A Randomized, Double-Blind, Placebo-Controlled Multi-Center Study to Evaluate the Safety and Efficacy of Three Dose Strengths of T3D-959 in Subjects With Mild-to-Moderate Alzheimer's Disease

A Randomized, Double-Blind, Placebo-Controlled Multi-Center Study to Evaluate the Safety and Efficacy of Three Dose Strengths of T3D-959 in Subjects with Mild-to-Moderate Alzheimer's Disease.

开始日期2021-03-01

申办/合作机构

T3D Therapeutics, Inc.

[+3]

NCT02560753 / Completed临床1/2期

Phase 2a Feasibility Study of T3D-959 in Subjects With Mild to Moderate Alzheimer's Disease

The study is a randomized, parallel, 4-dose design in subjects with mild-to-moderate Alzheimer's Disease. Subjects will be randomized to one of 4 doses of T3D-959. Subjects will be evaluated for changes from baseline in cerebral metabolic rate of glucose (FDG-PET imaging), functional connectivity of the hippocampus (BOLD-fMRI), and cognitive function (ADAS-Cog11 and DSST) as well as assessed for safety and tolerability to T3D-959.
An expanded access extension is planed to provide access to study medication to subjects who have completed the main study and requested continued use.

开始日期2015-07-01

申办/合作机构

T3D Therapeutics, Inc.

100 项与 DB-959Na 相关的临床结果

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100 项与 DB-959Na 相关的专利（医药）

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项与 DB-959Na 相关的文献（医药）

2020-02-04·Journal of Alzheimer's disease : JAD3区 · 医学

An Exploratory Phase IIa Study of the PPAR delta/gamma Agonist T3D-959 Assessing Metabolic and Cognitive Function in Subjects with Mild to Moderate Alzheimer’s Disease

3区 · 医学

Article

作者: Didsbury, John ; Gabriel, Hoda ; Small, Gary ; Chamberlain, Stanley ; Strittmatter, Warren

BACKGROUND:

T3D-959 is a chemically unique, brain penetrant, dual PPAR delta/gamma agonist with 15-fold higher PPAR delta selectivity. Ubiquitous brain expression of PPAR delta, its critical role in regulating glucose and lipid metabolism, and the Alzheimer's disease (AD)-like phenotype of PPAR delta null mice motivated this study.

OBJECTIVE:

To determine safety and tolerability of multiple doses of T3D-959 in subjects with mild to moderate AD, examine systemic and central drug pharmacology and in an exploratory manner, perform cognitive assessments.

METHODS:

Thirty-four subjects with mild-to-moderate AD were orally administered 3, 10, 30, or 90 mg of T3D-959 daily for 14 days. There was no inclusion of a placebo arm. Safety and tolerability were monitored. Systemic drug pharmacology was examined via plasma metabolomics LC-MS-MS analysis, cerebral drug pharmacology via FDG-PET measures of changes in Relative CMRgl (R CMRgl, AD-effected regions relative to brain reference regions), and cognitive function assessed before and after drug treatment and again one week after completion of drug treatment, by ADAS-cog11 and the Digit Symbol Substitution Test (DSST).

RESULTS:

T3D-959 was in general safe and well tolerated. Single point pharmacokinetics at the Tmax showed dose dependent exposure. Plasma metabolome profile changes showed dose-dependent systemic effects on lipid metabolism and metabolism related to insulin sensitization. Relative FDG-PET imaging demonstrated dose-dependent, regional, effects of T3D-959 on R CMRgl based on the use of multiple reference regions. ADAS-cog11 and DSST cognitive assessments showed improvements with possible ApoE genotype association and pharmacodynamics related to the mechanism of drug action.

CONCLUSIONS:

Exploratory data from this Phase IIa clinical trial supports further clinical investigation of T3D-959 in a larger placebo-controlled clinical study.

2016-11-19·Journal of Alzheimer's disease : JAD3区 · 医学

Improved Brain Insulin/IGF Signaling and Reduced Neuroinflammation with T3D-959 in an Experimental Model of Sporadic Alzheimer’s Disease

3区 · 医学

Article

作者: Didsbury, John ; de la Monte, Suzanne M ; Tong, Ming ; Schiano, Irio

BACKGROUND:

Alzheimer's disease (AD) is associated with progressive impairments in brain insulin, insulin-like growth factor (IGF), and insulin receptor substrate (IRS) signaling through Akt pathways that regulate neuronal growth, survival, metabolism, and plasticity. The intracerebral streptozotocin (i.c. STZ) model replicates the full range of abnormalities in sporadic AD. T3D-959, an orally active PPAR-delta/gamma agonist remediates neurocognitive deficits and AD neuropathology in the i.c. STZ model.

OBJECTIVE:

This study characterizes the effects of T3D-959 on AD biomarkers, insulin/IGF/IRS signaling through Akt pathways, and neuroinflammation in an i.c. STZ model.

METHODS:

Long Evans rats were treated with i.c. STZ or saline, followed by daily oral doses of T3D-959 (1 mg/kg) or saline initiated 1 day (T3D-959-E) or 7 days (T3D-959-L) later through Experimental Day 28. Protein and phospho-protein expression and pro-inflammatory cytokine activation were measured in temporal lobe homogenates by duplex or multiplex bead-based ELISAs.

RESULTS:

i.c. STZ treatments caused neurodegeneration with increased pTau, AβPP, Aβ42, ubiquitin, and SNAP-25, and reduced levels of synaptophysin, IGF-1 receptor (R), IRS-1, Akt, p70S6K, mTOR, and S9-GSK-3β. i.c. STZ also broadly increased neuroinflammation. T3D-959 abrogated or reduced most of the AD neuropathological and biomarker abnormalities, increased/normalized IGF-1R, IRS-1, Akt, p70S6K, and S9-GSK-3β, and decreased expression of multiple pro-inflammatory cytokines. T3D-959-E or -L effectively restored insulin/IGF signaling, whereas T3D-959-L more broadly resolved neuroinflammation.

CONCLUSION:

AD remediating effects of T3D-959 are potentially due to enhanced expression of key insulin/IGF signaling proteins and inhibition of GSK-3β and neuroinflammation. These effects lead to reduced neurodegeneration, cognitive impairment, and AD biomarker levels in the brain.

2016-02-27·Journal of Alzheimer's disease : JAD3区 · 医学

T3D-959: A Multi-Faceted Disease Remedial Drug Candidate for the Treatment of Alzheimer’s Disease

3区 · 医学

Article

作者: Didsbury, John ; de la Monte, Suzanne M ; Tong, Ming ; Deochand, Chetram

BACKGROUND:

T3D-959, a dual PPAR-δ/PPAR γ nuclear receptor agonist and former diabetes drug candidate, has been repositioned as an Alzheimer's disease (AD)-modifying therapy.

OBJECTIVE:

This study examines the effectiveness and mechanisms of T3D-959's therapeutic effects using in vivo and ex vivo rat models of sporadic AD.

METHODS:

A sporadic AD model was generated by intracerebral (i.c.) administration of streptozotocin (STZ). Control and i.c. STZ treated rats were gavaged with saline or T3D-959 (0.3 to 3.0 mg/kg/day) for 28 days. Spatial learning and memory were evaluated using the Morris water maze test. Frontal lobe slice cultures generated 24 hours after i.c. STZ or vehicle were used to study early effects of T3D-959 (0.5-1.0 μM) on viability and molecular markers of AD.

RESULTS:

T3D-959 significantly improved spatial learning and memory in i.c STZ-treated rats. Mechanistically, T3D-959 significantly improved culture viability and brain morphology, reduced levels of oxidative stress and Aβ, and normalized expression of phospho-tau, choline acetyltransferase, and myelin-associated glycoprotein. Protective effects occurred even at the lowest tested dose of T3D-959.

CONCLUSIONS:

Pre-clinical proof of concept has been demonstrated that T3D-959 can improve multiple pathologies of AD resulting in significant improvements in cognitive function and molecular and biochemical indices of neurodegeneration. These results support the theses that (1) effective disease modification in AD can be achieved by targeting relevant nuclear receptors, and (2) treating AD as a metabolic disease has the potential to be disease remedial. A Phase 2a trial of T3D-959 in mild-to-moderate AD patients has been initiated (ClinicalTrials.gov identifier NCT02560753).

项与 DB-959Na 相关的新闻（医药）

2023-11-06

·药研发

【药研发1107】信达VEGF/C3补体双抗眼科Ⅱ期临床积极 | 科越医药C5/FH1-5补体抑制剂II期临床积极...

「本文共：15条资讯，阅读时长约：3分钟」今日头条信达VEGF/C3补体双抗眼科Ⅱ期临床积极。信达生物在AAO2023年会上公布VEGF/C3补体双靶点药物IBI302治疗新生血管性年龄相关性黄斑变性的Ⅱ期临床最新数据。第36周时，与阿柏西普(2mg)相比，IBI302（2mg/4mg）治疗改善研究眼最佳矫正视力（BCVA）的效果达到非劣效标准，两组患者BCVA较基线变化均值分别为+10.6、+11.4和+12.0个字母；临床中，IBI302组无眼内炎或视网膜血管炎发生。该产品目前已处于Ⅲ期临床开发。国内药讯1.绿叶紫杉醇脂质体肺癌真实世界研究积极。绿叶制药自研紫杉醇脂质体（力扑素®）联合免疫一线治疗晚期非小细胞肺癌（NSCLC）的真实世界研究结果公布于SITC2023年会上。研究目前纳入100例至少接受2周期含紫杉醇脂质体联合免疫药物一线治疗的患者。中位随访时间为8.6个月。中位PFS为11个月（95% CI：8.9-16.8）。总体ORR为60.2%，疾病控制率（DCR）为91.5%。任意级别的不良事件发生率为91%，≥3级不良事件的发生率为34%。2.科越C5/FH1-5补体抑制剂II期临床积极。科越医药C5/FH1-5双靶点补体抑制剂KP104将在ASH2023年会上公布用于治疗阵发性睡眠性血红蛋白尿症(PNH)的II期试验积极结果。KP104旨在同时选择性抑制补体旁路和末端途径，具有协同治疗补体介导的疾病的潜力。科越医药计划在中国、美国和澳大利亚开展II期临床，适应症包括PNH、 IgA肾病、C3肾小球病和继发于系统性红斑狼疮的血栓性微血管病(SLE-TMA)。3.君实PD-1抑制剂联合治疗HNSCC早期临床积极。君实生物PD-1抑制剂特瑞普利单抗在SITC2023年会上公布与EGFR单抗西妥昔单抗联合治疗复发或转移性头颈部鳞状细胞癌（R/M-HNSCC）的Ⅰb/Ⅱ期临床积极结果。中位随访为10.0个月时，IRC评估的经确认的ORR为60%；DCR为80%，中位DOR为17.9个月；中位PFS为9.9个月，1年PFS率为40.7%。中位OS达15.4个月，1年OS率为54.4%。临床中，未报告与研究治疗相关的致死性AE。4.仁景mRNA疫苗获批HPV临床。仁景生物自主研发的HPV相关肿瘤治疗性mRNA疫苗RG002获FDA批准开展临床研究，用于治疗人乳头瘤病毒（HPV）16型和/或18型相关的2级或3级宫颈上皮内瘤变（CIN2/3）。RG002采用仁景生物自主知识产权的mRNA序列和脂质纳米颗粒（LNP）递送系统开发，已在临床前研究中显示出单药能诱导较强的特异性细胞免疫和肿瘤细胞杀伤作用。5.华夏英泰LILRB4靶向细胞疗法报IND。华夏英泰1类生物制品YTS104细胞注射液的临床试验申请获CDE受理。这是一款靶向LILRB4的自体型细胞治疗药物，通过慢病毒基因转导，将特定STAR基因导入自体T细胞内并经体外细胞扩增制备。该产品申报适应症包括复发/难治急性髓系白血病（AML）、慢性粒-单核细胞白血病（CMML）等。2022年年底，FDA已授予YTS104用于治疗R/R AML的孤儿药资格。国际药讯1.K药辅助治疗肾癌Ⅲ期临床成功。默沙东PD-1抑制剂Keytruda用于辅助治疗肾细胞癌（RCC）的Ⅲ期试验KEYNOTE-564达到主要终点和关键次要终点。与安慰剂相比，Keytruda辅助治疗显著改善患者的无病生存期，使疾病复发或死亡风险降低32%（HR=0.68，p=0.0010）；患者总生存期的统计也具有临床显著的改善。Keytruda的安全性与既往试验一致，没有出现新的安全性问题。2.细胞免疫疗法预防肾移植风险Ⅲ期临床积极。Medeor公司创新细胞疗法MDR-101在国际Ⅲ期临床中获积极中期结果。MDR-101由活体供肾者的血液和外周干细胞开发而来，旨在诱导供体特异性免疫耐受，预防肾移植肾的排斥反应。试验结果显示，接受HLA匹配活体捐献者肾移植的患者有63%的比例完成试验，并在两年内维持不使用免疫抑制药物状态。详细结果将公布于ASN2023年会上。3.体内CRISPR基因编辑疗法将启动Ⅲ期临床。Intellia公司CRISPR/Cas9基因编辑疗法NTLA-2001用于治疗转甲状腺素蛋白（ATTR）淀粉样变性的Ⅰ期试验最新结果积极。12个月随访分析显示，在接受≥0.3mg/kg剂量NTLA-2001单次给药的患者（n=62）中，其血清TTR中位降低91%，治疗后第28天的中位绝对残留血清TTR浓度为17 µg/mL；药物在总研究队列（包括多发性神经病和心肌病患者）中耐受性良好。该公司计划在今年年底启动NTLA-2001的Ⅲ期临床研究。4.创新APRIL单抗肾病Ⅱ期研究见刊NEJM。大冢制药和Visterra公司开发的APRIL单抗sibeprenlimab（VIS649）在ASN2023年会上公布用于治疗IgA肾病的Ⅱ期临床积极结果。与安慰剂相比，sibeprenlimab（2mg、4mg和8mg）治疗12个月时患者的蛋白尿水平显著减少，两组患者24小时尿蛋白/肌酐比值（UPCR）的几何平均比值降幅分别为47.2%、58.8%、62.0%和20.0%；两组治疗伴发不良事件（TEAE）的发生率也相似。详细结果同时发表于《新英格兰医学杂志》上。5.PPARδ/γ核受体激动剂老年痴呆Ⅱ期临床积极。T3D Therapeutics公司口服小分子PPARδ/γ核受体双重激动剂T3D-959治疗轻中度阿尔茨海默病（AD）的Ⅱ期PIONEER试验结果积极。在ITT人群中，与安慰剂相比， T3D-959（30mg）治疗24周时显著降低患者血浆Ab42/40比值（评估淀粉样斑块负荷的生物标志物）；患者认知水平量表ADAS-Cog11的评分改善了2分；药物总体安全性良好，未发生与卒中有关的药物相关不良事件。6.吉利德将开发血癌新一代CAR-T疗法。吉利德旗下Kite公司与Epic Bio公司将利用后者的基因调控平台（GEMS），针对Kite所选择靶向血癌的靶标开发载体，应用于新一代CAR-T细胞疗法。GEMS是一种表观遗传编辑的模块化平台，是一种允许通过单独AAV载体进行体内递送的CRISPR系统。根据协议，Epic Bio将获得预付款，开发、监管和销售里程碑潜在款项。医药热点。1.西湖大学启动创建医学院。近日，西湖大学董事会研究决定设立医学院，经校长施一公提名，医学院首任院长由中国科学院院士、著名免疫学家董晨教授担任。新成立的医学院将以培养顶尖医师科学家（Physician scientists）为目标，致力于医学创新和临床转化，重点聚焦微生物学与疫苗、免疫学与炎症、生理学与代谢、肿瘤生物学与治疗、医学遗传与罕见病、药物研发、公共健康等研究领域。2.南昌大学附一院乳腺专病中心成立。11月3日，南昌大学第一附属医院象湖院区“乳腺专病中心”成立。该中心是江西省首个由省级综合医院成立的乳腺专病中心，中心聚焦乳腺疾病，致力于为患者提供全流程、一站式的就诊服务。该中心除开展乳腺癌改良根治术、保乳术、前哨淋巴结活检术等常规手术之外，也开展了乳腺良恶性肿瘤的腔镜手术、乳腺癌保乳整形手术、乳房重建术（包括假体及自体皮瓣等）等。3.上海市外卖购药可刷医保。近日，上海相关部门已与饿了么、美团平台联系，试点互联网药店医保支付工作，有几十家药店纳入范畴。在上海通过美团外卖或饿了么 App下单带有“医保支付”字样的药品，页面显示可从个人电子医保卡账户付款，目前只有部分带有“医保支付”字样的药店才可使用医保。评审动态 1. CDE新药受理情况（11月06日) 2. FDA新药获批情况（北美11月03日）股市资讯上个交易日 A 股医药板块 +1.25%涨幅前三跌幅前三维康药业+19.99% *ST 太安-4.55%康为世纪+10.29% 奥泰生物-3.95%诺思兰德 +9.77% 珍宝岛 -3.85%【舒泰神]取得关于注射用STSP-0601的Ib/I期临床试验临床研究总结报告。剂型为注射用无菌冻干粉末，适应症为伴抑制物的血友病A或B患者出血按需治疗。【广济药业]收到国家药品监督管理局下发的化学原料药恩替卡韦《化学原料药上市申请批准通知书》，获批，登记号:Y20170000288。【华神科技]看展15000吨/年高端新材料和原料药(含医药中间体)绿色生产基地项目，在控股子公司山东凌凯药业有限公司进行项目一期建设，项目一期计划分阶段建设，其中第一阶段项目建设投资不超过4.8亿元，建设工期约12个月。- The End -戳“阅读原文”，了解更多医药研发及股市资讯。

临床2期临床结果疫苗临床3期临床1期

2023-11-03

·药明康德

速递 | 改善阿尔茨海默病患者认知！非淀粉样斑块靶向创新小分子2期试验积极

▎药明康德内容团队编辑T3D Therapeutics公布其2期PIONEER试验的积极顶线结果，分析显示其在研药物T3D-959具潜力改善轻中度阿尔茨海默病（AD）患者的疾病进程。在意向治疗（ITT）患者群体中，与安慰剂相比，T3D-959显著改善患者的治疗结局。接受30 mg T3D-959治疗的患者在评估淀粉样斑块负荷的生物标志物——血浆Ab42/40比值上，与安慰剂组患者相比显著降低（p=0.021）。▲PIONEER试验疗效结果（图片来源：参考资料[2]）55%的入组患者被确定为具有AD病理特征，证据是其pTau-217/非pTau-217比值等于或大于0.015（高pTau-217比率亚群）。这类患者在给予安慰剂时表现出认知功能下降，与典型AD进展一致。然而当该亚群患者接受30 mg T3D-959治疗（N=30）后表现出明显的认知改善。在24周时，与安慰剂相比，其在AD患者认知水平量表ADAS-Cog11的评分上改善了2分，达到的效果与靶向淀粉样斑块抗体在76-78周内观察到的效果相当或较好。▲PIONEER试验疗效结果（图片来源：参考资料[2]）药物在ITT人群中所显示的安全性特征良好，未发生与卒中有关的药物相关不良事件，也无淀粉样蛋白相关成像异常（ARIA）的临床指征。▲T3D-959药物机制（图片来源：参考资料[2]）T3D-959是一种每日一次的口服小分子，为PPARδ/γ核受体的双重激动剂。其机制旨在纠正AD和其他神经退行性疾病的糖脂代谢紊乱，为解决这些疾病提供了一种新方法。大家都在看药明康德为全球生物医药行业提供一体化、端到端的新药研发和生产服务，服务范围涵盖化学药研发和生产、生物学研究、临床前测试和临床试验研发、细胞及基因疗法研发、测试和生产等领域。如您有相关业务需求，欢迎点击下方图片填写具体信息。▲如您有任何业务需求，请长按扫描上方二维码，或点击文末“阅读原文/Read more”，即可访问业务对接平台，填写业务需求信息▲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] T3D Therapeutics Announces Positive Top-Line Results from the Phase 2 PIONEER Trial of T3D-959 in Mild-To-Moderate Alzheimer's Disease. Retrieved November 3, 2023 from https://www.prnewswire.com/news-releases/t3d-therapeutics-announces-positive-top-line-results-from-the-phase-2-pioneer-trial-of-t3d-959-in-mild-to-moderate-alzheimers-disease-301976115.html[2] LB3 - Topline Results From the Phase 2 PIONEER Trial of Oral T3D-959 for the Treatment of Patients Diagnosed With Mild-to-Moderate Alzheimer’s Disease. Retrieved November 3, 2023 from http://www.t3dtherapeutics.com/wp-content/uploads/2023/11/LB3_Didsbury_John-1-1.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

临床结果基因疗法临床2期

2023-11-03

·PRNewswire

T3D Therapeutics Announces Positive Top-Line Results from the Phase 2 PIONEER Trial of T3D-959 in Mild-To-Moderate Alzheimer's Disease

RESEARCH TRIANGLE PARK, N.C., Nov. 3, 2023 /PRNewswire/ -- T3D Therapeutics presented top-line results from its Phase 2 PIONEER study at the 16th international conference on Clinical Trials in Alzheimer's Disease (CTAD). The double-blind study compared 3 doses of T3D-959 versus placebo administered orally once a day for 24 weeks in 250 patients with mild to moderate Alzheimer's Disease (AD). Results suggest the potential of T3D-959 to be disease modifying in mild-to-moderate severity Alzheimer's patients. Biomarker data showed modification of multiple disease pathologies inherent in AD. Clinical evidence of improvement in cognition was shown in a sub-group of patients identified with a new blood biomarker of Alzheimer's disease (AD) pathology, pTau-217/Non-pTau-217 ratio. A high pTau-217 ratio in the blood defined an Alzheimer's disease population responsive to T3D-959 therapy. An excellent safety profile was demonstrated after 24-weeks of once daily oral dosing. Analyses showed: The ITT population (all randomized patients) had significant improvement with T3D-959 treatment vs. placebo: In a biomarker of amyloid plaque burden, plasma Ab42/40 ratio (PrecivityAD™), with 30mg of T3D-959 vs. placebo (p=0.021). In fasting plasma glucose, insulin, HDL and other lipids, indicators of an improved metabolic profile. In a plasma biomarker of neurodegeneration, neurogranin (p=0.013). In multiple plasma metabolomic biomarkers of AD neurodegeneration, inflammation, insulin resistance, mitochondrial dysfunction and oxidative stress. In multiple plasma proteomic biomarkers of AD, amyloid plaque formation, neurodegeneration, inflammation, mitochondrial dysfunction and oxidative stress as measured by LC-MS, The ITT population had an excellent safety profile with no drug -related adverse events related to stroke and no clinical signs of ARIA. 55% of subjects had a pTau-217/Non-pTau-217 ratio ≥0.015 indicating they had AD pathology (high pTau-217 ratio group) and exhibited cognitive decline in the placebo group consistent with AD. The high pTau-217 ratio group dosed with 30mg of T3D-959 (N=30) exhibited: An improvement of 2 points vs. placebo in ADAS-cog11 with an effect size at 24 weeks equivalent to or better than that observed for anti-amyloid plaque antibodies at 76-78 weeks. Stronger improvement in the plasma Ab42/40 ratio than the ITT population. A 30mg q.d. dose was identified as providing optimal safety and efficacy for further investigation in a Phase 2b/3 clinical trial in mild-to-moderate AD patients. John Didsbury, Ph.D., Chief Executive Officer of T3D said "PIONEER positive outcomes achieved the goal to inform the design of a larger and longer Phase 2b/3 trial, with dose selection, a 'responder' population of AD patients and biomarkers to assess. " "The exciting results of this study show potential to modify the course of Alzheimer's disease in a unique way. I look forward to seeing these results confirmed and expanded in a larger and longer Phase 2b/3 clinical trial" said Michael Weiner MD, Professor Emeritus at the University of California, San Francisco, and principal investigator of the Alzheimer's Disease Neuroimaging Initiative (ADNI). "The outcomes of this trial are encouraging and lay a foundation for advancing the further development of this new molecule to treat Alzheimer's disease" said Pierre N. Tariot MD, Director of Banner Alzheimer's Institute. About T3D-959: T3D-959, a small molecule, delivered orally once daily, is a brain-penetrating PPAR delta/gamma dual nuclear receptor agonist designed to improve both glucose and lipid metabolism dysfunctions present in AD and other neurodegenerative disorders. About the Study: The Phase 2 PIONEER study (Prospective therapy to Inhibit and Overcome Alzheimer's Disease Neurodegeneration via Brain EnErgetics and Metabolism Restoration) was a double-blind, placebo-controlled, parallel-group Phase 2 safety and efficacy study that enrolled 250 adults with mild-to-moderate Alzheimer's disease (MMSE 14-26). PIONEER was designed to assess the safety, tolerability, and effectiveness of T3D-959 in the treatment of Alzheimer's disease. T3D-959 was administered orally once daily over a 24-week dosing period. Subjects received one of three different doses of T3D-959 (15mg, 30mg, or 45mg) or a placebo. To learn more about this study please visit and reference study number NCT04251182. PIONEER is supported by the National Institute on Aging, part of the National Institutes of Health, under award number R01AG061122 and by the Alzheimer's Association's Part the Cloud Gates Partnership Grant Program. About T3D Therapeutics, Inc.: T3D Therapeutics, Inc. is a privately held, Research Triangle Park, NC-based company. The Company has an exclusive license to T3D-959, its lead product candidate, and a platform of structurally related molecules. T3D Therapeutics' mission is to develop and commercialize T3D-959 for the treatment of Alzheimer's disease. Additionally, T3D Therapeutics is targeting treatments for other neurodegenerative diseases with an emphasis on Huntington's Disease (HD). For more information visit . CONTACT: John Didsbury, Ph.D., CEO T3D Therapeutics, Inc. 1-919-237-4897 Email: [email protected]

临床结果临床2期引进/卖出

100 项与 DB-959Na 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
阿尔茨海默症	临床2期	美国	T3D Therapeutics, Inc.	2021-03-01
亨廷顿舞蹈病	临床1期	美国	T3D Therapeutics, Inc.	2019-05-13
非酒精性脂肪性肝炎	临床1期	美国	T3D Therapeutics, Inc.	2019-05-08
2型糖尿病	临床1期	美国	DARA BioSciences, Inc.	-
血脂障碍	临床1期	美国	DARA BioSciences, Inc.	-

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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


NCT04251182 (PIONEER, PRNewswire) 人工标引	临床2期	阿尔茨海默症	250	T3D-959	鹽鹹憲醖鬱壓膚選夢窪(餘醖鬱積製淵鬱衊獵廠) = 簾膚壓鬱觸製襯積齋齋鹹製顧蓋鬱鬱獵廠網餘 (壓觸選艱構衊願鏇壓鹹 )	积极	2023-11-03
				placebo	-
NCT02560753 (Pubmed \| J Alzheimers Dis) 人工标引	临床2期	阿尔茨海默症	34	T3D-959	廠遞窪願壓鹹窪艱窪鹽(構構遞築壓鹽膚蓋衊憲) = improvement 鬱鏇餘膚糧艱鏇衊醖網 (簾壓鏇夢鑰蓋網鹽製夢 ) 更多	积极	2020-01-01
NCT02560753 (CTgov)	临床1/2期	阿尔茨海默症	36	T3D-959 (T3D-959 3mg)	餘艱淵構廠築網築窪繭(蓋鹽網夢糧鏇選鹽積製) = 築簾顧蓋蓋淵淵淵鹽鹹鏇繭窪膚糧鏇簾選糧鑰 (窪顧簾膚鏇觸範製膚窪, 鬱製壓糧繭構鑰壓簾遞 ~ 觸鑰繭鏇窪網窪構鹹簾) 更多	-	2018-07-30
				T3D-959 (T3D-959 10mg)	餘艱淵構廠築網築窪繭(蓋鹽網夢糧鏇選鹽積製) = 願簾觸積壓範餘衊範鑰鏇繭窪膚糧鏇簾選糧鑰 (窪顧簾膚鏇觸範製膚窪, 選遞製遞鑰糧築積憲繭 ~ 鏇鏇憲獵醖醖遞壓蓋窪) 更多
NCT02560753 (AAIC2018)	临床1/2期	阿尔茨海默症	36	T3D-959 3mg	糧繭築艱艱膚夢鑰襯鹽(淵衊醖窪構膚淵膚築壓) = 蓋廠夢窪夢艱製艱築繭鹽網襯願選遞醖構窪廠 (積獵窪廠顧構願壓襯鬱 ) 更多	-	2018-07-01
				T3D-959 10mg	糧繭築艱艱膚夢鑰襯鹽(淵衊醖窪構膚淵膚築壓) = 襯衊蓋鹹構鏇壓醖鬱獵鹽網襯願選遞醖構窪廠 (積獵窪廠顧構願壓襯鬱 ) 更多