Background and Aims: Suzetrigine is the first class of non‐opioid analgesics that selectively targets and blocks a key mediator in pain signal transmission, NaV1.8, which is expressed in the peripheral nociceptive neurons. Suzetrigine received approval from the U.S. Food and Drug Administration (FDA) on January 30, 2025. This review aims to explore Suzetrigine, a newly FDA‐approved analgesic, by discussing its clinical opportunities, associated challenges, and future directions in pain management. Methods: We searched major databases (PubMed, Scopus, Web of Science, and ClinicalTrials.gov ) and FDA sources for information on Suzetrigine and its role in pain management. The collected preclinical, clinical, and regulatory data were reviewed and analyzed to highlight their current evidence, challenges, and future potential. Result and Discussion: Suzetrigine has been approved to treat acute pain after a sufficient and acceptable clinical trial. In terms of its usage in treating chronic pain, its effectiveness in cases of pregnant or lactating women and children, as well as whether it can be used in combination therapy, are still under observation. The brand name of Suzetrigine is JOURNAVX. So far, enough evidence has been provided to approve this drug only to treat acute pain for a short period of time. A lot of people with short‐term pain are concerned about getting addicted to opioid analgesics when they are used as postoperative pain relievers. The invention of Suzetrigine focused on combating these sorts of phenomena. Conclusion: Suzetrigine is considered an alternative option in the realm of acute pain management. Due to its selectivity, this medication does not interfere with other local anesthetics. Moreover, this selectivity also constrains this medication to act on other receptors, thus possessing the least amount of adverse effects. Although Suzetrigine created many opportunities for research in the field of pain management, but also opened a door for many uncertainties that cannot be ignored.

Background and Aims: Following the end of the COVID‐19 global emergency, concern has shifted to “Disease X,” a hypothetical, highly transmissible, and deadly pathogen, and Middle East Respiratory Syndrome Coronavirus (MERS‐CoV) is a prime candidate for this. This review explores its epidemiology, mutations, transmission, and potential to become a pandemic‐capable pathogen, aiming to support future research and public health preparedness against the disease. Methods: A comprehensive search of major databases was conducted for peer‐reviewed English articles (2000–2025) focusing on virology, outbreaks, treatments, and public health using relevant but definite keywords. Studies met strict inclusion criteria and standardized methods to ensure quality, reproducibility, and transparency. Results: Since it was identified in 2012, MERS‐CoV has spread across 27 countries, presenting a high case fatality rate (~34.5%) and zoonotic origin. It is primarily linked to dromedary camels, but shows limited human‐to‐human transmission ( R ₀ < 1). Unlike SARS‐CoV‐2, MERS‐CoV's spread is confined to close contact and healthcare settings, largely in the Middle East and parts of Africa. Its pathogenesis involves severe respiratory illness, driven by immune evasion and systemic inflammation, especially in individuals with comorbidities. While MERS‐CoV lacks pandemic‐level transmissibility, its genetic plasticity poses a risk for future evolution. Vaccine and therapeutic development remain limited due to sporadic outbreaks and low global urgency. Conclusion: Despite not currently fitting the Disease X archetype, MERS‐CoV's high mortality, zoonotic spillover potential, and possibility for increased transmissibility warrant continued surveillance, targeted research, and strengthened public health infrastructure to prevent localized outbreaks from escalating into broader crises.

Background: The apoptotic pathway mediated by mitochondria depends on the activation of pro‐apoptotic Bcl‐2 proteins Bax and Bak. When they permeabilize the outer mitochondrial membrane (OMM), mitochondrial dysfunction occurs, leading to caspase activation. A recent study proposed that Bax accumulation on mitochondria increases apoptotic susceptibility, with adhesion‐initiated signals regulating Bax. When adhesion signaling is inhibited, Bax translocates to the OMM, undergoes conformational change, and forms complexes that create pores. Although MOMP is well studied, mechanisms regulating Bax shuttling, non‐canonical partners, and mitochondrial dynamics remain poorly understood. Aims: This review aims to provide insights by discussing the mechanisms through which Bax regulates its mitochondrial targeting, the mitochondrial dynamics associated with Bax translocation, and their influence to apoptosis. Understanding these processes could reveal new insights into the decision‐making checkpoints that determine cell death. Methods: A comprehensive literature search was conducted across scientific databases for peer‐reviewed publications up to 2025. Search terms included Bax retrotranslocation , mitochondrial dynamics , Bcl‐2 family interactome , and apoptotic priming . Results: Recent evidence shows that Bax continuously retrotranslocates from mitochondria to the cytosol under survival conditions, a process driven by anti‐apoptotic Bcl‐2 proteins. When adhesion signaling or other survival cues are inhibited, this cycle is disrupted, leading to Bax accumulation on mitochondria, its oligomerization, and the onset of MOMP. Several mitochondrial proteins, including Drp1, MAVS, OCIAD1, PTPN1, and AKAP1, have also been linked to a mitochondrial interaction network that influences Bax localization and retrotranslocation. Proximity‐labeling approaches such as BioID are further identifying new proteins that may regulate Bax's mitochondrial targeting and apoptotic priming. Conclusion: The mechanisms driving Bax accumulation on mitochondria and its retrotranslocation remain unclear, especially the role of mitochondrial proteins. Evidence suggests mitochondrial interaction networks influence Bax and Bak regulation. Further research is needed to define how these networks integrate with the Bcl‐2 interactome to shape apoptotic decisions.

Neurological disorders involve complex interactions between neurotransmitters and immune signaling pathways, with serotonin (5-HT) and interleukins (ILs) playing crucial roles. This review explores the mixed pathway of 5-HT-IL signaling and its involvement in the pathophysiology of neurodegenerative and neuropsychiatric conditions. Dysregulated 5-HT and IL signaling has been implicated in Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, depression, anxiety, schizophrenia, autism spectrum disorder, and attention-deficit/hyperactivity disorder. 5-HT influences neuroinflammation, synaptic plasticity, and cognitive function, while ILs regulate immune responses and neuronal survival. Their interplay modulates neurotransmission, neuroinflammation, and neurodegeneration through mechanisms, such as cytokine-mediated 5-HT depletion and 5-HT receptor regulation. Understanding the 5-HT-IL pathway offers new insights into disease progression and potential therapeutic strategies, including selective 5-HT reuptake inhibitors, cytokine inhibitors, and combination therapies targeting neuroimmune interactions.

The increasing mortality from ovarian and lung cancers worldwide is largely due to late diagnosis and therapeutic resistance. Conventional biomarkers such as CA125 and CYFRA 21-1 lack the sensitivity or the specificity for monitoring real time disease progression or therapeutic response. This has prompted researchers to work on the development of relevant biomarkers that are minimally invasive for cancer diagnosis, prognosis and for therapeutic stratification. As such, liquid biopsies, which analyze tumor-derived components circulating in the blood including circulating tumor cells (CTCs), which are shed from primary or metastatic tumors into the bloodstream have emerged as a promising approach for detecting such cancers. This review critically analyzes the diagnostic and prognostic significance of CTCs in ovarian and lung cancers, highlighting technological advances, molecular characterization, and translational challenges associated with their clinical application. It briefly discusses the clinical utility of some biomarkers from liquid biopsies used in the diagnosis, prognosis as well as monitoring of ovarian and lung cancers with their detection methods. It highlights some of the relevant studies conducted in the field and finally it provides insights on the future of liquid biopsies. An extensive literature review analyzing papers between 2008 and 2026 was conducted using PubMed, Scopus, and Web of Science databases, that evaluated CTC detection methods, molecular profiling, and clinical outcomes in ovarian and lung cancer patients. Current literature reports that CTC enumeration and molecular characterization can provide significant insights into disease progression, therapeutic resistance and predict survival outcomes. Whilst the enrichment technologies such as CellSearch ^® , ISET, and microfluidic platforms have enhanced detection sensitivity, variability in assay performance and lack of a clinical standardization impede proper implementation. CTCs represent a powerful liquid biopsy tool with potential to revolutionize cancer diagnostics and precision medicine. Integration of multi-omics profiling, CTC-derived organoids, and AI-driven analytical models may further enhance their clinical utility in guiding personalized treatment strategies for ovarian and lung cancer patients.

Background and Aims: The integration of biosimilars into pediatric healthcare represents a significant evolution in treatment accessibility and cost‐effectiveness. Biosimilars—biological products highly similar to already approved biologics, have emerged as promising alternatives for managing chronic and rare pediatric conditions, including inflammatory bowel disease, juvenile idiopathic arthritis, psoriasis, asthma, lupus nephritis, and growth hormone deficiencies. Despite regulatory, clinical, and societal challenges, current data suggest biosimilars demonstrate comparable safety, efficacy, and immunogenicity profiles to their originator products. The review consolidates findings from recent clinical trials, real‐world data, and regulatory landscapes across the US and EU, emphasizing the growing role of biosimilars in pediatric pharmacotherapy. It also explores future directions in biosimilar development, highlighting the need for improved pediatric‐specific research, regulatory harmonization, and stakeholder education to ensure wider adoption and optimized outcomes in children. Method: A structured literature search of PubMed, Scopus, Web of Science, and Google Scholar (2003–March 2026) identified English‐language studies on pediatric biosimilars. Relevant clinical, regulatory, and review articles were thematically synthesized. Results: In pediatric patients with chronic conditions such as inflammatory bowel disease and rheumatologic disorders, biosimilars like infliximab and adalimumab offer efficacy and safety comparable to originator biologics, while lowering treatment costs. Economic analyses demonstrate that biosimilars are typically 15%–45% cheaper than reference products in Europe, and in some markets up to 85% lower, improving affordability and access to treatment in pediatric populations. Conclusion: Biosimilars have a great deal of promise to improve therapeutic access and lower medical expenses associated with pediatric care. However, to maximize results and guarantee therapeutic fairness in pediatric medicine, broader adoption necessitates increased age‐specific clinical trials, harmonized regulations, better training for healthcare providers, and increased stakeholder trust.