Abstract
Asthma represents a profoundly heterogeneous syndrome underpinned by multiple, distinct and overlapping immunopathological mechanisms. Nevertheless, prevailing management algorithms continue to adopt a largely uniform, stepwise approach in which pharmacotherapy is intensified only after clinical deterioration or recurrent exacerbations. Although the advent of targeted biologic agents has improved outcomes in severe asthma, the realisation of precision medicine - therapeutic selection directed by individual disease mechanisms - remains elusive. This is primarily attributable to the limited availability of validated biomarkers capable of defining endotypes and accurately predicting therapeutic responsiveness. Existing indicators of type-2 (T2) inflammation, including blood eosinophil counts, fractional exhaled nitric oxide, and serum Immunoglobulin E, provide only partial discrimination between T2 subtypes and are insufficient to guide the choice of specific T2-targeted biologics. Furthermore, robust non-T2 biomarkers are notably lacking. This review provides a critical appraisal of current biomarker paradigms and examines emerging molecular and cellular candidates with potential to enable precise endotyping. Integration of such biomarkers into early disease assessment offers the prospect of delivering truly individualised therapy, ensuring that appropriate treatment is instituted for the right patient at the optimal time.