Type 1 diabetes is caused by an autoimmune process resulting in a selective destruction of the pancreatic insulin-secreting beta-cell. DiaPep277® is a small, lyophilized powder containing 24 Amino-acids. We have proved in former studies that DiaPep277® can slow down beta cells destruction in the pancreas and therefore decelerate the progress of Diabetes.
The objective of the study is to assess the efficacy and safety of administrating DiaPep277® in type 1 diabetes patients.

开始日期2015-01-01

申办/合作机构

Hadassah University Hospital

NCT01898286

/ Terminated临床3期

Open-Label Study to Evaluate Long Term Safety and Treatment Effect of DiaPep277® in Subjects Who Have Completed Study 1001 (NCT01103284)

This is an extension study to evaluate the safety and tolerability of long-term treatment with DiaPep277® and to determine the long-term treatment effect of DiaPep277® on parameters of metabolic control and on preservation of beta-cell function in subjects who have long exposure to DiaPep277®.

开始日期2013-10-01

申办/合作机构

Andromeda Biotech Ltd.

NCT01460251

/ Terminated临床3期IIT

OPen Label Study to Evaluate Long Term Treatment Effect of DiaPep277 in Patients Who Have Completed Study 901 and Study 910 (Extension to 901 Phase III Study

The study is an open-label extension study, offering patients who participated and completed previous studies 901 and 910 (an extension to 901) to continue treatment with DiaPep277 and clinical follow-up, for up to 3 additional years.The aim of the study is to collect safety and efficacy data of long term treatment effect of Diapep277.Only patients who completed studies 901 or 910 and still have stimulated C-peptide level equal to or above 0.2 nmol/L will be eligible for this extension study

开始日期2012-01-01

申办/合作机构

Rabin Medical Center

100 项与 DiaPep-277 相关的临床结果

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100 项与 DiaPep-277 相关的转化医学

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100 项与 DiaPep-277 相关的专利（医药）

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项与 DiaPep-277 相关的文献（医药）

2016-12-01·Endocrine3区 · 医学

Antigen-based immunotherapies do not prevent progression of recent-onset autoimmune diabetes: a systematic review and meta-analysis

3区 · 医学

Review

作者: Rika, Maria ; Rizava, Chrysoula ; Galli-Tsinopoulou, Asimina ; Haidich, Anna Bettina ; Sarigianni, Maria ; Liakos, Aris ; Tsapas, Apostolos ; Bekiari, Eleni

We performed a systematic review and meta-analysis to assess the efficacy and safety of antigen-based immunotherapies in tertiary prevention of autoimmune diabetes. We searched for randomised controlled trials testing antigen-based immunotherapies in patients with recent-onset type 1 diabetes or latent autoimmune diabetes of adults in MEDLINE, COCHRANE and EMBASE databases, trial registries, conference proceedings and reference lists of pertinent records. Primary outcomes were fasting and stimulated C-peptide (after glucagon or mixed meal stimulation). Change in glycosylated haemoglobin (HbA_1c), daily insulin needs and incidence of any or severe hypoglycaemic events or severe adverse events were secondary outcomes. Fifteen studies were included in the meta-analysis. Overall, there was no difference in fasting [weighted mean difference (WMD) 0.01 nmol/L; 95 % confidence interval (CI) -0.09, 0.11; I ² = 73 %] or mixed meal stimulated C-peptide (WMD 0.02 nmol/L/min; 95 % CI -0.08, 0.12; I ² = 50 %) compared with placebo. Glucagon stimulated C-peptide was maintained higher (WMD 0.13 nmol/L/min; 95 % CI 0.05, 0.21; I ² = 0 %) in patients treated with Diapep277. Moreover, there was no change in daily insulin needs (WMD 0.02 IU/kg; 95 % CI -0.04, 0.09; I ² = 51 %) or HbA_1c (WMD -0.06 %; 95 % CI -0.35, 0.23; I ² = 42 %) vs. placebo. Finally, there was no effect on the incidence of severe hypoglycaemic events or overall serious adverse events [risk ratio 0.94, 95 % CI 0.62, 1.41; I ² = 0 % and 0.87; 95 % CI 0.53, 1.44; I ² = 0 %, respectively). Antigen-based immunotherapies are not effective in preventing the progression of autoimmune diabetes in newly diagnosed patients.

2015-10-20·Oncotarget

HSP60 - a double edge sword in autoimmunity

作者: Landstein, Dorit ; Ulmansky, Rina ; Naparstek, Yaakov

Human autoimmune inflammatory diseases are usually characterized by a chronic course. Antigen-induced experimental animal models for these diseases, on the other hand, typically present an acute or sub-acute course and after spontaneous recovery the animal may become resistant to reinduction of the disease. One explanation for this course of events may be that the antigen that induces the disease has a dual effect; on one hand it may serve as the target for the pathogenic immune attack whereas on the other it may lead to the development of protective immune mechanisms. Deficiency in these protective immune pathways may lead to the development of chronic autoimmune diseases. In the editorial below we will address this phenomenon by describing an example of one such antigen, HSP60 that has been shown to have a dual role in immune-mediated disorders, being involved in the induction and propagation of autoimmune diseases as well as in suppressing them [1]. HSP60 is a highly conserved protein, which was initially characterized as a mitochondrial chaperone. Upon exposure to stress or immune activation, HSP60 is also found in the cytosol, cell surface, extracellular space and biological fluids. HSP60 activates innate and adaptive immune responses, and can function as an endogenous danger signal to the immune system. It binds to cell surface receptors, including CD14 and members of the TLR family [reviewed by 1]. Overexpression of HSP60 has been described in tissues of various inflammatory diseases suggesting a possible pathogenic role of this antigen in their pathogenesis. Increased expression of human HSP60 is observed in intestinal ulcer of Behcet's Disease (BD) [2], in inflamed bowel of Crohn's disease patients, in muscle tissue of juvenile dermatomyositis (JDM) patients, and in synovial fluid and synovial tissue of juvenile idiopathic arthritis (JIA) and Rheumatoid arthritis (RA) patients [3]. HSP60 is also overexpressed in inflamed lesions of atopic dermatitis where it is co-localized with CD3 positive cells [4]. Peripheral mononuclear cells (PBMCs) taken from patients with various inflammatory diseases can be activated by HSP60. For instance, HSP60 induces IFNγ secretion from atopic dermatitis patients' PBMCs [4] and PBMCs of patients with BD, stimulated with various epitopes of HSP60, resulted in excess amounts of Th1 cytokine production [2]. Several supporting evidence for the pathogenicity of HSP60 have also been reported in experimental animal models of inflammatory diseases. HSP60 is upregulated in animal model of glomerulonephritis (NTN) as shown by increased HSP60 secretion in the urine and into the extracellular space of the diseased kidney. In addition, administration of HSP60 aggravates the disease in the NTN model and in experimental autoimmune uveitis in mice [5, 6]. Contrary to its role as a target for pathogenic autoimmune inflammatory processes, HSP60 has been shown to activate immunoregulatory pathways that may lead to suppression of these diseases. The finding that immunization with whole MT HSP60 prior to induction of adjuvant arthritis (AA) leads to protection against the disease attributed many experiments aimed at revealing the mechanism of this phenomenon, using mammalian and MT whole protein or synthetic peptides of the proteins. HSP60 based treatment ameliorated or suppressed several animal models of inflammatory diseases such as AA, collagen induced arthritis, insulin-dependent diabetes mellitus and atherosclerosis. Preventive as well as therapeutic HSP60 peptide treatment included various regimens, modes of administration and adjuvants and resulted in suppression of inflammatory cytokines, elevation of Th2 cytokines, and induction of regulatory T cells (CD4+CD25+Foxp3+) [3]. Interestingly, the presence of antibodies against peptide 6, a specific peptide derived from MT-HSP60, generated resistance to the induction of AA. We have recently shown that Prozumab, a humanized mAb targeting HSP60, is effective in ameliorating animal models of autoimmune inflammatory diseases such as RA and IBD. In vitro studies performed on human PBMCs were also indicative of an anti-inflammatory effect of Prozumab: Treatment of naive PBMCs resulted in suppression of anti CD3-induced INFγ and IL-6 secretion [7]. Immune reactivity against HSP60 has been found to have a disease suppressing effect in human autoimmune inflammatory diseases as well. The presence of self-HSP60-specific T cell responses in JIA patients correlates with a benign disease course. Self-HSP-specific T cell responses have also been reported to be immunoregulatory in various other autoimmune diseases, such as RA and JDM, by the production of anti-inflammatory cytokines such as interleukin (IL)-10, IL-4 and TGF-β [3]. A phase 2 clinical trial testing the effect of Diapep277 (a human HSP60 derived peptide) in type 1 diabetes, has shown promising results. A phase 3 trial is currently ongoing [1, 3]. In summary HSP60 has been identified as a target for both pathogenic as well as protective immune mechanisms in many experimental and human inflammatory diseases. The upregulation of this protein at the sites of inflammation on one hand and its ability to skew the immune system towards suppression of disease on the other hand may explain the spontaneous remission of many experimental models of these inflammatory diseases. Understanding the putative mechanisms of disease suppression in animal models may lead to novel immunotherapeutic approaches to human autoimmune inflammatory diseases.

2015-01-01·Diabetes Care

Treatment of Recent-Onset Type 1 Diabetic Patients With DiaPep277: Results of a Double-Blind, Placebo-Controlled, Randomized Phase 3 Trial. Diabetes Care 2014;37:1392–1400. DOI: 10.2337/dc13-1391

作者: Giordano, Carla ; Elias, Dana ; Peled, Dana ; Avron, Ann ; Raz, Itamar ; Mauricio, Didac ; Eren, Rachel ; Bonnici, Francois ; Pozzilli, Paolo ; Tamir, Merana ; Schernthaner, Guntram ; Distiller, Larry A. ; Linn, Thomas ; Dagan, Shlomo ; Wainstein, Julio ; Procházka, Vlastimil ; Cohen, Irun R. ; Ziegler, Anette G. ; de Vries, Liat ; Giorgino, Francesco

On behalf of the authors identified below, the corresponding author has formally requested to retract the above-cited article. An accompanying article (1) has also been retracted. The article reports on the DIA-AID 1 trial, which examined the safety and efficacy of DiaPep277 to treat type 1 diabetes. The DIA-AID 1 trial, as noted in the Duality of Interest section, was funded by Andromeda Biotech, Ltd. On 8 September 2014, Hyperion Therapeutics, Inc., which acquired Andromeda Biotech in June 2014, announced that it had chosen to terminate the DiaPep277 program. As stated in the press release …

项与 DiaPep-277 相关的新闻（医药）

2024-08-28

·凯莱英药闻

29亿美元收购所得！赛诺菲靶向CD3药物替利珠单抗国内申报上市，可预防/延缓1型糖尿病

欢迎关注凯莱英药闻 2024年8月28日，根据中国国家药监局药品审评中心（CDE）官网公示，赛诺菲公司的替利珠单抗注射液的上市申请获得受理。替利珠单抗是一款抗CD3单克隆抗体，2023年3月，赛诺菲曾以每股25.00美元现金，股权价值约为 29 亿美元收购Provention Bio，将包含替利珠单抗在内多款自免药物收入囊中。关于替利珠单抗替利珠单抗（teplizumab）是人源化IgG1抗体，通过靶向CD4+或CD8+T淋巴细胞上CD3分子，抑制T细胞活性，从而调节1型糖尿病（T1D）的病理性免疫反应。Teplizumab的Fc段经氨基酸修饰后，构成了Fc受体非结合区域，减少与补体和Fc受体的结合，并降低了相关毒性反应。 2022年11月，teplizumab（商品名：Tzield）获FDA批准延迟2 期T1D成人患者和8 岁及以上儿童患者的3 期T1D的发病。Tzield是第一种可预防/延缓特定人群发展为临床T1D（3 期T1D）的疗法，是继一个世纪前胰岛素问世以来，T1D治疗方面取得的第一个重大进展。 Tzield的获批是基于一项关键的随机、双盲、事件驱动、安慰剂对照试验，衡量疗效的主要标准，是从随机入组到诊断为3期1型糖尿病的时间。结果显示：在51个月的中位随访中，接受Tzield的患者中有45%进展为3期1型糖尿病，而接受安慰剂有72%被诊断为3期糖尿病。接受Tzield的患者诊断为3期1型糖尿病的中位时间是50个月，接受安慰剂的病人是25个月。 C-peptide 相比安慰剂有显著提升，说明治疗促进了患者自身胰岛素的生成。患者每日胰岛素所需剂量相比安慰剂，有明显下降，第一年时teplizumab 组有5%的患者不再需要使用胰岛素（安慰剂组为0）。关于1型糖尿病糖尿病是危害人类健康最常见的慢性疾病之一，我国已经成为全球糖尿病患病人数增长最快的国家，18岁以上人群糖尿病患病率超过10%。近年来，糖尿病发病年轻化也是不容小窥的公共卫生问题。根据2019年世界卫生组织（WHO）最新的糖尿病分型标准，糖尿病分为1型糖尿病、2型糖尿病、妊娠糖尿病、混合型糖尿病、未分类型糖尿病、特殊类型糖尿病。 1型糖尿病的病人是由于免疫系统的破坏导致的，主要是免疫系统对胰岛β细胞的破坏，造成绝大部分的胰岛β细胞受到严重的损害，导致胰岛β细胞死亡。残留的胰岛β细胞比较少，产生的胰岛素，不能满足身体的需要，造成血糖的升高。据推测，全球可能有230万人患有1型糖尿病。根据翁建平教授等人在2010~2013年调查发现，中国所有年龄段的T1DM发病率估计为1.01/10万人年。除了每天注射胰岛素外，T1D患者还需要采取严格的管理计划，包括定期监测血糖、健康饮食和体育锻炼。近年来，我国针对1型糖尿病开展了相关的研究，以期对T1D药物的开发起到推动作用：翁建平教授团队对55例T1DM患者进行外周血T细胞亚群分布分析，结果提示CD4+ T细胞、调节性CD4+ T细胞、CD8+ T细胞比例及其表面Notch受体表达与HLA分型、病程、起病年龄均无明显相关性，且Notch信号分子在T细胞表面表达量较低。回顾文献提示外周血中T1DM相关致病性T细胞比例较低，后续对共刺激分子功能学研究难度较大，因此需重新寻找被高度活化的T1DM相关自身免疫性CD4+ T细胞克隆或细胞系的分离培养方法，并重新考虑Notch信号分子等共刺激分子在T1DM发病机制中作用。中南大学湘雅二院周智广教授团队在国内首次建立四次跨膜蛋白7（Tetraspanin 7）抗体的检测平台，并发现Tetraspanin 7抗体阳性是LADA患者C肽衰竭的独立预测因子。南京医科大学、中山大学和中南大学团队通过对2596例抗体阳性汉族T1DM患者和5082例对照进行全基因组关联分析（GWAS），在中国人群中发现了3个此前未报道的T1DM易感位点：BTN3A1基因附近的rs4320356位点、GATA3基因的rs3802604位点和HLA-C 275，并利用鉴定出的8个易感位点构建了T1DM风险预测模型，曲线下面积达到0.86。进一步分析发现，预测模型的遗传风险评分（GRS）越高，T1DM发病年龄越早、初诊时空腹C肽水平越低。此外，在高加索人群中报道的易感位点中，近一半与中国人群T1DM无关联或者频率较低，这可能是中国T1DM发病率较低的原因。关于自疫治疗1型糖尿病策略近年关于T1DM免疫调节治疗的研究主要集中在T效应细胞和B细胞免疫调节等方面。抗CD3单克隆抗体：通过与效应T细胞表面的CD3结合，激发或阻断细胞活化的信号，清除效应T细胞或诱导调节性T细胞（Treg）产生，诱导免疫耐受，抑制T细胞对胰岛β细胞的攻击，从而延缓β细胞被破坏的进程。目前，主要研究药物包括奥昔珠单抗和替利珠单抗；临床试验结果提示，奥昔珠单抗具有一定延缓T1DM患者β细胞功能减退的作用，然而低剂量对新确诊的T1DM患者C肽水平的下降速度又没有改善，因此该药物在T1DM的进展落后于替利珠单抗。抗CD20单克隆抗体：CD20是位于B细胞表面的标志性分子，能够调节B细胞活化；将抗CD20单克隆抗体作用于B细胞上表达的CD20抗原，启动介导B细胞溶解的免疫反应，减少自身抗原向T细胞的递呈，从而延缓β细胞的损伤。代表药物利妥昔单抗在一项II期临床显示，新诊断的T1DM患者接受1个疗程的利妥昔单抗治疗，可以将C肽的下降延迟8.2个月，但随访至30个月时两组之间无明显差异；此外，将利妥昔单抗与Treg疗法联用，延缓T1DM进展方面始终优于单一治疗。目前，针对利妥昔单抗治疗T1DM患者的III期研究正在进行中。嵌合抗原受体T细胞疗法：该疗法通过从患者血液中收集免疫细胞，对其进行基因改造使之识别特定的靶细胞，被改造后被重新输注到患者体内，从而发挥免疫调节作用。目前，美国Abata 公司开发的新型Treg细胞疗法的候选药物ABA-201正在进行IND审批，有望于2025年进入临床。人热休克蛋白60（Diapep277）：是源自人热休克蛋白60序列上的一段肽段，能够调节免疫系统，使胰岛细胞免受破坏并保护胰岛的分泌功能。III期临床显示，DiaPep277治疗组在不增加胰岛素剂量的情况下达到目标糖化血红蛋白的患者比例明显增加，降低了低血糖事件风险；与对照组相比，治疗组胰高糖素刺激的C肽曲线下面积下降幅度显著降低，说明DiaPep277在一定程度上能够减缓胰岛功能的衰退。抗胸腺细胞球蛋白（ATG）：是一种多克隆IgG，能够破坏T细胞的活化，诱导免疫耐受从而可能治疗新发T1DM。临床研究表明，在诊断T1DM的3个月内使用1个疗程的小剂量ATG（2.5 mg/kg），可减缓β细胞的减少。由于目前低剂量ATG所提供的保护时间并不确定，需要更长时间的临床观察。参考资料 1、公司官网、CDE 2、Weng J, Zhou Z, Guo L, et al.; T1D China Study Group. Incidence of type 1 diabetes in China, 2010-13: population based study. BMJ 2018;360:j5295 3、Yingxin Xian, Haixia Xu, Yifang Gao, Jinhua Yan, Jing Lv, Wenqian Ren, Qianwen Huang, Ziyu Jiang, Fen Xu, Bin Yao, Jianping Weng. Diabetes Metab Res Rev. 2019;e3228. 4、Shi X, Huang G, Wang Y, Liu Z, Deng C, Li X, Zheng P, Zhou Z Tetraspanin 7 autoantibodies predict progressive decline of beta cell function in individuals with LADA. Diabetologia. 2019 Mar;62(3):399-407. 5、Zhu, M., et al., Identification of Novel T1D Risk Loci and Their Association With Age and Islet Function at Diagnosis in Autoantibody-Positive T1D Individuals: Based on a Two-Stage Genome-Wide Association Study. Diabetes Care, 2019. 42(8): p. 1414-1421. 6、公众号：中华糖尿病杂志、1型糖尿病学组感谢关注、转发，转载授权、加行业交流群，请加管理员微信号“hxsjjf1618”。 “在看”点一下

临床3期并购临床结果

2015-10-07

·BioSpace

Clal Biotech Opts Out of Re-Acquiring Andromeda from Hyperion After Phase III Diabetes Drug Tanks

October 7, 2015 By Alex Keown , BioSpace.com Breaking News Staff YAVNE, Israel – Applied Genetic Technologies Corporation will not exercise its option to purchase its former subsidiary Andromeda Biotech from Hyperion Therapeutics and its parent company Horizon Pharma following the late-stage failure of the company’s experimental treatment for juvenile diabetes, Globes, an Israel-based business publication reported . Clal Biotech had an option to purchase Andromeda for a price tag of $2.5 million to $36.5 million, depending on clinical trial outcomes. However, Andromeda ’s Phase III trial for DiaPep277, a drug for the treatment of type 1 diabetes in juveniles, failed to achieve efficacy, Globes said. There is no indication yet if research will continue on the drug to see if it is a more effective diabetes treatment for other age groups. Clal Biotechnology is a life-sciences holding company. Its main holdings include Gamida Cell Ltd. , MediWound Ltd. and CureTech Ltd. , Globes reported. Clal ’s , traded on the Tel Aviv Stock Exchange, was down this morning. The stock was trading at 280.10 ILS (Israeli Shekels) down from a day’s high of 288.70 ILS. Clal ’s option to purchase Andromeda was part of an agreement with Hyperion the two companies entered into after a dispute over DiaPep277 stemming back to 2014. In April 2014, Hyperion acquired Andromeda from Clal for up to $570 million, but then scuttled trials for DiaPep277, arguing the drug’s data was not complete as it omitted results from 34 patients in violation of trial protocols. Clal sued Hyperion for $200 million, arguing that the company’s claims against them caused damage to the company’s reputation. The two companies negotiated a truce to complete trials for DiaPep277, giving Clal the option to repurchase Andromeda and the drug. In 2007, DeveloGen AG sold all rights to DiaPep277 to Andromeda, which at the time was a subsidiary of Clal Biotechnology . After Andromeda acquired the drug from DeveloGen , it c-o-developed the medication with Israel-based Teva Pharmaceutical Industries Ltd. until that company relinquished its rights to the drug in 2014, Globes reported. Teva financed most of the clinical trials surrounding DiaPep277, Globes said . After the latest DiaPep277 drama, the drug is scheduled to revert to Yeda Research and Development Company , the place where it was originally discovered. In May, Hyperion was acquired by Ireland-based Horizon Pharma for $1.1 billion. Hyperion ’s pipeline included Ravicti and Buphenyl, both used for the treatment of urea cycle disorders. Buphenyl, also known as sodium phenylbutyrate, helps by removing nitrogen from the body. Ravicti, or glycerol phenylbutyrate, eliminates ammonia in patients over 24 hours. Urea cycle disorders and metabolic disorders impact more than 2,100 people in the U.S. Earlier this year, Novo Nordisk pulled the plug on an expansion of Victoza (liraglutide) for use in type 1 diabetes after disappointing Phase III trial results. Victoza is a GLP-1 analogue used to treat type 2 diabetes. In the latest study, dubbed Adjunct One, Victoza (liraglutide) combined with an insulin improved blood glucose control in attempts to treat type 1 diabetes actually worsened episodes of low blood sugar, the company reported.

并购临床3期临床2期上市批准

2014-02-24

·BioSpace

Andromeda Biotech Acquires DiaPep277 Rights From Teva Pharmaceutical Industries Limited

YAVNE, Israel, Feb. 24, 2014 (GLOBE NEWSWIRE) -- Andromeda Biotech Ltd. announces that it entered into an agreement with Teva Pharmaceutical Industries Ltd. for the acquisition of Teva's rights for Andromeda's drug, DiaPep277®, for the treatment of Type 1 Diabetes. Help employers find you! Check out all the jobs and post your resume.

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100 项与 DiaPep-277 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
1型糖尿病	临床3期	-	Weizmann Institute of Science	-
1型糖尿病	临床3期	-	Weizmann Institute of Science	-

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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


NCT00615264 (DIA-AID 1 \| DIA-AID, CTgov)	临床3期	1型糖尿病	457	DiaPep277 (DiaPep277)	糧願築築顧鏇衊憲積網(醖餘鏇餘顧築鑰遞鏇鬱) = 壓壓膚衊廠鏇遞壓廠構鹹窪範齋襯網鹹築製醖 (膚鏇壓餘範簾餘簾遞積, 簾鹹齋艱鏇選糧選網觸 ~ 簾醖齋築鬱蓋醖築構艱) 更多	-	2016-06-06
				Placebo (Placebo)	糧願築築顧鏇衊憲積網(醖餘鏇餘顧築鑰遞鏇鬱) = 範範襯膚窪鏇鹹選襯遞鹹窪範齋襯網鹹築製醖 (膚鏇壓餘範簾餘簾遞積, 獵齋構鑰醖艱糧鏇衊壓 ~ 衊膚範窪鹽壓襯遞壓夢) 更多
NCT01103284 (DIA-AID2, CTgov)	临床3期	1型糖尿病	475	DiaPep277 (DiaPep277)	膚顧簾襯製憲蓋選鏇簾(鹽獵艱獵膚鑰獵糧遞憲) = 夢艱獵糧繭窪淵遞鏇鏇簾遞製獵鑰衊鏇網顧餘 (廠壓齋鏇願顧蓋艱顧鬱, 膚夢鬱餘窪顧積糧窪選 ~ 鏇衊範壓齋窪壓鹹淵齋) 更多	-	2016-05-26
				Placebo (Placebo)	膚顧簾襯製憲蓋選鏇簾(鹽獵艱獵膚鑰獵糧遞憲) = 蓋顧鹹網襯膚範構衊觸簾遞製獵鑰衊鏇網顧餘 (廠壓齋鏇願顧蓋艱顧鬱, 鏇觸遞願夢願構顧製鹹 ~ 夢鹽鬱範遞繭襯構膚製) 更多
NCT01898286 (DIA-AID 2, CTgov)	临床3期	1型糖尿病	38	DiaPep	齋窪糧憲製淵積襯鏇廠(構願壓艱願膚獵艱膚齋) = 壓蓋憲鑰獵糧窪醖觸膚鏇夢繭鹽築餘壓襯糧鏇 (艱艱獵壓衊齋襯鬱範餘, 獵製廠衊簾鬱淵壓網襯 ~ 憲窪鏇憲獵膚壓夢糧廠) 更多	-	2016-05-26
NCT00615264 (DIA-AID 1, EASD2013)	临床3期	stimulated C-peptide levels	43	DiaPep277®	膚糧夢窪淵積淵鬱鹽淵(鬱醖鹹積餘膚糧遞遞鑰) = Out of 81 adverse events reported by 31 subjects, only two were related to the study drug, both of which were resolved. Only one severe adverse event was reported which was not considered related to the study medication. The most common non-related adverse events were infections and infestations (35/81, 43%) followed by gastrointestinal disorders (9/81, 11%) 鑰願襯鏇構鏇願構願憲 (艱醖艱觸鹽鹽襯蓋製糧 )	积极	2013-09-25
				Placebo
NCT00615264 (DIA-AID 1, EASD2012)	临床3期	1型糖尿病 C-peptide \| islet autoantibodies	457	DiaPep277	顧製壓選製憲願淵憲鹽(齋齋顧選淵齋窪餘願築) = 衊積廠窪觸範製齋夢鑰糧襯鏇顧積餘網選願壓 (糧窪鹹膚醖網繭鑰醖鬱 ) 更多	积极	2012-10-04
				Placebo	顧製壓選製憲願淵憲鹽(齋齋顧選淵齋窪餘願築) = 範積網艱鏇淵顧壓範鹽糧襯鏇顧積餘網選願壓 (糧窪鹹膚醖網繭鑰醖鬱 ) 更多