A Phase 2b, Randomized, Double-Blind, Parallel Group, Placebo-Controlled 60-Week Study to Evaluate the Efficacy and Safety of Rezpegaldesleukin in the Treatment of Severe to Very Severe Alopecia Areata in Adult Patients (Rezolve AA)

This is an interventional, randomized, double blind, parallel group, placebo-controlled, Phase 2b, 3-arm study to assess the effect of pegylated-recombinant-human interleukin-2 (rezpegaldesleukin) in adult participants with severe to very severe alopecia areata.
The estimated duration includes a screening period of up to 35 days, a 36-week treatment period, and a 24-week follow-up period. The maximum study duration is approximately 65 weeks for all participants.

开始日期2024-04-02

申办/合作机构

Nektar Therapeutics

NCT06136741 / Recruiting临床2期

A Phase 2b, Randomized, Double-Blind, Parallel-Group, Placebo-Controlled 54-Week Study to Evaluate the Efficacy and Safety of Rezpegaldesleukin in the Treatment of Adult Patients With Moderate-to-Severe Atopic Dermatitis

This is an interventional, randomized, parallel group, treatment, Phase IIb, double blind, 4-arm study to assess the effect of pegylated-recombinant-human interleukin-2 (rezpegaldesleukin) in adult participants with moderate to severe atopic dermatitis.
The estimated duration is 15-35 days for screening and then up to approximately day 378 (last dose on day 280 + 98 days safety follow-up) for all patients. Patients with a response at Week 16 (end of induction therapy) will be re-randomized for the maintenance therapy period.

开始日期2023-10-23

申办/合作机构

Nektar Therapeutics

NCT05565729 / Completed临床1期

A Phase 1, Randomized, Placebo-controlled, Participant- and Investigator-blind, Single-dose Study of the Pharmacokinetics of LY3471851 Following Subcutaneous Dosing of LY3471851 in Healthy Participants

The purpose of this study is to compare two different formulations (test & reference) of LY3471851 in healthy participants. This study will compare how much of each formulation gets into the blood stream and how long it takes the body to remove it. Information about any side effects that may occur will also be collected. Participants will remain in the study for about 12 weeks, after receiving the study drug that is LY3471851.

开始日期2022-10-05

申办/合作机构

Nektar Therapeutics

[+1]

100 项与 Rezpegaldesleukin 相关的临床结果

登录后查看更多信息

100 项与 Rezpegaldesleukin 相关的转化医学

登录后查看更多信息

100 项与 Rezpegaldesleukin 相关的专利（医药）

登录后查看更多信息

项与 Rezpegaldesleukin 相关的文献（医药）

2022-01-01·Journal of translational autoimmunity

Selective expansion of regulatory T cells by NKTR-358 in healthy volunteers and patients with systemic lupus erythematosus

Article

作者: Furie, Richard ; Levin, Robert ; Diab, Isam ; Fanton, Christie ; Chindalore, Vishala ; Hanan, Nathan ; Zalevsky, Jonathan ; Dickerson, Daniel ; Dixit, Neha ; Haglund, Cat ; Kotzin, Brian L ; Gibbons, Jacqueline

Objective:

To evaluate NKTR-358, a polyethylene glycol-interleukin-2 conjugate composition designed to selectively induce regulatory T cells (Tregs), in first-in-human studies.

Methods:

Healthy volunteers and patients with systemic lupus erythematosus (SLE) received single- or multiple-dose (biweekly) NKTR-358 or placebo in two sequential, randomized, phase 1 studies (single ascending dose [SAD; NCT04133116] and multiple ascending dose [MAD; NCT03556007]). Primary objectives were safety and tolerability; secondary objectives included pharmacokinetics (PK) and immune effects of NKTR-358; exploratory objectives included effects on SLE disease activity.

Results:

There were eight ascending dose cohorts in the SAD study (0.3-28.0 μg/kg: n = 76; placebo: n = 24) and four in the MAD study (3-24.0 μg/kg: n = 36; placebo: n = 12). Most adverse events (AEs) were grade 1-2 injection-site reactions, with no treatment-related serious or severe AEs, or deaths. PK data showed dose proportionality and prolonged exposure (mean half-life: 7.4-12.9 days). Dose-dependent, selective, and sustained increases in percentages and absolute numbers of total CD4⁺ Tregs and CD25^bright Tregs were observed, with no significant changes in conventional CD4⁺ and CD8⁺ T cells, and low-level increases in natural killer cells. At the highest doses tested, administration of NKTR-358 resulted in a 12-17-fold increase in CD25^bright Tregs over baseline that was sustained for 20-30 days.

Conclusion:

NKTR-358 was well tolerated, had a suitable PK profile for biweekly dosing, and led to marked and selective dose-dependent increases in CD25^bright Tregs, with no significant changes in conventional T cells. These results provide strong support for further testing in SLE and other inflammatory diseases.

2021-01-01·Journal of translational autoimmunity

NKTR-358: A novel regulatory T-cell stimulator that selectively stimulates expansion and suppressive function of regulatory T cells for the treatment of autoimmune and inflammatory diseases

Article

作者: Zhang, Ping ; Dixit, Neha ; Kuo, Peiwen ; Lee, Myong ; Fanton, Christie ; Doberstein, Stephen K ; Cetz, Janet ; Sweeney, Theresa D ; VanderVeen, Laurie A ; Kamihara, Yusuke ; Chang, Thomas ; Dixit, Vidula ; Rubas, Werner ; Langowski, John L ; Kirksey, Yolanda ; Ritz, Jerome ; Tang, Yinyan ; Zalevsky, Jonathan ; Maiti, Mekhala ; Ji, Chunmei ; Kim, Grace ; Kirk, Peter

Impaired interleukin-2 (IL-2) production and regulatory T-cell dysfunction have been implicated as immunological mechanisms central to the pathogenesis of multiple autoimmune and inflammatory diseases. NKTR-358, a novel regulatory T-cell stimulator, is an investigational therapeutic that selectively restores regulatory T-cell homeostasis in these diseases. We investigated NKTR-358's selectivity for regulatory T-cells, receptor-binding properties, ex vivo and in vivo pharmacodynamics, ability to suppress conventional T-cell proliferation in mice and non-human primates, and functional activity in a murine model of systemic lupus erythematosus. In vitro, NKTR-358 demonstrated decreased affinity for IL-2Rα, IL-2Rβ, and IL-2Rαβ compared with recombinant human IL-2 (rhIL-2). A single dose of NKTR-358 in cynomolgus monkeys produced a greater than 15-fold increase in regulatory T-cells, and the increase lasted until day 14, while daily rhIL-2 administration for 5 days only elicited a 3-fold increase, which lasted until day 7. Repeated dosing of NKTR-358 over 6 months in cynomolgus monkeys elicited cyclical, robust increases in regulatory T-cells with no loss in drug activity over the course of treatment. Regulatory T-cells isolated from NKTR-358-treated mice displayed a sustained, higher suppression of conventional T-cell proliferation than regulatory T-cells isolated from vehicle-treated mice. NKTR-358 treatment in a mouse model (MRL/MpJ-Fas^lpr) of systemic lupus erythematosus for 12 weeks maintained elevated regulatory T-cells for the treatment duration and ameliorated disease progression. Together, these results suggest that NKTR-358 has the ability to elicit sustained and preferential proliferation and activation of regulatory T-cells without corresponding effects on conventional T-cells, with improved pharmacokinetics compared with rhIL-2.

2019-01-14·ACS biomaterials science & engineering3区 · 工程技术

Folic-Acid-Adorned PEGylated Graphene Oxide Interferes with the Cell Migration of Triple Negative Breast Cancer Cell Line, MDAMB-231 by Targeting miR-21/PTEN Axis through NFκB

3区 · 工程技术

Article

作者: Chattopadhyay, Dipankar ; Ghosh, Avijit ; Upadhyay, Priyanka ; Basu, Arijita ; Adhikary, Arghya

Triple negative breast cancer (TNBC), characterized by its aggressive and highly metastatic nature, is difficult to cure by the currently available therapies. In our investigation, folic-acid-adorned PEGylated graphene oxide (FA-PEG-GO) was synthesized by modifying graphene oxide (GO) with folic acid-PEG conjugate (FA-PEG-NH₂) by EDC/NHS coupling reaction. FA-PEG-GO exhibited an exceptional potential to attenuate cell migration of TNBC cell line ,MDAMB-231 as compared to GO because of the adorned folic acid moiety, which rendered better targeting. FA-PEG-GO inhibited cell migration by actin depolymerization and perturbing lamellipodia formation. The immunocytochemistry and western blot data unraveled the fact that FA-PEG-GO inhibited cell migration by targeting miR-21 by restricting the nuclear translocation of NFκB. The downregulation of miR-21 resulted in the elevation of PTEN expression which sequentially downregulated pFAK resulting in inhibition of cell migration. Moreover, upregulation of PTEN in FA-PEG-GO treated cells led to the decrease in expression of the downstream regulators including pAkt(Ser473) and pERK1/2, which contributed to the retardation of cell migration. Interestingly, the overexpression of NFκB-p65 by the transfection of NFκB-p65 expression plasmid in TNBC cells reversed the inhibitory effect of FA-PEG-GO on the nuclear translocation of NFκB-p65 which stabilized miR-21 expression and successively downregulated PTEN expression in FA-PEG-GO treated cells. Furthermore, miR-21 overexpression by transfection of miR-21 mimic in turn downregulated PTEN expression and sequentially restored the expression of pFAK even upon FA-PEG-GO treatment. miR-21 overexpression also compensated the inhibitory effect of FA-PEG-GO on pAkt(Ser473) and pERK1/2 which was evident from their significant expression in FA-PEG-GO-treated cells. The studies on chick embryo model ratified the ex ovo antimigratory efficacy of FA-PEG-GO. Altogether, our study unveiled the enormous potential of FA-PEG-GO to attenuate migration of TNBC cell line, MDAMB-231 by targeting the miR-21/PTEN axis through NFκB and thereby providing insights on cancer treatment.

项与 Rezpegaldesleukin 相关的新闻（医药）

2024-06-12

·PRNewswire

Nektar Therapeutics Presents First Preclinical Data on NKTR-0165, a TNFR2 Agonist Antibody Being Developed for the Treatment of Inflammatory Diseases, at EULAR 2024

– NKTR-0165 Demonstrates Selective Enhancement of Treg Cell Function Through Novel Agonistic Mechanism – – IND-Enabling Studies Underway for NKTR-0165 with First-in-Human Studies Planned in First Half of 2025 - SAN FRANCISCO, June 12, 2024 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) today announced the presentation of a poster highlighting new preclinical data on NKTR-0165 at the European Alliance of Associations for Rheumatology (EULAR) 2024 Congress. NKTR-0165 is a novel, first-in-class tumor necrosis factor receptor 2 (TNFR2) agonist and bivalent antibody designed to selectively stimulate TNFR2 receptor activity, without modulation of the TNFR1 signaling. TNFR2 signaling has been shown to be an important gatekeeper of inflammation and its absence or deficit is associated with a broad range of autoimmune diseases. TNFR2 is highly expressed on Tregs, neuronal cells and endothelial cells and has been shown to potentiate the suppressive effects and overall functional properties of regulatory T cells (Tregs). "The preclinical data presented at EULAR show that NKTR-0165 is a unique antibody that selectively binds to TNFR2 on Tregs to enhance its immunosuppressive activities, and could potentially become a first-in-class treatment for various autoimmune diseases, including ulcerative colitis and vitiligo," said Jonathan Zalevsky, Ph.D., Senior Vice President and Chief Research & Development Officer at Nektar. "By selectively binding to TNFR2, NKTR-0165 upregulates expression of proteins that are critical to Treg proliferation and function. Animal models show that NKTR-0165 reduces inflammation through the selective enhancement of Treg cell function via TNFR2 agonism. These data demonstrate a unique and differentiated profile for this bivalent antibody in the field of TNFR2 agonists." The poster presentation is available for download at . Key details and takeaways from the presentation are as follows: Abstract 3174: "A Novel Therapeutically Active Anti-TNFR2 Agonistic Antibody Promotes Treg Proliferation and Induction of Treg Functional Markers", Miyazaki, et al. NKTR-0165 shows selective TNFR2 binding and receptor agonism in human Tregs, with minimal binding and signaling activity in other TNFR2-expressing immune cells in vitro and in vivo. NKTR-0165 agonistic activity enhances Treg lineage stabilization and upregulates expression of proteins involved in Treg proliferation and function. NKTR-0165 demonstrates therapeutic efficacy in a KLH-induced delayed type hypersensitivity (DTH) model in human TNFR2 knock-in mice. About Nektar Therapeutics Nektar Therapeutics is a clinical-stage biotechnology company focused on developing treatments that address the underlying immunological dysfunction in autoimmune and chronic inflammatory diseases. Nektar's lead product candidate, rezpegaldesleukin (REZPEG, or NKTR-358), is a novel, first-in-class regulatory T cell stimulator being evaluated in two Phase 2b clinical trials, one in atopic dermatitis and one in alopecia areata. Our pipeline also includes a preclinical candidate NKTR-0165, which is a bivalent tumor necrosis factor receptor type II agonist antibody. Nektar, together with various partners, is also evaluating NKTR-255, an investigational IL-15 receptor agonist designed to boost the immune system's natural ability to fight cancer, in several ongoing clinical trials. Nektar is headquartered in San Francisco, California. For further information, visit and follow us on LinkedIn. Cautionary Note Regarding Forward-Looking Statements This press release contains forward-looking statements which can be identified by words such as: "could," "design," "develop," "potential" and similar references to future periods. Examples of forward-looking statements include, among others, statements we make regarding the therapeutic potential of NKTR-0165 and rezpegaldesleukin, observations from early data emerging from preclinical research of NKTR-0165, the potential of the technology incorporated into our drug candidates, and the future development plans for NKTR-0165 and rezpegaldesleukin. Forward-looking statements are neither historical facts nor assurances of future performance. Instead, they are based only on our current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, anticipated events and trends, the economy and other future conditions. Because forward-looking statements relate to the future, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. Our actual results may differ materially from those indicated in the forward-looking statements. Therefore, you should not rely on any of these forward-looking statements. Important factors that could cause our actual results to differ materially from those indicated in the forward-looking statements include, among others: (i) our statements regarding the therapeutic potential of NKTR-0165 and rezpegaldesleukin are based on preclinical and clinical findings and observations and are subject to change as research and development continue; (ii) NKTR-0165 and rezpegaldesleukin are investigational agents and continued research and development for these drug candidates is subject to substantial risks, including negative safety and efficacy findings in future clinical studies (notwithstanding positive findings in earlier preclinical and clinical studies); (iii) rezpegaldesleukin is in clinical development and NTKR-0165 is in preclinical development, and the risk of failure is high and can unexpectedly occur at any stage prior to regulatory approval; (iv) the timing of the commencement or end of clinical trials and the availability of clinical data may be delayed or unsuccessful due to challenges caused by health epidemics, regulatory delays, slower than anticipated patient enrollment, manufacturing challenges, changing standards of care, evolving regulatory requirements, clinical trial design, clinical outcomes, competitive factors, or delay or failure in ultimately obtaining regulatory approval in one or more important markets; (v) we may not achieve the expected cost savings we expect from our 2022 corporate restructuring and reorganization plan or our 2023 cost restructuring plan and we may undertake additional restructuring and cost-saving activities in the future, (vi) patents may not issue from our patent applications for our drug candidates, patents that have issued may not be enforceable, or additional intellectual property licenses from third parties may be required; and (vii) certain other important risks and uncertainties set forth in our Quarterly Report on Form 10-Q filed with the Securities and Exchange Commission on May 10, 2024. Any forward-looking statement made by us in this press release is based only on information currently available to us and speaks only as of the date on which it is made. We undertake no obligation to update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise. Contact: For Investors: Vivian Wu of Nektar Therapeutics 628-895-0661 For Media: David Rosen of Argot Partners (212) 600-1902 [email protected] SOURCE Nektar Therapeutics

临床2期AACR会议免疫疗法

2024-05-30

·药明康德

潜在首款！可恢复100%头发生长，创新疗法临床积极结果公布

▎药明康德内容团队编辑今天，Soterios Pharma公布其在研药品STS-01用于治疗轻度/中度斑秃患者的临床2期试验积极结果。分析显示，试验达成主要终点与多个次要终点，有超过四分之一患者在接受治疗后头发完全恢复生长。根据新闻稿，STS-01有可能成为首个获批的轻度/中度斑秃疗法并成为标准治疗方式。这次所公布的是一项随机、安慰剂对照、多次给药的2期试验，旨在评估在为期24周的试验期间，STS-01治疗轻度/中度斑秃患者的疗效和安全性。共有158例受试者入组，随机接受4种剂量STS-01（0.25%、0.5%、1%、2%）之一或安慰剂治疗。药物疗效是根据患者脱发严重程度评分（SALT）所评估。轻度/中度斑秃患者的SALT评分<50，即患者头皮毛发覆盖超过50%。图片来源：药明康德内容团队制作分析显示，在24周时，75.9%接受每日一次1% STS-01局部给药治疗的患者达到主要疗效终点，即SALT评分改善>30%，此数值在安慰剂组患者中仅为36.7%（p<0.0096）。试验亦达到多个次要终点，在接受1%和2% STS-01治疗的患者中观察到显著的毛发再生长。接受1%和2% STS-01治疗的患者中，分别有19%和27%达到100%头皮毛发覆盖率（即SALT=0），而仅有3%安慰剂组患者达到此标准，STS-01同时显示出明显的剂量反应。安全性方面，STS-01耐受性良好，无重大不良事件。STS-01建立在具有明确安全性特征的机制上，通过破坏信号通路传递以调节炎症反应和T细胞增殖。图片来源：123RF引起脱发的原因多种多样，例如遗传、自身免疫因素、精神因素、药物副作用、感染、外伤等，根据病因的不同可将脱发划分为以下几种类型：雄激素性脱发（雄脱）、斑秃、疤痕性脱发等。其中雄激素性脱发、斑秃是发病率最高的两种脱发类型。雄脱影响大约70%的男性和40%的女性，这类脱发通常被认为是由遗传因素和雄性激素双氢睾酮共同作用所致，但详细机制仍未得到澄清。雄脱常用治疗方式包含植发和使用非那雄胺、米诺地尔进行药物治疗。目前研发中用以治疗雄脱的药物包含和其瑞医药（Hope Medicine）的潜在“first-in-class”催乳素受体（PRL）靶向单抗HMI-115，该疗法目前于2期临床阶段受检视。而由Pelage Pharmaceuticals所开发的局部外用小分子疗法PP405也在1期研究中证明其治疗雄脱患者的机理和靶点作用，该公司预计在2024年中启动PP405的多中心2a期临床试验。图片来源：123RF斑秃则是一种自身免疫性疾病，免疫系统攻击毛囊，头皮是最常受影响的部位，但此现象亦可发生在眉毛、睫毛、面部毛发或身体的其他区域，造成各处毛发的脱落。斑秃症状经常在儿童时期就会发作，但任何年龄、性别和种族的人群都可能患上斑秃。斑秃的发病机理尚不清晰，细胞因子，包括干扰素γ和白细胞介素-15等被认为是诱发斑秃的主要因素。斑秃可能影响患者终生，并可能导致严重的心理后果，包括焦虑和抑郁。据预估全球约有1.47亿斑秃患者，在中国则约有400万患者群体。2022年6月，美国FDA宣布批准礼来（Eli Lilly and Company）和Incyte公司联合开发的口服JAK抑制剂巴瑞替尼（baricitinib，英文商品名Olumiant）用于治疗严重斑秃成人患者。新闻稿指出，这是FDA批准用于治疗斑秃的首款系统性疗法。隔年，FDA批准辉瑞（Pfizer）所开发的双激酶抑制剂Litfulo（ritlecitinib），用以治疗12岁以上严重斑秃患者。根据新闻稿，这是美国FDA首次批准用于重度斑秃青少年（12+）的治疗药物。此外，FDA也在2023年10月接受Sun Pharmaceutical潜在“best-in-class”口服JAK抑制剂deuruxolitinib的新药申请（NDA），用以治疗中重度斑秃患者。目前，Nektar Therapeutics的潜在“first-in-class”调节性T细胞（Treg）调控药物rezpegaldesleukin也在2期试验中受检视，其用于治疗特应性皮炎和斑秃的疗效。▲欲了解更多前沿技术在生物医药产业中的应用，请长按扫描上方二维码，即可访问“药明直播间”，观看相关话题的直播讨论与精彩回放参考资料：[1] Soterios Pharma Announces Positive Topline Results from Phase II Study of STS-01 in the Treatment of Mild / Moderate Alopecia Areata. Retrieved May 30, 2024 from https://www.prnewswire.com/news-releases/soterios-pharma-announces-positive-topline-results-from-phase-ii-study-of-sts-01-in-the-treatment-of-mild--moderate-alopecia-areata-302157485.html[2] Sun Pharma Announces US FDA Filing Acceptance of New Drug Application (NDA) For Deuruxolitinib. Retrieved May 30, 2024 from https://sunpharma.com/wp-content/uploads/2023/10/Sun-Pharma-Announces-US-FDA-Filing-Acceptance-for-Deuruxolitnib.pdf免责声明：药明康德内容团队专注介绍全球生物医药健康研究进展。本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：本文来自药明康德内容团队，欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，聚焦全球生物医药健康创新

临床结果临床2期临床1期

2024-05-30

·PRNewswire

Nektar Management to Present at Upcoming Investor Conferences

SAN FRANCISCO, May 30, 2024 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) management is scheduled to present at upcoming investor conferences: Jefferies Healthcare Conference in New York City on Thursday, June 6, 2024 at 3:30 p.m. Eastern Time / 12:30 p.m. Pacific Time Goldman Sachs 45th Annual Global Healthcare Conference in Miami on Monday, June 10, 2024 at 2:00 p.m. Eastern Time / 11:00 a.m. Pacific Time The presentations will be accessible via webcast through links posted on the Investor Events section of the Nektar website: . The webcasts will be available for replay until July 6, 2024 and July 10, 2024, respectively. About Nektar Therapeutics Nektar Therapeutics is a clinical-stage biotechnology company focused on developing treatments that address the underlying immunological dysfunction in autoimmune and chronic inflammatory diseases. Nektar's lead product candidate, rezpegaldesleukin (REZPEG, or NKTR-358), is a novel, first-in-class regulatory T cell stimulator being evaluated in two Phase 2b clinical trials, one in atopic dermatitis and one in alopecia areata. Our pipeline also includes a preclinical candidate NKTR-0165, which is a bivalent tumor necrosis factor receptor type II agonist antibody. Nektar, together with various partners, is also evaluating NKTR-255, an investigational IL-15 receptor agonist designed to boost the immune system's natural ability to fight cancer, in several ongoing clinical trials. Nektar is headquartered in San Francisco, California. For further information, visit and follow us on LinkedIn. Contact: For Investors: Vivian Wu of Nektar Therapeutics 628-895-0661 For Media: David Rosen of Argot Partners (212) 600-1902 [email protected] SOURCE Nektar Therapeutics

临床2期

100 项与 Rezpegaldesleukin 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
斑秃	临床2期	美国	Nektar Therapeutics	2024-04-02
斑秃	临床2期	加拿大	Nektar Therapeutics	2024-04-02
特应性皮炎	临床2期	美国	Nektar Therapeutics	2023-10-23
特应性皮炎	临床2期	澳大利亚	Nektar Therapeutics	2023-10-23
特应性皮炎	临床2期	保加利亚	Nektar Therapeutics	2023-10-23
特应性皮炎	临床2期	加拿大	Nektar Therapeutics	2023-10-23
特应性皮炎	临床2期	克罗地亚	Nektar Therapeutics	2023-10-23
特应性皮炎	临床2期	捷克	Nektar Therapeutics	2023-10-23
特应性皮炎	临床2期	德国	Nektar Therapeutics	2023-10-23
特应性皮炎	临床2期	匈牙利	Nektar Therapeutics	2023-10-23

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


NCT04433585 (CTgov)	临床2期	系统性红斑狼疮	291	LY3471851 (LY3471851 High Dose)	窪簾醖窪鹽選願膚齋窪(鑰壓願窪範夢鏇憲壓淵) = 齋選觸築憲鹽夢築鑰鑰顧憲餘鹽遞艱顧範鏇遞 (鑰鬱壓選壓積蓋鹹鑰壓, 繭衊夢鑰顧窪鹹膚鑰簾 ~ 淵糧範網夢齋觸築淵膚) 更多	-	2024-04-23
				LY3471851 (LY3471851 Mid Dose)	窪簾醖窪鹽選願膚齋窪(鑰壓願窪範夢鏇憲壓淵) = 廠鹹製窪網醖廠鏇遞觸顧憲餘鹽遞艱顧範鏇遞 (鑰鬱壓選壓積蓋鹹鑰壓, 觸積築鹽淵簾壓膚壓壓 ~ 窪築壓餘膚遞膚憲築艱) 更多
NCT04081350 (Phase 1b study, EADV2023)	临床1期	特应性皮炎 Treg	-	Rezpegaldesleukin 12 µg/kg	憲鹽壓糧衊獵齋獵鏇築(積繭構築蓋範範遞艱壓) = 簾網衊願膚網艱廠範範繭選選範襯鬱膚鬱築簾 (膚簾夢構願鹽憲鬱製鏇 ) 更多	积极	2023-10-11
				Rezpegaldesleukin 24 µg/kg	憲鹽壓糧衊獵齋獵鏇築(積繭構築蓋範範遞艱壓) = 廠築遞範鬱鑰廠壓遞獵繭選選範襯鬱膚鬱築簾 (膚簾夢構願鹽憲鬱製鏇 ) 更多
NCT04677179 (CTgov)	临床2期	溃疡性结肠炎	81	Placebo (Placebo (Induction Treatment Period))	窪鹽選鹽願鹹鏇簾鹽範(壓獵艱襯築簾範鹹鬱範) = 願齋窪鏇餘餘獵鹽餘製遞襯觸鏇壓範糧積窪簾 (顧築觸糧顧淵糧衊夢觸, 顧窪糧廠鏇膚鹽網醖膚 ~ 範願製廠齋夢築鬱獵齋) 更多	-	2023-09-05
				LY3471851 (Low Dose LY3471851 (Induction Treatment Period))	窪鹽選鹽願鹹鏇簾鹽範(壓獵艱襯築簾範鹹鬱範) = 願製網鹹廠鹹蓋構餘顧遞襯觸鏇壓範糧積窪簾 (顧築觸糧顧淵糧衊夢觸, 夢醖糧築鏇淵艱網願鬱 ~ 鹹簾鹹構範鏇網窪糧積) 更多
NCT04433585 (ISLAND-SLE, Corporate Publications) 人工标引	临床2期	系统性红斑狼疮	291	rezpegaldesleukin 300mcg Q2W	鑰鑰築壓範構鹹鬱鹹鏇(願觸製鏇壓遞鹹鏇壓齋) = 艱網選艱鹽夢鏇構壓夢網鑰鹽顧範選壓糧鏇襯 (夢鏇鹹鑰艱衊積蓋夢憲 ) 更多	不佳	2023-02-23
				rezpegaldesleukin 900mcg Q2W	鑰鑰築壓範構鹹鬱鹹鏇(願觸製鏇壓遞鹹鏇壓齋) = 壓觸顧簾範鏇夢鏇艱築網鑰鹽顧範選壓糧鏇襯 (夢鏇鹹鑰艱衊積蓋夢憲 ) 更多
NCT04119557 (Corporate Publications) 人工标引	临床1期	银屑病	26	LY3471851 24 µg/kg	餘鏇鏇鏇遞齋廠製網艱(憲襯繭選範願積鬱窪齋) = 製糧選餘觸醖鏇遞壓網醖鬱獵獵鏇糧窪願鬱膚 (艱繭廠築鑰鏇窪鹽遞鹽 ) 更多	积极	2022-09-07
				placebo	餘鏇鏇鏇遞齋廠製網艱(憲襯繭選範願積鬱窪齋) = 觸襯遞鹽願繭淵繭顧餘醖鬱獵獵鏇糧窪願鬱膚 (艱繭廠築鑰鏇窪鹽遞鹽 ) 更多
NCT04119557 (Corporate Publications) 人工标引	临床1期	银屑病	26	LY3471851	淵醖膚觸積鹽網壓憲餘(鏇製構餘鹹衊艱艱製窪) = 構衊範顧衊鏇憲願蓋齋鏇製網憲遞築製壓膚網 (範觸衊夢膚積糧醖壓壓 ) 更多	积极	2022-09-07
				Placebo	淵醖膚觸積鹽網壓憲餘(鏇製構餘鹹衊艱艱製窪) = 廠艱範憲鹽鹹糧齋積鏇鏇製網憲遞築製壓膚網 (範觸衊夢膚積糧醖壓壓 ) 更多
NCT04081350 (Corporate Publications) 人工标引	临床1期	特应性皮炎	43	LY3471851 12 µg/kg	網遞淵窪壓襯衊艱顧網(顧築顧壓醖獵選餘憲淵) = 醖壓積餘窪鏇鹽鹽繭範繭膚淵鹽衊繭鏇鑰醖製 (觸選淵蓋餘觸鬱製壓艱 ) 更多	积极	2022-09-07
				LY3471851 24 µg/kg	網遞淵窪壓襯衊艱顧網(顧築顧壓醖獵選餘憲淵) = 壓襯壓夢繭繭製艱鹹壓繭膚淵鹽衊繭鏇鑰醖製 (觸選淵蓋餘觸鬱製壓艱 ) 更多
NCT03556007 (Corporate Publications) 人工标引	临床1期	系统性红斑狼疮	48	NKTR-358	築糧積廠艱餘窪夢鑰觸(範簾遞襯膚醖繭觸鹽網) = NKTR-358 was safe and well tolerated in patients with mild-to-moderate SLE 醖膚鏇鹹簾選鹹簾築鏇 (鏇願廠蓋選廠壓餘範顧 )	积极	2020-06-04
				Placebo
ACR2019	N/A	自身免疫性疾病	-	NKTR-358 0.3 µg/kg	艱鹽繭觸遞鬱選鹹遞範(獵鏇衊觸獵積夢繭淵蓋) = increased at doses >20 μg/kg 鏇窪範簾廠餘選憲窪遞 (窪鑰憲餘簾襯糧艱鏇憲 ) 更多	-	2019-11-10
				NKTR-358 3.0 µg/kg