NI-0101

Enables expansion of ongoing vitiligo clinical study to U.S. investigational sites Topline data anticipated Q4 2027 TORONTO, Oct. 15, 2026 (GLOBE NEWSWIRE) -- Edesa Biotech, Inc. (Nasdaq:EDSA), a clinical-stage biopharmaceutical company focused on developing host-directed therapeutics for immuno-inflammatory diseases, today reported that the U.S. Food and Drug Administration (FDA) has cleared the company's Investigational New Drug (IND) application for its Phase 2 clinical study of EB06 in vitiligo, enabling Edesa to expand recruitment to the United States. Patient recruitment is underway in Canada and the first U.S. investigational sites are expected to begin enrolling subjects next quarter. Edesa anticipates that topline data will be available fourth quarter 2027. The double-blind, placebo-controlled clinical study is evaluating EB06, a monoclonal antibody targeting CXCL10, in up to 80 adults with moderate-to-severe nonsegmental vitiligo. Participants are randomized 1:1 to receive either EB06 or placebo every two weeks through Week 22. The primary efficacy endpoint is the mean percent change from baseline in the Facial Vitiligo Area Scoring Index (F-VASI) at Week 28. Secondary and exploratory measures include facial and total-body scoring benchmarks, as well as assessments of safety, tolerability, pharmacokinetics and immunogenicity. “FDA clearance of our IND represents an important regulatory and operational milestone for our vitiligo program,” said Par Nijhawan, MD, Chief Executive Officer of Edesa. “With recruitment already underway in Canada and U.S. enrollment expected to begin next quarter, we believe we are well positioned to complete the study and report topline results in the fourth quarter of next year.” EB06 is a fully human monoclonal antibody targeting CXCL10, a signaling protein implicated in vitiligo. By inhibiting CXCL10, EB06 is designed to interrupt immune-cell recruitment and melanocyte loss through a targeted mechanism that is distinct from broader immunomodulatory approaches. The safety and efficacy of EB06 remain subject to clinical evaluation. About EB06 EB06 is a fully human monoclonal antibody candidate that binds specifically to chemokine ligand 10 (CXCL10) with high affinity and inhibits the interaction of CXCL10 with its receptors, CXCR3A and CXCR3B. CXCL10 is highly expressed in vitiligo patients and has been shown to play both a key role in the CXCR3A-mediated trafficking of anti-melanocytic CD8+ T-cells to the epidermis and in inducing melanocyte apoptosis (cell death) via CXCR3B. EB06 has been evaluated in 65 subjects across three prior clinical studies, in which it demonstrated the pharmacodynamic activity relevant to its mechanism and was generally safe and well tolerated. EB06 is currently formulated for intravenous administration, with a subcutaneous formulation anticipated to be ready for follow-on clinical evaluation. About Vitiligo Vitiligo is a chronic autoimmune disease that causes the loss of skin pigmentation in patches. It occurs when melanocytes, the pigment-producing skin cells, die or stop producing melanin. The extent of color loss from vitiligo is unpredictable and can affect the skin on any part of the body. Vitiligo is estimated to affect up to 2% of the global population. Vitiligo patients are not born with lesioned skin. Rather, unpigmented spots appear over time, with about 50% of patients having symptom onset before 20 years of age. At present, there are limited treatment options for patients, and no approved systemic drug therapies in the U.S. About Edesa Biotech, Inc. Edesa Biotech, Inc. (Nasdaq: EDSA) is a clinical-stage biopharmaceutical company developing innovative ways to treat inflammatory and immune-related diseases. Its clinical pipeline is focused on two therapeutic areas: Medical Dermatology and Respiratory. In Medical Dermatology, Edesa is developing EB06, an anti-CXCL10 monoclonal antibody candidate, as a therapy for vitiligo, a common autoimmune disorder that causes skin to lose its color in patches. Its medical dermatology assets also include daniluromer, a Phase 3-ready asset developed for use as a potential therapy for moderate-to-severe chronic Allergic Contact Dermatitis (ACD), a common occupational skin condition. The company’s most advanced Respiratory drug candidate is paridiprubart, which is being developed as a potential treatment for Acute Respiratory Distress Syndrome, a life-threatening form of respiratory failure. The paridiprubart program has been the recipient of two funding awards from the Government of Canada to support the further development of this asset, and is currently being evaluated in a U.S. government-funded platform study. Edesa is also pursuing additional uses for paridiprubart. Sign up for news alerts . Connect with us on X and LinkedIn . Edesa Forward-Looking Statements This press release may contain forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. Forward-looking statements may be identified by the use of words such as "anticipate," "believe," "plan," "estimate," "expect," "intend," "may," "will," "would," "could," "should," "might," "potential," or "continue" and variations or similar expressions, including statements related to: the company's plans and timing to activate U.S. investigational sites; the design, enrollment and anticipated timing of topline data from the company's Phase 2 study of EB06; the potential of EB06's mechanism of action; and the company's timing and plans regarding its development pipeline and clinical studies, in general. Readers should not unduly rely on these forward-looking statements, which are not a guarantee of future performance. There can be no assurance that forward-looking statements will prove to be accurate, as all such forward-looking statements involve known and unknown risks, uncertainties and other factors which may cause actual results or future events to differ materially from the forward-looking statements. Such risks include: the ability of Edesa to obtain regulatory approval for or successfully commercialize any of its product candidates, the risk that access to sufficient capital to fund Edesa's operations may not be available or may be available on terms that are not commercially favorable to Edesa, the risk that Edesa's product candidates may not be effective against the diseases tested in its clinical trials, the risk that Edesa fails to comply with the terms of license agreements with third parties and as a result loses the right to use key intellectual property in its business, Edesa's ability to protect its intellectual property, the timing and success of submission, acceptance and approval of regulatory filings, and the impacts of public health crises. Many of these factors that will determine actual results are beyond the company's ability to control or predict. For a discussion of further risks and uncertainties related to Edesa's business, please refer to Edesa's public company reports filed with the U.S. Securities and Exchange Commission and the British Columbia Securities Commission. All forward-looking statements are made as of the date hereof and are subject to change. Except as required by law, Edesa assumes no obligation to update such statements. CONTACT: Contact: Gary Koppenjan Edesa Biotech, Inc. investors@edesabiotech.com

本文要点 研究背景与设计 针对细菌内共生体如何增强真菌致病性的问题，利用无菌/自然土壤盆栽模型、16S测序及代谢组学，解析了番茄尖孢镰刀菌（FOL）、内共生体与根际微生物组的三方互作。 核心发现与意义 FOL携带的Achromobacter属内共生体驱动白僵菌素合成，特异性抑制疾病抑制型Streptomyces菌群，从而削弱微生物组介导的植物免疫，揭示了跨界共生重编程病原体代谢以破坏植物微生物组防御的新机制。 内共生体鉴定 FOL菌丝内检出活体Achromobacter sp. EB05；抗生素清除内共生体导致致病性显著降低，而回补后致病性恢复，且该效应在自然土壤中更强。 微生物组抑制 内共生体阳性FOL显著降低根际Streptomyces丰度，而清除内共生体则促进其富集， 且分离出的Streptomyces sp. St52在体内外均显著抑制FOL并减轻萎蔫病。 代谢重编程机制 内共生体显著上调FOL中BEAS基因表达以提升白僵菌素产量；外源添加白僵菌素重现了菌群失衡，且BEAS基因敲除完全消除了内共生体介导的致病性增强及对Streptomyces的抑制。 核心关键词 细菌内共生菌　　真菌致病性　　尖孢镰刀菌　　根际微生物组　　白僵菌素　　链霉菌　　枯萎病 科普解读 在植物与土传病原菌的战争中，根际微生物组是植物仰赖的第一道防线。然而，顶尖病原菌似乎早已破解了这道防线。 在一项发表于 Cell Host & Microbe 的研究中，南京农业大学韦中团队与东北农业大学周新刚团队的合作揭示了一个令人惊叹的机制：番茄枯萎病菌 Fusarium oxysporum f. sp. lycopersici （FOL）通过其胞内栖息的细菌共生体，能够 精准打击 根际中的有益菌，从而瓦解微生物组的防御屏障。 三重角色的“生化战争” 研究团队首先发现，FOL菌丝内部寄生着 无色杆菌属 （Achromobacter spp.）的活细菌。当这些“房客”被抗生素清除后，真菌的致病力显著下降。但有趣的是，这种致病力差异在 天然土壤中更为显著 ——去除共生菌的FOL在天然土壤中引起的病害严重度远低于其在无菌土中的表现。这暗示，内共生菌的“贡献”并非直接损伤植物，而是通过破坏根际微生物组来实现的。 通过16S rRNA基因测序，该研究发现，携带内共生菌的FOL感染后，根际中多个 链霉菌属 （Streptomyces spp.）的丰度显著下降。而链霉菌恰恰是公认的 植物守护者 ，它们能产生抗菌物质、诱导植物系统抗性。团队从根际分离出一株高丰度的链霉菌St52，验证了其能有效抑制FOL生长并降低枯萎病严重度。然而，当St52面对携带内共生菌的FOL时，其保护效力大打折扣。 白僵菌素：分子层面的“精准武器” 内共生菌本身并不直接攻击St52。那么，它是如何帮助真菌削弱有益菌的？代谢组学分析揭示了答案：内共生菌的存在，会 显著上调 FOL体内白僵菌素合成基因 BEAS 的表达，促使真菌大量分泌 白僵菌素 （beauvericin）——一种具有抗菌活性的环状六肽。 数据显示，只有携带内共生菌的FOL，其培养上清液才能强烈抑制St52生长。而外源添加白僵菌素，则能完全恢复“无菌”FOL的抑制能力。更关键的是，团队敲除了FOL的 BEAS 基因后，这种内共生菌介导的致病力增强效应 几乎消失殆尽 。这直接证实了白僵菌素是内共生菌增强FOL毒力的核心媒介。 重塑根际微生物组 研究进一步发现，外源施加白僵菌素本身就足以搅乱根际的菌群结构。它导致多个链霉菌类群的丰度下降，并被证实能 削弱微生物组的抑病功能 。在土壤移植实验中，来自白僵菌素处理过的根际土，其保护植物抵御枯萎病的能力明显变差。 这意味着，白僵菌素通过抑制根际有益菌，为病原菌的入侵扫清了关键障碍。 从实验室到田间的新思路 这项研究刷新了我们对病原菌致病策略的认知。它表明，病原菌-细菌共生体-根际微生物组之间存在着一场 三方博弈 。病原菌并非单打独斗，而是会借助胞内共生菌来“武装”自己，生产出能够定向清除有益菌的化学武器。 这一发现为防治土传病害提供了全新视角——未来的策略或许不应只盯着病原菌本身，而应考虑如何加固根际微生物组这道防线，或直接 干扰这种共生关系 ，从而阻断毒素的生产链条。 图片摘要 相关文章推荐 01 Science · IF: 47.3 Science：凝集素介导细菌与真核生物共生 02 American Journal of Respiratory and Critical Care Medicine · IF: 21.7 气道黏膜内暗藏共生菌，或成哮喘免疫调节新开关 03 PNAS · IF: 9.5 细菌如何改造宿主，单只蟑螂藏匿超三千外来片段 原文链接 https://rbase.chinagut.cn/base/article/c4cbfa62867043e4af8d5890da075ec2