tissue (WAT), thereby increasing energy expenditure. They are associated with reductions in adipocyte size, particularly within visceral fat depots, alongside improvements in metabolic health markers. The aim of this publication is to provide a literature review on the effects of GLP-1RAs and dual incretin agonists on adipocyte type and size, adipose tissue functional remodeling, and their implications for obesity management. These findings highlight the capacity of incretin-based therapies to modulate adipose tissue biology, offering metabolic benefits that extend beyond weight reduction.
Glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1RAs) and dual incretin agonists have demonstrated significant potential in improving adipose tissue function beyond their established effects on appetite suppression and weight loss. These agents not only reduce overall fat mass but also induce favorable changes in fat distribution and adipose tissue quality. Notably, they enhance brown adipose tissue (BAT) activity and promote the browning of white adipose tissue (WAT), thereby increasing energy expenditure. They are associated with reductions in adipocyte size, particularly within visceral fat depots, alongside improvements in metabolic health markers. The aim of this publication is to provide a literature review on the effects of GLP-1RAs and dual incretin agonists on adipocyte type and size, adipose tissue functional remodeling, and their implications for obesity management. These findings highlight the capacity of incretin-based therapies to modulate adipose tissue biology, offering metabolic benefits that extend beyond weight reduction.
DOI: https://doi.org/10.37349/eemd.2025.101452
Apparent increases in autism and other forms of neurodivergence are often interpreted as a rise in incidence. Yet demographic expansion, diagnostic broadening, and growing cultural awareness all contribute to higher prevalence estimates. At the same time, contemporary sensory and digital environments have become increasingly overstimulating, characterized by persistent noise, visual saturation, hyperconnectivity, and unpredictable social rhythms. These conditions heighten sensory and cognitive load for many individuals, making neurodivergent traits more visible and increasing the urgency of diagnosis. Drawing on cognitive ecology, sensory neuroscience, and neuroaffirmative scholarship, this perspective proposes that neurodivergence can be understood as an adaptive response to environments that exceed nervous-system thresholds. Autistic regulatory behaviors—including withdrawal, shutdown, sensory avoidance, and monotropism-driven focus—may serve as mechanisms for maintaining coherence in overstimulating contexts. Interpreting neurodivergence as an ecological signal offers new pathways for public health, accessibility design, and social policy. It reframes autistic embodiment not as internal dysfunction but as meaningful information about the livability of contemporary environments.
Apparent increases in autism and other forms of neurodivergence are often interpreted as a rise in incidence. Yet demographic expansion, diagnostic broadening, and growing cultural awareness all contribute to higher prevalence estimates. At the same time, contemporary sensory and digital environments have become increasingly overstimulating, characterized by persistent noise, visual saturation, hyperconnectivity, and unpredictable social rhythms. These conditions heighten sensory and cognitive load for many individuals, making neurodivergent traits more visible and increasing the urgency of diagnosis. Drawing on cognitive ecology, sensory neuroscience, and neuroaffirmative scholarship, this perspective proposes that neurodivergence can be understood as an adaptive response to environments that exceed nervous-system thresholds. Autistic regulatory behaviors—including withdrawal, shutdown, sensory avoidance, and monotropism-driven focus—may serve as mechanisms for maintaining coherence in overstimulating contexts. Interpreting neurodivergence as an ecological signal offers new pathways for public health, accessibility design, and social policy. It reframes autistic embodiment not as internal dysfunction but as meaningful information about the livability of contemporary environments.
DOI: https://doi.org/10.37349/ent.2025.1004130
Aim:
To determine whether PepTivator® melanoma-associated antigen-A3 (MAGE-A3) primes early T-cell activation and memory skewing in human peripheral blood mononuclear cells (PBMCs).
Methods:
PBMCs from 10 donors were stimulated with MAGE-A3 (manufacturer-recommended dose), negative control (NC), or CD3/CD28 and CytoStim™ (PC: positive control). Activation [CD69, CD25, HLA-DR (human leukocyte antigen-DR isotype)], proliferation, cytokines [24 h; GM-CSF (granulocyte-macrophage colony-stimulating factor), IFN-γ (interferon-gamma), IL-2 (interleukin-2), TNF-α (tumor necrosis factor-alpha)], and memory phenotypes (CD45RO/CD27 at days 0/7/14) were quantified by flow cytometry and MACSPlex. Paired statistics used repeated-measures models with Šidák correction; cytokines were analyzed on log10 scale.
Results:
MAGE-A3 significantly increased early activation (CD69 ↑, CD25 ↑) and modestly increased proliferation, with selective IL-2/TNF-α rise and minimal IFN-γ and modest HLA-DR. Across two weeks, 6/10 donors showed increased central memory T cell (TCM)/effector memory T cell (TEM) with a corresponding decline in naïve cells relative to NC. Variability across donors was evident.
Conclusions:
MAGE-A3 primes partial activation and memory skewing of human T cells in vitro, suggesting utility as a component antigen that likely benefits from professional antigen-presenting cell (APC) presentation and/or costimulation. We discuss limitations (single dose, in vitro context, donor variability) and implications for future dose-response, HLA-stratified, and APC-supported studies.
Aim:
To determine whether PepTivator® melanoma-associated antigen-A3 (MAGE-A3) primes early T-cell activation and memory skewing in human peripheral blood mononuclear cells (PBMCs).
Methods:
PBMCs from 10 donors were stimulated with MAGE-A3 (manufacturer-recommended dose), negative control (NC), or CD3/CD28 and CytoStim™ (PC: positive control). Activation [CD69, CD25, HLA-DR (human leukocyte antigen-DR isotype)], proliferation, cytokines [24 h; GM-CSF (granulocyte-macrophage colony-stimulating factor), IFN-γ (interferon-gamma), IL-2 (interleukin-2), TNF-α (tumor necrosis factor-alpha)], and memory phenotypes (CD45RO/CD27 at days 0/7/14) were quantified by flow cytometry and MACSPlex. Paired statistics used repeated-measures models with Šidák correction; cytokines were analyzed on log10 scale.
Results:
MAGE-A3 significantly increased early activation (CD69 ↑, CD25 ↑) and modestly increased proliferation, with selective IL-2/TNF-α rise and minimal IFN-γ and modest HLA-DR. Across two weeks, 6/10 donors showed increased central memory T cell (TCM)/effector memory T cell (TEM) with a corresponding decline in naïve cells relative to NC. Variability across donors was evident.
Conclusions:
MAGE-A3 primes partial activation and memory skewing of human T cells in vitro, suggesting utility as a component antigen that likely benefits from professional antigen-presenting cell (APC) presentation and/or costimulation. We discuss limitations (single dose, in vitro context, donor variability) and implications for future dose-response, HLA-stratified, and APC-supported studies.
DOI: https://doi.org/10.37349/ei.2025.1003231
Fibroblast growth factor receptor 1 (FGFR1) is crucial in the progression of various cancers, participating in the processes of cell proliferation, survival, and differentiation. FGFR1 plays a role in the resistance to immune checkpoint inhibitors (ICIs) such as pembrolizumab and nivolumab. Therefore, using monoclonal antibodies and tyrosine kinase inhibitors to target FGFR1 and enhancing ICIs by modifying the tumor microenvironment and combating immune suppression represents a potential therapeutic strategy. Based on the FGFR1-related research and the active targeting strategy, we believe that modifying the surface of nanomedicines with anti-FGFR1 antibodies (such as OM-RCA-01) is an effective targeted treatment method for tumors with high expression of FGFR1. Although there have been relevant studies confirming the feasibility of this approach, there are challenges in clinical application, especially in terms of maintaining uniform quality during large-scale production. Therefore, we suggest conducting further optimization studies in the future to accelerate the clinical application of such drug delivery systems and provide more efficient and cost-effective options for tumor treatment.
Fibroblast growth factor receptor 1 (FGFR1) is crucial in the progression of various cancers, participating in the processes of cell proliferation, survival, and differentiation. FGFR1 plays a role in the resistance to immune checkpoint inhibitors (ICIs) such as pembrolizumab and nivolumab. Therefore, using monoclonal antibodies and tyrosine kinase inhibitors to target FGFR1 and enhancing ICIs by modifying the tumor microenvironment and combating immune suppression represents a potential therapeutic strategy. Based on the FGFR1-related research and the active targeting strategy, we believe that modifying the surface of nanomedicines with anti-FGFR1 antibodies (such as OM-RCA-01) is an effective targeted treatment method for tumors with high expression of FGFR1. Although there have been relevant studies confirming the feasibility of this approach, there are challenges in clinical application, especially in terms of maintaining uniform quality during large-scale production. Therefore, we suggest conducting further optimization studies in the future to accelerate the clinical application of such drug delivery systems and provide more efficient and cost-effective options for tumor treatment.
DOI: https://doi.org/10.37349/etat.2025.1002353
