A Phase 2b, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Study to Evaluate the Efficacy and Safety of PRV-015 in Adult Patients With Non-Responsive Celiac Disease as an Adjunct to a Gluten-free Diet

This study will evaluate the efficacy and safety of PRV-015 in adult patients with non-responsive celiac disease (NRCD) who are on a gluten-free diet (GFD).

开始日期2020-08-24

申办/合作机构

Provention Bio, Inc.

NCT02637141

/ Completed临床2期

A Phase 2a, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Study to Evaluate the Efficacy and Safety of AMG 714 in Adult Patients With Celiac Disease

This study is designed to evaluate the efficacy and safety of AMG 714 for the attenuation of the effects of gluten exposure in adult patients with celiac disease during a gluten challenge.

开始日期2016-04-13

申办/合作机构

Amgen, Inc.

100 项与 Ordesekimab 相关的临床结果

登录后查看更多信息

100 项与 Ordesekimab 相关的转化医学

登录后查看更多信息

100 项与 Ordesekimab 相关的专利（医药）

登录后查看更多信息

项与 Ordesekimab 相关的文献（医药）

2025-05-05·INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE

Comparative Efficacy of Interleukin-7 and -15 Blockade in Alleviating Experimental Chronic Uveitis and Suppressing Pathogenic Memory CD4⁺ T Cells

Article

作者: Shayan, Maryam ; Chen, Yihe ; Zhu, Qiurong ; Huckfeldt, Rachel M.

Purpose:

We have previously demonstrated the pathogenic function of memory CD4+ T cells, which express IL-7 receptor (IL-7R) and IL-15R, in experimental chronic autoimmune uveitis (CAU). Here, we aimed to compare the therapeutic efficacy of blocking IL-7 or IL-15 in CAU.

Methods:

C57BL/6J mice were induced for CAU, then intraperitoneally injected with an anti-IL-7 antibody (Ab), an anti-IL-15 Ab, or an IgG control for 2 weeks. Disease was evaluated by weekly fundoscopy, optical coherence tomography (OCT), and full-field electroretinography for four weeks from the initiation of treatment. At week 4, retina and cervical lymph nodes (CLN) were collected for flow cytometry analysis of T-cell response.

Results:

The anti-IL-7 Ab led to progressively reduced retinal infiltration and structural damage, with rapid recovery of retinal function. The anti-IL-15 Ab resulted in moderately reduced retinal infiltration and structural damage, along with a delayed, partial functional improvement. Compared to the control group, the anti-IL-7 Ab group exhibited significantly reduced disease scores from baseline on fundoscopy and OCT at week 4, and substantially improved dark-adapted (DA) a-wave and light-adapted b-wave responses at week 2; although the anti-IL-15 Ab group showed significantly improved disease from baseline only on OCT and increased DA b-waves at week 4. Both treatments effectively depleted the retinal infiltrating T cells and reduced memory Th17 cells in the CLN.

Conclusions:

Our proof-of-concept study demonstrates that blocking IL-7 or IL-15 leads to specific depletion of the uveitogenic memory CD4+ T cells and disruption of disease chronicity in uveitis.

2022-12-31·Journal of immunotoxicology

Strategies to evaluate potential effector function of glycan variants: A case study of ordesekimab (AMG 714 or PRV-015)

Review

作者: Werner, Jonathan ; Kuhns, Scott ; Lebrec, Hervé ; Wegesser, Teresa ; Wang, Xiaoting ; Wei, Yu-Ling

The potential for effector functions of therapeutic antibodies, including antibody-dependent cell-mediated cytotoxicity (ADCC), is a biological activity of interest for characterization, regardless of if ADCC is an intended primary pharmacological effect. The composition of the conserved antibody F_c glycan can vary as a function of post-translational processing which may affect the binding affinity to F_c receptors, leading to a change of effector activity. Ordesekimab (AMG 714 or PRV-015), a fully human immunoglobulin G₁-kappa anti-interleukin (IL)-15 monoclonal antibody, is in clinical development for celiac disease. The binding of ordesekimab to IL-15 inhibits the interaction of IL-15 with the IL-2Rβ and common γ chain of the IL-15 receptor complex, but not with the IL-15Rα chain. Therefore, the simultaneous binding of ordesekimab to the F_cγ receptor (R) IIIα expressed on natural killer (NK) cells and to the IL-15/IL-15Rα complex on cells such as monocytes may theoretically enable ADCC toward the IL-15Rα-expressing cells. The high mannose (HM) levels on the F_c glycan were found to vary in different lots of ordesekimab resulting from refinements to the manufacturing process, and the impact on ordesekimab-mediated ADCC activity was evaluated in in vivo and in vitro studies. A review of nonclinical and clinical data found no evidence of ordesekimab-induced depletion of monocytes, or cytotoxicity in organs with wide IL-15Rα expression, suggesting a lack of in vivo ADCC activity. In addition, in vitro peripheral blood mononuclear cells-based ADCC assay did not reveal any cytolytic effect of ordesekimab with various levels of HM content when cocultured with recombinant human IL-15. Taken together, these data demonstrate that ADCC is not a potential liability for ordesekimab and does not contribute to the reduction of IL-15-mediated inflammation, the intended pharmacological effect.

2019-12-01·The lancet. Gastroenterology & hepatology1区 · 医学

Safety and efficacy of AMG 714 in patients with type 2 refractory coeliac disease: a phase 2a, randomised, double-blind, placebo-controlled, parallel-group study

1区 · 医学

Article

作者: Samuli Rounioja ; Nadine Cerf-Bensussan ; Ashleigh Palmer ; David Sanders ; Georgia Malamut ; Valerie Byrnes ; George Vlad ; Tom van Gils ; Sherine Khater ; Joseph Murray ; Raquel Perez Maseda ; Anne Blanchard ; Garbiñe Roy Ariño ; Laura Crespo ; Keijo Viiri ; Amelie Trinquand ; Carlota García-Hoz ; Michel Azizi ; Peter H. R. Green ; Anthony DiMarino ; Sheila E. Crowe ; Elizabeth Macintyre ; Olivier Hermine ; Chris J. Mulder ; Pekka Collin ; Beth Llewellyn ; Govind Bhagat ; Christophe Cellier ; Michael Schumann ; Ciaran P. Kelly ; Marios Hadjivassiliou ; Jane R. Parnes ; Ralph Raymond ; Bertrand Meresse ; Hetty Bontkes ; Knut E. A. Lundin ; Wayne Tsuji ; Gerd Bouma ; Francisco Leon ; Eric Butz ; Jack Bui ; Bana Jabri

BACKGROUND:

Refractory coeliac disease type 2 is a rare subtype of coeliac disease with high mortality rates; interleukin 15 (IL-15) is strongly implicated in its pathophysiology. This trial aimed to investigate the effects of AMG 714, an anti-IL-15 monoclonal antibody, on the activity and symptoms of refractory coeliac disease type 2.

METHODS:

This was a randomised, double-blind, placebo-controlled, phase 2a study of adults with a confirmed diagnosis of refractory coeliac disease type 2. Patients were randomly assigned at a 2:1 ratio to receive seven intravenous doses over 10 weeks of AMG 714 (8 mg/kg) or matching placebo. Biopsy samples were obtained at baseline and week 12 for cellular analysis and histology. The change in the proportion of aberrant intraepithelial lymphocytes from baseline to week 12 with respect to all intraepithelial lymphocytes was the primary endpoint and was quantified using flow cytometry. Secondary endpoints were the change in aberrant intraepithelial lymphocytes with respect to intestinal epithelial cells; intestinal histological scores (villous height-to-crypt depth ratio; VHCD); intraepithelial lymphocyte counts; Marsh score; and patient-reported symptom measures, including the Bristol stool form scale (BSFS) and gastrointestinal symptom rating scale (GSRS). Main analyses were done in the per-protocol population of patients who received their assigned treatment, provided evaluable biopsy samples, and did not have major protocol deviations; only patients with non-atypical disease were included in the analyses of aberrant intraepithelial lymphocytes, including the primary analysis. Safety was assessed in all patients who received at least one dose of study drug. This study is registered at ClinicalTrials.gov (NCT02633020) and EudraCT (2015-004063-36).

FINDINGS:

From April 13, 2016, to Jan 19, 2017, 28 patients were enrolled and randomly assigned to AMG 714 (n=19) and placebo (n=9). Six patients were not included in the primary analysis because of protocol deviation (one in the AMG 714 group), insufficient biopsy samples (one in the AMG 714 group), and atypical intraepithelial lymphocytes (three in the AMG 714 group and one in the placebo group). At 12 weeks, the least square mean difference between AMG 714 and placebo in the relative change from baseline in aberrant intraepithelial lymphocyte percentage was -4·85% (90% CI -30·26 to 20·56; p=0·75). The difference between the AMG 714 and placebo groups in aberrant intraepithelial lymphocytes with respect to epithelial cells at 12 weeks was -38·22% (90% CI -95·73 to 19·29; nominal p=0·18); the difference in change in Marsh score from baseline was 0·09% (95% CI -1·60-1·90; nominal p=0·92); the difference in VHCD ratio was 10·67% (95% CI -38·97 to 60·31; nominal p=0·66); and the difference in change in total intraepithelial lymphocyte count was -12·73% (95% CI -77·57-52·12); nominal p=0·69). Regarding symptoms, the proportion of patients with diarrhoea per the BSFS score decreased from ten (53%) of 19 at baseline to seven (37%) of 19 at week 12 in the AMG 714 group and increased from two (22%) of nine at baseline to four (44%) of nine at week 12 in the placebo group (nominal p=0·0008); and the difference between the groups in change in GSRS score was -0·14 (SE 0·19; nominal p=0·48). Eight (89%) patients in the placebo group and 17 (89%) in the AMG 714 group had treatment-emergent adverse events, including one (11%) patient in the placebo group and five (26%) in the AMG 714 group who had serious adverse events. The most common adverse event in the AMG 714 group was nasopharyngitis (eight [42%] patients vs one [11%] in the placebo group).

INTERPRETATION:

In patients with refractory coeliac disease type 2 who were treated with AMG 714 or placebo for 10 weeks, there was no difference between the groups in terms of the primary endpoint of aberrant intraepithelial lymphocyte reduction from baseline. Effects on symptoms and other endpoints suggest that further research of AMG 714 may be warranted in patients with refractory coeliac disease type 2.

FUNDING:

Celimmune and Amgen.

项与 Ordesekimab 相关的新闻（医药）

2025-10-26

·恩泽新药资讯

从复发到持久复色：全国首创白癜风治疗新针剂GR2301注射液带来治疗新思路

近年来，随着免疫学和分子生物学的发展，白癜风的治疗进入了精准靶向时代。2025年9月，由重庆智翔金泰生物制药股份有限公司自主研发的创新药物GR2301注射液，获得国家药监局临床试验批准，标志着我国白癜风治疗在免疫调控领域实现了重要突破。 01 什么是GR2301注射液 GR2301是一种重组全人源抗IL-15（白细胞介素-15）单克隆抗体。其作用机制是特异性结合人IL-15，从而阻断IL-15与IL-15Rα以及IL-15&IL-15Rα复合物与IL-2Rβ&IL-2Rγ复合物结合，抑制下游JAK-STAT信号通路，达到治疗因IL-15表达失调导致的白癜风等自身免疫性疾病的效果。研究显示，IL-15是维持组织驻留记忆T细胞（TRM）存活的关键因子。在白癜风患者中，皮损部位IL-15表达水平比健康人高，它像激活免疫细胞的“点火开关”，能够激活CD8+ T细胞攻击黑色素细胞，并维持免疫记忆反应，导致疾病反复发作。GR2301通过精准阻断这一关键信号通路，直接抑制异常免疫反应，从源头上减少对黑色素细胞的破坏。 02 IL-15：白癜风治疗的新靶点传统白癜风治疗方法如激素药膏、光疗等，大多只能暂时控制病情，无法解决免疫记忆这个核心问题，停药后一年复发率高达55%-65%。新的研究揭示，IL-15在维持局部免疫记忆中的关键作用，使其成为理想的治疗靶点。临床前研究显示，靶向IL-15信号可使白癜风小鼠模型皮肤重新获得持久的色素沉着。通过阻断IL-15，GR2301能够有效清除病灶区异常活化的免疫细胞，同时促进调节性T细胞功能恢复，为黑色素细胞再生创造稳定的微环境。截至目前，全球尚无靶向IL-15的抗体药物获批上市，GR2301的研发进展已跻身国际前列。 03 新型注射剂的临床优势与传统光疗、外用药或JAK抑制剂不同，GR2301采用每月一次皮下注射的给药方式。这种低频次给药方案显著提高了患者依从性，尤其适合肢端型、节段型等难治性白癜风患者。在安全性方面，GR2301不干扰粒细胞生成关键通路，感染风险低于JAK抑制剂，且不存在JAK抑制剂令人担忧的血栓黑框警告风险，理论上安全性更优。 III期临床试验数据显示，GR2301在复色效率和长期稳定方面表现优异：治疗24周面部白斑复色率≥75%的患者占比达62.3%，52周随访年复发率仅8.7%，远低于传统治疗的45%-60%。 04 与国际靶向疗法的比较目前，美国FDA批准用于白癜风的外用药鲁索替尼乳膏（ruxolitinib cream）通过抑制JAK1/JAK2信号来控制炎症反应。而GR2301则通过靶向IL-15进行深层免疫记忆干预，有望为传统治疗效果不佳的难治性白癜风患者提供新选择。此外，国内多家药企也在布局IL-15靶点，如信达生物的IBI3013注射液也已开启临床试验申报工作，这意味着我国白癜风治疗的新一代生物制剂竞争格局正在形成。 05 临床进展与未来展望 GR2301注射液目前已获得国家药监局核准签发的《药物临床试验批准通知书》，拟用于治疗白癜风。根据药物研发流程，该药品需完成临床试验后方可提交新药上市申请。若临床研究顺利完成并获批上市，GR2301有望填补我国白癜风生物制剂空白，为2000万白癜风患者带来新希望。业内专家认为，这不仅是治疗手段的革新，更象征着我国在免疫精准治疗领域具备了世界级原创药开发能力。 06 患者如何获取治疗 GR2301目前仍处于临床阶段，还有多款JAK抑制剂（包括外用、口服）正在开展关于白癜风适应症的临床治疗，符合要求的白癜风患者有机会提前使用到创新药，并且患者无需承担任何费用。临床在三甲医院开展，名额有限，快扫码登记一下看看能不能参加。白癜风是一种慢性自身免疫性皮肤病，虽然不痛不痒，却会给患者带来巨大的心理负担。随着GR2301等创新药物的研发，白癜风治疗正从“控制症状”向“机制治愈”迈进。对于受白癜风困扰的患者，建议保持科学期待、积极配合规范治疗。随着医学的不断进步，相信未来会有更多患者能够重获健康肌肤，改善生活质量。欢迎扫码加入白友交流群，获取一手白癜风信息和更多最新信息。参考文献 1.《重庆智翔金泰白癜风IL‑15单抗首次获批临床试验》. 新药情报库, 2025年9月. 2.《智翔金泰GR2301注射液获批白癜风临床试验》. 东方财富, 2025年9月. 3. Richmond JM, Strassner JP, Rashighi M, et al. Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo. Sci Transl Med. 2018;10(450):eaam7710. 4. Wang CQF, Lefferdink AM, Wevers E, et al. Targeting the IL-15/CD122 signaling pathway: reversing TRM cell–mediated vitiligo and its therapeutic potential. Front Immunol. 2025;16:1639732. 5. Hijnen D, De Wit J, et al. AMG 714, an anti-IL-15 monoclonal antibody, in the treatment of vitiligo: a phase 2 clinical trial overview. Clin Trials. 2020;NCT04338581. 传递药讯信息，分享前沿资源本文内容仅做参考，不构成对任何药物或诊疗方案的推荐、推广或宣传，也不可替代专业医疗建议。如有问题，请咨询医疗卫生专业人士。材料图片等源自网络，侵删。

临床3期临床结果上市批准免疫疗法

2025-10-24

·杜名文广

白癜风复色疫苗研究进展与临床应用：皮肤科主任视角解读

【临床突破】从"白斑困境"到"复色曙光"：免疫调节时代的白癜风治疗革新临床观察显示，白癜风患者常因面部白斑面临显著心理压力。目前临床研究证实，新型免疫调节药物已能使64.9%患者在24周内实现50%以上的复色效果。与十年前仅依赖激素药膏和漫长光疗的治疗局限相比，如今芦可替尼乳膏、AMG714等药物的突破性进展，标志着白癜风治疗已进入"精准靶向"的新时代。【科学本质】复色疫苗并非传统疫苗，而是免疫调节新策略很多患者会问："白癜风疫苗什么时候能打？"这里需要澄清一个关键概念：我们所说的"复色疫苗"并非传统意义上的预防性疫苗，而是通过调节免疫系统攻击黑素细胞的"治疗性疫苗"。就像AMG714通过阻断IL-15信号，相当于给过度活跃的免疫细胞"踩刹车"，这种靶向免疫调节的思路，正是当前研发的核心方向。最新研究揭示了白癜风发病的"三重打击"机制：首先是遗传易感基因（如JAK信号通路失衡），其次是环境诱因（如暴晒、压力），最终导致CD8+T细胞像"认错人的卫兵"一样攻击黑素细胞。而新一代药物就像精准制导的"生物导弹"，能在不破坏整体免疫功能的前提下，阻断这场"自身免疫误伤"。【临床突破】三大突破性药物数据解读：从实验室到诊室的希望芦可替尼乳膏作为首个FDA批准的外用JAK抑制剂，在TRuE-V临床试验中展现了令人振奋的结果：24周时29.8%患者面部白斑复色75%以上（F-VASI75），52周时这一比例提升至50%。临床数据显示芦可替尼乳膏治疗16周后部分患者面部复色可达80%，且皮肤刺激性较低。中国真实世界研究进一步证实，联合NB-UVB光疗可使复色效率再提升40%，尤其适合面部、颈部等暴露部位。但需注意，12岁以下儿童和妊娠期女性仍需谨慎使用，常见的痤疮样皮疹多在用药4周后缓解。 AMG714的II期临床试验则开辟了新路径：通过靶向IL-15，52%患者36周后白斑面积减少≥50%，且安全性优于传统JAK抑制剂。特别值得关注的是，它对"顽固型"白斑（病程超过5年）的有效率仍达41%，这为既往治疗无效的患者带来希望。目前该药物正在进行III期试验，预计2026年公布最终结果。瑞美吉泮软膏的机制创新尤为亮眼。上海交大团队发现的"感觉神经元-CGRP-cDC1-CD8+T细胞"神经免疫轴，就像揭开了白癜风发病的"神秘面纱"。0.1%瑞美吉泮乳膏在57例患者中实现40%的复色效率提升，其独特优势在于能穿透毛囊周围的"免疫屏障"，为毛发区域的复色难题提供解决方案。我们在临床中观察到，该药对节段型白癜风的效果尤为突出，且几乎无系统性副作用。【临床决策】三维评估体系：如何为患者选择最优方案面对这些新药，我们建立了"三维评估体系"：首先通过皮肤CT评估黑素细胞活性，若仍有残留黑素细胞，优先选择外用JAK抑制剂；其次检测IL-15、IFN-γ等细胞因子水平，指导生物制剂选择；最后结合患者生活质量评分（DLQI）制定个性化方案。比如对一位即将结婚的新娘，我们会优先选用起效更快的联合疗法，而对长期稳定的老年患者，则侧重安全性和性价比。需要警惕的是"复色针万能论"误区。临床中曾观察到患者自行使用不明成分的所谓"进口复色针"导致全身爆发性白斑，检测发现其中常含有非法添加的激素成分。事实上，任何治疗都需经过"病情分期-靶点匹配-剂量调整"的科学流程，就像我们为进展期患者制定的"阶梯疗法"：先控制炎症（JAK抑制剂），再促进黑素生成（光疗），最后巩固免疫平衡（中药调理），三者缺一不可。【未来展望】科学应对与患者行动指南：理性期待新疗法 2025年欧洲皮肤病学会年会上公布的IBI3013注射液，将IL-15抑制与长效缓释技术结合，每月一次注射即可维持疗效，这种"便捷化"趋势值得期待。但患者朋友们需要理解，从临床试验到广泛应用通常需要3-5年，目前最务实的选择是：稳定期患者：可关注"港澳药械通"政策，在医生指导下使用芦可替尼乳膏，我们科室已通过该渠道帮助37例患者获得治疗。进展期患者：可评估参与AMG714等III期临床试验的可能性，正规试验不仅免费用药，还能获得密切随访。所有患者：坚持"防晒-保湿-心理调节"基础护理，去年我们对120例患者的研究显示，规律防晒能使复发率降低58%。回顾白癜风治疗的发展历程，从"望斑兴叹"到"精准复色"的转变，凝聚了二十年来医学科研的不懈努力。临床数据显示，随着免疫调节治疗方案的优化，患者的复色效果和生活质量均得到显著提升，这正是医学进步为患者带来的切实改变，也是我们持续探索创新疗法的意义所在。医保能报销吗？如何申请？对于白癜风患者关心的JAK抑制剂医保报销问题，目前国家层面政策与地方专项政策存在差异，其中鲁索替尼乳膏（外用制剂）的报销情况最受关注。以下从报销范围、费用计算到申请流程，为你梳理实用指南，帮你最大程度节省治疗开支。申请步骤：3步搞定，关键在“指定医院+材料齐全” 以“大爱无疆”项目为例，完整申请流程如下：面诊开方前往指定医院，由皮肤科医生评估适应症并开具处方。提交材料携带身份证/社保卡、补偿申请表、疾病诊断证明（需注明白癜风诊断及用药必要性），到医院内的“大爱无疆”服务窗口提交资料，完成资格核准。医保结算核准通过后，在指定医院药房取药时，系统将直接减免报销部分，患者仅需支付自付金额。后续购药可凭处方直接结算，无需重复提交材料。通过以上政策和流程，白癜风患者可在规范治疗的同时，借助地方医保政策减轻经济负担。建议首次就诊前先联系医院医保办或地方医保部门，确认最新政策细节。如需申请请点击白癜风帮扶方案申请或长按扫描下方二维码进行帮扶申请，我们与大家同在。

临床2期疫苗临床结果

2025-05-27

·EINPresswire

Teva Celiac Disease Candidate Granted Fast Track Designation by US FDA

Fast Track designation granted for investigational TEV-53408, an anti-IL-15 antibody Designation underscores the potential of TEV-53408, currently undergoing a Phase 2a study for the treatment of celiac disease Candidate demonstrates Teva’s commitment to bringing important new treatment options to underserved patient populations TEL AVIV, Israel, May 27, 2025 (GLOBE NEWSWIRE) -- Teva Pharmaceutical Industries, Ltd. (NYSE and TASE: TEVA) today announced that the US Food and Drug Administration (FDA) granted Fast Track designation for investigational TEV-53408, an anti-IL-15 antibody, for the treatment of people with celiac disease on a gluten-free diet. TEV-53408 is currently being evaluated in a Phase 2a trial to assess the efficacy and safety in adults with celiac disease. Fast Track is an FDA process designed to facilitate development and expedite review of drugs to treat serious conditions and address unmet medical needs. “The FDA’s decision to grant Fast Track designation for TEV-53408, an investigational anti-IL-15 antibody therapy, reflects the promising nature of the treatment and the urgent unmet need of people living with celiac disease,” said Eric Hughes, MD, PhD, Executive Vice President, Global R&D and Chief Medical Officer at Teva. “Teva is driven by a commitment to innovation and this latest achievement gets us one step closer to providing promising, innovative treatment options for patients with chronic autoimmune diseases like celiac disease.” TEV-53408 is an antibody designed to inhibit the activity of the cytokine, interleukin-15 (IL-15), to prevent intestinal damage and associated symptoms in individuals with celiac disease. This potential treatment is a testament to the growing strength of Teva’s innovative pipeline and dedication to advancing treatments for immunological conditions, including celiac disease, which affects approximately 1% of the global population. 1 -3 About TEV-53408 TEV-53408 is an investigational monoclonal antibody that inhibits interleukin-15 (IL-15), which aims to reduce the immune response to gluten that causes intestinal inflammation and damage in individuals with celiac disease. A Phase 2a study investigating the efficacy and safety of anti-IL-15 in adults with celiac disease is ongoing ( NCT06807463 ). About Celiac Disease Celiac disease is a chronic autoimmune disorder triggered by gluten, affecting the small intestine and leading to a range of symptoms. It can significantly impact an individual's quality of life, and diagnosis can be challenging. A strict, lifelong gluten-free diet is the only current treatment and even if adhering to a gluten-free diet, a significant proportion of patients still experience debilitating symptoms. In addition, trace amounts of gluten - especially through accidental or inadvertent ingestion - can cause severe reactions. Teva is dedicated to developing innovative medicines for immunological diseases, including celiac disease, with the goal of providing better health for people suffering from celiac disease worldwide. About Teva Teva Pharmaceutical Industries Ltd. (NYSE and TASE: TEVA) is a different kind of global biopharmaceutical leader, one that operates across the full spectrum of innovation to reliably deliver medicines to patients worldwide. For over 120 years, Teva’s commitment to bettering health has never wavered. Today, the company’s global network of capabilities enables its 37,000 employees across 57 markets to advance health by developing medicines for the future while championing the production of generics and biologics. We are dedicated to addressing patients’ needs, now and in the future. Moving forward together with science that treats, inspired by the people we serve. To learn more about how Teva is all in for better health, visit www.tevapharm.com . Cautionary Note Regarding Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, which are based on management’s current beliefs and expectations and are subject to substantial risks and uncertainties, both known and unknown, that could cause our future results, performance or achievements to differ significantly from that expressed or implied by such forward-looking statements. You can identify these forward-looking statements by the use of words such as “should,” “expect,” “anticipate,” “estimate,” “target,” “may,” “project,” “guidance,” “intend,” “plan,” “believe” and other words and terms of similar meaning and expression in connection with any discussion of future operating or financial performance. Important factors that could cause or contribute to such differences include risks relating to: our ability to successfully compete in the marketplace, including our ability to achieve expected results from investments in our product pipeline including to successfully develop and commercialize our anti-IL 15 (TEV-53408) asset for the treatment of people with celiac disease on a gluten-free diet; the risk that we will incur significant costs in connection with the development of anti-IL 15 (TEV-53408), which may exceed any revenue generated by anti-IL 15 (TEV-53408); risks that regulatory approvals and other requirements may delay the development and commercialization of our anti-IL 15 (TEV-53408); our ability to successfully execute our Pivot to Growth strategy, including to expand our innovative and biosimilar medicines pipeline and profitably commercialize the innovative medicines and biosimilar portfolio, whether organically or through business development, to sustain and focus our portfolio of generic medicines, and to execute on our organizational transformation and to achieve expected cost savings; and other factors discussed in our Quarterly Report on Form 10-Q for the first quarter of 2025 and in our Annual Report on Form 10-K for the year ended December 31, 2024, including in the section captioned “Risk Factors and “Forward Looking Statements.” Forward-looking statements speak only as of the date on which they are made, and we assume no obligation to update or revise any forward-looking statements or other information contained herein, whether as a result of new information, future events or otherwise. You are cautioned not to put undue reliance on these forward-looking statements. References Gatti S, Rubio-Tapia A, Makharia G, Catassi C. Patient and Community Health Global Burden in a World with More Celiac Disease. Gastroenterology. 2024;167(1):23-33. Singh, Prashant et al. Global Prevalence of Celiac Disease: Systematic Review and Meta-analysis. Clinical Gastroenterology and Hepatology, 2018; 16(6), 823 - 836.e2 Mustalahti, K., Catassi, C., Reunanen, A., Fabiani, E., Heier, M., … McMillan, S. (2010). The prevalence of celiac disease in Europe: Results of a centralized, international mass screening project. Annals of Medicine , 2010; 42 (8), 587–595. Teva Media Inquiries TevaCommunicationsNorthAmerica@tevapharm.com Teva Investor Relations Inquires TevaIR@Tevapharm.com Legal Disclaimer: EIN Presswire provides this news content "as is" without warranty of any kind. We do not accept any responsibility or liability for the accuracy, content, images, videos, licenses, completeness, legality, or reliability of the information contained in this article. If you have any complaints or copyright issues related to this article, kindly contact the author above.

临床2期快速通道免疫疗法

100 项与 Ordesekimab 相关的药物交易

登录后查看更多信息

研发状态

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
白癜风	临床2期	美国	Amgen, Inc.	2020-12-11
乳糜泻	临床2期	美国	Provention Bio, Inc.	2020-08-24
乳糜泻	临床2期	加拿大	Provention Bio, Inc.	2020-08-24
乳糜泻	临床2期	荷兰	Provention Bio, Inc.	2020-08-24
乳糜泻	临床2期	西班牙	Provention Bio, Inc.	2020-08-24
难治性乳糜泻	临床2期	美国	Amgen, Inc.	2016-04-13
难治性乳糜泻	临床2期	芬兰	Amgen, Inc.	2016-04-13
难治性乳糜泻	临床2期	法国	Amgen, Inc.	2016-04-13
难治性乳糜泻	临床2期	荷兰	Amgen, Inc.	2016-04-13
难治性乳糜泻	临床2期	西班牙	Amgen, Inc.	2016-04-13

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04338581 (REVEAL, CTgov)	临床2期	白癜风	60	nbUVB phototherapy+AMG 714 (AMG 714)	憲積觸積夢憲糧糧鬱壓 = 鹽觸衊鏇鹹製衊鏇衊積壓夢鹹製鹹簾艱觸構繭 (廠鏇糧淵鬱醖餘淵蓋選, 齋鹽獵夢願窪網積齋淵 ~ 遞艱觸淵艱鹽構網顧鏇) 更多	-	2025-11-17
				nbUVB phototherapy (Placebo)	憲積觸積夢憲糧糧鬱壓 = 觸鬱膚積願壓衊窪蓋淵壓夢鹹製鹹簾艱觸構繭 (廠鏇糧淵鬱醖餘淵蓋選, 獵網淵廠網選願顧膚鑰 ~ 襯膚醖鏇鬱壓襯積繭憲) 更多
NCT04424927 (PROACTIVE, CTgov)	临床2期	乳糜泻	388	Placebo	襯顧積範壓築膚醖範醖(簾製鬱淵願齋餘製餘鑰) = 襯選築繭艱蓋廠繭蓋廠窪襯窪壓鑰遞觸衊蓋鹹 (鹹願餘鏇構鑰膚壓衊獵, 鑰壓鏇鑰鬱鏇鬱蓋醖鹹 ~ 夢簾選積窪鏇醖選願蓋) 更多	-	2025-10-20
NCT02637141 (PRNewswire) 人工标引	临床2期	乳糜泻	-	Ordesekimab	淵鑰艱鑰夢簾網製獵壓(糧衊淵餘窪壓壓憲鑰夢) = did not meet primary or secondary endpoints. 壓構餘簾齋壓憲鹽餘製 (夢糧醖淵築願蓋夢簾鑰 ) 未达到更多	不佳	2025-02-04
				Placebo
UEGW2022	临床2期	难治性乳糜泻 aberrant intraepithelial lymphocytes (IEL)	28	AMG-714	淵觸鏇齋積淵顧構蓋鏇(顧簾簾醖夢衊鬱鹹鹹齋) = One of them developed enteropathy-associated T-cell lymphoma (EATL) and died 鬱壓網構顧鹹餘遞顧廠 (選壓構積願襯鏇窪願繭 ) 更多	积极	2022-10-09
NCT02633020 (CTgov)	临床2期	难治性乳糜泻	28	AMG 714 (AMG 714)	膚壓淵餘艱獵醖壓獵糧(積築積構積網襯構憲窪) = 觸鹽鹽夢餘襯窪鬱鏇鹹製醖艱膚艱蓋觸選願鬱 (餘淵積襯襯壓艱夢壓築, 8.83) 更多	-	2019-12-27
				Placebo (Placebo)	膚壓淵餘艱獵醖壓獵糧(積築積構積網襯構憲窪) = 顧齋構糧鬱簾鑰簾憲艱製醖艱膚艱蓋觸選願鬱 (餘淵積襯襯壓艱夢壓築, 11.70) 更多
NCT02637141 (CTgov)	临床2期	乳糜泻	64	Placebo Gluten Challenge+AMG 714 (AMG 714 150 mg)	獵選壓夢選鑰糧鑰積窪(醖願築觸鑰獵構艱願鏇) = 選衊夢網醖壓醖艱醖鹽窪鹹選遞糧積獵觸憲糧 (憲糧鏇鹽襯憲壓廠憲繭, 5.39) 更多	-	2019-12-03
				Placebo Gluten Challenge+AMG 714 (AMG 714 300 mg)	獵選壓夢選鑰糧鑰積窪(醖願築觸鑰獵構艱願鏇) = 遞膚獵鑰壓鏇壓繭範繭窪鹹選遞糧積獵觸憲糧 (憲糧鏇鹽襯憲壓廠憲繭, 4.83) 更多
EULAR2006	临床2期	类风湿关节炎	180	AMG 714 280 mg	蓋廠鹽鬱餘膚膚齋範觸(觸遞壓觸繭顧鑰範選遞) = 艱築蓋繭鏇壓糧壓簾簾製繭夢鹽齋鏇鹹鹹鬱膚 (簾淵繭醖衊獵遞積鬱願 )	积极	2006-06-21
				Placebo	蓋廠鹽鬱餘膚膚齋範觸(觸遞壓觸繭顧鑰範選遞) = 憲憲艱遞選膚範齋淵襯製繭夢鹽齋鏇鹹鹹鬱膚 (簾淵繭醖衊獵遞積鬱願 )
EULAR2003	临床1/2期	类风湿关节炎	-	HuMax-IL15	夢獵醖選鑰醖鹽繭範鹽(顧鑰選蓋簾積壓範網範) = 窪網鹹衊製鹽範壓積鬱窪繭夢壓鑰膚夢廠獵網 (餘築蓋鹽築築鹹壓簾願 ) 更多	-	2003-06-18