A Randomized, Double-Blind, Placebo-Controlled Phase 3 Study to Evaluate the Efficacy and Safety of Blisibimod Administration in Subjects With Systemic Lupus Erythematosus With or Without Nephritis

The purpose of this study is to evaluate the clinical efficacy of blisibimod as measured by a composite responder index in subjects who, despite corticosteroid use, continue to have seropositive, clinically-active Systemic Lupus Erythematosus (SLE) as defined by SELENA-SLEDAI score ≥10, and positive for anti-double stranded DNA and low complement (C3 or C4).

开始日期2016-06-01

申办/合作机构

Anthera Pharmaceuticals, Inc.

NCT01609452

/ Withdrawn临床2/3期

MONICA-SC: A Randomized, Double-Blind, Placebo-Controlled Phase 2/3 Study to Evaluate the Efficacy, Safety and Tolerability of Blisibimod (A-623) Administration in Subjects With Immune Thrombocytopenic Purpura (ITP)

The purpose of this study is to evaluate efficacy, safety and tolerability of blisibimod when administered on top of standard-of-care to subjects with Immune Thrombocytopenic Purpura (ITP).

开始日期2015-12-01

申办/合作机构

Anthera Pharmaceuticals, Inc.

NCT02074020

/ Withdrawn临床3期

A Randomized, Double-Blind, Placebo-Controlled Phase 3 Study to Evaluate the Efficacy and Safety of Blisibimod Administration in Subjects With Systemic Lupus Erythematosus With or Without Nephritis

The purpose of this study is to evaluate the clinical efficacy of blisibimod as measured by a composite responder index in subjects who, despite corticosteroid use, continue to have autoantibody positive, clinically-active Systemic Lupus Erythematosus (SLE) as defined by SELENA SLEDAI score ≥10.

开始日期2015-12-01

申办/合作机构

Anthera Pharmaceuticals, Inc.

100 项与比利莫德相关的临床结果

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100 项与比利莫德相关的转化医学

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100 项与比利莫德相关的专利（医药）

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项与比利莫德相关的文献（医药）

2023-12-01·Clinical rheumatology

A narrative review of potential drug treatments for nephritis in children with IgA vasculitis (HSP)

Review

作者: Lamond, Megan ; Marro, Julien ; Chetwynd, Andrew J ; Oni, Louise ; Williams, Chloe E C

Abstract:

Immunoglobulin A (IgA) vasculitis (IgAV, also known as Henoch-Schoenlein purpura, HSP) is the most common vasculitis of childhood. It usually presents with a simple, self-limiting disease course; however, a small subset of patients may develop kidney involvement (IgAV-N) which occurs 4–12 weeks after disease onset and is the biggest contributor to long-term morbidity. Treatment currently targets patients with established kidney involvement; however; there is a desire to work towards early prevention of inflammation during the window of opportunity between disease presentation and onset of significant nephritis. There are no clinical trials evaluating drugs which may prevent or halt the progression of nephritis in children with IgAV apart from the early use of corticosteroids which have no benefit. This article summarises the latest scientific evidence and clinical trials that support potential therapeutic targets for IgAV-N that are currently being developed based on the evolving understanding of the pathophysiology of IgAV-N. These span the mucosal immunity, B-cell and T-cell modulation, RAAS inhibition, and regulation of complement pathways, amongst others. Novel drugs that may be considered for use in early nephritis include TRF-budesonide; B-cell inhibiting agents including belimumab, telitacicept, blisibimod, VIS649, and BION-1301; B-cell depleting agents such as rituximab, ofatumumab, and bortezomib; sparsentan; angiotensin converting enzyme inhibitors (ACE-Is); and complement pathway inhibitors including avacopan, iptacopan, and narsoplimab. Further clinical trials, as well as pre-clinical scientific studies, are needed to identify mechanistic pathways as there may be an opportunity to prevent nephritis in this condition.Key Points• Kidney involvement is the main cause of long-term morbidity and mortality in IgA vasculitis despite the current treatment recommendations.• The evolving understanding of the pathophysiology of IgA vasculitis is allowing exploration of novel treatment options which target underlying immune pathways.• Novel treatments currently being trialled in IgA nephropathy may have benefit in IgA vasculitis due to the similarities in the underlying pathophysiology, such as TRF-budesonide, B-cell modulators, and complement inhibitors.• Further studies, including clinical trials of novel drugs, are urgently needed to improve the long-term outcomes for children with IgA vasculitis nephritis.

2023-01-01·Frontiers in pharmacology

Advances in natural products and antibody drugs for SLE: new therapeutic ideas.

Review

作者: Zhao, Xinyue ; Liu, Bin ; Han, Yibing ; Liu, Lingwei ; Liang, Ruiwen ; Zang, Bo

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune systemic disease with a wide range of clinical symptoms, complex development processes, and uncertain prognosis. The clinical treatment of SLE is mainly based on hormones and immunosuppressants. Research on novel therapy strategies for SLE has flourished in recent years, especially the emergence of new targeted drugs and natural products that can modulate related symptoms. This review discusses the current experience including B-cell targeted drugs (belimumab, tabalumab, blisibimod, atacicept, rituximab, ofatumumab, ocrelizumab, obexelimab, and epratuzumab), T-cell targeted drugs (abatacept, dapirolizumab, and inhibitor of syk and CaMKIV), cytokines targeted drugs (anifrolumab and sifalimumab), and natural products (curcumin, oleuropein, punicalagin, sulforaphane, icariin, apigenin, and resveratrol). The aim of this paper is to combine the existing in vitro and in vivo models and clinical research results to summarize the efficacy and mechanism of natural drugs and targeted drugs in SLE for the reference and consideration of researchers.

2021-07-01·Annals of the rheumatic diseases

Correspondence to ‘Time to change the primary outcome of lupus trials’

Letter

作者: Oon, Shereen ; Nikpour, Mandana ; Huq, Molla

We note with interest and express our principle agreement with the views put forward by Professor Frederic Houssiau in the recent Editorial ‘Time to change the primary outcome of lupus trials’ published in Annals of the Rheumatic Diseases .1 Professor Houssiau advocated using steroid reduction as a primary outcome measure in systemic lupus erythematosus (SLE) clinical trials, or as a minimum, incorporating a steroid reduction target into the primary endpoint. This proposal was prompted by the observation that, like many other recent phase 3 clinical trials conducted with drugs that have a sound biological mechanism for benefit in SLE, the recently published CHABLIS-SC phase 3 clinical trial of subcutaneous blisibimod in SLE2 failed to meet its primary endpoint of a week 52-SLE Responder Index (SRI)-6. However, a significant steroid sparing effect was seen, with a modified endpoint of a week 52-SRI-6 combined with a reduction in steroid dose during weeks 40–52 compared with study entry, showing a trend to benefit for the blisibimod …

项与比利莫德相关的新闻（医药）

2023-11-01

·CPHI制药在线

靶向B细胞治疗系统性红斑狼疮的研究进展

关注并星标CPHI制药在线系统性红斑狼疮 ( SLE) 是一种慢性全身性自身免疫性疾病。B细胞过度活化导致免疫失衡是SLE发病的直接原因。靶向B细胞治疗可抑制B细胞的活化、增殖，减少自身抗体的产生，因此B细胞在近些年成为了SLE治疗的新型靶点。目前临床针对B细胞特异性治疗 SLE的靶点主要包括B细胞表面抗原、B 细胞相关细胞因子和其辅助分子等，而细胞内小分子靶向药物也极具临床潜力。 1、抗CD19靶向治疗 CD19是B细胞表面的一种跨膜糖蛋白，其广泛存在于前 B 细胞到浆细胞的整个发育过程，可影响B细胞的活化、信号传导及生长，并参与B细胞内Ca2+的转运，故被普遍用作白血病、淋巴瘤及免疫系统相关疾病的诊断和预后评估，亦可作为免疫治疗的重要靶点。FcγR Ⅱ b是B 细胞表面的低亲和力IgG受体，是一种可逆的B细胞抑制剂。Obexelimab ( XmAb5871) 是一种双特异性抗体，对B细胞表面CD19 和Fc受体FcγRⅡB 两种不同的靶分子都具有结合特异性。通过靶向 CD19可以抑制B细胞的活化和增殖，清除分泌自身抗体的浆细胞。在 FcγRⅡB 的协同作用下还可以抑制抗原提呈细胞 (APC) 功能、T细胞活化以及Toll 样受体9 (TLR9) 介导的信号传导。抗CD19嵌合抗原受体T细胞 (抗 CD19CAR-T) 疗法是通过基因转染技术使T淋巴细胞表达抗 CD19 的嵌合型抗原受体 ( chimeric antigen receptor，CAR)，来识别并攻击 CD19+B 细胞。 2、抗CD20靶向治疗 CD20是成熟B细胞表面的一种糖基磷酸化蛋白，其表达限于前B细胞到记忆性B细胞，不影响长寿命浆细胞。由于浆细胞维持抗体产生，给予CD20 抑制剂可几乎耗尽外B细胞，但免疫球蛋白水平没有显著降低。 ①利妥昔单抗（rituximab，RTX）是一种选择性靶向CD20的人鼠嵌合型单克隆抗体，具有人IgG1结构域和鼠类CD20 可变区，已成为表达 CD20 的 B 细胞淋巴瘤和类风湿性关节炎标准疗法中的一种药物。RTX 治疗SLE的机制是通过抗体依赖的细胞介导的细胞毒性作用和补体介导的细胞毒性作用来诱导细胞凋亡，通过持续消耗 B 细胞来削弱自身免疫对机体的损伤。虽然在两项SLE大型随机对照试验 ( EXPLORER) 和 ( LUNAR) 中利妥昔单抗均未能达到主要终点，但大量治疗SLE的开放性研究报告了其良好的疗效。2019年EULAR指南推荐，在严重肾脏、血液系统、神经系统受累的重症患者和难治性SLE中建议应用利妥昔单抗。它的一个主要问题是人抗嵌合抗体( HACA)的产生，会使药物疗效降低并导致后续治疗失效。 ②奥瑞珠单抗（ocrelizumab，OCZ）是新一代Fc段修饰的人源化抗CD20单克隆抗体，与RTX 相比，在SLE 患者中具有更高的ADCC活性和更低的CDC效应，而且不产生HACA。但在几项 SLE 的临床研究中因严重不良事件而提前终止，但初步结果表明 OCZ 可能对 LN有一定疗效，目前 OCZ 在 SLE 方面的应用还需要大量的临床研究来验证。 ③奥比妥珠单抗（obinutuzumab，OBZ）是最新一代具有糖修饰Fc的完全人源化的Ⅱ型抗 CD20 单克隆抗体，其与Ⅰ型抗 CD20 抗体相比，免疫原性更低，对效应细胞上的 FcγR Ⅲ具有更高的亲和力，故其具有更强的 ADCC 和更好的直接 B 细胞杀伤能力。研究证实，OBZ在类风湿性关节炎和 SLE 体外全血试验中诱导B细胞毒性的效率至少是RTX 的2 倍。目前一项有关 OBZ 用于治疗增殖性 LN的临床试验结果表明 OBZ 有助于改善增殖性 LN 患者的临床反应。 ④奥法木单抗（ofatumumab）是完全人源化 Ⅰ型IgG1 抗CD20 单克隆抗体，已被批准用于治疗慢性淋巴细胞白血病、自身免疫性溶血性贫血和免疫介导的血小板减少症。部分病例报道说明其在不耐受 RTX的 SLE 患者中可取得较好的疗效。 3、抗CD22靶向治疗 CD22膜受体是一种B细胞限制性黏附分子，其可与B细胞抗原受体形成复合物，并作为抑制性辅助受体发挥作用。依帕珠单抗（epratuzumab）是一种抗人CD22 IgG1抗体，可使B 细胞亚群的激活和分化受到抑制，但B 细胞数量不会显著减少。故与RTX 相比，其感染风险的概率相对降低。一项长期安全性和有效性的扩展研究显示Epratuzumab 对SLE 治疗耐受性良好，可持续改善疾病活动度，并降低激素剂量。然而，另两项Ⅲ期临床研究中Epratuzumab对中至重度 SLE 患者的治疗与安慰剂比较无显著差异，但对B细胞有特异的免疫调节作用。因此，Epratuzumab 可能在SLE 患者中具有可接受的安全性，但是仍需大样本量和长随访时间的随机对照试验来验证其疗效。 4、靶向B淋巴细胞刺激因子及增殖诱导配体相关生物制剂 BAFF也被称为B淋巴细胞刺激因子 ( BLyS)，属于肿瘤坏死因子家族，可以调节外周血B 细胞稳态。它与B细胞上的BAFF 受体、跨膜激活剂和亲环素配体相互作用物 (TACI)、B 细胞成熟抗原( BCMA) 结合，在促进B细胞存活、分化和自身免疫中发挥关键作用。特别是在SLE中，研究发现血清 BAFF 水平与SLE 疾病活动呈正相关。 ①贝利尤单抗（belimumab）于2011年3月获得美国食品和药物管理局（Food and Drug Administration，FDA）和欧洲药品监管局（European Medicines Agency，EMA）的正式批准，用于治疗接受标准疗法的自身抗体阳性的活动性成人 SLE 患者，这是50多年来被 FDA批准用于治疗SLE 的第一个生物制剂。belimumab是针对 BAFF 的重组人 IgG1-λ 单克隆抗体，其治疗SLE主要是通过影响 BAFF 与受体结合，使B细胞成熟和存活受到抑制，减少浆细胞的数目，最终减少自身抗体的产生。目前，关于belimumab治疗 SLE的5项大型Ⅲ期临床研究已经证实了其耐受性和安全性。 ②阿他西普（atacicept）是完全人源重组融合蛋白，可结合并中和 BAFF和APRIL。它的独特四价 "蛋白体"结构，对 BAFF 亲和力更高。在一项活动性 SLE 患者的Ⅲ期随机对照研究中，Blisibimod 在减少激素用量方面与对照组差异有统计学意义，且成功地降低了蛋白尿和自身抗体水平，耐受性良好，虽然未能达到主要终点，但仍显示出了临床疗效。 ③泰它西普（telitacicept）是一种新型重组融合蛋白，可中和BAFF和APRIL的活性，从而抑制浆细胞和成熟B细胞的发育和存活。2020年4月，FDA 授予telitacicept 用于治疗SLE。2021年3月，中国国家药品监督管理局批准 telitacicept 用于活动性自身抗体阳性 SLE 成人患者的治疗。 ④比利莫德（blisibimod）是一种抑制 BlyS 的新型IgG1单克隆抗体，具有肽和抗体的特征，其对BAFF的亲和力更高。一项在中度至重度 SLE 中使用 blisibimod的Ⅱ期临床试验在第 24周时虽未达到其主要终点，但接受最高剂量 blisibimod（每周200 mg）的患者在第20周时的SLE 应答者指数（SLE responder index，SRI）-5 反应率差异有统计学意义。一项评价 blisibimod 治疗合并有 LN 的 SLE 患者的有效性和安全性的Ⅲ期临床试验结果虽然未达到 SRI-6终点，但是使用 blisibimod 成功减少了GU 用量、蛋白尿的产生和生物标志物反应，且耐受性良好。 5、针对Ⅰ型干扰素（IFN-Ⅰ） IFN- Ⅰ被认为是SLE 发病机制中的关键干扰素，但不同类别的IFN- Ⅰ可能在SLE的调节中具有不同功能。其中IFN-α 由B细胞和浆细胞样树突状细胞产生，其可刺激 B 细胞分化并通过产生 BAFF 来促进自身抗体的产生。故阻断IFN-α 信号传导通路可间接调节B细胞，减少自身抗体生成。anifrolumab 是一种完全人源化单克隆抗体，其以高特异性和高亲和力与 IFN- Ⅰ受体亚基1结合，阻断IFN-α和IFN-β信号。Anifrolumab 是一种完全人源化的IgG1K单克隆抗体，能结合IFNAR，通过阻断IFN-Ⅰ自扩增环，抑制促炎细胞因子，有效抑制 IFN-Ⅰ依赖的信号传导，从而抑制浆细胞分化。在一项中至重度 SLE 的Ⅱ期随机对照研究中，Anifrolumab 可有效减少口服激素用量，并达到主要终点。在一项多国、多中心的Ⅲ期双盲随机对照研究中，SLE 患者根据疾病活动度、IFN 刺激基因(ISG) 表达水平和口服激素用量进行分层，Anifrolumab 与安慰剂对比有显著疗效，并可持续减少激素用量，ISG 高表达的患者对 Anifrolumab 治疗反应更佳。 6、靶向CD40 配体 (CD40L) T细胞表面的CD40L与B细胞上的CD40相互作用，对B细胞的生长、分化、激活至关重要。CD40L 广泛表达于初始和激活的CD4+ T 细胞和血小板上。靶向 CD40L会影响B细胞功能。两种针对CD40L 的单克隆抗体 Ruplizumab 和 Toralizumab在 SLE 研究中均因血栓事件被终止。一种聚乙二醇化的抗 CD40LFab 片段 Dapirolizumab pegol，因其没有 Fc 片段，不能结合血小板受体，从而减少了血小板聚集的风险。在针对 SLE 患者的Ⅰ期试验中，未发现血栓栓塞事件，且报告了良好的疗效。Dapirolizumab 对中至重度 SLE 患者的疗效和安全性的Ⅱ期临床试验正在进行中，其治疗SLE 的潜力有待进一步明确。 7、靶向B细胞内的分子靶点最近，SLE 的治疗已经进入了一个新的阶段，即靶向致病B细胞内的分子。布鲁顿酪氨酸激酶( Bruton's tyrosine kinase，BTK) 是B细胞信号通路中的重要组成，在SLE中起多种致病作用，包括促进B细胞分化和产生自身抗体。在一些狼疮模型中，BTK 的小分子抑制剂可以有效降低自身抗体水平并减轻肾脏损伤。因此，BTK 抑制剂是一种很有前途的 SLE 治疗药物。Evobrutinib是一种新型高选择性的 BTK 抑制剂，在SLE小鼠模型中，口服 Evobrutinib 可以减轻疾病的严重程度和组织学损伤，有效改善肾脏、皮肤和神经系统症状。目前，一项评估该药治疗 SLE 的有效性及安全性的Ⅱ期临床试验正在进行中。相关阅读：《贝利尤单抗治疗系统性红斑狼疮的研究进展》参考资料 [1]张英杰,王春芳.靶向B细胞的生物制剂治疗系统性红斑狼疮的研究进展[J].中国医药科学,2022,12(19):42-46. [2]李赫,尹晶,李崇巍.靶向B细胞治疗系统性红斑狼疮的研究进展[J].沈阳医学院学报,2021,23(05):482-485. 作者简介：小泥沙，食品科技工作者，食品科学硕士，现就职于国内某大型药物研发公司，从事营养食品的开发与研究。来源：CPHI制药在线声明：本文仅代表作者观点，并不代表制药在线立场。本网站内容仅出于传递更多信息之目的。如需转载，请务必注明文章来源和作者。投稿邮箱：Kelly.Xiao@imsinoexpo.com▼更多制药资讯，请关注CPHI制药在线▼点击阅读原文，进入智药研习社~

细胞疗法免疫疗法

2016-12-28

·BioSpace

Anthera Pharma Plunges After Cystic Fibrosis Drug Fails Late-Stage Trial

December 28, 2016 By Mark Terry , BioSpace.com Breaking News Staff Hayward, Calif. – Anthera Pharmaceuticals announced that its Sollpura to treat cystic fibrosis patients with exocrine pancreatic insufficiency (EPI) failed to meet its primary endpoint in a Phase III study. The company emphasized that it only narrowly missed the primary endpoint, which was non-inferiority for change in the Coefficient of Fat Absorption (CFA). And that the drug did meet the non-inferiority criterion. It also confirmed that the ratio of the three enzymes in the drug showed an appropriate response in the coefficient of nitrogen absorption (CNA). Anthera indicated that during its analysis, the patients were unable to increase their doses because of time restrictions and the protocol design. In addition, other patients couldn’t increase their dose to the daily limit for porcine pancreatic enzyme replacement therapies (PERTs). As a result, and because of faith in the analyzed Sollpura activity data, the company will launch an additional trial of the drug that it believes will optimize dosing and dose titration. It’s expected to start in the first quarter of 2017 and will result in “only a modest delay in the filing of the BLA” around the first quarter of 2018. Anthera took a dive at the news. Shares traded for $1.99 on December 27 and are currently trading for $0.72. The company faced another setback in November when it announced the CHABLIS-SC1 clinical trial with blisibimod to treat systemic lupus erythematosus (SLE) didn’t meet its primary endpoint. And shortly afterwards, the company shook up its leadership team. J. Crag Thompson stepped in as chief executive officer, replacing Paul Truex . Truex took over as chairman of the board, replacing Christopher Henney , who is remaining on the company’s board of directors. The company at the time indicated that Thompson’s promotion was in preparation for the commercial launch of Sollpura and the continued development of blisibimod for IgA nephropathy. Of Sollpura, John Carroll , writing for Endpoints News, said, “This is a drug with multiple failures to contend with. Eli Lilly tried the pancreatic enzyme replacement therapy liprotomase in a Phase III and failed in 2011. Anthera acquired the drug in 2014. It is designed to treat low digestive enzyme levels, or Exocrine Pancreatic Insufficiency, caused by CF.” Investors weren’t terribly happy in November when blisibimod failed its clinical trial, and the recent plunge indicated they’re even less happy about the results of the Sollpura trial. And in quoting from an optimistic investors’ note by Jefferies ’ Matthew Andrews written several weeks ago, Carroll speculates on whether the backlash will be even worse. Andrews wrote, “We believe the Phase III study has a high likelihood of success based on its non-inferiority design, a well-controlled patient population enrolled in the study (potential for less variability in efficacy), improved formulation (higher lipase dose), and weight-based dosing (vs. fixed dosing in the prior Lilly-sponsored Phase III study). The study has successfully passed two safety reviews by the data monitoring board.” It’s possible, of course, that the additional trial will solve the problem, although if it doesn’t, the company is going to have some explaining to do. “Although we are disappointed to narrowly miss the primary endpoint, we remain encouraged by the overall SOLUTION study results and look forward to releasing final data from its 12-week extension phase in the future, the SIMPLICITY study and the continuation of the open-label EASY study,” said William Shanahan , Anthera’s chief medical officer, in a statement. “We would like to thank the patients, investigators and study staff for their hard work and dedication to our study. We are most grateful for their commitment to our shared hope of developing new treatments for exocrine pancreatic insufficiency, and believe that the shortcomings of Sollpura in SOLUTION can be addressed in the new study that we plan to initiate in 1Q’17.”

临床3期高管变更临床2期

2016-12-07

·BioSpace

Bay Area’s Anthera Names a New CEO in Shakeup

December 7, 2016 By Alex Keown , BioSpace.com Breaking News Staff HAYWARD, Calif. – Shares of Anthera Pharmaceuticals are up more than 48 percent this morning after the company announced changes in leadership as it moves closer to commercializing its cystic fibrosis drug, Sollpura. On Tuesday, the Bay Area-based company announced it promoted announced J. Craig Thompson to Chief Executive Officer. He takes over for Paul Truex , who will now assume the responsibilities of the Chairman of the Board and continue to provide guidance to Anthera’s senior executive team. After 10 years as chairman, Christopher Henney is stepping down from that role, but will remain on the company’s board of directors. In a statement Tuesday, Truex said Thompson’s promotion will prepare the company for the commercialization of Sollpura and the continued development of blisibimod for IgA nephropathy. Thompson joined the company at the beginning of 2016. Truex said over the course of the year Thompson “has proven his ability to lead and to fully integrate his experiences into the operation of Anthera.” Prior to Anthera, Thompson served as chief operating officer for Tetraphase Pharmaceuticals where he oversaw the development and implementation of the marketing, sales strategy, business development and the commercial manufacturing for Tetraphase. Before Tetraphase, Thompson served as chief commercial officer for Trius Therapeutics until the company was acquired by Cubist Pharmaceuticals, Inc. in September 2013. Thompson said he looks forward to executing the company’s strategy to “commercialize Sollpura while further exploring opportunities for blisibimod.” “This is an exciting time for Anthera with new data emerging on both Sollpura and blisibimod, which could transform the company’s future,” Thompson said in a statement. Sollpura is an enzyme replacement therapy being developed for cystic fibrosis patients who suffer from exocrine pancreatic insufficiency. The drug is designed for patients who are either unable to swallow multiple pills or are forced to use gastric tubes in order to maintain appropriate nutritional health, according to the company’s website. The company expects to announce Phase III results before the end of the year, or in early 2017. Anthera is preparing to begin a Phase III clinical trial for Sollpura in toddlers. In a separate announcement on Tuesday, Anthera also reported positive trends from its Phase II proof-of-concept study blisibimod for IgA nephropathy. Blisibimod is a selective peptibody antagonist of the B-cell activating factor (BAFF) cytokine. In its announcement, Anthera said patients taking the drug through 48 weeks demonstrated “stable to slightly decreasing levels of estimated 24 hour urinary protein excretion… as compared to slowly increasing levels of proteinuria in the placebo group.” No safety or tolerability concerns were observed with blisibimod during routine reviews, the company added. Development of blisibimod suffered a small setback earlier this year when Anthera’s Japanese development partner, Zenyaku , ended a two-year-old collaboration agreement. Shares of Anthera are trading at $2.17 as of 10:50 a.m. The stock closed at $1.47 on Tuesday, Dec. 6.

临床2期高管变更临床结果临床3期并购

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KEGG	Wiki	ATC	Drug Bank
D10311	比利莫德	-	DB12330

研发状态

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适应症	最高研发状态	国家/地区	公司	日期
肾炎	临床3期	格鲁吉亚	Anthera Pharmaceuticals, Inc.	2016-06-01
免疫性血小板减少症	临床3期	-	Anthera Pharmaceuticals, Inc.	2015-12-01
免疫球蛋白a肾病	临床3期	美国	Anthera Pharmaceuticals, Inc.	2013-06-01
免疫球蛋白a肾病	临床3期	德国	Anthera Pharmaceuticals, Inc.	2013-06-01
免疫球蛋白a肾病	临床3期	英国	Anthera Pharmaceuticals, Inc.	2013-06-01
系统性红斑狼疮	临床3期	美国	Anthera Pharmaceuticals, Inc.	2013-02-01
系统性红斑狼疮	临床3期	白俄罗斯	Anthera Pharmaceuticals, Inc.	2013-02-01
系统性红斑狼疮	临床3期	巴西	Anthera Pharmaceuticals, Inc.	2013-02-01
系统性红斑狼疮	临床3期	哥伦比亚	Anthera Pharmaceuticals, Inc.	2013-02-01
系统性红斑狼疮	临床3期	格鲁吉亚	Anthera Pharmaceuticals, Inc.	2013-02-01

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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


NCT01395745 (CHABLIS-SC1, Pubmed) 人工标引	临床3期	系统性红斑狼疮	442	blisibimod	鑰製艱齋憲廠鬱壓襯遞(鹽繭襯遞糧淵鏇網艱遞) = The SRI-6 primary end point was not met 範衊顧願顧繭淵獵觸廠 (繭衊範築窪願顧願鬱蓋 ) 更多	不佳	2018-06-01
				Placebo
NCT01395745 (CHABLIS-SC1, EULAR2017)	临床3期	系统性红斑狼疮 anti-nuclear antibodies \| anti-dsDNA \| complement C3	442	Blisibimod 200 mg	網醖顧襯簾壓顧廠顧餘(顧鹹鹹獵繭鬱網範糧鑰) = 選襯襯齋繭襯窪網製艱繭夢廠餘齋餘鏇簾醖繭 (醖積網觸衊糧糧繭餘範 ) 更多	不佳	2017-06-14
				Placebo	網醖顧襯簾壓顧廠顧餘(顧鹹鹹獵繭鬱網範糧鑰) = 壓膚餘範鹹築襯繭餘鹹繭夢廠餘齋餘鏇簾醖繭 (醖積網觸衊糧糧繭餘範 ) 更多
NCT01395745 (CHABLIS-SC1, EULAR2016)	临床3期	系统性红斑狼疮 anti-double-stranded DNA (dsDNA) \| low complement C3 or C4	442	Blisibimod	憲淵願壓淵鏇鹹網糧壓(製艱糧糧繭鬱網窪醖獵) = 繭願鹽窪鬱淵積憲憲顧範遞膚餘夢鬱壓簾襯鹹 (觸簾壓夢廠製範窪襯遞 ) 更多	积极	2016-06-08
NCT02411136 \| NCT02443506 (Pubmed \| Arthritis Res Ther)	临床1期	系统性红斑狼疮 BAFF	-	Blisibimod	鹹鹹壓鏇繭築蓋窪繭鹽(獵襯鬱簾鏇遞繭憲選觸) = With time, memory B cells reverted to baseline, leading to a calculated 30 % reduction in total B cells by approximately 160 days after the first dose 顧淵襯遞襯顧繭膚鹽襯 (製淵遞願膚獵鏇鹽醖範 )	-	2015-12-01
NCT01162681 (PEARL-SC, Pubmed \| Arthritis Rheumatol \| Ann Rheum Dis) 人工标引	临床2期	系统性红斑狼疮	547	blisibimod	膚襯鬱觸構積製選膚糧(餘鑰製夢築範襯蓋壓鹽) = SRI-5 response rates were not significantly improved in the pooled blisibimod groups 蓋窪廠願糧築淵夢顧築 (獵鏇鑰夢鏇襯選艱築網 )	积极	2015-09-01
				Placebo
NCT01162681 (PEARL-SC, EULAR2015)	临床2期	系统性红斑狼疮 anti-double-stranded DNA \| anti-nuclear antibodies	547	Blisibimod 200 mg QW	範範繭選觸齋蓋糧膚顧(蓋齋夢淵築鬱觸鑰鹽襯) = 顧鬱衊鬱願淵膚鏇選遞獵網鹹積憲夢餘選醖窪 (餘膚醖窪鏇憲壓醖築願 ) 更多	积极	2015-06-10
				Placebo	範範繭選觸齋蓋糧膚顧(蓋齋夢淵築鬱觸鑰鹽襯) = 齋憲遞夢夢鹹繭蓋醖積獵網鹹積憲夢餘選醖窪 (餘膚醖窪鏇憲壓醖築願 ) 更多
PEARL-SC and OLE (EULAR2014)	临床2期	系统性红斑狼疮 proteinuria \| renal biomarkers \| inflammation biomarkers ... 更多	547	Blisibimod 200 mg monthly SC	糧築餘醖衊鹹壓鹽衊遞(鏇簾獵齋淵築廠醖觸蓋) = Blisibimod was safe and well-tolerated at all dose levels with no meaningful imbalances in serious adverse events or infections between blisibimod and placebo in the PEARL-SC study, and continued to be well-tolerated through the OLE study. 願襯衊網獵鑰鹹積廠鏇 (窪範選壓糧選蓋鬱範顧 ) 更多	-	2014-06-11
				Blisibimod 100 mg weekly SC
NCT01162681 (PEARL-SC, ACR2013)	临床2期	系统性红斑狼疮 anti-double-stranded DNA \| anti-nuclear antibodies	547	Blisibimod 100 mg QW	艱鹹窪鏇構繭範糧製積(衊繭艱窪淵願廠餘衊鏇) = During the placebo-controlled study, critically low IgG levels (<4g/L) were observed in 1/280 subjects in blisibimod group compared with 0/266 subjects on placebo 鑰窪憲願範衊齋觸構鏇 (繭鏇膚醖選選築鹽顧憲 ) 更多	积极	2013-10-25
				Blisibimod 200 mg QW
ACR2013	N/A	系统性红斑狼疮	-	Blisibimod	餘範獵艱網築範醖鹽願(壓襯範積襯積糧膚顧遞) = no meaningful imbalances in serious adverse events or infections between blisibimod and placebo in the PEARL-SC study, and continued to be well-tolerated through the OLE study 願艱獵鏇廠醖鏇顧壓網 (鏇範鑰齋夢艱淵膚繭齋 ) 更多	-	2013-10-25
				Placebo
EULAR2013	临床2期	系统性红斑狼疮 proteinuria \| inflammation \| anti-dsDNA antibodies ... 更多	547	Blisibimod	衊夢築積淵鹽構願遞艱(醖襯獵顧網餘壓觸獵艱) = 鏇範鬱夢膚廠夢襯遞鹽齋衊觸壓醖醖觸糧鑰齋 (衊製鬱衊襯衊醖廠築積, -35.0%)	积极	2013-06-12
				Placebo	衊夢築積淵鹽構願遞艱(醖襯獵顧網餘壓觸獵艱) = 淵製鬱選顧願觸醖廠獵齋衊觸壓醖醖觸糧鑰齋 (衊製鬱衊襯衊醖廠築積, -5.1%)