A Randomized, Balanced, Phase 1, Multiple-dose, Open-label, Two-treatment, Two-period, Two-sequence, Crossover, Relative Bioavailability Study to Investigate Lithium Brain/Plasma Pharmacokinetics and Safety of an AL001 Oral Capsule Compared to a Marketed Immediate-release Lithium Carbonate Capsule in Healthy Adult Subjects

The goal of this clinical trial is to assess the safety and effects of a crystalized form of lithium, AL001, when compared to commonly used Lithium Carbonate in healthy volunteers. The main questions this study aims to answer are:
How safe and effective is AL001 when compared to Lithium Carbonate? How is AL001 broken down in the brain and body compared to Lithium Carbonate?
Participants will be asked to:
* Take both the study drug (AL001) and Lithium Carbonate each for a period of 14 days
* Stay overnight at MGH's research unit for two separate 2-week periods
* Participate in two separate 24 hour periods of multiple MRIs and blood draws

开始日期2025-05-01

申办/合作机构

Alzamend Neuro, Inc.

[+1]

CTR20250683

/ RecruitingN/A

碳酸锂片人体生物等效性研究

主要目的：比较空腹和餐后给药条件下湖南省湘中制药有限公司提供的碳酸锂片（规格：0.25 g）与LABORATOIRES DELBERT持证的碳酸锂片（商品名：TERALITHE®；规格：0.25 g）在中国健康人群吸收程度和吸收速度的差异。次要目的：评价空腹及餐后条件下，湖南省湘中制药有限公司提供的碳酸锂片（规格：0.25 g）与LABORATOIRES DELBERT持证的碳酸锂片（商品名：TERALITHE®；规格：0.25 g）在中国健康人群体内的安全性。

开始日期2025-03-29

申办/合作机构

湖南省湘中制药有限公司

NCT06776848

/ Not yet recruiting临床1/2期IIT

A Placebo-controlled Evaluation of Low Dose Lithium Carbonate in Patients with TBR1-related Neurocognitive Disorders: a 24-month Multi-centre Pilot Study

TBR1 is a human gene encoding a brain-specific transcription factor, principally expressed in the excitatory neurons of the neocortex. It regulates development of axonal projection and expression of numerous genes involved in autism spectrum disorders (ASD) and intellectual disability (ID). Recent progress in detection and analysis of rare variants allowed to identify group of genes with strong statistical evidence for association with ASD risk, of which TBR1. Numerous studies on mice showed that TBR1 heterozygous mice display autistic traits as deficiencies in social interaction, in cognitive flexibility, and in associative memory. Functional analyses on human cell lines have demonstrated that de novo truncating variants in TBR1 identified in patients with sporadic ASD disrupt transcriptional repression activity, localization, homodimerization of TBR1 product.
In 2019, only 12 single nucleotide variants (SNVs) and few copy number variations (CNVs) involving TBR1 have been reported in the literature and clinical descriptions were poor. To provide details on the phenotype linked to TBR1 mutations, we and others gathered 25 new individuals with de novo TBR1 SNV and CNV, complemented by a review of individuals previously reported in the literature. On 38 individuals, all presented developmental delay (DD)/ID, ranging from mild to severe, and 76% of them presented autistic traits. Additional behaviour disorders were observed in 85% of individuals, mainly attention deficit and aggressive behaviour. However, the natural history of patients with TBR1 variations is not well known.
Development of RNA-Seq allowed a better understanding of its transcription factor role and revealed that Tbr1 promotes expression of layer 6 markers as Wnt7b. In heterozygous and homozygous TBR1 mutant mice, Fazel Darbandi et al (1), observed that Wnt7b expression is reduced in cortical layer 6 and that neurons have reduced excitatory and inhibitory synaptic density. They showed that lithium chloride and lithium carbonate, WNT-signalling agonists, rescue the dendritic spines, the synaptic and the axonal defects in Tbr1layer5, Tbr1layer6 and Tbr1 constitutive (Tbr1+/-) mutant mice. They also observed an improvement of social interactions in mice after treatment by lithium. These results suggest an important and novel biological mechanism underlying ASD that may have implications for the treatment of patients with TBR1 variants.
Moreover, lithium treatment has already been evaluated in patients with neurocognitive disorders not linked to TBR1 showing an improvement in the adaptative behaviour and cognition function.
As of today, only symptomatic treatments are available. As lithium increase neuronal activity in mice, and may thus improve the symptoms of this disorder, we propose a clinical trial to study the security and efficacy of lithium carbonate targeting the patients with TBR1-related disorders, with specific and adapted endpoints. Lithium carbonate treatment will be administered after an observation period of 6 to 12 months, allowing to ascertain the stability of neurocognitive abnormalities.

开始日期2025-02-01

申办/合作机构

Centre Hospitalier Universitaire de Dijon

100 项与碳酸锂相关的临床结果

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100 项与碳酸锂相关的转化医学

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100 项与碳酸锂相关的专利（医药）

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23,776

项与碳酸锂相关的文献（医药）

2025-12-01·Nano-Micro Letters

Photo-Energized MoS2/CNT Cathode for High-Performance Li–CO2 Batteries in a Wide-Temperature Range

Article

作者: Li, Qiuju ; Hu, Kang ; Hu, Tingsong ; Yao, Tengyu ; Lian, Wenyi ; Shen, Laifa ; Cui, Xueliang

AbstractLi–CO2 batteries are considered promising energy storage systems in extreme environments such as Mars; however, severe performance degradation will occur at a subzero temperature owning to the sluggish reaction kinetics. Herein, a photo-energized strategy adopting sustainable solar energy in wide working temperature range Li–CO2 battery was achieved with a binder-free MoS2/carbon nanotube (CNT) photo-electrode as cathode. The unique layered structure and excellent photoelectric properties of MoS2 facilitate the abundant generation and rapid transfer of photo-excited carriers, which accelerate the CO2 reduction and Li2CO3 decomposition upon illumination. The illuminated battery at room temperature exhibited high discharge voltage of 2.95 V and mitigated charge voltage of 3.27 V, attaining superior energy efficiency of 90.2% and excellent cycling stability of over 120 cycles. Even at an extremely low temperature of − 30 °C, the battery with same electrolyte can still deliver a small polarization of 0.45 V by the photoelectric and photothermal synergistic mechanism of MoS2/CNT cathode. This work demonstrates the promising potential of the photo-energized wide working temperature range Li–CO2 battery in addressing the obstacle of charge overpotential and energy efficiency.

2025-12-01·Nano-Micro Letters

An Efficient Boron Source Activation Strategy for the Low-Temperature Synthesis of Boron Nitride Nanotubes

Article

作者: Zuo, Hui ; Songfeng, E ; Wang, Ying ; He, Qian ; Wang, Nanyang ; Hu, Yue ; Wu, Liyun ; Zhang, Kai ; Yao, Yagang ; Ding, Feng ; Zhang, Jin ; Ding, Liping ; Zhou, Zhengyang

AbstractLowering the synthesis temperature of boron nitride nanotubes (BNNTs) is crucial for their development. The primary reason for adopting a high temperature is to enable the effective activation of high-melting-point solid boron. In this study, we developed a novel approach for efficiently activating boron by introducing alkali metal compounds into the conventional MgO–B system. This approach can be adopted to form various low-melting-point AM–Mg–B–O growth systems. These growth systems have improved catalytic capability and reactivity even under low-temperature conditions, facilitating the synthesis of BNNTs at temperatures as low as 850 °C. In addition, molecular dynamics simulations based on density functional theory theoretically demonstrate that the systems maintain a liquid state at low temperatures and interact with N atoms to form BN chains. These findings offer novel insights into the design of boron activation and are expected to facilitate research on the low-temperature synthesis of BNNTs.

2025-09-01·Journal of the European Ceramic Society

Research on optimizing the crystal structure and enhancing the performance of LLTO solid electrolyte through doping with high-electronegativity Fe3+

作者: Kwame, Yadzo Emmanuel ; Jiang, Binxuan ; Yuan, Jiale ; Guo, Xu ; Li, Yueming ; Li, Kai

The excellent bulk conductivity of the perovskite-type (Li_0.33-xFe_xLa_0.56TiO₃, LLTO) solid electrolyte makes it one of the most valuable solid electrolyte materials.However, in the current research, there are few studies examining how electronegativity factors influence the crystal structure of LLTO.In this paper, the solid phase reaction method was adopted to adjust the lattice structure of the material by the chem. formula Li_0.33-xFe_xLa_0.56TiO₃(x = 0.01, 0.03,0.05, 0.07 mol) by substituting strong electronegativity Fe³⁺ ions for Li⁺ ions in LLTO.The effects of Fe³⁺ con the structure and properties of LLTO were studied.The results show that the addition of Fe³⁺ can successfully replace Li+ in the lattice, effectively improve the cubic phase content, crystal integrity, grain size uniformity and bulk d. of LLTO, and further improve the grain conductance.However, increasing the doping amount of Fe³⁺ c results in excessive unequal substitution, facilitating the formation of many cation vacancies in the lattice which is detrimental to the growth and perfection of cubic crystals.Also, excess Fe³⁺ c causes exaggerated grain growth, reduction of grain size uniformity and the d. of the material, thereby reducing the bulk conductance of the material.In this work, optimal comprehensive performance is achieved when the sample is doped with 0.01 mol of Fe³⁺ c and sintered at 1220 °C for 6 h.The c-LLTO content reaches 93%, bulk d. of 4.75 g cm^-3, and bulk conductivity of 1.42 mS cm^-1 which is 63.22% higher than that of the undoped sample.This study demonstrates that the incorporation of Fe³⁺ significantly enhances the bulk conductivity of the material′s grains.

项与碳酸锂相关的新闻（医药）

2025-05-02

·美中药源

唇齿相依的药物与靶点？

现代新药研发是个漫长、复杂、且昂贵的高风险过程，将其分割成多个风险可控步骤系统去风险化是一个实操的需求。您不能把一个成功率未知的化合物直接推进耗资上亿美元的三期，如同不能让一个没有经过各种比赛环境考验的球队去打世界杯。药物靶点是一个非常重要的去风险机制，靶点为中心因此成为新药研发的主流模式。成为主流是有其深刻原因和合理理由的。首先有很多药物的确有明确可靠靶点，比如以PCSK9抗体为代表的抗体药物。其次靶点提供了理性药物设计和开发的基础、降低了开发总风险，根据药物与靶点结合能力和药代性质就能大概判断你的药物在什么剂量、哪些人群可能产生疗效。另外如果药物的动物疗效来自患者没有的靶点也就不要盲目把这样药物推进临床了，比如最早的STING激动剂DMXAA只对鼠源STING有活性、到人体显然无法重复小鼠疗效，后来就没有人继续浪费资源优化DMXAA了。但是有些药物有明确靶点不等于所有药物开发都需要靶点， Arash Sadri最新的分析说只有9.4%小分子新药有是通过靶点驱动发现的、尽管这个比例存在争议。有些药物靶点是否与药物疗效有关也存疑，比如紫杉醇在肿瘤患者癌细胞内的浓度不足以抑制微管蛋白、这是它公认的作用靶点。靶向药物鼻祖格列卫是个BCL-ABL抑制剂，后来发现脱靶活性贡献了一些疗效。HER2 ADC在HER2阴性乳腺癌有效，PD-1药物在某些适应症选择PD-L1阳性患者需要加上非肿瘤细胞PD-L1。这些例子说明即使所谓精准医学药物也存在灰色地带。不仅很多药物的靶点我们不知道，甚至并不是所有成功药物背后都有一个传统意义上的生物学靶点。比如40年代发现的碳酸锂到现在还是双相情感障碍的一线用药，难以想象锂离子在人体高浓度金属离子竞争下能与哪个蛋白高强度结合。这并非孤例，下表这些分子量小于200的药物除了几个共价药物大多不会与生物分子以超过10nM亲和力结合，因为每个原子提供的结合自由能是有上限的（~0.3千卡/摩尔/重原子）、能够达到这个上限的分子很少见。这里面不乏二甲双胍、阿司匹林这样的大药，所以药物与靶点并非唇亡齿寒、或horse and carriage的共生关系。尽管制药界为搭建现在靶点为中心研发模式倾注了大量心血和投入，但最近与业界一些朋友聊天一个基本共识是这个体系不可持续。虽然这个模式提供了一个10%的临床开发成功率，但随着开发成本和支付端压力的不断提升新药开发已经开始向负回报率挺进。雪上加霜的是，研发技术的普及令跟踪靶点为中心药物变得越来越容易，导致你九死一生验证的靶点可在瞬间成为内卷中心，FIC与me-too药物上市间隔越来越短。生物体是一个复杂的系统、很多性质不能还原成部件功能，发生故障（疾病）并不一定是某个零件出了问题、而是多个零件的配合失调了。多年前冷泉实验室的Yuri Lazebnik教授写了一篇比较靶点为中心药物发现与修理收音机的文章，值得大家一读[1]。如同足球比赛，进攻丢球了不一定是传球线路上某个球员突然晕倒，更多情况是传球队员过度盘带错过最佳传球机会、接球队员占位不合理、队员体力下降动作变形等。系统故障要在系统水平排除，多年来靶点为中心模式的还原论基础不断受到质疑。系统生物学（Systems Biology）、表型筛选、高内涵筛选可能解决靶点为中心还原主义面临的一些问题，尤其在迅速成熟的AI支撑下。不可否认的是靶点为中心模式雷打不动除了正当理由外也有制药业的一些行为因素作怪，比如有了明确靶点令我们觉得药物设计的理性、精准性、可控性都增加了，这为挑战高度不确定的药物开发提供一些安全感。靶点也是药物开发失败的一个主要甩锅对象，否定靶点比否定开发能力更容易接受。靶点作为研发主线也更容易评价进展，活性、选择性、生物标记物的改变都是成药前的里程碑，助力了现在追求进展（progress-seeking）而非真相（truth-seeking）的开发文化。靶点对于某些药物是非常重要的，但不是所有药物都需要靶点、甚至不一定都有一个现在思考框架下的靶点。为了找到一个化合物的靶点我们发明各种化学生物学技术、如胞内卡宾蛋白标记，为了解决靶点不可成药性我们用尽了可能办法，从PROTAC、RNAi、到天文数字的DEL、多肽化合物库。这些技术固然重要，但我们不能忽略来自业界各领域观察者的共同体会，即过度依赖现有模式不可持续、我们需要关注主流之外的其它模式。四分卫长传技术是橄榄球比赛最重要因素，但是没有看似低效的running game再怎么提高QB的长传水平也难以持续赢得比赛。因为你注定会遇到擅长防守长传的队伍，如同有些疾病不是因为单个靶点功能异常造成。Deming说过“It is not necessary to change. Survival is not mandatory” ，继续沉醉于靶点相关技术进展可能忽略行业面临的生存危机。是时候看看那些通过非靶点驱动发现的药物能给我们哪些生存启示。[1]Lazebnik, Yuri. "Can a biologist fix a radio?—Or, what I learned while studying apoptosis." Cancer cell 2.3 (2002): 179-182.

抗体药物偶联物

2025-03-09

·医学新视点

巴西风湿病学会：干燥综合征患者神经、认知、精神表现的临床评估及管理建议

原发性干燥病（Sjögren′s disease，SjD）是一种免疫介导的慢性、炎症性疾病，临床表现极为复杂。除常见的外分泌腺功能障碍外，神经和精神系统也常受影响，严重影响患者的生活质量、社会参与度和预后。然而，在SjD患者中，其神经和精神症状常被忽视，且尚未得到全面、系统的评估。鉴于SjD引起的神经、精神和认知障碍的病理生理学基础尚不完全清楚，且缺乏明确的诊断、调查及管理标准，当前的治疗策略主要遵循一般指导方针。因此，深入探索SjD患者神经和精神系统病变的病理机制，寻找共同的分子特征，并结合临床参数进行综合分析，对于提高诊断准确性、优化治疗方案及改善患者预后具有重要意义。巴西风湿病学会工作小组对原发性SjD的中枢、周围和自主神经系统表现的诊断和患病率进行了系统回顾，并提出针对性的诊断和管理建议，以期为临床实践提供新的思路与参考。研究共纳入51项研究，重点关注并分析了周围神经系统和中枢神经系统相关内容，并在此基础上制定了10条建议。 ▲选择用于荟萃分析的关于SjD的神经和精神表现的诊断和流行的研究流程图（图片来源：参考文献[1]) 主要观点 SjD的神经系统受累在解剖学上分为三大类：中枢神经系统、周围神经系统和自主神经系统。尽管欧洲抗风湿病联盟干燥综合征疾病活动指数（ESSDAI）这一疾病活动评估工具纳入了部分神经系统表现，但其并未对某些神经和精神方面的表现进行评估。神经系统症状可能比干燥症状早几年出现，这进一步增加了诊断SjD的困难性。与干燥综合征相关的神经和精神障碍展现了一个广泛且高度异质性的临床表现谱系，其中一些症状往往未被识别为潜在疾病的一部分。推荐意见 01 建议将ESSDAI作为诊断和评估SjD期间神经系统疾病活动的辅助工具。（同意度100%） 02 建议对患有神经系统综合征的患者进行SjD检查，即使患者没有出现干燥症状，尤其是当其他诊断线索无明显进展时。（同意度100%） 03 对于有自身免疫证据（如抗核抗体、抗Ro/SSA抗体、抗La/SSB抗体、冷球蛋白、类风湿因子）、存在生物标志物（高γ球蛋白血症、低补体水平）、有干燥症状或既往诊断为SjD的患者，建议关注神经系统疾病。（同意度100%） 04 建议对SjD和神经系统疾病患者进行管理，或与专业知识中心密切合作，采用多学科方法。（同意度100%）周围神经系统主要观点周围神经系统的表现通常与体质和内脏症状以及血清生物标志物的改变有关。这些情况可能与ESSDAI评估的较高疾病活动率相关，尽管该工具没有考虑到许多潜在的表现。周围神经系统受累比中枢神经受累更常见，其中一些可导致较差的生活质量和淋巴瘤的风险增加。周围神经病变患者的生存率似乎降低，尤其是那些患有多发性单神经炎的患者。 SjD的神经学表现需要特别注意与感染性疾病（麻风病和丙型肝炎病毒感染、人类免疫缺陷病毒感染、人类嗜T淋巴细胞病毒感染）、代谢性疾病（糖尿病）、遗传性疾病（法布雷病、淀粉样变性）、副蛋白血症和肿瘤、维生素B12和硒缺乏、酒精或药物毒性以及其他自身免疫性炎症性疾病（乳糜泻、重症肌无力和桥本氏甲状腺炎）进行鉴别诊断。一些与周围神经症状有关的药物包括抗生素（异烟肼、甲硝唑、乙胺丁醇、呋喃妥因、粘菌素、氨苯砜）、抗有丝分裂药物（长春新碱、顺铂、紫杉醇、阿霉素）、抗病毒药物（双脱氧肌苷、双脱氧胞苷、干扰素）以及其他药物（沙利度胺、秋水仙碱、金制剂、青霉胺、氯喹、环孢素、胺碘酮、苯妥英、双硫仑、碳酸锂片、西咪替丁）。推荐意见 05 建议在诊断时准确评估每位患者的神经体征和症状以及随访期间的任何不适。（同意度100%） 06 建议对患有SjD和神经系统疾病的患者进行最全面的评估，首先进行完整的神经系统检查。在根据综合征和病变部位进行临床诊断后，应采用适当的辅助检查。（同意度100%） 07 由于淋巴瘤风险增加，建议对SjD和周围神经损伤患者进行血清生物标志物（细胞减少、冷球蛋白、补体C4部分、γ球蛋白血症）、涎腺肿大、淋巴结病和体质症状（发热、盗汗、体重减轻）的评估。（同意度100%）中枢神经系统主要观点 SjD的中枢神经系统表现多样，影像学和脑脊液分析是诊断和鉴别诊断的重要工具。中枢神经系统受累可分为局灶性/多灶性受累（如卒中、视神经炎、多发性硬化样病变和假性肿瘤病变）和弥漫性受累（无菌性脑膜脑炎、认知功能障碍和精神障碍）。中枢神经系统受累可能导致严重的功能丧失以及更高的发病率和死亡率。认知障碍、抑郁症、脑病和脑膜炎是弥漫性受累的特征，这种情况更常见，但不是特别严重。血管炎、脱髓鞘疾病伴脊髓炎、视神经炎和运动神经元损伤是局灶性受累的特征，这些疾病罕见且危及生命。 SjD患者神经系统表现的主要危险因素是以前发生过另一种神经系统受累。辅助诊断评估和管理推荐意见 08 建议进行辅助检查以明确神经疾病的综合征和病变部位特征，避免误诊。（同意度100%） Ⅰ. 脑脊液对于感染和中枢神经系统肿瘤的鉴别诊断至关重要。在大多数神经精神性SjD病例中，脑脊液检查结果在参考范围内。蛋白升高、淋巴细胞增多和寡克隆带均为非特异性表现，在多达1/4的中枢、颅神经或周围神经系统受累的患者中被观察到。 Ⅱ. 影像学检查，如脑部和神经轴的磁共振成像（MRI），有助于检测局灶性和弥漫性、血管性和脱髓鞘病变。在约80%的有症状或无症状个体的检查中，主要发现是白质中的血管源性病变，这些病变不具有特异性。 Ⅲ. 单光子发射计算机断层成像（SPECT）在评估受损脑区的灌注情况时具有一定价值，尽管其结果并不具有特异性，但当与磁共振成像（MRI）结合分析时，可提供有用信息。 Ⅳ. 肌电图（EMG）和神经传导研究（NCS）是诊断和验证病变部位的重要工具，特别是对于周围神经病变，应在神经系统体格检查之外进行。 Ⅴ. 神经、背神经节、肌肉和皮肤的活检和组织病理学检查分别有助于发现血管炎、神经血管坏死、炎性T细胞浸润和表皮无髓纤维密度降低。 Ⅵ. 建议所有视神经炎或脊髓炎患者进行抗水通道蛋白4抗体筛查。 09 建议对患有SjD并主诉听力损失（无论是否伴有认知障碍）的患者进行早期筛查和定期随访，通过纯音测听检查感音神经性听力损失。（同意度100%）治疗周围神经系统管理周围神经病变的治疗方案应根据临床表现进行个体化调整，以缓解疼痛并优化功能。对于感觉及感觉运动轴索性神经病，治疗策略依据病情轻重及进展而异。轻度、稳定患者多采取对症处理；对于常规治疗无效或病情进展伴运动障碍的严重患者，静脉注射免疫球蛋白（IVIg）以每月2 g/kg剂量治疗有效。对于难治性病例，可考虑甲泼尼龙和环磷酰胺冲击治疗作为二线选择。利妥昔单抗及疾病修饰药物如吗替麦考酚酯和硫唑嘌呤等疗效有限。小纤维神经病的治疗重点在于缓解疼痛，一线药物包括加巴喷丁和普瑞巴林，疼痛控制不佳时可考虑5-羟色胺-去甲肾上腺素再摄取抑制剂替代或联用。三环类抗抑郁药虽有效但可能加重干燥症状，阿片类镇痛药疗效存疑。症状治疗无效时，可尝试实验性免疫调节或免疫抑制疗法，个案报告显示IVIg有效，但治疗持续时间不明。在治疗感觉共济失调神经病时，免疫抑制药物、IVIg、抗TNF、抗CD20疗法及糖皮质激素的使用存在争议。其中，糖皮质激素使用较广泛，IVIg常作为一线药物与其联用；免疫疗法、合成药物及血浆置换的研究结果相互矛盾，或与治疗延迟有关。多发性单神经炎常用环磷酰胺和大剂量糖皮质激素治疗。利妥昔单抗可用于冷球蛋白血症性血管炎病变。颅神经病变可用糖皮质激素治疗，根神经节病变可能对IVIg有反应。慢性炎症性脱髓鞘性多发性神经病可采用糖皮质激素、血浆置换和IVIg治疗。自主神经病变目前仅支持性治疗有效。中枢神经系统管理中枢神经系统表现相对罕见，其治疗多为经验性治疗。对于严重、急性或快速进展的中枢神经系统受累患者，首选大剂量糖皮质激素和环磷酰胺，随后逐渐减少糖皮质激素剂量。替代疗法和维持缓解药物包括硫唑嘌呤和霉酚酸酯等，但由于缺乏直接比较免疫抑制剂疗效和安全性的对照研究，因此无法推荐优先使用某一种药物。利妥昔单抗可用于冷球蛋白相关血管炎和NMOSD的抢救治疗。EM样病例应接受特异性EM治疗。对于精神疾病或精神模糊等惰性症状，应进行适当的监测和支持性治疗。主要观点对于神经系统表现的治疗多为经验性，其依据主要来自于非对照研究的小病例系列中获得的证据，并以专家意见为指导，这些意见是从治疗SjD本身的其他腺体外表现或治疗其他自身免疫性疾病的类似表现中推断出来。免疫抑制剂主要用作糖皮质激素保留剂，很少有证据支持选择一种药物优于另一种药物。由于缺乏比较其在SjD中疗效的研究，因此除了考虑患者的特征和合并症的安全性问题外，无法给出具体的推荐。关于剂量、给药途径和治疗持续时间，目前尚无可用的信息。推荐意见 10 建议神经系统表现的药物管理应侧重于致病机制，而致病机制因受累类型而异。（同意度100%）相关阅读《柳叶刀》：皮肤干燥、剧烈瘙痒？别担心，这类单克隆抗体治疗效果好！瘙痒、糜烂、水疱……《柳叶刀》：4大类措施，早日摆脱手部湿疹嗜睡、疲劳、怕冷、变胖……多半是甲状腺出问题了！《柳叶刀》：关注甲减治疗的5大问题欢迎投稿：学术成果、前沿进展、临床干货等主题均可，点此了解投稿详情。参考资料 [1] de Oliveira FR, Appenzeller S, Pasoto SG, et al. Recommendations on neurologic, cognitive, and psychiatric manifestations in patients with Sjögren's disease by the Brazilian Society of Rheumatology. Adv Rheumatol. 2025 Feb 11;65(1):7. doi: 10.1186/s42358-025-00438-7. PMID: 39934881. 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。分享，点赞，在看，传递医学新知

2024-12-18

·ir.alzamend.com

Alzamend Neuro to Present Non-Clinical Data Update at the Society of Toxicology 2025 Annual Meeting and ToxExpo

Presentation Topic is the Pharmacokinetics of AL001, a Lithium Salicylate/L-Proline Co-crystal, as a Potentially Beneficial Lithium Sparing Treatment for Bipolar Disorder Type 1, Alzheimer’s Disease, Major Depressive Disorder and Post-Traumatic Stress Disorder ATLANTA--(BUSINESS WIRE)-- Alzamend Neuro, Inc. (Nasdaq: ALZN) (“Alzamend”), a clinical-stage biopharmaceutical company, focused on developing novel products for the treatment of Alzheimer’s disease (“Alzheimer’s”), bipolar disorder (“BD”), major depressive disorder (“MDD”) and post-traumatic stress disorder (“PTSD”), today announced it will have a poster presentation at the Society of Toxicology (“SOT”) Annual Meeting and ToxExpo, being held from March 16-20, 2025, in Orlando, Florida. “Our poster presentation at SOT in 2025 with data from our non-clinical study: Comparing Brain and Plasma Lithium Exposures between AL001 and Lithium Carbonate in Alzheimer’s Transgenic Mice, demonstrates the potential of AL001 to enhance brain-specific lithium delivery while minimizing systemic exposure in an Alzheimer’s disease mouse model, guiding development of enhanced lithium effectiveness and safety in human diseases,” said Stephan Jackman, Chief Executive Officer of Alzamend. “Following successful results from this study and our Phase I and IIA trials, AL001 is positioned for five Phase II trials in partnership with Massachusetts General Hospital in 2025. These trials aim to redefine lithium therapy across neurodegenerative and neuropsychiatric conditions by leveraging a lower-dose, high-efficacy approach anticipated to qualify for the U.S. Food and Administration 505(b)(2) approval pathway.” Abstract 3266/H393 – Poster presentation: Title: Pharmacokinetics of AL001, Lithium Salicylate/L-Proline Co-crystal: A Potentially Beneficial Lithium Sparing Treatment for Bipolar Disorder Type 1 (BD1), Alzheimer’s Disease (AD), Major Depressive Disorder (MDD) and Post-traumatic Stress Disorder (PTSD) Session Title: Pharmaceutical Safety and Drug Discovery Session Date and Time: Monday, March 17, 2025; 9:15AM ET – 11:45AM ET Session Location: Orange County Convention Center, ToxExpo Hall Presenting Author: Darrell Sawmiller, Ph.D, Assistant Professor, Center of Excellence for Aging & Brain Repair, University of South Florida, Tampa, FL, USA Summary: No Undue Adverse Effects: Both treatments had no negative impact on the mice's body weight or clinical signs during the treatment period. Reduced Systemic Exposure: AL001 showed lower plasma lithium levels than lithium carbonate, reducing the risk of adverse systemic effects, suggesting an expansion for safety of lithium’s therapeutic index. Enhanced Brain Penetration: AL001 showed consistently higher lithium concentrations in brain tissues, particularly at lower doses, compared to lithium carbonate. Targeted Brain Structures: The study found that different brain regions absorb and retain lithium differently. This means treatments can potentially be tailored to target specific brain areas, allowing for more precise treatment of various brain-related conditions when applied in human studies. Further information can be found at https://www.toxicology.org/events/am/AM2025/index.asp. About AL001 Non-Clinical Study The study involved administering AL001, a good manufacturing practices-quality active pharmaceutical ingredient (“API”) to 5XFAD mice, a recognized model for Alzheimer’s research, to compare its effects against lithium carbonate, a U.S. Food and Drug Administration approved and marketed API. Mice received either high or low doses scaled to humans of both AL001 and lithium carbonate over a 14-day period to observe pharmacokinetic steady-state drug conditions. On the 15th day, the mice were analyzed to assess how the treatments affected lithium concentrations in different brain regions and in their plasma. The results mentioned in the summary highlight the potential clinical advantages of AL001 for conditions like Alzheimer’s, BD, MDD and PTSD at low doses. By reducing the systemic burden, AL001 could lessen the risk of side effects such as thyroid and kidney complications often associated with extant lithium therapies. This positions AL001 as a promising candidate for safer long-term treatment options, without the need for routine blood lithium monitoring. This innovation is specifically designed to address the needs of fragile populations, such as elderly and Alzheimer’s patients, by offering a potentially more efficient and safer alternative to existing treatments. About Alzamend Neuro Alzamend Neuro is a clinical-stage biopharmaceutical company focused on developing novel products for the treatment of Alzheimer’s, BD, MDD and PTSD. Our mission is to rapidly develop and market safe and effective treatments. Our current pipeline consists of two novel therapeutic drug candidates, AL001 - a patented ionic cocrystal technology delivering lithium via a therapeutic combination of lithium, salicylate and L-proline, and ALZN002 - a patented method using a mutant-peptide sensitized cell as a cell-based therapeutic vaccine that seeks to restore the ability of a patient’s immunological system to combat Alzheimer’s. Both of our product candidates are licensed from the University of South Florida Research Foundation, Inc. pursuant to royalty-bearing exclusive worldwide licenses. Forward-Looking Statements This press release contains “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. These forward-looking statements generally include statements that are predictive in nature and depend upon or refer to future events or conditions, and include words such as “believes,” “plans,” “anticipates,” “projects,” “estimates,” “expects,” “intends,” “strategy,” “future,” “opportunity,” “may,” “will,” “should,” “could,” “potential,” or similar expressions. Statements that are not historical facts are forward-looking statements. Forward-looking statements are based on current beliefs and assumptions that are subject to risks and uncertainties. Forward-looking statements speak only as of the date they are made, and Alzamend undertakes no obligation to update any of them publicly in light of new information or future events. Actual results could differ materially from those contained in any forward-looking statement as a result of various factors. More information, including potential risk factors, that could affect Alzamend’s business and financial results are included in Alzamend’s filings with the U.S. Securities and Exchange Commission. All filings are available at www.sec.gov and on Alzamend’s website at www.Alzamend.com. View source version on businesswire.com: https://www.businesswire.com/news/home/20241218800562/en/ Email: Info@Alzamend.com or call: 1-844-722-6333 Source: Alzamend Neuro, Inc. Released December 18, 2024

临床2期疫苗临床结果

100 项与碳酸锂相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
D00801	碳酸锂	N05AN01	DB14509

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适应症	国家/地区	公司	日期
躁郁症1型	美国	Hikma Pharmaceuticals USA, Inc.	1982-01-29
躁郁症	美国	ANI Pharmaceuticals, Inc.	1979-04-27

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适应症	最高研发状态	国家/地区	公司	日期
克莱恩-莱文综合征	临床前	欧盟	Laboratoires Delbert SAS	2023-08-16

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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


NCT02862210 (Lithium, CTgov)	临床2期	额颞痴呆	17	Lithium Carbonate (Lithium Carbonate)	壓夢積壓膚鹹構齋構積(衊鑰築廠積窪範窪獵艱) = 壓積觸窪窪餘遞構廠窪淵鑰窪齋衊鏇簾構窪選 (壓衊築製壓鬱獵鏇襯鏇, 製衊蓋遞蓋繭構製壓顧 ~ 齋構範廠鹽網鑰網鬱醖) 更多	-	2025-02-03
NCT02862210 (Lithium, CTgov)	临床2期	额颞痴呆	17	Placebo (Placebo)	壓夢積壓膚鹹構齋構積(衊鑰築廠積窪範窪獵艱) = 選齋範願餘窪顧觸簾蓋淵鑰窪齋衊鏇簾構窪選 (壓衊築製壓鬱獵鏇襯鏇, 艱鏇繭製願壓遞顧鬱醖 ~ 齋憲廠蓋夢淵鹹鹽夢鏇) 更多	-	2025-02-03
ASN2022	N/A	肾性尿崩症	-	Lithium Carbonate 300 mg	襯網襯觸齋顧顧窪齋顧(網憲觸願膚憲廠網築艱) = 築鹹構衊觸選製製糧鬱夢壓糧糧鹹醖鹹鹽衊憲 (衊獵範衊繭鏇範鹹鹹觸 )	-	2022-11-06
ASN2022	N/A	肾性尿崩症	-	Thiazide diuretic	襯網襯觸齋顧顧窪齋顧(網憲觸願膚憲廠網築艱) = 築襯鑰衊廠繭蓋鬱醖選夢壓糧糧鹹醖鹹鹽衊憲 (衊獵範衊繭鏇範鹹鹹觸 )	-	2022-11-06
ISN WCN2022	N/A	中毒 \| 间质性肾炎	-	Lithium carbonate 900 mg/day	鏇艱鑰鹹選夢衊願憲壓(衊願願夢蓋鬱積夢簾蓋) = The diagnosis of chronic interstitial nephritis was made based on suggestive clinical and biological signs 鑰積觸構襯遞鏇壓願獵 (鑰鏇艱壓膚壓積製鹹簾 )	-	2022-02-01
ISN WCN2022	N/A	中毒 \| 间质性肾炎	-	No lithium therapy		-	2022-02-01
ENDO2021	N/A	甲状腺功能亢进症 \| 粒细胞减少症一线	-	Methimazole	範顧齋網鹹積憲膚鹽鹽(獵壓醖淵廠襯製憲製鹽) = 鑰餘餘獵鹽窪窪鹹築艱繭壓憲衊範鏇膚窪衊蓋 (鬱鹹選積憲襯願襯願繭 ) 更多	-	2021-05-03
ENDO2021	N/A	甲状腺功能亢进症 \| 粒细胞减少症一线	-	Lithium Carbonate	範顧齋網鹹積憲膚鹽鹽(獵壓醖淵廠襯製憲製鹽) = 醖餘齋鏇壓廠膚壓顧壓繭壓憲衊範鏇膚窪衊蓋 (鬱鹹選積憲襯願襯願繭 )	-	2021-05-03
NCT02918097 (CTgov)	临床4期	躁郁症	78	Lithium Carbonate+Risperidone+Nortriptyline+Sertraline	醖餘範壓餘艱糧衊獵襯(顧餘襯鬱艱齋築顧餘夢) = 糧選膚醖鏇願構鏇鏇顧願醖遞憲膚膚構齋膚夢 (齋壓鬱齋衊淵簾艱選築, 鬱願淵齋範繭製積壓鏇 ~ 鬱憲鹹夢廠獵構簾窪獵) 更多	-	2020-10-14
NCT01820624 (Pubmed) 人工标引	临床1期	急性髓性白血病	9	lithium carbonate+tretinoin	(齋膚鑰積膚築顧範遞顧) = 觸積餘衊築膚鹹餘襯獵窪遞壓齋淵蓋壓鏇築壓 (艱遞鏇願範簾觸衊遞觸 )	不佳	2020-03-10
NCT01553916 (CTgov)	临床1/2期	小细胞肺癌	19	Prophylactic cranial irradiation+Lithium Carbonate	憲網蓋簾遞壓夢選簾顧(廠衊醖遞鹹願鏇衊壓蓋) = 簾鹹網壓淵艱繭鑰簾網鹹範衊獵襯願獵蓋鬱齋 (衊顧齋憲窪繭衊艱窪襯, 鹹選壓簾鹹願鑰簾鹽衊 ~ 鹹築醖遞壓觸襯簾憲餘) 更多	-	2017-11-08
NCT00501540 (CTgov)	临床2期	神经内分泌肿瘤	15	Lithium Carbonate	(膚廠築顧憲襯衊糧憲壓) = 鹹醖簾獵範鑰築淵壓製簾簾壓鹹網憲齋範構蓋 (獵製繭齋遞鏇糧積鬱餘, 鑰夢遞艱積壓壓繭製鏇 ~ 糧獵齋觸鹹選餘齋遞齋) 更多	-	2017-05-03
NCT00408681 (GVHD, CTgov)	N/A	复发性急性髓细胞白血病 \| 复发性边缘区淋巴瘤 \| 妊娠滋养细胞疾病 \| 成人急性髓性白血病 \| 伯基特淋巴瘤 \| BCR/ABL阴性非典型性慢性髓系白血病 \| 难治性成人急性淋巴细胞白血病 \| 加速期慢性骨髄性白血病 \| 复发性霍奇金淋巴瘤 \| 继发性骨髓增生异常综合征 \| 毛细胞白血病 \| 幼年型骨髓单核细胞白血病 \| 多发性骨髓瘤 \| 原发性皮肤间变性大细胞淋巴瘤 \| 塞扎里综合征 \| 难治性慢性淋巴细胞白血病 \| 慢性嗜酸性粒细胞白血病 \| 小淋巴细胞淋巴瘤 \| 原发性骨髓纤维化 \| 淋巴母细胞淋巴瘤 \| 3型乳腺癌 \| 慢性期慢性髓性白血病 \| 急性移植物抗宿主病 \| 复发性成人急性淋巴细胞白血病 \| 肾母细胞瘤 \| 并发症 \| 慢性粒单核细胞白血病 \| 弥漫性大B细胞淋巴瘤 \| 卵巢生殖细胞癌 \| 急性转化期慢性粒细胞性白血病 \| 复发性套细胞淋巴瘤 \| 睾丸生殖细胞肿瘤 \| 急性早幼粒细胞白血病 \| 复发性 B 细胞急性淋巴细胞白血病 \| 小儿横纹肌肉瘤 \| 复发性卵巢癌 \| 复发性神经母细胞瘤 \| 未经治疗的小儿急性非淋巴细胞白血病 \| 慢性中性粒细胞白血病 \| 免疫母细胞大细胞淋巴瘤 \| 伴有 11q23 异常的急性髓系白血病 \| 复发性 3a 级滤泡性淋巴瘤 \| 转移性乳腺癌 \| 小儿淋巴母细胞非霍奇金淋巴瘤 \| 卵巢上皮癌 \| II 期非连续成人弥漫性小裂细胞淋巴瘤	20	laboratory biomarker analysis+lithium carbonate	鬱網膚範醖夢鬱鬱構遞(憲廠餘淵構糧獵醖夢夢) = 廠遞獵網蓋膚夢繭築鏇築鏇鏇糧齋遞願淵顧網 (願鹽願願衊繭築餘鹽範, 遞膚願鑰廠艱鑰鬱獵壓 ~ 蓋簾襯艱餘製製顧鹹鏇)	-	2017-01-20
NCT00582712 (CTgov)	临床2期	甲状腺髓样癌	5	Lithium carbonate	選範蓋鹹鑰鹹艱壓醖鏇(範糧遞鑰糧繭繭膚願遞) = 齋製窪餘齋鏇繭憲淵網積簾鹽壓願廠觸鑰糧鹽 (齋齋獵艱製獵廠獵觸鹽, 遞壓鹹蓋淵齋蓋範網鑰 ~ 積艱築鹽鹽襯壓糧鑰顧) 更多	-	2016-12-12