{"id":82813,"date":"2026-07-16T00:01:43","date_gmt":"2026-07-16T00:01:43","guid":{"rendered":"https:\/\/english.saigonbiz.com\/vn\/neutrolis-announces-new-england-journal-of-medicine-publication-demonstrating-first-clinical-evidence-for-net-degrading-therapy-in-severe-treatment-refractory-systemic-lupus-erythematosus-sle-cause\/"},"modified":"2026-07-16T00:01:43","modified_gmt":"2026-07-16T00:01:43","slug":"neutrolis-announces-new-england-journal-of-medicine-publication-demonstrating-first-clinical-evidence-for-net-degrading-therapy-in-severe-treatment-refractory-systemic-lupus-erythematosus-sle-cause","status":"publish","type":"post","link":"https:\/\/english.saigonbiz.com\/vn\/neutrolis-announces-new-england-journal-of-medicine-publication-demonstrating-first-clinical-evidence-for-net-degrading-therapy-in-severe-treatment-refractory-systemic-lupus-erythematosus-sle-cause\/","title":{"rendered":"Neutrolis Announces New England Journal of Medicine Publication Demonstrating First Clinical Evidence for NET-Degrading Therapy in Severe, Treatment-Refractory Systemic Lupus Erythematosus (SLE) Caused by DNASE1L3 Deficiency"},"content":{"rendered":"<div>\n<p align=\"center\"><em>Treatment with investigational DNASE1L3 analog NTR-441, which degrades neutrophil extracellular traps (NETs), resulted in rapid clinical improvement in a patient with\u00a0<\/em><em>treatment-refractory<\/em><em> SLE <\/em><\/p>\n<p align=\"center\"><em>Results provide first human proof-of-concept that enzymatic NET degradation may address a key driver of disease activity in SLE, with broader implications for other NET-driven autoimmune and inflammatory diseases<\/em><\/p>\n<p align=\"center\"><em>Observations from this single-patient compassionate-use treatment support Neutrolis&#8217; broader exDNASE&#x2122; platform, including NTR-1011, now advancing in clinical studies in SLE and rheumatoid arthritis (RA)<\/em><\/p>\n<p>CAMBRIDGE, Mass., July  15, 2026  (GLOBE NEWSWIRE) &#8212; Neutrolis, Inc., a biotechnology company pioneering therapies that target neutrophil extracellular traps (NETs), today announced a clinical report published in <em>The New England Journal of Medicine<\/em> demonstrating that administration of NTR-441, an investigational DNASE1L3 analog, resulted in rapid clinical improvement in a patient with severe, treatment-refractory SLE and hypocomplementemic urticarial vasculitis caused by congenital DNASE1L3 deficiency.<\/p>\n<p>The publication, titled \u201cTargeted Degradation of NETs in Lupus with DNASE1L3 Deficiency,\u201d reported rapid clinical and pharmacodynamic effects following weekly intravenous administration of NTR-441 in a 16.5-year-old patient whose long-standing disease, including recurrent vasculitic rash, polyarthritis, episcleritis, inflammatory bowel disease, autoimmune hepatitis and persistent inflammation, had not achieved sustained remission despite extensive prior immunosuppressive therapy. The patient\u2019s disease manifestations began at 1.5 years of age, and genetic testing at age 11 confirmed a homozygous loss-of-function DNASE1L3 variant as the cause.<\/p>\n<p>Clinical symptoms resolved within six hours of the first infusion of NTR-441. A transient recurrence of rash and episcleritis occurred within 24 hours and subsequently improved. Over four weeks, the patient experienced continued clinical improvement: vasculitic rash decreased from 76% to 20% of body surface area, joint inflammation and episcleritis resolved, and disease-activity scores (SLEDAI-2K, BILAG) and patient-, parent- and physician-reported assessments all improved.<\/p>\n<p>\u201cPatients with DNASE1L3 deficiency can experience severe, early-onset autoimmune disease with limited treatment options,\u201d said author Andreas Reiff, MD, PhD, Chief Medical Officer of Neutrolis<strong>.<\/strong> \u201cThe speed and extent of improvement for this patient after NTR-441 treatment are an important proof-of-concept for how NET-degrading therapy can benefit patients across autoimmune and inflammatory indications.\u201d<\/p>\n<p>DNASE1L3 analogs are designed to enzymatically degrade NETs by dismantling their DNA backbone. In the publication, plasma DNASE1L3 levels rose rapidly after NTR-441 administration, confirming systemic exposure. Target engagement was demonstrated by increases in circulating DNA and myeloperoxidase-DNA complexes, consistent with degradation of NETs in tissues. These biomarker changes correlated with clinical improvement, supporting NETs as a direct driver of disease activity in SLE with DNASE1L3 deficiency.<\/p>\n<p>\u201cThe pharmacodynamic biomarker data in this publication confirm that restoring DNASE1L3 activity degrades NETs as designed,\u201d said author Tobias A. Fuchs, PhD, Co-Founder and Chief Scientific Officer of Neutrolis. \u201cThe tight temporal link between NET degradation and clinical response supports our strategy of targeting NETs as a non-immunosuppressive approach to directly target the trigger of disease inflammation in the tissue for the first time in a patient.\u201d<\/p>\n<p>During the fifth infusion, the patient developed an infusion reaction with anti-drug antibodies, likely reflecting the immune system&#8217;s lack of prior exposure to native DNASE1L3 given the patient&#8217;s congenital deficiency. Doses were reduced using a desensitization protocol; clinical response was preserved until discontinuation after the eighth infusion due to shortened drug exposure.<\/p>\n<p>Building upon these findings, Neutrolis completed a Phase 1a study of NTR-1011, an improved DNASE1L3 fusion protein, showing favorable safety and tolerability in April 2026. Neutrolis is initiating a Phase 1b study of NTR-1011 (LIBERATE-I, NCT07237659) in SLE and RA to evaluate the safety and establish proof-of-concept in a broader autoimmune population.<\/p>\n<p>\u201cThis is a turning point built on twenty years of foundational NET biology, and on a growing recognition that NETs are drivers of many of the diseases we most need to treat,\u201d said author Abdul Hakkim, PhD, Co-Founder and Chief Operating Officer of Neutrolis.<\/p>\n<p>\u201cThis publication is a defining moment for Neutrolis,\u201d said Anthony Aiudi, Chief Executive Officer of Neutrolis. \u201cIt validates the scientific thesis our platform was built on, and it strengthens our conviction as we advance NTR-1011 into broader patient populations with SLE and RA.\u201d<\/p>\n<p><strong>About DNASE1L3 Deficiency and NETs<\/strong><\/p>\n<p>Neutrophil extracellular traps, or NETs, are extracellular DNA scaffolds released by neutrophils that can perpetuate inflammation, autoimmunity and tissue injury. DNASE1L3, secreted by macrophages and dendritic cells, is the principal extracellular DNase of the immune system, responsible for clearing NETs and preventing their pathologic accumulation. Loss-of-function variants in DNASE1L3 are associated with severe early-onset SLE and hypocomplementemic urticarial vasculitis.<\/p>\n<p><strong>About DNASE1L3 Analogs<\/strong><\/p>\n<p>Neutrolis\u2019 DNASE1L3 analogs are investigational recombinant molecules designed to restore extracellular DNASE1L3 activity and degrade NETs by dismantling their DNA backbone. Neutrolis&#8217; portfolio includes, among others, NTR-441, used in the compassionate-use treatment described in the publication, and NTR-1011, an improved, first-in-class DNASE1L3 fusion protein.<\/p>\n<p><strong>About Neutrolis<\/strong><\/p>\n<p>Neutrolis is a clinical-stage biotechnology company pioneering a new class of rapid-acting, non-immunosuppressive therapies that directly target neutrophil extracellular traps (NETs), a root cause of tissue damage and chronic inflammation. The company&#8217;s exDNASE&#x2122; platform powers the development of analogs of naturally occurring enzymes that disassemble NETs. For more information, visit https:\/\/neutrolis.com\/.<\/p>\n<p><strong>Forward-Looking Statements<\/strong><\/p>\n<p>This press release contains forward-looking statements, including regarding the potential implications of the published findings, the scientific rationale for DNASE1L3 analogs, and the timing and design of the planned Phase 1b portion of the LIBERATE-I trial. These statements are subject to risks and uncertainties that could cause actual results to differ materially. Findings described in the publication are based on compassionate-use treatment in one patient and may not be predictive of results in additional patients or future studies. DNASE1L3 analogs, including NTR-441 and NTR-1011, are investigational and have not received marketing authorization from any regulatory authority. Neutrolis undertakes no obligation to update forward-looking statements, except as required by law.<\/p>\n<p><strong>Media Contact<\/strong><\/p>\n<p>press@neutrolis.com<\/p>\n<p><img decoding=\"async\" alt=\"\" src=\"https:\/\/ml.globenewswire.com\/media\/ZmQxNjFjMDMtZDAxZi00MTc3LTk0YzAtOGMzZWE0MGQzMDYwLTEzMDg4NjktMjAyNi0wNy0xNS1lbg==\/tiny\/Neutrolis-Inc-.png\" referrerpolicy=\"no-referrer-when-downgrade\"><\/div>\n","protected":false},"excerpt":{"rendered":"<p>Treatment with investigational DNASE1L3 analog NTR-441, which degrades neutrophil extracellular traps (NETs), resulted in rapid clinical improvement in a patient with\u00a0treatment-refractory SLE Results provide first human proof-of-concept that enzymatic NET degradation may address a key driver of disease activity in SLE, with broader implications for other NET-driven autoimmune and inflammatory diseases Observations from this single-patient [&#8230;]\n","protected":false},"author":1,"featured_media":85254,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[5],"tags":[],"class_list":["post-82813","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-people"],"yoast_head":"<!-- This site is optimized with the Yoast SEO Premium plugin v21.6 (Yoast SEO v21.6) - 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