# Emerging Therapeutic Strategies in Asthma: Advances in Treatment, Drug Delivery, Drug Adherence, and Disease Management

**Authors:** Ying Xuan Lim, Yi Ning Choo, Yuet Thong Looi, Yap Wern Chuan, Kai Xin Chiam, Rebecca Shin-Yee Wong, Nancy Choon-Si Ng, Bey Hing Goh

PMC · DOI: 10.1007/s11882-026-01265-6 · 2026-03-06

## TL;DR

This review explores new asthma treatments, including biologics, nanomedicine, and digital tools, highlighting their benefits and challenges in improving patient outcomes.

## Contribution

The paper provides a comprehensive synthesis of recent advances in asthma therapies, emphasizing precision medicine and technology-enabled care.

## Key findings

- Biologics targeting IgE, IL-5, and IL-4/IL-13 significantly reduce asthma exacerbations and corticosteroid use.
- Regenerative and gene-based therapies remain largely preclinical with limited clinical application.
- Digital health tools improve adherence and asthma management but face challenges in cost and long-term effectiveness.

## Abstract

This review synthesises evidence published between 2020 and 2025 on emerging therapeutic strategies for asthma, with a focus on three interrelated domains: targeted treatments across asthma endotypes, advances in drug delivery aimed at improving pulmonary deposition and therapeutic efficiency, and technology-enabled tools to support adherence and disease management. We examine how biologics, regenerative and gene-based approaches, nanomedicine platforms, and digital health interventions are reshaping asthma care, while critically appraising their clinical maturity and implementation challenges.

Advances in precision therapy have substantially improved outcomes for patients with severe asthma, particularly through biologics targeting IgE, IL-5 or its receptor, IL-4/IL-13 signalling, and the upstream epithelial alarmin thymic stromal lymphopoietin. These agents consistently reduce exacerbation frequency and systemic corticosteroid use in selected populations, with favourable short- to medium-term safety profiles. In contrast, regenerative strategies such as mesenchymal stem cell–based therapies, gene-based interventions including miRNA and siRNA modulation, and tolerogenic mRNA vaccines remain largely preclinical, offering mechanistic insight but limited clinical readiness. Nanoparticle-enabled drug delivery systems show potential to enhance pulmonary targeting and controlled release, though evidence is predominantly experimental. In parallel, smart inhalers, digital therapeutics, and environmental monitoring technologies address behavioural and environmental determinants of asthma control by improving adherence, inhaler technique, and trigger identification. However, their real-world impact is constrained by cost, integration into clinical workflows, and limited long-term effectiveness data.

Asthma management is increasingly moving toward precision, endotype-informed care supported by targeted biologics, advanced delivery systems, and digital self-management tools. While biologics represent the most clinically established advances, regenerative, gene-based, and nanomedicine approaches remain exploratory and require robust long-term evaluation. Key priorities for future research include effective therapies for non–Type 2 and steroid-resistant asthma, improved affordability and equitable access, and integrated care models that combine biomarkers with adherence and environmental monitoring to optimise sustained disease control.

## Linked entities

- **Proteins:** IGHE (immunoglobulin heavy constant epsilon), IL5 (interleukin 5), IL4 (interleukin 4), IL13 (interleukin 13)
- **Diseases:** asthma (MONDO:0004979)

## Full-text entities

- **Genes:** IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, TSLP (thymic stromal lymphopoietin) [NCBI Gene 85480], IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, MAPK14 (mitogen-activated protein kinase 14) [NCBI Gene 1432] {aka CSBP, CSBP1, CSBP2, CSPB1, EXIP, Mxi2}, CXCL12 (C-X-C motif chemokine ligand 12) [NCBI Gene 6387] {aka IRH, PBSF, SCYB12, SDF1, TLSF, TPAR1}, IL9 (interleukin 9) [NCBI Gene 3578] {aka HP40, IL-9, P40}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}, CXCR4 (C-X-C motif chemokine receptor 4) [NCBI Gene 7852] {aka CD184, D2S201E, FB22, HM89, HSY3RR, LCR1}, Serpinb1-ps1 (serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene) [NCBI Gene 282665] {aka EID, ovalbumin}, Il33 (interleukin 33) [NCBI Gene 77125] {aka 9230117N10Rik, Il-33, Il1f11, NF-HEV}, Il4 (interleukin 4) [NCBI Gene 16189] {aka BSF-1, Il-4}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, POSTN (periostin) [NCBI Gene 10631] {aka OSF-2, OSF2, PDLPOSTN, PN}, NOTCH1 (notch receptor 1) [NCBI Gene 4851] {aka AOS5, AOVD1, TAN1, hN1}, IL33 (interleukin 33) [NCBI Gene 90865] {aka C9orf26, DVS27, IL1F11, NF-HEV, NFEHEV}, IL25 (interleukin 25) [NCBI Gene 64806] {aka IL17E}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, MIR1825 (microRNA 1825) [NCBI Gene 100302183] {aka MIRN1825, hsa-mir-1825}, Ifng (interferon gamma) [NCBI Gene 15978] {aka IFN-g, If2f, Ifg}, Il25 (interleukin 25) [NCBI Gene 140806] {aka IL-17e, IL-25, Il17e}, Il13 (interleukin 13) [NCBI Gene 16163] {aka Il-13}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, NOX4 (NADPH oxidase 4) [NCBI Gene 50507] {aka KOX, KOX-1, RENOX}, IL5RA (interleukin 5 receptor subunit alpha) [NCBI Gene 3568] {aka CD125, CDw125, HSIL5R3, IL5R}, CSF3 (colony stimulating factor 3) [NCBI Gene 1440] {aka C17orf33, CSF3OS, GCSF}, Il5 (interleukin 5) [NCBI Gene 16191] {aka Il-5}, IGHE (immunoglobulin heavy constant epsilon) [NCBI Gene 3497] {aka IgE}
- **Diseases:** chronic (MESH:D002908), wheeze (MESH:D012135), Type 2 disease (MESH:C536595), nasopharyngitis (MESH:D009304), fibrotic remodelling (MESH:D020257), hypertrophy (MESH:D006984), infections (MESH:D007239), hypersensitivity reactions (MESH:D006967), cytotoxicity (MESH:D064420), cough (MESH:D003371), epithelial injury (MESH:D009375), angioedema (MESH:D000799), anaphylaxis (MESH:D000707), urticaria (MESH:D014581), obesity (MESH:D009765), rash (MESH:D005076), chest tightness (MESH:D002637), fatigue (MESH:D005221), airflow limitation (MESH:D029424), lung damage (MESH:D008171), breathlessness (MESH:D004417), eosinophilia (MESH:D004802), Asthma (MESH:D001249), fibrosis (MESH:D005355), Type 2 inflammation (MESH:D007249), respiratory tract infections (MESH:D012141), airway inflammation and remodelling (MESH:D056151), mitochondrial dysfunction (MESH:D028361), asthmatic (MESH:D013224), corticosteroid dependence (MESH:C565152)
- **Chemicals:** Dupilumab (MESH:C582203), PLGA (MESH:D000077182), reactive oxygen species (MESH:D017382), Omalizumab (MESH:D000069444), berberine (MESH:D001599), Baicalein (MESH:C006680), steroid (MESH:D013256), carbon dioxide (MESH:D002245), Mepolizumab (MESH:C434107), Zafirlukast (MESH:C062735), naringenin (MESH:C005273), nucleoside (MESH:D009705), lipid (MESH:D008055), doxofylline (MESH:C029797), dexamethasone (MESH:D003907), celastrol (MESH:C050414), Cyranose (-), rhynchophylline (MESH:C052714), indacaterol (MESH:C510790), glycyrrhizic acid (MESH:D019695), nitric oxide (MESH:D009569), volatile organic compounds (MESH:D055549), Reslizumab (MESH:C515492), polyethylene glycol (MESH:D011092), Tezepelumab (MESH:C000622721), Benralizumab (MESH:C571386), polyamide (MESH:D009757), Chitosan (MESH:D048271)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12966251/full.md

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Source: https://tomesphere.com/paper/PMC12966251