Phase 2 Clinical Platform Trial Investigating Multiple Therapeutic Options for the Treatment of Hospitalized Patients With Acute Respiratory Distress Syndrome (ARDS)

This is a Phase 2 multicenter, randomized, double-blinded, placebo-controlled study that will evaluate the safety and efficacy of host-directed therapeutics in hospitalized adults diagnosed with Acute Respiratory Distress Syndrome (ARDS) utilizing a platform trial design. Participants will be randomized to receive either a placebo or one of the active treatments.
This record describes the default procedures and analyses for all cohorts. Each specific cohort may have additional eligibility requirements, safety and efficacy procedures, or endpoints, which will be described in the corresponding intervention-specific records on clinicaltrials.gov listed below in the detailed description.

开始日期2025-06-10

申办/合作机构

PPD Development LP

[+4]

NCT06701669

/ Recruiting临床2期

Phase 2 Clinical Platform Trial Investigating Multiple Therapeutic Options for the Treatment of Hospitalized Patients With Acute Respiratory Distress Syndrome (ARDS)

This is a Phase 2 multicenter, randomized, double-blinded, placebo-controlled study that will evaluate the safety and efficacy of host-directed therapeutics in hospitalized adults diagnosed with Acute Respiratory Distress Syndrome (ARDS) utilizing a platform trial design.
Cohort B: Participants will be randomized to receive either a placebo or paridiprubart.
This record describes the default procedures and analyses for Cohort B. Please see NCT06703073 for information on the BP-ARDS-P2-001 Master Protocol.

开始日期2025-06-10

申办/合作机构

PPD Development LP

[+4]

NCT04401475

/ Suspended临床2/3期

A Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Safety and Efficacy of EB05 + SOC Vs. Placebo + SOC in Adult Hospitalized Patients with COVID-19

COVID-19 patients who develop severe disease often develop acute respiratory distress syndrome (ARDS) as a result of a dysregulated immune response. This in turn stimulates a pro-inflammatory cascade ("cytokine storm") as well as emergency myelopoiesis.
This proinflammatory cascade is activated when viral-mediated cell damage occurs in the lungs, resulting in the release of damage-signaling alarmin molecules such as S100A8/A9 (Calprotectin), HMGB1, Resistin, and oxidized phospholipids. These damage-associated molecular patterns (DAMPs) are recognized by the pattern recognition receptor Toll-Like Receptor 4 (TLR4) found on macrophages, dendritic cells and other innate immune cells and result in additional release of pro-inflammatory molecules. Several recent studies have shown that S100A8/A9 serum levels in hospitalized COVID-19 patients positively correlate with both neutrophil count and disease severity. Taken together the DAMP-TLR4 interaction forms a central axis in the innate immune system and is a key driver of the pathological inflammation observed in COVID-19. We hypothesis that targeting the initial step in the signalling pathways of these DAMPs in innate immunity offers the best hope for controlling the exaggerated host response to SARS-CoV-2 infection.
EB05 has demonstrated safety in two clinical studies (>120 patients) and was able to block LPS-induced (TLR4 agonist) IL-6 release in humans. Given, this extensive body of evidence we believe EB05 could ameliorate ARDS due to COVID-19, significantly reducing ventilation rates and mortality.

开始日期2020-11-25

申办/合作机构

Edesa Biotech, Inc.

[+1]

100 项与 NI-0101 相关的临床结果

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100 项与 NI-0101 相关的转化医学

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100 项与 NI-0101 相关的专利（医药）

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项与 NI-0101 相关的文献（医药）

2026-05-01·VACCINE

Pharmacovigilance analysis of vaccination errors during pregnancy using VAERS data

Article

作者: Campisi, Lucrecia M ; Asmar, Lisa O ; Gallo, Kirsten J ; Lynch, Sarah E ; McCall, Kenneth L ; Khalla, Sandi S ; Steinberg, Joshua D ; Park, Jae Hee ; Clark, Taylor M

BACKGROUND/OBJECTIVE:

Vaccination during pregnancy protects both pregnant individuals and infants, yet real-world data on administration errors in this population are limited. We aimed to identify and characterize safety signals for vaccination errors during pregnancy using the Vaccine Adverse Event Reporting System (VAERS).

METHODS:

We conducted a retrospective analysis of VAERS reports from January 1, 2023, to May 30, 2025, involving vaccinations administered during pregnancy. Disproportionality was assessed using PRR (>2), ROR (signal if lower 95% CI > 1), EB05 (>2), and IC025 (>0) for error types with ≥5 reports.

RESULTS:

Of 171,958 unique VAERS reports, 1413 involved vaccinations during pregnancy. Several vaccine-error pairs showed moderate to strong signals: RSV-wrong product (PRR 6.8; ROR 10.3, 95% CI 7.4-14.6; EB05 1.8; IC025 0.8), TDAP-extra dose (PRR 9.7; ROR 11.6, 95% CI 6.7-20.3; EB05 3.0; IC025 1.6), TDAP-storage error (PRR 15.4; ROR 17.7, 95% CI 8.5-36.6; EB05 3.2; IC025 1.7), and influenza-expired product (PRR 8.3; ROR 8.8, 95% CI 3.4-22.4, EB05 1.8; IC025 0.9). Live vaccine administrations (MMR n = 35, varicella n = 42) were reported, with 47.6% unaware of pregnancy at vaccination. No birth defects or deaths were reported among vaccine-error pairs.

CONCLUSIONS:

Vaccine administration during pregnancy showed disproportionate reporting of specific errors, especially RSV-wrong product, multiple TDAP-related errors (extra dose, storage) and live vaccine administration, with no severe outcomes reported. Findings suggest practical targets for error prevention to reduce wrong-product and scheduling errors while maintaining access to indicated maternal immunizations.

2024-07-01·Pharmaceutical Medicine

Statistical Signal Detection Algorithm in Safety Data: A Proprietary Method Compared to Industry Standard Methods

Article

作者: Allen, Jeff K ; Philip, Jeff ; Bastos, Eugenia

INTRODUCTION:

Several quantitative methods have been established, in pharmacovigilance, to detect signals of disproportionate reporting (SDRs) from databases containing reports of adverse drug reactions (ADRs). The signal detection algorithms (SDAs) and the source of the reporting per product vary, but it is unclear whether any algorithm can provide satisfactory performance using data with such large variance factors.

OBJECTIVE:

Determine the appropriate SDA for Biogen's internal Global Safety Database (GSD) given the characteristics of the database including frequencies of events, data skewness, outliers, and missing information. Compare performance of standard approaches (EBGM, EB05, PRR, and ROR), well accepted by industry, to a Biogen-developed Machine Learning (ML) Regression Decision Tree (RDT) model, across several Biogen products, to determine a champion SDA.

METHODS:

All data associated with seven marketed Biogen products were chosen and a historical subset of reported ADRs were considered. Six SDAs (five common industry disproportionality methods) and RDT were evaluated. The SDRs were calculated on training and test data composed of quarterly reporting intervals from 2004-2019. The performance measures used were sensitivity, precision, time to detect new events, and frequency of detected cases for each algorithm for each product. Outcomes in the test data are known a priori and easily compared to predicted outcomes. Validation was performed via rates of misclassification. This work solely represents Biogen's internal information, intentionally chosen to serve the performance review of its signal detection systems, and results will not necessarily be generalizable to other external sources.

RESULTS:

Several algorithms performed differently among products, but no one method dominated any other. Performance was dependent on the thresholds used to define a signal according to different criteria. However, those different statistics subtly influenced the achievable performance. The relative performance of RDT and Medicines and Healthcare products Regulatory Agency (MHRA) algorithms were superior and paired across products. A reduction in precision for all methods spanning the products was present. Hence, companies evaluating signal detection approaches, search for innovative methods to minimize this effect.

CONCLUSIONS:

In designing signal detection systems, careful consideration should be given to the criteria that are used to define SDRs. The choice of disproportionality statistics does not affect the achievable range of signal detection performance. These choices should consider mainly ease of implementation and interpretation. The implementation of a method is specific to its accuracy. The RDT attempted to take advantage of known methods and compare results on a per-product basis. Many factors influencing ADRs may improve RDT in future efforts. In this experiment, RDT demonstrated superiority in terms of quickest time to detect and capturing of the highest number of ADRs. Next steps include expansion of data for products representing other indications and testing models in external databases to investigate generalizability of estimates when comparing SDAs.

2020-03-01·Annals of the rheumatic diseases1区 · 医学

Efficacy and safety of NI-0101, an anti-toll-like receptor 4 monoclonal antibody, in patients with rheumatoid arthritis after inadequate response to methotrexate: a phase II study

1区 · 医学

Article

作者: Ernest H Choy ; Cristina de Min ; Philippe Jacqmin ; Tamta Kobakhidze ; Iain McInnes ; Geneviève Lapeyre ; Kathy de Graaf ; Emmanuel Monnet

Objectives:

Anti-citrullinated protein antibodies (ACPAs) form immune complexes with citrullinated proteins binding toll-like receptor (TLR) 4, which has been proposed as a mediator of rheumatoid arthritis (RA). NI-0101 is a first-in-class humanised monoclonal antibody blocking TLR4, as confirmed by inhibition of in vivo lipopolysaccharide-induced cytokine release in healthy volunteers. This study was design to confirm preclinical investigations supporting a biomarker-driven approach for treatment of patients with RA who present positive for these immune complexes.

Methods:

Placebo-controlled, double-blind, randomised (2:1) trial of the tolerability and efficacy of NI-0101 (5 mg/kg, every 2 weeks for 12 weeks) versus placebo in ACPA-positive RA patients with inadequate response to methotrexate. Efficacy measures included Disease Activity Score (28-joint count) with C reactive protein (DAS28-CRP), European League Against Rheumatism (EULAR) good and moderate responses, and American College of Rheumatology (ACR) 20, ACR50 and ACR70 responses. Subgroup analyses defined on biomarkers were conducted. Pharmacokinetics, pharmacodynamics and safety were reported.

Results:

90 patients were randomised (NI-0101 (61) and placebo (29)); 86 completed the study. No significant between-group difference was observed for any of the efficacy endpoints. Subgroup analyses using baseline parameters as covariants did not reveal any population responding to NI-0101. Treatment-emergent adverse events occurred in 51.7% of patients who received placebo versus 52.5% for NI-0101.

Conclusions:

We demonstrate for the first time that in RA, a human immune-mediated inflammatory disease, blocking the TLR4 pathway alone does not improve disease parameters. Successful targeting of innate immune pathways in RA may require broader and/or earlier inhibitory approaches.

项与 NI-0101 相关的新闻（医药）

2026-08-26

·今日头条

病原真菌利用内共生菌，毒杀植物保护菌 | 热心肠日报

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

微生物疗法临床研究

2026-08-20

·BioSpace

Edesa Biotech Announces Pricing of $25.0 Million Public Offering

TORONTO, Aug. 19, 2026 (GLOBE NEWSWIRE) -- Edesa Biotech, Inc. (Nasdaq: EDSA) (the “Company” or “Edesa”), a clinical-stage biopharmaceutical company focused on developing host-directed therapeutics for immuno-inflammatory diseases, today announced the pricing of an underwritten public offering consisting of (i) 3,870,500 common shares and accompanying common share warrants to purchase an aggregate of 3,870,500 common shares and (ii) in lieu of common shares to investors who so choose, pre-funded warrants to purchase up to 675,000 common shares and accompanying common share warrants to purchase an aggregate of 675,000 common shares, at an exercise price of $0.0001 per pre-funded warrant. Each common share and pre-funded warrant is being sold in combination with an accompanying common share warrant to purchase one common share. The common share warrants will have an exercise price of $7.50 per share, will be immediately exercisable from the date of issuance and will expire on the earlier of (x) the 18-month anniversary of the original issuance date and (y) 30 days following the Company’s public announcement of Phase 2 vitiligo topline data for EB06. The combined public offering price of each common share and accompanying common share warrant is $5.50. The combined public offering price of each pre-funded warrant and accompanying common share warrant is $5.4999, which represents the combined public offering price for the common shares and accompanying common share warrants less the $0.0001 per share exercise price for each pre-funded warrant. The gross proceeds are expected to be approximately $25.0 million, before deducting underwriting discounts and commissions and other estimated offering expenses. In addition, Edesa has granted the underwriters a 30-day option to purchase up to an additional 681,825 common shares and accompanying common share warrants to purchase up to 681,825 common shares at the public offering price, less underwriting discounts and commissions. All common shares, pre-funded warrants and accompanying common share warrants are being offered by Edesa. The offering is expected to close on or about August 21, 2026, subject to the satisfaction of customary closing conditions. Guggenheim Securities is acting as the sole book-running manager for the offering. Edesa intends to use the net proceeds from the offering for general corporate purposes, which may include working capital, capital expenditures and research and development and manufacturing expenses. The offering is being made pursuant to a shelf registration statement on Form S-3 (File No. 333-288966), including a base prospectus, that was declared effective by the Securities and Exchange Commission (“SEC”) on September 9, 2025. A preliminary prospectus supplement and accompanying prospectus relating to the offering have been filed with the SEC and a final prospectus supplement with the final terms of the offering will be filed with the SEC and will be available for free on the SEC’s website, located at Copies of the final prospectus supplement and the accompanying prospectus relating to the offering may be obtained, when available, from Guggenheim Securities, LLC, Attention: Equity Syndicate Department, 330 Madison Avenue, 8th Floor, New York, NY 10017, or by telephone at (212) 518-9544, or by email at GSEquityProspectusDelivery@guggenheimpartners.com. This press release does not constitute an offer to sell or the solicitation of an offer to buy these securities, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of that state or jurisdiction. 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 EB01 (1.0% daniluromer cream), 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. 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 regarding the Company’s expectations regarding the satisfaction of customary closing conditions related to the offering, the expected closing of the offering and the anticipated use of proceeds therefrom. 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: market and other conditions, those relating to the anticipated use of proceeds, 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 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: Gary Koppenjan Edesa Biotech, Inc. investors@edesabiotech.com

临床2期

2026-08-19

·发现报告

Edesa Biotech Inc美股招股说明书(2026-08-20版)

Edesa Biotech Inc美股招股说明书(2026-08-20版) 2026-08-20 美股招股说明书 Zt 核心观点： Edesa Biotech, Inc. (EDSA) 是一家生物制药公司，专注于治疗炎症和免疫相关疾病。公司目前有两个主要治疗领域：医疗皮肤科和呼吸系统疾病。医疗皮肤科：公司正在开发 EB06，一种抗 CXCL10 单克隆抗体候选药物，用于治疗白癜风，这是一种常见的自身免疫性疾病，会导致皮肤出现脱色斑块。 EB06 已显示出良好的安全性和耐受性特征。公司已获得加拿大卫生部的批准，可以进行 EB06 在中度至重度非节段性白癜风患者中的 2 期概念验证研究。公司正在与美国食品药品监督管理局 (FDA) 讨论相同研究的 IND 申请。公司还拥有 EB01 (1.0% daniluromer 乳膏)，这是一种用于治疗中度至重度慢性过敏性接触性皮炎 (ACD) 的 3 期准备资产，ACD 是一种常见的职业性皮肤疾病。呼吸系统疾病：公司最先进的呼吸系统药物候选药物是 paridiprubart，它代表了一种名为“宿主导向疗法”（HDT）的新兴疗法类别，旨在调节身体自身的免疫反应，以应对感染性疾病甚至化学制剂。在 2025 年 10 月，公司报告称，paridiprubart 在一项针对住院 ARDS 患者的截断 3 期临床研究中达到了主要和次要终点，并具有统计学意义，提供了临床上有意义的生存和康复改善。公司还报告了来自同一研究的积极额外数据。这些结果代表了更广泛的 278 名患者人群，其中包括先前报告的 104 名需要机械通气 (IMV) 的患者以及 174 名非 IMV 患者。在这个完整的人群中，paridiprubart 显示出统计学上显著的 28 天死亡率降低。治疗益处在不同严重程度组之间以及患有严重合并症的患者中是一致的。由于 TLR4 介导的炎症在肺和肾损伤中起着核心作用，公司进行了额外的探索性分析，以评估 paridiprubart 对同时患有急性肾损伤 (AKI) 的 ARDS 患者的效果。在公司 2 期和 3 期研究中，101 名来自 ARDS 患者群体，在基线时出现 AKI，paridiprubart 加上标准治疗与显著的死亡率降低相关，并由肾脏特异性 MAKE30 复合终点的一致性改善所支持。 paridiprubart 正在被评估中，一项由美国政府资助的平台研究正在评估三种新型威胁无关的 HDT，用于治疗住院 ARDS 患者。公司已启动制造准备活动，包括工艺开发和规模放大计划，为未来的药物生产做准备。财务状况：公司计划将本次发行的净收益用于一般公司目的，包括营运资金、资本支出和研发及制造费用。公司目前没有计划支付现金股息，并打算将未来的收益用于未来的运营和业务扩张。风险因素：投资公司证券涉及高风险，投资者应仔细考虑风险和不确定性，包括管理对净收益使用的广泛自由裁量权、潜在稀释、缺乏公开市场以及未来资金筹集的不确定性。关键数据：公司计划发行 3,870,500 股普通股，以及伴随的普通股认股权证，认股权证可购买最多 3,870,500 股普通股。公司还提供替代方案，向某些投资者发行最多 675,000 股普通股的预资助认股权证，以及伴随的普通股认股权证。普通股认股权证可随时行使，并可在以下两者中较早者行使：(i) 原始发行日期后 18 个月周年纪念日，以及 (ii) 公司公布 EB06 2 期顶线数据后的 30 天内。普通股认股权证的行使价格为每股 7.50 美元。预资助认股权证可立即行使，无需支付任何费用。公司普通股在纳斯达克资本市场上交易，代码为“EDSA”。结论： Edesa Biotech, Inc. 是一家处于临床开发阶段的生物制药公司，拥有多个潜在的治疗炎症和免疫相关疾病的产品。公司最先进的产品 EB06 和 paridiprubart 分别处于 2 期和 3 期临床研究阶段，并显示出有希望的临床结果。然而，公司也面临着一些风险和不确定性，投资者应仔细考虑这些因素。点击免费查看完整报告

临床3期临床2期临床申请临床成功

100 项与 NI-0101 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D12624	-	-	-

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
成人呼吸窘迫综合征	临床3期	美国	Edesa Biotech, Inc.	2022-07-11
成人呼吸窘迫综合征	临床3期	加拿大	Edesa Biotech, Inc.	2022-07-11
成人呼吸窘迫综合征	临床3期	哥伦比亚	Edesa Biotech, Inc.	2022-07-11
急性呼吸窘迫综合征	临床3期	美国	Edesa Biotech, Inc.	2020-11-25
急性呼吸窘迫综合征	临床3期	加拿大	Edesa Biotech, Inc.	2020-11-25
新型冠状病毒感染	临床3期	美国	Edesa Biotech, Inc.	2020-11-25
类风湿关节炎	临床2期	美国	NovImmune SA	2017-05-10
类风湿关节炎	临床2期	波斯尼亚和黑塞哥维那	NovImmune SA	2017-05-10
类风湿关节炎	临床2期	保加利亚	NovImmune SA	2017-05-10
类风湿关节炎	临床2期	匈牙利	NovImmune SA	2017-05-10

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临床结果

适应症

分期

评价

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


ATS2026	临床3期	新型冠状病毒感染	104	Paridiprubart (TLR4 inhibitor) + Standard of Care (SOC)	蓋選淵醖齋廠憲鬱鏇鹽(廠網憲衊鏇鏇淵襯淵願) = 積範憲鏇壓衊齋網夢餘積獵網壓顧願廠齋築鏇 (築齋壓願鏇顧膚繭積繭, 35 ~ 44) 更多	积极	2026-05-15
				Placebo + Standard of Care (SOC)	蓋選淵醖齋廠憲鬱鏇鹽(廠網憲衊鏇鏇淵襯淵願) = 襯鹹製遞憲衊醖憲鬱築積獵網壓顧願廠齋築鏇 (築齋壓願鏇顧膚繭積繭, 47 ~ 58) 更多
Company_Website 人工标引	临床3期	急性呼吸窘迫综合征	278	Paridiprubart + SOC	願簾淵獵積餘蓋襯選積(廠鏇簾鹽襯窪醖選鬱構) = 願醖獵積構範鏇願齋憲構窪積遞醖壓鑰鹽艱繭 (鹽鑰窪顧積選衊餘觸遞, 21 ~ 27) 达到更多	积极	2026-02-24
				Placebo + SOC	願簾淵獵積餘蓋襯選積(廠鏇簾鹽襯窪醖選鬱構) = 範簾顧構夢觸廠顧鏇鹹構窪積遞醖壓鑰鹽艱繭 (鹽鑰窪顧積選衊餘觸遞, 29 ~ 37) 达到更多