A Phase 1, randomized, double-blind, placebo-controlled study of BMS-984923 administered orally twice daily (BID) for 28 days in participants with Parkinson's disease.

开始日期2024-03-15

申办/合作机构

Allyx Therapeutics, Inc.初创企业

[+1]

NCT05804383 / Recruiting临床1期

A Phase 1B Multiple Ascending Dose Study of The Safety and Tolerability of BMS-984923 in Healthy Older Adults and Patients With Alzheimer's Disease

A Phase 1b Multiple Ascending Dose Study of the Safety and Tolerability of BMS-984923 in Healthy Older Adults and Patients with Alzheimer's Disease

开始日期2023-03-28

申办/合作机构

Allyx Therapeutics, Inc.初创企业

[+2]

NCT05817643 / Active, not recruiting临床1期

A Randomized, Open-label, 2-period, Crossover, Pilot Food Effect Study of BMS-984923 in Healthy Older Adult Volunteers

This project is developing a novel disease-modifying compound for Alzheimer's disease (AD).

开始日期2023-01-10

申办/合作机构

Allyx Therapeutics, Inc.初创企业

[+1]

100 项与 BMS-984923 相关的临床结果

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100 项与 BMS-984923 相关的转化医学

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100 项与 BMS-984923 相关的专利（医药）

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项与 BMS-984923 相关的文献（医药）

2022-06-01·Science translational medicine1区 · 医学

Reversal of synapse loss in Alzheimer mouse models by targeting mGluR5 to prevent synaptic tagging by C1Q

1区 · 医学

Article

作者: Toyonaga, Takuya ; Spurrier, Joshua ; Laird, William ; Chiasseu, Marius ; Nies, Sarah Helena ; Allnutt, Mary Alice ; Siegert, Timothy R. ; Zhang, Le ; Fang, Xiaotian T. ; Lee, Supum ; Strittmatter, Stephen M. ; Sadasivam, Pragalath ; Cai, Zhengxin ; Holden, Daniel ; Nicholson, LaShae ; Brody, A. Harrison ; Pérez-Cañamás, Azucena ; Takahashi, Hideyuki ; Carson, Richard E. ; Huang, Yiyun H. ; Stoner, Austin J. ; Li, Songye

Microglia-mediated synaptic loss contributes to the development of cognitive impairments in Alzheimer’s disease (AD). However, the basis for this immune-mediated attack on synapses remains to be elucidated. Treatment with the metabotropic glutamate receptor 5 (mGluR5) silent allosteric modulator (SAM), BMS-984923, prevents β-amyloid oligomer–induced aberrant synaptic signaling while preserving physiological glutamate response. Here, we show that oral BMS-984923 effectively occupies brain mGluR5 sites visualized by [ 18 F]FPEB positron emission tomography (PET) at doses shown to be safe in rodents and nonhuman primates. In aged mouse models of AD ( APPswe/PS1 Δ E9 overexpressing transgenic and App NL-G-F / hMapt double knock-in), SAM treatment fully restored synaptic density as measured by [ 18 F]SynVesT-1 PET for SV2A and by histology, and the therapeutic benefit persisted after drug washout. Phospho-TAU accumulation in double knock-in mice was also reduced by SAM treatment. Single-nuclei transcriptomics demonstrated that SAM treatment in both models normalized expression patterns to a far greater extent in neurons than glia. Last, treatment prevented synaptic localization of the complement component C1Q and synaptic engulfment in AD mice. Thus, selective modulation of mGluR5 reversed neuronal gene expression changes to protect synapses from damage by microglial mediators in rodents.

2017-07-01·Cell reports1区 · 生物学

Silent Allosteric Modulation of mGluR5 Maintains Glutamate Signaling while Rescuing Alzheimer’s Mouse Phenotypes

1区 · 生物学

ArticleOA

作者: Herber, Charlotte S ; Haas, Laura T ; Smith, Levi M ; Macor, John E ; Balakrishnan, Anand ; Strittmatter, Stephen M ; Degnan, Andrew P ; Albright, Charles F ; Cox, Timothy O ; Zhao, Helen R ; Salazar, Santiago V

Metabotropic glutamate receptor 5 (mGluR5) has been implicated in Alzheimer's disease (AD) pathology. We sought to understand whether mGluR5's role in AD requires glutamate signaling. We used a potent mGluR5 silent allosteric modulator (SAM, BMS-984923) to separate its well-known physiological role in glutamate signaling from a pathological role in mediating amyloid-β oligomer (Aβo) action. Binding of the SAM to mGluR5 does not change glutamate signaling but strongly reduces mGluR5 interaction with cellular prion protein (PrP^C) bound to Aβo. The SAM compound prevents Aβo-induced signal transduction in brain slices and in an AD transgenic mouse model, the APPswe/PS1ΔE9 strain. Critically, 4 weeks of SAM treatment rescues memory deficits and synaptic depletion in the APPswe/PS1ΔE9 transgenic mouse brain. Our data show that mGluR5's role in Aβo-dependent AD phenotypes is separate from its role in glutamate signaling and silent allosteric modulation of mGluR5 has promise as a disease-modifying AD intervention with a broad therapeutic window.

bioRxiv : the preprint server for biology

Aging-Dependent Loss of Connectivity in Alzheimer’s Model Mice with Rescue by mGluR5 Modulator

作者: Papademetris, Xenophon ; Onofrey, John ; Mukherjee, Bandhan ; Mandino, Francesca ; Desrosiers-Gregoire, Gabriel ; Strittmatter, Stephen M ; Shen, Xilin ; Lake, Evelyn MR ; Qu, An ; Chakravarty, M. Mallar ; O’Connor, David ; Owens, Ashley

Abstract:

Amyloid accumulation in Alzheimer’s disease (AD) is associated with synaptic damage and altered connectivity in brain networks. While measures of amyloid accumulation and biochemical changes in mouse models have utility for translational studies of certain therapeutics, preclinical analysis of altered brain connectivity using clinically relevant fMRI measures has not been well developed for agents intended to improve neural networks. Here, we conduct a longitudinal study in a double knock-in mouse model for AD (AppNL-G-F/hMapt), monitoring brain connectivity by means of resting-state fMRI. While the 4-month-old AD mice are indistinguishable from wild-type controls (WT), decreased connectivity in the default-mode network is significant for the AD mice relative to WT mice by 6 months of age and is pronounced by 9 months of age. In a second cohort of 20-month-old mice with persistent functional connectivity deficits for AD relative to WT, we assess the impact of two-months of oral treatment with a silent allosteric modulator of mGluR5 (BMS-984923) known to rescue synaptic density. Functional connectivity deficits in the aged AD mice are reversed by the mGluR5-directed treatment. The longitudinal application of fMRI has enabled us to define the preclinical time trajectory of AD-related changes in functional connectivity, and to demonstrate a translatable metric for monitoring disease emergence, progression, and response to synapse-rescuing treatment.

项与 BMS-984923 相关的新闻（医药）

2024-06-11

·GlobeNewswire-Health Care

Allyx Therapeutics Announces First Alzheimer’s Disease Patient Treated with Lead Compound ALX-001

With Growing Body of Clinical Evidence, ALX-001 is Ready to Commence Phase 2 StudiesNEW HAVEN, Conn., June 11, 2024 (GLOBE NEWSWIRE) -- Allyx Therapeutics, a clinical-stage biotechnology company working to deliver a novel approach to preserve and protect synapses for people living with neurodegenerative diseases, announced that the first Alzheimer’s disease patient has been dosed with its lead compound, ALX-001, in a clinical study. ALX-001 is a highly selective, first-in-class, synapse-targeted, disease-modifying oral therapy that is ready for Phase 2 clinical development. “Administering the first dose in patients is a watershed moment for a new therapeutic, and we are pleased to begin research in Alzheimer’s disease patients as we continue to advance clinical development of ALX-001 to become the first-ever disease-modifying small molecule for neurodegenerative diseases,” commented Stephen Bloch, M.D., chief executive officer and co-founder of Allyx Therapeutics. Individuals with Alzheimer’s disease are being enrolled in a 28-day study which will evaluate the safety of ALX-001 dosed twice daily at either 50 mg or 100 mg versus placebo in adults between 50 and 80 years of age. This is the second phase of an ongoing study which previously assessed multiple ascending doses in healthy volunteers (NCT05804383) and is being conducted at Yale School of Medicine with support from the National Institute on Aging. “Every neuroscientist hopes for the moment that an asset they believe in and fight for advances to the critical stage of testing in patients,” stated Stephen Strittmatter M.D., Ph.D., scientific founder of Allyx Therapeutics and professor and chair of Neuroscience at the Yale School of Medicine. “The unique mechanism of action of ALX-001 and its promising early data have brought us to this point, and bolster our hope that it has the potential to be a difference-maker in Alzheimer’s disease.” ALX-001 is ready to proceed to phase 2 clinical development, and is not restricted by completion of ongoing studies. Building on twelve years of clinical research, ALX-001 continues to demonstrate promise in studies supported by highly reputable third parties. The ALX-001 program has received more than $20 million in grant funding from the National Institutes of Health, the U.S. Government’s highly competitive Small Business Innovation Research (SBIR) programs, the Alzheimer’s Association, and The Michael J. Fox Foundation for Parkinson’s Research, among others. About ALX-001ALX-001 (previously BMS-984923) is a silent allosteric modulator of mGluR5, and is a first-in-class compound that selectively blocks the pathogenic activation of the receptor while preserving the normal physiological glutamate signaling that is required for cognition. As such, ALX-001 has a wide therapeutic window that can saturate receptors while avoiding on-target toxicity observed with negative allosteric modulators. mGluR5 has been shown to be essential for mediating synaptic dysfunction and loss caused by multiple misfolded extracellular protein species, and as such, presents a novel approach for treating Alzheimer's and Parkinson’s disease. Importantly, ALX-001 is an orally bioavailable and brain penetrant small molecule with demonstrated mGluR5 selective engagement. The molecule was originally identified by Bristol Myers Squibb, but the mechanism of action for neurodegenerative diseases and the identification of ALX-001 as disease-modifying for Alzheimer’s disease was discovered by Allyx scientific founder Stephen Strittmatter at Yale School of Medicine. Allyx Therapeutics obtained an exclusive worldwide license for ALX-001 from Bristol Myers Squibb and Yale School of Medicine. About Allyx Therapeutics Allyx Therapeutics was founded in 2019 by a group of seasoned biopharma industry executives, venture capitalists, and scientific experts. The company aims to deliver a novel approach to preserve and protect synapses for people living with neurodegenerative diseases. Its lead compound, ALX-001, is a first-in-class oral therapy with a unique mechanism of action at mGluR5 in clinical development for Alzheimer’s disease and Parkinson’s disease. Learn more at allyxthera.com. Contact Media: Eliza Schleifstein917.763.8106Eliza@schleifsteinpr.com Investors: Tim Siegert203-691-6543tsiegert@allyxthera.com

引进/卖出临床2期

2024-06-11

·BioSpace

Allyx Therapeutics Announces First Alzheimer’s Disease Patient Treated with Lead Compound ALX-001With Growing Body of Clinical Evidence, ALX-001 is Ready to Commence Phase 2 Studies

NEW HAVEN, Conn., June 11, 2024 (GLOBE NEWSWIRE) -- Allyx Therapeutics, a clinical-stage biotechnology company working to deliver a novel approach to preserve and protect synapses for people living with neurodegenerative diseases, announced that the first Alzheimer’s disease patient has been dosed with its lead compound, ALX-001, in a clinical study. ALX-001 is a highly selective, first-in-class, synapse-targeted, disease-modifying oral therapy that is ready for Phase 2 clinical development. “Administering the first dose in patients is a watershed moment for a new therapeutic, and we are pleased to begin research in Alzheimer’s disease patients as we continue to advance clinical development of ALX-001 to become the first-ever disease-modifying small molecule for neurodegenerative diseases,” commented Stephen Bloch, M.D., chief executive officer and co-founder of Allyx Therapeutics. Individuals with Alzheimer’s disease are being enrolled in a 28-day study which will evaluate the safety of ALX-001 dosed twice daily at either 50 mg or 100 mg versus placebo in adults between 50 and 80 years of age. This is the second phase of an ongoing study which previously assessed multiple ascending doses in healthy volunteers (NCT05804383) and is being conducted at Yale School of Medicine with support from the National Institute on Aging. “Every neuroscientist hopes for the moment that an asset they believe in and fight for advances to the critical stage of testing in patients,” stated Stephen Strittmatter M.D., Ph.D., scientific founder of Allyx Therapeutics and professor and chair of Neuroscience at the Yale School of Medicine. “The unique mechanism of action of ALX-001 and its promising early data have brought us to this point, and bolster our hope that it has the potential to be a difference-maker in Alzheimer’s disease.” ALX-001 is ready to proceed to phase 2 clinical development, and is not restricted by completion of ongoing studies. Building on twelve years of clinical research, ALX-001 continues to demonstrate promise in studies supported by highly reputable third parties. The ALX-001 program has received more than $20 million in grant funding from the National Institutes of Health, the U.S. Government’s highly competitive Small Business Innovation Research (SBIR) programs, the Alzheimer’s Association, and The Michael J. Fox Foundation for Parkinson’s Research, among others. About ALX-001 ALX-001 (previously BMS-984923) is a silent allosteric modulator of mGluR5, and is a first-in-class compound that selectively blocks the pathogenic activation of the receptor while preserving the normal physiological glutamate signaling that is required for cognition. As such, ALX-001 has a wide therapeutic window that can saturate receptors while avoiding on-target toxicity observed with negative allosteric modulators. mGluR5 has been shown to be essential for mediating synaptic dysfunction and loss caused by multiple misfolded extracellular protein species, and as such, presents a novel approach for treating Alzheimer's and Parkinson’s disease. Importantly, ALX-001 is an orally bioavailable and brain penetrant small molecule with demonstrated mGluR5 selective engagement. The molecule was originally identified by Bristol Myers Squibb, but the mechanism of action for neurodegenerative diseases and the identification of ALX-001 as disease-modifying for Alzheimer’s disease was discovered by Allyx scientific founder Stephen Strittmatter at Yale School of Medicine. Allyx Therapeutics obtained an exclusive worldwide license for ALX-001 from Bristol Myers Squibb and Yale School of Medicine. About Allyx Therapeutics Allyx Therapeutics was founded in 2019 by a group of seasoned biopharma industry executives, venture capitalists, and scientific experts. The company aims to deliver a novel approach to preserve and protect synapses for people living with neurodegenerative diseases. Its lead compound, ALX-001, is a first-in-class oral therapy with a unique mechanism of action at mGluR5 in clinical development for Alzheimer’s disease and Parkinson’s disease. Learn more at allyxthera.com. Contact Media: Eliza Schleifstein 917.763.8106 Eliza@schleifsteinpr.com Investors: Tim Siegert 203-691-6543 tsiegert@allyxthera.com

引进/卖出临床2期

2024-03-19

·药明康德

毛发再生疗法7天即可激活休眠毛囊干细胞；疾病控制率达100%的小分子抑制剂… | 一周盘点

▎药明康德内容团队编辑本期看点1. 新型局部外用小分子疗法PP405的早期临床结果表明，该疗法能重新激活休眠的毛囊干细胞，诱发毛发生长，有望治疗各类型脱发。2. 第三代小分子MEK抑制剂IMM-1-104用于治疗晚期携带RAS突变的实体肿瘤患者的早期临床结果亮眼，100%的患者未产生获得性RAS变异，超半数患者观察到靶病灶的消退。3. 口服HSF1信号通路抑制剂NXP800用于治疗铂类耐药、携带ARID1a突变的卵巢癌患者的1b期试验结果积极，疾病控制率达100%。药明康德内容团队整理PP405：公布1期临床试验数据Pelage Pharmaceuticals公司公布了其新型局部外用小分子疗法PP405的转化研究和1期临床研究的积极数据。PP405是一种强效的局部线粒体丙酮酸载体（MPC）抑制剂，可作用于细胞代谢通路以上调乳酸脱氢酶（LDH）。干细胞对LDH尤为敏感，LDH的上调能够激活干细胞并促进毛发生长。此次公布的数据证明该公司的新型局部外用小分子疗法PP405能重新激活休眠的毛囊干细胞，诱发毛发生长。在接受过面部提升去皱手术的皮肤上，单次外用0.006%和0.06%的PP405可在24小时内提高毛囊干细胞的LDH活性。LDH活性与毛发隆起处Ki67信号的显著增加相对应，表明毛囊干细胞有增殖反应。此外，1期研究还在雄激素性脱发患者中证明了机理和靶点作用。仅在0.05% PP405局部治疗7天后，Ki67信号与基线相比就出现了具有统计学意义的升高。研究人员还观察到新生毛基质（毛发生长周期中由休止期向生长期转变的标志）。Pelage公司将于2024年中期启动PP405的多中心2a期临床试验，招募患有雄激素性脱发的男女患者。PP405还可用于其他类型的脱发，包括休止期脱发（由压力引起的脱发）和化疗引起的脱发。IMM-1-104：公布1/2a期临床试验数据Immuneering公司宣布，其高选择性第三代小分子MEK抑制剂IMM-1-104治疗晚期携带RAS突变的实体肿瘤患者的1/2a期试验取得了积极的顶线结果。IMM-1-104是一款靶向MAPK通路中重要激酶MEK的抑制剂，旨在通过每日一次给药对MAPK通路进行抑制。这次所公布的试验共有41位患者入组，其中胰腺癌患者占63.4%、结直肠癌患者占12.2%、肺癌患者占9.76%。试验中有82%的患者在接受过往治疗时未曾达到部分缓解（PR）或完全缓解（CR）。截至2024年2月20日的数据，IMM-1-104在41例受试者中的耐受性良好，且具有差异化的安全性。22名接受循环肿瘤DNA（ctDNA）检测并接受IMM-1-104治疗的可评估患者中，100%未出现新的获得性RAS变异，支持其具有泛RAS活性。在每天320 mg或240 mg剂量组中，53%的患者观察到靶病灶的消退。在二线治疗中，320 mg剂量组的最佳的患者肿瘤病变消退为-35.7%，240 mg剂量组中为-11.4%；320 mg剂量组的最佳RECIST肿瘤最长直径之和（SLD）减少了18.9%，240 mg剂量组中减少了7.1%。候选的推荐2期剂量（RP2D）为每日一次320 mg，该RP2D得到耐受性、ctDNA、药代动力学（PK）和药效（PD）特征和初始抗肿瘤活性等积极结果的支持。NXP800：公布1b期临床试验的初步数据Nuvectis Pharma公司公布了其开发的口服HSF1通路小分子抑制剂NXP800用于治疗铂类耐药、携带ARID1a突变的卵巢癌患者的1b期临床试验的积极结果。HSF1是一款应激诱导的转录因子，HSF1信号通路在肿瘤发生中起到重要作用，是多项研究验证的抗癌药物靶点。在针对多种类型的晚期实体肿瘤患者开展的1a期试验中，NXP800的临床概况与临床前实验的预期高度一致，没有报告与药物相关的4级或5级事件。此前，NXP80在铂类耐药、携带ARID1a突变卵巢癌中的开发项目已被美国FDA授予快速通道资格。此次公布的结果显示，3名可评估患者的疾病控制率为100%，缓解率为33%。其中，1名达到未确认的PR患者的淋巴结非靶病灶获得了CR。ATSN-201：公布1/2期临床试验首个队列的数据ATSN-201是Atsena Therapeutics公司利用其新型扩散衣壳AAV.SPR开发的基因疗法，用于治疗X连锁视网膜劈裂症（XLRS）。XLRS是由RS1基因的突变引起的，该基因编码一种名为retinoschisin的蛋白，这是一种主要由光感受器分泌的蛋白质，位于视杆细胞、视锥细胞和双极细胞的外表面。XLRS的特点是视网膜层的异常分裂，这会导致视力受损，且无法通过眼镜矫正，随后会导致进行性的视力丧失。该病目前尚无批准的治疗方法。ATSN-201使用的病毒衣壳能够横向扩散到视网膜下注射点以外的位置，实现对中央视网膜的安全和有效的基因递送（在XLRS患者的视网膜中，分裂腔主要集中在中央视网膜部位）。此前的研究显示，AAV.SPR在临床剂量下能够有效递送载荷至视网膜中央凹上的视锥细胞，无需手术分离，并且不会引起炎症。此次公布的数据显示，ATSN-201在1/2期临床试验首个队列的所有3名患者中耐受性良好，没有报告严重不良事件。数据和安全监测委员会建议继续进行第二组，以测试下一个剂量水平的ATSN-201。RGLS8429：公布1b期临床试验数据Regulus Therapeutics公司公布了其开发的新型下一代寡核苷酸疗法RGLS8429用于治疗常染色体显性多囊肾病（ADPKD）的1b期临床试验的新数据。常染色体显性多囊肾病是由PKD1或PKD2基因突变引起的，也是最常见的人类单基因疾病之一，同时是终末期肾病的主要原因。RGLS8429旨在抑制miR-17并优先靶向肾脏，在临床前研究中已被证明能够明显改善肾脏功能、大小和其他疾病严重程度指标，并具有优越的药理学特征。此前，该公司已公布1期单次递增剂量临床试验的结果，结果显示，RGLS8429具有良好的安全性、耐受性和PK特征。此次公布的是1b期研究中第二个队列的结果，患者对RGLS8429的耐受性良好，未发现令人担忧的安全性问题。基于尿液生物标志物分析结果，在2 mg/kg剂量水平下观察到RGLS8429的生物活性。基于影像学的生物标志物的探索性结果令人鼓舞，在PC1和PC2增加最多的患者中，总肾脏体积减少的幅度最大。PC1和PC2是PKD1和PKD2基因的蛋白质产物，已被证明与疾病严重程度呈负相关。Sabirnetug（ACU193）：公布1期临床试验的新数据Acumen Pharmaceuticals公司公布了其新药sabirnetug用于治疗阿尔茨海默病（AD）的1期临床试验的新数据。Sabirnetug是一种选择性靶向毒性可溶性β淀粉样蛋白寡聚体（AβOs）的选择性人源化单克隆抗体。Sabirnetug能够结合AβOs，由于其独特的结合特性，sabirnetug有可能在产生淀粉样蛋白相关成像异常（ARIA，一种抗体疗法产生的常见主要副作用）风险较低的情况下提供治疗益处，因为sabirnetug可以在不直接靶向淀粉样斑块的情况下阻断AβOs的毒性作用。2023年7月公布的结果显示，该试验的初步结果达到了主要和次要目标，为sabirnetug的临床机制验证提供了证据。在较高剂量组的患者中观察到淀粉样斑块快速、剂量相关的显著减少（p=0.01），每四周给药一次60 mg/kg sabirnetug组患者的淀粉样斑块在第63天减少了25%，每两周给药一次25 mg/kg sabirnetug组患者的淀粉样斑块在第70天减少了20%。这一结果与已批准的Aß单克隆抗体在其临床开发阶段相似时间点的平均淀粉样蛋白斑块减少相当。此次公布的脑脊液生物标志物结果显示，与接受安慰剂治疗的患者相比，接受sabirnetug治疗的早期AD患者大脑中与AD病理学相关的生物标志物得到了改善，神经粒蛋白（neurogranin）水平降低了13.9%，p-tau181水平降低了13.0%，Aβ42/40比率呈上升趋势。在所有剂量中，AβOs的靶点作用与神经粒蛋白以及p-tau181的变化之间均存在显著的相关性，高度支持sabirnetug在早期AD患者大脑中的下游药理作用。该公司计划在2024年上半年启动sabirnetug的2期临床试验。ATR-258 Atrogi：公布1a/b期临床试验数据Atrogi公司宣布，其新型β2肾上腺素受体（β2-AR）激动剂ATR-258治疗2型糖尿病（T2D）患者的1a/b期临床试验达到了所有终点。ATR-258可与β2-AR结合，启动葡萄糖向骨骼肌运输的过程，从而降低血糖水平，并对受T2D影响的多个器官产生积极影响。这种专有的小分子化合物以一种新颖的方式激活受体，导致选择性调节和独特的信号传导特征。这种创新方法使解决2型糖尿病的核心问题成为可能。临床前研究表明，它能有效地将2型糖尿病状态逆转到健康水平。KIO-101：公布1期临床试验数据KIO-101是Kiora Pharmaceuticals公司的一种靶向二氢乳清酸脱氢酶（DHODH）的下一代非甾体类免疫调节小分子抑制剂，旨在克服市售的DHODH抑制剂的相关脱靶副作用和安全问题。此次公布的结果显示，使用12天KIO-101滴眼液在24名健康受试者中的安全性和耐受性良好，没有观察到严重的不良事件。与安慰剂组相比，治疗组的结膜充血明显减少。结膜充血是眼部炎症的体征，由多种非感染性和感染性原因引起。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（可上下滑动查看）[1] Pelage Presents Late-Breaking Data at AAD 2024 Meeting Demonstrating PP405 Activates Human Hair Follicle Stem Cells Ex Vivo and in Phase 1 Clinical Study. Retrieved March 11, 2024, from https://www.prnewswire.com/news-releases/pelage-presents-late-breaking-data-at-aad-2024-meeting-demonstrating-pp405-activates-human-hair-follicle-stem-cells-ex-vivo-and-in-phase-1-clinical-study-302084610.html[2] Arrowhead Pharmaceuticals Initiates Phase 1/2a Study of ARO-DM1 for Treatment of Type 1 Myotonic Dystrophy. Retrieved March 11, 2024, from https://www.businesswire.com/news/home/20240308355853/en/[3] Acumen Pharmaceuticals Presents Sabirnetug (sabirnetug) Fluid Biomarker and Target Engagement Analyses from Phase 1 INTERCEPT-AD Study in Early Alzheimer’s at the AD/PD™ 2024 Annual Meeting. Retrieved March 11, 2024, from https://investors.acumenpharm.com/news-releases/news-release-details/acumen-pharmaceuticals-presents-sabirnetug-acu193-fluid[4] Kiora Announces Publication of Phase 1 Study Demonstrating Safety, Tolerability and Anti-Inflammatory Activity of KIO-101 in the Treatment of Inflammation of the Eye. Retrieved March 11, 2024, from https://ir.kiorapharma.com/news-events/press-releases/detail/207/kiora-announces-publication-of-phase-1-study-demonstrating[5] ImmunAbs Announces Conclusion of Phase 1 Clinical Trial, Revealing Positive Topline Results. Retrieved March 11, 2024, from https://www.prnewswire.com/news-releases/immunabs-announces-conclusion-of-phase-1-clinical-trial-revealing-positive-topline-results-302084998.html[6] Allyx Therapeutics Announces Positive Phase 1b Multiple Ascending Dose Data and Advances ALX-001 to Patients. Retrieved March 11, 2024, from https://www.globenewswire.com/news-release/2024/03/11/2843754/0/en/Allyx-Therapeutics-Announces-Positive-Phase-1b-Multiple-Ascending-Dose-Data-and-Advances-ALX-001-to-Patients.html[7] Aprea Therapeutics Announces FDA Clearance of IND for APR-1051, its Next Generation WEE1 Kinase Inhibitor for Cyclin E Overexpressing Cancers. Retrieved March 11, 2024, from https://www.globenewswire.com/news-release/2024/03/11/2843764/0/en/Aprea-Therapeutics-Announces-FDA-Clearance-of-IND-for-APR-1051-its-Next-Generation-WEE1-Kinase-Inhibitor-for-Cyclin-E-Overexpressing-Cancers.html[8] Sonnet BioTherapeutics Announces Early Safety Data from the Company’s Phase 1b/2a Clinical Trial of SON-080 in Chemotherapy-Induced Peripheral Neuropathy (CIPN) Met the Study’s Initial Pre-Specified Objective. Retrieved March 11, 2024, from https://www.sonnetbio.com/news-media/press-releases/detail/84/sonnet-biotherapeutics-announces-early-safety-data-from-the[9] Sonnet BioTherapeutics Announces Early Safety Data from the Company’s Phase 1b/2a Clinical Trial of SON-080 in Chemotherapy-Induced Peripheral Neuropathy (CIPN) Met the Study’s Initial Pre-Specified Objective. Retrieved March 11, 2024, from https://www.sonnetbio.com/news-media/press-releases/detail/84/sonnet-biotherapeutics-announces-early-safety-data-from-the[10] EILEAN THERAPEUTICS APPROVED TO INITIATE FIRST PATIENT TRIAL WITH BALAMENIB (ZE63-0302), A SELECTIVE BEST-IN-CLASS MENIN INHIBITOR. Retrieved March 11, 2024, from https://www.prnewswire.com/news-releases/eilean-therapeutics-approved-to-initiate-first-patient-trial-with-balamenib-ze63-0302-a-selective-best-in-class-menin-inhibitor-302085538.html[11] Synnovation Therapeutics Announces First Patient Dosed in Phase I Trial with SNV1521, a PARP1 Selective Inhibitor for the Treatment of Solid Tumors. Retrieved March 11, 2024, from https://www.businesswire.com/news/home/20240311306666/en/[12] Nurix Therapeutics Announces U.S. FDA Lifts Partial Clinical Hold on NX-2127 Phase 1 TrialNurix cleared to introduce new chirally controlled NX-2127 drug product and resume enrollment of new patients into the study. Retrieved March 11, 2024, from https://ir.nurixtx.com/news-releases/news-release-details/nurix-therapeutics-announces-partial-clinical-hold-nx-2127-phase[13] Replay’s cell therapy product company Syena announces first patient dosed in Phase 1/2 study of TCR-NK cell therapy for multiple myeloma. Retrieved March 11, 2024, from https://replay.bio/news/replays-cell-therapy-product-company-syena-announces-first-patient-dosed-in[14] Regulus Therapeutics Announces Positive Topline Data from the Second Cohort of Patients in its Phase 1b Multiple-Ascending Dose (MAD) Clinical Trial of RGLS8429 for the Treatment of Autosomal Dominant Polycystic Kidney Disease (ADPKD). Retrieved March 11, 2024, from https://www.prnewswire.com/news-releases/regulus-therapeutics-announces-positive-topline-data-from-the-second-cohort-of-patients-in-its-phase-1b-multiple-ascending-dose-mad-clinical-trial-of-rgls8429-for-the-treatment-of-autosomal-dominant-polycystic-kidney-disease-ad-302086081.html[15] Atsena Therapeutics Announces Initiation of Dosing in Second Cohort of Phase I/II Clinical Trial Evaluating ATSN-201 Gene Therapy for the Treatment of X-linked Retinoschisis (XLRS). Retrieved March 14, 2024, from https://www.tmcnet.com/usubmit/2024/03/13/9977428.htm [16] Ocugen, Inc. Announces Dosing Completion of Subjects with Geographic Atrophy in Cohort 1 of Phase 1/2 Clinical Trial Evaluating the Safety and Efficacy of OCU410. Retrieved March 14, 2024, from https://ir.ocugen.com/news-releases/news-release-details/ocugen-inc-announces-dosing-completion-subjects-geographic[17] Clearmind Medicine Obtains Clearance for its Psychedelic- Based Alcoholism Clinical Trial. Retrieved March 14, 2024, from https://www.clearmindmedicine.com/news-release/clearmind-medicine-obtains-clearance-for-its-psychedelic--based-alcoholism-clinical-trial[18] Immuneering Announces Positive Topline Results from Phase 1 Portion of its Phase 1/2a Clinical Trial of IMM-1-104 in RAS-Mutant Solid Tumors. Retrieved March 14, 2024, from https://www.globenewswire.com/news-release/2024/03/14/2846143/0/en/Immuneering-Announces-Positive-Topline-Results-from-Phase-1-Portion-of-its-Phase-1-2a-Clinical-Trial-of-IMM-1-104-in-RAS-Mutant-Solid-Tumors.html[19] Nuvectis Pharma Announces Encouraging Preliminary Data from the NXP800 Phase 1b Clinical Trial in Platinum-Resistant ARID1a-Mutated Ovarian Cancer. Retrieved March 14, 2024, from https://www.globenewswire.com/news-release/2024/03/14/2846324/0/en/Nuvectis-Pharma-Announces-Encouraging-Preliminary-Data-from-the-NXP800-Phase-1b-Clinical-Trial-in-Platinum-Resistant-ARID1a-Mutated-Ovarian-Cancer.html[20] Atrogi Announces Positive Clinical Data from First-in-Class Insulin-Independent Treatment for Type 2 Diabetes. Retrieved March 14, 2024, from https://www.globenewswire.com/news-release/2024/03/14/2846027/0/en/Atrogi-Announces-Positive-Clinical-Data-from-First-in-Class-Insulin-Independent-Treatment-for-Type-2-Diabetes.html[21] Atrogi Announces Positive Clinical Data from First-in-Class Insulin-Independent Treatment for Type 2 Diabetes. Retrieved March 14, 2024, from https://www.globenewswire.com/news-release/2024/03/14/2846027/0/en/Atrogi-Announces-Positive-Clinical-Data-from-First-in-Class-Insulin-Independent-Treatment-for-Type-2-Diabetes.html[22] Nuvation Bio Doses First Patient in Phase 1/2 Study of NUV-1511 for the Treatment of Advanced Solid Tumors. Retrieved March 14, 2024, from https://www.businesswire.com/news/home/20240314331030/en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

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100 项与 BMS-984923 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
帕金森病	临床1期	美国	Allyx Therapeutics, Inc.初创企业	2024-03-15
阿尔茨海默症	临床1期	美国	Bristol Myers Squibb Co.	2021-03-18

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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


NCT04805983 (CTgov)	临床1期	阿尔茨海默症	36	BMS-984923 (10 mg BMS-984923)	壓衊選鹽鹽簾淵鑰蓋糧(襯淵壓鹽壓鑰築築繭夢) = 顧襯壓網繭鏇鹽範觸遞鬱願夢壓淵淵鹽選築遞 (衊築鬱餘淵繭壓窪蓋憲, 衊壓衊簾顧窪壓淵壓顧 ~ 膚壓製窪築繭鏇顧蓋憲) 更多	-	2023-04-13
				BMS-984923 (40 mg BMS-984923)	壓衊選鹽鹽簾淵鑰蓋糧(襯淵壓鹽壓鑰築築繭夢) = 鹽網積構艱壓蓋鬱簾廠鬱願夢壓淵淵鹽選築遞 (衊築鬱餘淵繭壓窪蓋憲, 蓋鹽繭築願網襯鑰膚鏇 ~ 範淵膚鹽鑰願蓋鏇窪艱) 更多