Stroke is the third leading cause of death in the developed world and a major cause of chronic disability, especially among the elderly population. The major biomarkers of stroke which are the most promising for predicting onset time and independently differentiating ischemic from hemorrhagic and other stroke subtypes are at present limited to a few. This review aims to emphasize on the prognostic role of S100 calcium-binding protein b (S100B), and Glial Fibrillary Acidic Protein (GFAP) in patients with stroke. An electronic search of the published research from January 2000 to February 2024 was conducted using the MEDLINE, Scopus, and Cochrane databases. The implementation of S100B and GFAP in existing clinical scales and imaging modalities may be used to improve diagnostic accuracy and realize the potential of blood biomarkers in clinical practice. The reviewed studies highlight the potential of S100B and GFAP as significant biomarkers in the prognosis and diagnosis of patients with stroke and their ability of predicting long-term neurological deficits. They demonstrate high sensitivity and specificity in differentiating between ischemic and hemorrhagic stroke and they correlate well with stroke severity and outcomes. Several studies also emphasize on the early elevation of these biomarkers post-stroke onset, underscoring their value in early diagnosis and risk stratification. The ongoing research in this field should aim at improving patient outcomes and reducing stroke-related morbidity and mortality by developing a reliable, non-invasive diagnostic tool that can be easily implemented in several healthcare settings, with the ultimate goal of improving stroke management.

Intravitreal inhibition of vascular endothelial growth factor (VEGF) has transformed the management of neovascular age-related macular degeneration, diabetic macular oedema and macular oedema secondary to retinal vein occlusion, but frequent monitoring and retreatment remain major burdens. Ocular half-life is often used as shorthand for durability, although the clinical interval is produced by a wider molecular and biological system. This narrative review examines how dose, molecular format, hydrodynamic size, binding affinity, valency, ligand spectrum, target turnover, tissue distribution and delivery architecture determine the time for which an eye remains controlled. Human ocular pharmacokinetic and pharmacodynamic evidence is interpreted according to compartment, assay and model provenance, with particular attention to the distinction between drug elimination, free-ligand suppression, anatomical control and protocol-assigned treatment interval. Trial evidence for ranibizumab, aflibercept, conbercept, brolucizumab and faricimab shows that extended dosing can arise from greater starting exposure, altered binding architecture or pathway expansion without a proportionate change in intrinsic ocular half-life. Patient phenotype and retreatment rules further modify the observed interval. Refillable reservoirs, biodegradable depots and ocular gene therapy change the governing kinetics from bolus elimination to controlled release or sustained local production, thereby increasing the importance of reversibility and cumulative safety. We propose that durability be defined as a time-to-threshold phenotype integrating active target-site exposure, biological demand, anatomical recurrence, all treatment-related procedures and safety. Standardised estimands, longitudinal human ocular sampling, spatial exposure methods and externally validated mechanism-informed models are needed to make molecular durability comparable and clinically actionable.