---
title: "Inhaled ARO-RAGE siRNA for pulmonary inflammation: first-in-human randomized trial"
id: "nature-2-inhaled-sirna-therapy-targeting-rage-for-pulmonary-inflammation-a-first-in"
canonical_url: "https://medichelpline.com/clinical-feed/nature-2-inhaled-sirna-therapy-targeting-rage-for-pulmonary-inflammation-a-first-in"
content_type: "clinical_feed_article"
specialty: "Pulmonology"
source_name: "Nature Medicine"
source_url: "https://www.nature.com/articles/s41591-026-04607-z"
published_at: "2026-09-09T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Inhaled ARO-RAGE siRNA for pulmonary inflammation: first-in-human randomized trial
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/nature-2-inhaled-sirna-therapy-targeting-rage-for-pulmonary-inflammation-a-first-in
- **Specialty:** [Pulmonology](https://medichelpline.com/clinical-feed/pulmonology.md)
- **Primary Source:** Nature Medicine
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41591-026-04607-z)
- **Published At:** 2026-09-09T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The study reports development of **ARO-RAGE**, an inhaled, epithelium-targeted siRNA designed to silence pulmonary RAGE (AGER) mRNA and reduce RAGE protein expression in the lung. - Preclinical work showed deep, durable RAGE silencing and reduced pulmonary inflammation in multiple animal models: rat models of asthma, COPD and acute lung injury, and mouse models assessing inflammatory responses. - In nonhuman primates (macaques), ARO-RAGE produced dose-dependent reductions in membrane-bound RAGE in lung tissue and in soluble RAGE (**sRAGE**) in serum, with bronchoalveolar lavage (BAL) showing post-dose decreases in sRAGE consistent with lung target silencing. - The delivery platform links siRNA to a ligand targeting epithelial ανβ6 integrins to preferentially deliver RNAi to the pulmonary epithelium after inhalation. - A phase 1/2a randomized, double-blind, placebo-controlled trial (ClinicalTrials.gov NCT05276570) evaluated safety/tolerability (primary), pharmacokinetics (secondary) and pharmacodynamics (exploratory) in healthy volunteers (n = 58; male n = 14) and patients with asthma (n = 19; male n = 6). - In both cohorts, inhaled ARO-RAGE was reported as safe and well tolerated with no clinically relevant changes on chest x-ray, pulmonary function tests or systemic inflammation markers. - Plasma ARO-RAGE levels were low, consistent with lung retention and minimal systemic bioavailability. - Dose-responsive and prolonged decreases in serum and BAL **sRAGE** levels indicated effective pulmonary target engagement. - The data support feasible pulmonary delivery and target engagement of an inhaled epithelial-targeted therapeutic siRNA and justify continued clinical development. - Source article is truncated in the provided text; detailed numerical results, dosing regimens, specific adverse event listings and longer-term follow-up data were not reported in the provided extract.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [nature medicine](https://www.nature.com/nm) 3. [articles](https://www.nature.com/nm/articles?type=article) 4. article Inhaled siRNA therapy targeting RAGE for pulmonary inflammation: a first-in-human randomized trial [ Download PDF ](https://www.nature.com/articles/s41591-026-04607-z.pdf) [ Download PDF ](https://www.nature.com/articles/s41591-026-04607-z.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 09 September 2026 # Inhaled siRNA therapy targeting RAGE for pulmonary inflammation: a first-in-human randomized trial * [Mark O’Carroll](https://www.nature.com/articles/s41591-026-04607-z#auth-Mark-O_Carroll-Aff1) [ORCID: orcid.org/0009-0009-3904-8590](https://orcid.org/0009-0009-3904-8590)[1](https://www.nature.com/articles/s41591-026-04607-z#Aff1), * [David Kasahara](https://www.nature.com/articles/s41591-026-04607-z#auth-David-Kasahara-Aff2)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [John Huetsch](https://www.nature.com/articles/s41591-026-04607-z#auth-John-Huetsch-Aff2) [ORCID: orcid.org/0000-0003-0045-5833](https://orcid.org/0000-0003-0045-5833)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [Taylor Reed](https://www.nature.com/articles/s41591-026-04607-z#auth-Taylor-Reed-Aff2)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [Timothy N. Perkins](https://www.nature.com/articles/s41591-026-04607-z#auth-Timothy_N_-Perkins-Aff3)[3](https://www.nature.com/articles/s41591-026-04607-z#Aff3), * [Rong Zhou](https://www.nature.com/articles/s41591-026-04607-z#auth-Rong-Zhou-Aff2)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [Lindsey Moser](https://www.nature.com/articles/s41591-026-04607-z#auth-Lindsey-Moser-Aff2)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [Bianca Tomasini-Johansson](https://www.nature.com/articles/s41591-026-04607-z#auth-Bianca-Tomasini_Johansson-Aff2)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [Anh Ta](https://www.nature.com/articles/s41591-026-04607-z#auth-Anh-Ta-Aff2) [ORCID: orcid.org/0009-0004-1293-3112](https://orcid.org/0009-0004-1293-3112)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [Tim D. Oury](https://www.nature.com/articles/s41591-026-04607-z#auth-Tim_D_-Oury-Aff3)[3](https://www.nature.com/articles/s41591-026-04607-z#Aff3), * [Tao Pei](https://www.nature.com/articles/s41591-026-04607-z#auth-Tao-Pei-Aff2)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [James Hamilton](https://www.nature.com/articles/s41591-026-04607-z#auth-James-Hamilton-Aff2)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [Erik W. Bush](https://www.nature.com/articles/s41591-026-04607-z#auth-Erik_W_-Bush-Aff2)[2](https://www.nature.com/articles/s41591-026-04607-z#Aff2), * [Nicholas J. Leeper](https://www.nature.com/articles/s41591-026-04607-z#auth-Nicholas_J_-Leeper-Aff4) [ORCID: orcid.org/0000-0002-0905-2806](https://orcid.org/0000-0002-0905-2806)[4](https://www.nature.com/articles/s41591-026-04607-z#Aff4) & * [Matthias Salathe](https://www.nature.com/articles/s41591-026-04607-z#auth-Matthias-Salathe-Aff5) [ORCID: orcid.org/0000-0001-9092-4861](https://orcid.org/0000-0001-9092-4861)[5](https://www.nature.com/articles/s41591-026-04607-z#Aff5) * [on behalf of the RAGE study consortium](https://www.nature.com/articles/s41591-026-04607-z#group-1) Show authors [_Nature Medicine_](https://www.nature.com/nm) (2026) [Cite this article](https://www.nature.com/articles/s41591-026-04607-z#citeas) [ Save article ](https://www.nature.com/articles/s41591-026-04607-z/save-research?_csrf=2f1Am42Pz-j2Of2XtbD6AkxVQoqYKTyT) [ View saved research ](https://www.nature.com/saved-research) ## Abstract The receptor for advanced glycation end products (RAGE), a multiligand receptor that is abundantly expressed by lung alveolar type-1 cells, amplifies and sustains the innate immune response in a variety of pulmonary disorders, including asthma and chronic obstructive pulmonary disease. Here we developed ARO-RAGE, an inhaled, lung-epithelium-targeted siRNA directed against pulmonary RAGE mRNA. Preclinical data from rat models of asthma, chronic obstructive pulmonary disease and acute lung injury, as well as mouse models for assessment of inflammatory responses, demonstrated deep and durable silencing of RAGE, limiting pulmonary inflammation. In macaques, ARO-RAGE produced dose-dependent reductions in membrane-bound RAGE levels in lung tissue and soluble RAGE (sRAGE) levels in serum; moreover, bronchoalveolar lavage showed post-dose decreases in sRAGE levels, consistent with robust silencing of lung membrane-bound RAGE. We then tested ARO-RAGE in a phase 1/2a, randomized, double-blinded, placebo-controlled trial designed to assess safety and tolerability (primary endpoint), pharmacokinetics (secondary endpoint) and pharmacodynamics (exploratory endpoint). In healthy volunteers (total _n_ = 58, male _n_ = 14) and in patients with asthma (total _n_ = 19, male _n_ = 6), inhaled ARO-RAGE was safe and well tolerated. No clinically relevant changes in chest x-ray findings, pulmonary function tests or systemic markers of inflammation were observed in the two cohorts. Plasma levels of ARO-RAGE were low, consistent with drug retention in the lung and minimal systemic bioavailability. Prolonged dose-responsive decreases in serum and bronchoalveolar lavage sRAGE levels indicated effective pulmonary target engagement. Together, these results demonstrate safe pulmonary delivery and target engagement of an inhaled, epithelial-targeted therapeutic siRNA, and support continued clinical development of ARO-RAGE. ClinicalTrials.gov registration: [NCT05276570](https://clinicaltrials.gov/study/NCT05276570). ### Explore related subjects Discover the latest articles and news in related subjects. * [Asthma](https://www.nature.com/subjects/asthma) * [Drug development](https://www.nature.com/subjects/drug-development) * [Preclinical research](https://www.nature.com/subjects/pre-clinical-studies) * [Target validation](https://www.nature.com/subjects/target-validation) * [Translational research](https://www.nature.com/subjects/translational-research) ## Main Inflammatory pulmonary diseases, including asthma and chronic obstructive pulmonary disease (COPD), represent substantial global health burdens, characterized by chronic airway inflammation, airflow obstruction and frequent exacerbations[1](https://www.nature.com/articles/s41591-026-04607-z#ref-CR1 "Global strategy for asthma management and prevention. GINA www.ginasthma.org \(2025\)."),[2](https://www.nature.com/articles/s41591-026-04607-z#ref-CR2 "GOLD. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease 215 \(Global Initiative for Chronic Obstructive Lung Disease, 2025\)."). Asthma affects approximately 300 million individuals worldwide, with severe asthma—defined as persistent symptoms despite inhaled corticosteroid and long-acting beta agonist therapy—occurring in roughly 4% of patients with asthma[1](https://www.nature.com/articles/s41591-026-04607-z#ref-CR1 "Global strategy for asthma management and prevention. GINA www.ginasthma.org \(2025\)."). Traditional therapies, such as bronchodilators and corticosteroids, provide symptomatic relief but are limited by systemic side effects such as osteoporosis and incomplete efficacy in severe disease[3](https://www.nature.com/articles/s41591-026-04607-z#ref-CR3 "Barnes, P. J. Inhaled corticosteroids are not beneficial in chronicobstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 161, 342–344 \(2000\)."),[4](https://www.nature.com/articles/s41591-026-04607-z#ref-CR4 "Pace, W. D., Callen, E., Gaona-Villarreal, G., Shaikh, A. & Yawn, B. P. Adverse outcomes associated with inhaled corticosteroid use in individuals with chronic obstructive pulmonary disease. Ann. Fam. Med. 23, 127–135 \(2025\)."). Biologic therapies targeting type 2 (T2) inflammatory pathways, including monoclonal antibodies against thymic stromal lymphopoietin, interleukin (IL)-5 and IL-4Rα, have demonstrated efficacy in reducing asthma exacerbations and improving symptom control. However, clinical remission rates remain modest (14–43%)[5](https://www.nature.com/articles/s41591-026-04607-z#ref-CR5 "Lugogo, N. L. et al. Are we ready for asthma remission as a clinical outcome? Chest 164, 831–834 \(2023\)."), and these therapies are notably less effective or ineffective in patients with T2-low inflammation, a phenotype characterized by neutrophilic or mixed inflammatory profiles. Thus, there remains a critical unmet need for novel therapeutic strategies capable of addressing airway inflammation across both T2-high and T2-low asthma phenotypes. The receptor for advanced glycation end-products (RAGE) has emerged as a potential target in inflammatory pulmonary diseases[6](https://www.nature.com/articles/s41591-026-04607-z#ref-CR6 "Sukkar, M. B. et al. Rage: A new frontier in chronic airways disease. Br. J. Pharmacol. 167, 1161–1176 \(2012\)."). RAGE is a pattern recognition receptor expressed on pulmonary epithelial cells that binds to several damage-associated molecular patterns, including advanced glycation end-products, high-mobility group box-1 (HMGB1) protein, complement components and S100 proteins. Upon activation, RAGE triggers a diverse array of intracellular signaling mechanisms including nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK) and Janus kinase/signal transducers and activators of transcription (JAK/STAT)-related pathways[7](https://www.nature.com/articles/s41591-026-04607-z#ref-CR7 "Perkins, T. N. et al. The receptor for advanced glycation end products is a critical mediator of type 2 cytokine signaling in the lungs. J. Allergy Clin. Immunol. 144, 796–808 \(2019\)."). RAGE has been implicated in the pathogenesis of a wide range of inflammatory diseases, including several pulmonary disorders[6](https://www.nature.com/articles/s41591-026-04607-z#ref-CR6 "Sukkar, M. B. et al. Rage: A new frontier in chronic airways disease. Br. J. Pharmacol. 167, 1161–1176 \(2012\)."). In mouse models of allergic asthma, RAGE is necessary for airway influx of canonical T2 inflammatory mediators such as IL-33, IL-5, IL-13 and eosinophils[8](https://www.nature.com/articles/s41591-026-04607-z#ref-CR8 "Killian, K. N. et al. Rage contributes to allergen driven severe neutrophilic airway inflammation via nlrp3 inflammasome activation in mice. Front. Immunol. 14, 1039997 \(2023\)."). Further, in models of neutrophilic airways disease, RAGE is necessary for inflammasome activation and upregulation of non-T2 inflammatory mediators including recruitment of neutrophils[8](https://www.nature.com/articles/s41591-026-04607-z#ref-CR8 "Killian, K. N. et al. Rage contributes to allergen driven severe neutrophilic airway inflammation via nlrp3 inflammasome activation in mice. Front. Immunol. 14, 1039997 \(2023\)."). RAGE knockout mice are also protected against inflammatory response and destruction of parenchyma in several models of COPD-emphysema[9](https://www.nature.com/articles/s41591-026-04607-z#ref-CR9 "Waseda, K. et al. Emphysema requires the receptor for advanced glycation end-products triggering on structural cells. Am. J. Respir. Cell Mol. Biol. 52, 482–491 \(2015\)."),[10](https://www.nature.com/articles/s41591-026-04607-z#ref-CR10 "Caraher, E. J. et al. Receptor for advanced glycation end-products and world trade center particulate induced lung function loss: a case–cohort study and murine model of acute particulate exposure. PLoS ONE 12, e0184331 \(2017\)."),[11](https://www.nature.com/articles/s41591-026-04607-z#ref-CR11 "Lee, H. et al. Blockade of rage ameliorates elastase-induced emphysema development and progression via rage-damp signaling. FASEB J. 31, 2076–2089 \(2017\)."),[12](https://www.nature.com/articles/s41591-026-04607-z#ref-CR12 "Sambamurthy, N., Leme, A. S., Oury, T. D. & Shapiro, S. D. The receptor for advanced glycation end products \(rage\) contributes to the progression of emphysema in mice. PLoS ONE 10, e0118979 \(2015\)."). Despite its promise as a therapeutic target, the structural and functional complexity of RAGE has posed considerable challenges to traditional drug discovery[13](https://www.nature.com/articles/s41591-026-04607-z#ref-CR13 "Armando, R., Miguel, M., Ileana, G. & Paulina, A. Inhibition of rage axis signaling: a pharmacological challenge. Curr. Drug Targets 20, 340–346 \(2019\)."). Therapeutic small interfering RNA (siRNA), however, can overcome limitations of protein-interacting small molecules and biologics by directly reducing target mRNA translation. Here we report the development and testing of ARO-RAGE, a synthetic, double-stranded siRNA designed to specifically silence advanced glycosylation end-product receptor messenger RNA (_AGER_ , aka _RAGE_ mRNA) via an RNA interference (RNAi) mechanism to reduce RAGE expression[14](https://www.nature.com/articles/s41591-026-04607-z#ref-CR14 "Nicholas, A., Bush, E. W., Kasahara, D. I. & Schienebeck, C. M. RNAi agents for inhibiting expression of receptor for advanced glycation end-products, compositions thereof, and methods of use. US Patent 20220396791/A1 \(Arrowhead Pharmaceuticals, 2022\)."). This novel lung delivery platform comprises siRNA linked to a targeting ligand that binds epithelial ανβ6 integrins and facilitates selective delivery of siRNA to the pulmonary epithelium, enhancing target engagement when administered via inhalation[15](https://www.nature.com/articles/s41591-026-04607-z#ref-CR15 "Kasahara, D. et al. A clinical-stage inhaled rnai therapeutic for pulmonary inflammation mediates durable rage silencing in nonhuman primates \(NHP\). Eur. Respir. J. 62, PA1289 \(2023\)."),[16](https://www.nature.com/articles/s41591-026-04607-z#ref-CR16 "Bush, E. W. et al. A novel targeted rnai molecule delivery platform for the therapeutic inhibition of enac in cystic fibrosis lung disease. Pediatr. Pulmonol. 53, 256 \(2018\)."). We hypothesized that an RNAi therapeutic that effectively and safely silences RAGE in the pulmonary compartment could provide broad anti-inflammatory effects in the airway and allow for the development of a novel therapy relevant to both T2-high and T2-low asthma. We describe the preclinical development pathway and provide results from the first-in-human trial of ARO-RAGE in healthy human volunteers and patients with asthma. ## Results ### Silencing pulmonary _RAGE_ with an epithelium-targeted siRNA limits inflammation in rat models of allergic asthma, COPD and acute lung injury Preclinical rat studies utilized a species-specific siRNA targeting the rat _RAGE_ mRNA conjugated to an integrin ανβ6-selective ligand (Supplementary Data Fig. [1](https://www.nature.com/articles/s41591-026-04607-z#MOESM1)) to facilitate epithelial uptake. Based on tissue concentrations obtained in rat, the siRNA was predominantly distributed to the lung after inhaled-dose administration. The next highest concentration was observ
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