This is a single-site, single-arm, single-dose, Phase 1 study of the safety of bryostatin in participants with multiple sclerosis (MS) receiving any disease modifying therapy (DMT).

开始日期2024-06-26

申办/合作机构

The Cleveland Clinic Foundation

[+1]

NCT04538066

/ Completed临床2期

A Randomized, Double-Blind, Placebo-Controlled, Phase 2 Study Assessing Safety, Tolerability and Long-term Efficacy of Bryostatin in the Treatment of Moderately Severe Alzheimer's Disease Subjects Not Receiving Memantine Treatment

To evaluate the safety, tolerability, and long-term efficacy of bryostatin 1 (hereafter referred to as bryostatin) for the treatment of moderately severe Alzheimer's disease (AD).

开始日期2020-08-30

申办/合作机构

TAO Synergies, Inc.

[+2]

NCT03560245

/ Completed临床2期

A Randomized, Double-Blind, Placebo-Controlled, Phase 2 Study Assessing the Safety, Tolerability and Efficacy of Bryostatin in the Treatment of Moderately Severe to Severe Alzheimer's Disease Subjects Not Receiving Memantine Treatment

This is a randomized double-blind Placebo-controlled, Phase 2 study comparing bryostatin to placebo for the treatment of moderately severe to severe Alzheimer's disease in subjects not receiving memantine treatment. The study is 15 weeks in duration, including a safety and efficacy evaluation 30 days after the last dose of study drug. Subjects will receive 7 doses of study drug during the study. The primary efficacy endpoint is defined as the change from baseline to Week 13 in the Severe Impairment Battery (SIB) total score.

开始日期2018-06-20

申办/合作机构

TAO Synergies, Inc.

[+1]

100 项与草苔虫内酯１相关的临床结果

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100 项与草苔虫内酯１相关的转化医学

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100 项与草苔虫内酯１相关的专利（医药）

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项与草苔虫内酯１相关的文献（医药）

2025-12-08·JCI Insight

Regulation of selective class switching provides long-term therapeutic benefits for hay fever

Article

作者: Nagatake, Takahiro ; Kojima, Hirotatsu ; Sugai, Manabu ; Inomata, Takenori ; Huang, Tianxiang ; Shinkura, Reiko ; Gao, Peng ; Nakayama, Keiichi I ; Morita, Naoki ; Adachi, Takahiro ; Tamano, Ryutaro ; Yamada, Yasuhiro ; Yamamoto, Kohta

IgA protects the body from invaders in the mucosal sites, but its role in allergic diseases, such as hay fever, is poorly understood. We demonstrate an increased susceptibility to cedar-pollen-induced hay fever associated with increasing pollen penetration into the body in IgA-deficient mice, indicating that IgA prevents pollen invasion in the mucosa. We identified bryostatin 1, an anticarcinogenic protein kinase Cδ (PKCδ) activator, as an IgA/IgE class-switching regulator in B cells. Bryostatin 1 enhanced IgA production through induction of germline transcript α (GLTα) via the PKCδ/MEK/ERK/RUNX1 pathway and suppressed IgE by reducing GLTε through the PKCδ/STAT5/ID2 pathway. Production of Th2 cytokines and eosinophil infiltration in the lungs was also reduced. Furthermore, hay fever alleviation by bryostatin 1 demonstrated diminished symptoms in mice in vivo 3 months subsequent to intranasal administration.

2025-12-01·Journal for ImmunoTherapy of Cancer

Affinity-matured CD72-targeting nanobody CAR T cells enhance elimination of antigen-low B-cell malignancies

Article

作者: Serrano, Juan Antonio Camara ; Wiita, Arun P ; Phojanakong, Paul ; Carpenter, Christopher ; Shah, Nirali N ; Maus, Marcela V ; Larson, Rebecca C ; Wang, Hao-Wei ; Ramos, Emilio ; Steri, Veronica ; Sahu, Srabani ; Zakraoui, Ons ; Tariq, Isa ; Verma, Amit ; Nix, Matthew A ; Johnson, Haley ; Gil-Alós, Daniel ; Izgutdina, Adila ; Martinez-Lopez, Joaquin ; Parekh, Samir ; Kang, Amrik S ; Naik, Akul ; Chen, Szu-Ying ; Yuan, Constance M ; Salangsang, Fernando ; Patiño-Escobar, Bonell ; Rashid, Tasfia ; Valeri, Antonio ; Temple, William C ; Li, Mingcheng ; Walunj, Sujata ; Aminov, Sarah ; Takamatsu, Hiroyuki ; Geng, Huimin

Background:

Chimeric antigen receptor (CAR) T-cell therapies are highly efficacious for several different hematologic cancers. However, for most CAR T targets it is observed that low surface antigen density on tumors can significantly reduce therapeutic efficacy. In this study, we explore this dynamic in the context of CD72, a surface antigen we recently found as a promising target for refractory B-cell cancers, but for which CD72 low antigen density can lead to therapeutic resistance in preclinical models.

Methods:

Primary samples were accessed via institutional review board-approved protocols. Affinity-matured and humanized nanobody clones were previously described in Temple et al. (2023). CAR T cells were generated via lentiviral transduction. In vitro cytotoxicity assays were performed using luciferase-labeled cell lines. In vivo studies were performed using cell line-derived or patient-derived xenografts implanted in NOD scid gamma mice.

Results:

We first confirmed ubiquitous CD72 expression across a range of primary B-cell non-Hodgkin lymphomas. We further found that after resistance to CD19-directed therapies, across both B-cell acute lymphoblastic leukemia (B-ALL) models and primary tumor samples, surface CD72 expression was largely preserved while CD22 expression was significantly diminished. Affinity maturation of a nanobody targeting CD72, when incorporated into CAR T cells, led to more effective elimination in vitro of isogenic models of CD72 low-expressing tumors. These results suggested that nanobody-based CAR T cells (nanoCARs) may exhibit a similar relationship between binder affinity, antigen expression, and efficacy as previously demonstrated only for single chain variable fragment-based CAR T cells. Surprisingly, however, this significantly improved in vitro efficacy only translated to modest in vivo survival benefit. As a parallel strategy to enhance CAR T function, we found that the small molecule bryostatin could also significantly increase CD72 surface antigen density on B-cell malignancy models. Structural modeling and biochemical analysis identified critical residues improving CD72 antigen recognition of our lead affinity-matured nanobody.

Conclusions:

Together, these findings support affinity-matured CD72 nanoCARs as a potential immunotherapy product for CD19-refractory B-cell cancers. Our results also suggest that for B-ALL in particular, CD72 may be a preferable second-line immunotherapy target over CD22.

2025-11-28·JOURNAL OF NATURAL PRODUCTS

Targeting the PKC-Gli Axis: Bryostatin 1 as a Hedgehog Pathway Inhibitor

Article

作者: Billingsley, Kelvin L. ; Tran, UyenPhuong

Aberrant Hedgehog (Hh) signaling contributes to multiple cancers, yet current Smoothened (Smo)-targeted therapies are limited by resistance and relapse. This study investigates bryostatin 1, a clinically relevant natural product from Bugula neritina, for its ability to inhibit Hh signaling downstream of Smo. Bryostatin 1 robustly suppresses Gli transcriptional activity and significantly reduces the expression of key Hh pathway components in a time- and dose-dependent manner. Additionally, it selectively impairs viability in Hh-driven cancer cells while sparing healthy fibroblasts. These compelling results highlight bryostatin 1 as a promising therapeutic candidate for overcoming resistance in aggressive Hh-driven diseases.

项与草苔虫内酯１相关的新闻（医药）

2026-05-29

·BioSpace

Aphios Corporation Announces Notice of Allowance for Novel Bryoid Composition Patent Targeting Alzheimer’s Disease, Multiple Sclerosis, HIV Latency and Cancer

NORTH READING, Mass.--(BUSINESS WIRE)-- #Alzheimers -- Aphios Corporation today announced that the United States Patent and Trademark Office (USPTO) has issued a Notice of Allowance for a divisional patent application titled “Bryoid Compositions, Methods of Making and Use Thereof” covering novel Bryoid compounds with potential therapeutic applications in neurodegenerative diseases, HIV latency, cancer, and other amyloid-mediated disorders. The allowed claims relate to a novel Bryoid composition designated B14B, including methods of isolation, purification, and manufacture. The USPTO determined that the claimed Bryoid composition demonstrated novelty and non-obviousness over prior bryostatin-related art. The patent application is part of Aphios’ expanding Bryoid intellectual property portfolio derived from marine bryozoan natural products and advanced purification technologies. The invention was developed with support from the National Institute on Aging and the National Institutes of Health (NIH). Bryoids are structurally related to bryostatins, a class of complex macrocyclic compounds known to modulate protein kinase C (PKC) pathways involved in neurodegeneration, viral latency, and oncology. According to the patent specification, several novel Bryoid compositions demonstrated biological activity comparable to or greater than Bryostatin-1 in stimulating alpha-secretase activity and PKC signaling pathways associated with Alzheimer’s disease and other CNS disorders. The application describes multiple proprietary Bryoid analogs with molecular weights distinct from known Bryostatins 1–20. Experimental data presented in the application demonstrated enhanced alpha-secretase activity and PKC modulation in SHSY-5Y neuroblastoma cells. “Our Bryoid platform represents a significant advancement in the discovery and development of novel marine-derived therapeutics,” said Dr. Trevor P. Castor, Founder and CEO of Aphios Corporation. “This Notice of Allowance further validates the novelty of our Bryoid technology and strengthens our intellectual property estate in neurodegenerative disease therapeutics, HIV latency reversal strategies, and oncology applications.” Aphios’ Bryoid platform combines proprietary extraction, purification, and characterization technologies, including its SuperFluids™ processing platform, to isolate highly pure Bryoid compounds from Bugula neritina and related marine sources. The company believes these compounds may serve as next-generation therapeutics for Alzheimer’s disease, Multiple sclerosis, Parkinson’s disease, HIV-1 latency reversal, and other serious disorders with significant unmet medical need. The Notice of Allowance follows Aphios’ previously issued patents covering Bryoid compositions and expands the company’s growing portfolio of more than 85 issued and pending U.S. and international patents. About Aphios Corporation Aphios Corporation is an emerging growth biotechnology company developing enhanced therapeutics and enabling technologies for drug discovery, drug delivery, and pathogen safety. The company’s proprietary platforms include SuperFluids™ extraction and purification, nanotechnology-based drug delivery systems, and novel therapeutics targeting cancer, infectious diseases, and CNS disorders including Alzheimer’s disease, addiction, pain, and anxiety. This research was in part funded by an SBIR Grant from the National Institute on Aging (NIA), NIH. The content of this release is solely the responsibility of the authors and does not represent the official views of NIA and NIH. For more information, visit . Forward-Looking Statements This press release contains forward-looking statements regarding future events and the future performance of Aphios Corporation, including statements related to the therapeutic potential, development, commercialization, and intellectual property protection of Bryoid compounds and related technologies. Actual results may differ materially from those expressed or implied by these forward-looking statements due to various risks and uncertainties, including scientific, regulatory, clinical, financial, and business factors. Aphios undertakes no obligation to update any forward-looking statements except as required by law. Contacts Dr. Trevor P. Castor Founder & CEO Aphios Corporation (781) 858-7520 tcastor@aphios.com

2026-05-27

·今日头条

把潜伏HIV“激活”？一种源于海洋的化合物获得美国专利

点击了解HIV暴露前预防（PrEP），主动守护健康源于海洋生物的HIV治愈研究。 briefglance.com消息，美国生物技术公司Aphios Corporation近日宣布，其研发的一类来源于海洋生物的新型化合物——Bryoid ，获得了美国专利授权通知。这类化合物正在被探索用于潜伏性HIV感染、阿尔茨海默病和癌症等疾病治疗的研究。 Bryoid化合物这类Bryoid化合物，是从一类从海洋苔藓动物Bugula neritina中分离出的复杂分子。 Bugula neritina是一种微小的水生无脊椎动物，看起来并不起眼，体内能产生一些结构复杂、具有潜在药用价值的分子。这类Bryoid化合物与此前被研究多年的Bryostatin（苔藓虫素）关系密切。其中，Bryostatin-1曾被用于、阿尔茨海默病和癌症相关研究，但其临床结果并不稳定，而且天然来源有限，提取困难。 Aphios公司此次获得专利保护的，是一种特定的Bryoid组合物——B14B，及其制造工艺。从专利获批到临床应用，还有很远的路要走。 PKC通路：细胞里的“信号开关” Bryostatins和较新的Bryoids都可以作为“蛋白激酶C（PKC）”的强效激活剂。 PKC是一类酶，可以理解为细胞内部的“信号开关”。而PKC通路，则像是一套“总开关系统”，参与细胞生长、免疫反应、记忆形成等多种过程。当这些通路发生异常时，可能会导致神经退行性改变、病毒持续存在，以及癌细胞不受控制地生长。相反，如果这些开关能被合理调控，就可能影响一些疾病的发展过程。 Aphios公司称，临床前数据显示，Bryoid化合物在激活某些关键细胞通路方面，可能具有与Bryostatin-1相当甚至更强的生物活性。 PKC可能参与激活潜伏病毒库的过程。 Bryoid化合物与HIV治愈研究同一类化合物之所以可能被用于多种疾病研究，关键在于其基础作用机制。通过靶向PKC，Bryoid可能为一些当前治疗手段仍不足的疾病，提供新的研究方向。潜伏病毒库是HIV治愈研究中的一大拦路石。很多HIV感染者即使长期接受抗病毒治疗，病毒载量已经控制到检测不到，体内仍可能存在少量“沉睡”的病毒。这些病毒藏在免疫细胞里，不活跃、不复制，因此既不容易被免疫系统发现，也难以被现有抗病毒药物清除。对此，科学界提出了一种“激活并清除”策略——先用某种药物把潜伏的HIV“叫醒”，使其从隐藏状态中暴露出来；再配合其他治疗手段，把这些被激活的病毒细胞清除掉。 Bryoid作为PKC激活剂，正是因为可能参与“激活”这一步，所以被认为具有进一步研究价值。它未来或许有机会成为帮助清除潜伏病毒库的候选工具之一。这仍然只是研究方向，并不是成熟疗法。从专利到临床应用一种化合物从“看起来有前景”，到真正成为临床用药，中间还要经过毒理学研究、动物实验、人体临床试验等多个阶段，不仅周期长、投入大，而且充满风险，任何一步失败都可能让研发停下来。尤其是在海洋天然产物药物研发领域，过去也有很多案例：实验室数据很好，但到了人体试验并不理想。不过，Aphios公司的优势在于——它并不是完全从零开始，而是在一类已有研究基础的化合物上进行改进，并围绕较明确的生物靶点、制造工艺和专有技术进行布局。这可能帮助其克服天然产物研发中常见的提取难、供应难、稳定生产难等问题。这项进展值得关注，但不能被简单理解为“海洋药物即将治愈HIV”。更准确地说，它代表了HIV治愈研究中的一个重要方向：科学家正在继续寻找突破潜伏病毒库的方法。同时，也说明这类海洋来源化合物在药物研发和知识产权保护上迈出了重要一步。 HIV 未发生高危的朋友不要仅凭“检测阴性”或主观判断放松警惕规范防护 + PrEP （暴露前预防）可将感染风险大幅降低（有效性可达99%+）已经发生高危的朋友请在72小时内尽快采取PEP（暴露后阻断）措施 ——越早越有效关于艾滋，我们想多说一句不必恐惧，也不应忽视因为正视，所以不歧视因为了解，所以能预防因为治疗，所以有希望 AIDS

2026-04-22

·化学经纬

Hoveyda组Science：应用大环烯烃复分解反应实现复杂大环发散性可编程骨架重组

导读最近，法国斯特拉斯堡大学&美国波士顿学院Amir H. Hoveyda课题组，报道了一种简洁、高效、精准、可编程大环化物（MCs）骨架重组策略。该策略基于多种催化烯烃复分解反应实现，包括：1）大环开环/交叉复分解（MROCM），用于切断大环烯烃以生成二烯；2）交叉复分解（CM）和烯丙基取代，用于实现一个单位链同系化（即增加一个碳）；3）烯烃异构化和乙烯解，用于实现一个单位链剪切（即减少一个碳）；4）大环关环复分解（MRCM），用于重新关环。应用此发散性方法，作者成功得到14种抗癌药埃博霉素C类似物。相关研究成果于近期在线发表在《科学》杂志上（Science, 2026, DOI: 10.1126/science.aee3540）。背景大环化物（MCs，≥12元）兼具刚性和柔性构象，能更好适应不同形状结合位点，并能与相对平坦表面进行更有效相互作用，因而被视为针对“不可成药”靶点的极具吸引力候选药物分子。尽管大环化物分子量相对较大，不符合“Lipinski类药性五规则”（分子量小于500），但仍可具有足够生物利用度以实现口服给药。后期烯烃关环复分解（RCM）反应在大环化物合成中应用广泛。抗丙肝病毒药物Simeprevir和各种活性大环天然产物例如Phorboxazole A、Bryostatin 1，其合成中都应用过RCM反应（Fig. 1A）。然而，大环化物的微小骨架改变，可能会对生物活性产生不可预测影响，且会引入构效关系分析难题，这为大环药物开发带来极大挑战性。从头合成法虽能构建大环类似物骨架，但存在效率低下等问题。如果能发展出一种实用、简洁且可编程的大环化物骨架重组方法，将极大简化大环化合成和相关药物发现。概述此文作者分析了已报道的三例大环天然产物骨架重组合成案例（Fig. S1），认为这些方法存在中间体无法分离或不安全、需要多步操作等问题，因而不适用于大环化物发散性骨架重组。作者认为以催化烯烃复分解反应为关键反应，以二烯烃为发散性枢纽，能够实现大环化物的可编程骨架重组。如Fig. 1B所示，首先通过大环开环/交叉复分解（MROCM）反应，将购买或多步合成所得大环烯烃转化成二烯，然后发生如下转化实现发散性大环骨架重组，包括：1）通过同系化的增碳反应，在二烯左侧（L）插入CH₂得到hub(+CH₂)ᴸ，经大环关环复分解（MRCM）反应得到大环扩环产物MC(+CH₂)ᴸᶻ；2）通过增碳反应，在二烯右侧（R）插入CHOH得到hub(+CHOH)R，经MRCM反应得到大环扩环产物MC(+CHOH)RE；3）通过删碳反应，在二烯左侧（L）删除一个CH₂得到hub(–CH₂)ᴸ，经MRCM反应得到大环缩环产物MC(–CH₂)ᴸᴱ，并可继续迭代删除CH₂得到MC(–2CH₂)ᴸᶻ，实现可编程骨架重组。（Fig. 1，来源：Science）（Fig. S1，来源：Science）图文解析二烯生成和大环烯烃异构化：如Fig. 2所示，1）在钌催化下，能直接通过乙烯解（ethenolysis）反应，将epothilone C和Simeprevir高效开环（Open）转化成对应二烯Epo-Hub和Sim-Hub（Fig. 2A-a）；2）zearalenone直接经钌催化乙烯解反应收率太低，为此作者通过光催化烯烃异构化、乙烯解两步反应，或酚羟基保护、和Z-丁烯发生大环开环/交叉复分解（MROCM）反应、乙烯解（Clip）三步反应，优化了对应二烯生成收率（Fig. 2A-b）；3）所得二烯Epo-Hub，经TBS硅醚化、和E-丁烯发生MROCM反应（Cap）、大环关环复分解（MRCM）反应（Close）、脱TBS，可实现Epo的烯烃Z/E异构化得到产物E-Epo（Fig. 2B）；4）Epo和Z-Zea，可分别与dicarb发生MROCM反应，高效得到对应同系化碳酸酯类二烯（Fig. 2C-a）；5）二烯Epo-Hub和Epo-Hub(Si)，也可与烯醇发生交叉复分解（CM）反应，得到三种同系化烯丙醇类二烯（Fig. 2C-b）。（Fig. 2，来源：Science）扩环反应研究：基于Fig. 3A所示二烯链增长策略，作者开展如下扩环反应研究：1）二烯Epo-Hub(Si)和烯醇发生交叉复分解（CM）反应得到烯丙醇类二烯，然后经醇还原去氧化反应（10.1021/jo062325p）实现烯丙基取代（Substitute）得到三种同系化二烯，最后发生大环关环复分解（MRCM）和脱TBS反应得到对应扩环产物。二烯Epo-Hub(+2CH₂OH)ᶻᶻ也可经类似多步反应转化成对应扩环产物（Fig. 3B）；2）二烯Epo-Hub(Si)所得烯丙醇类二烯，也可经碳酸酯化、硼化反应和氧化反应、MRCM反应、脱TBS，转化成多个含烯丙位羟基扩环产物（Fig. 3C）。（Fig. 3，来源：Science）缩环和烯烃换位反应研究：基于Fig. 4A所示二烯链缩短策略，作者开展如下缩环和烯烃换位反应研究：1）二烯Epo-Hub经烯烃异构化（shift）、乙烯解反应（Clip），在左侧（L）删除一个碳得到末端二烯，然后与Z-丁烯发生交叉复分解（CM）反应（Cap）得到Z型二烯（不交换无法关环），最后发生大环关环复分解（MRCM）反应（Close）得到对应删一个碳Z型缩环产物（Fig. 4B-a）；2）二烯Epo-Hub(Si)经烯烃异构化、乙烯解反应、烯烃异构化、乙烯解反应，可得到4个二烯前体。4个二烯前体分别经MRCM/脱TBS、MRCM/脱TBS、CM/MRCM/脱TBS反应、MRCM/脱TBS反应，得到对应删一个或两个碳的E或Z型型缩环产物（Fig. 4B-b）；3）大环化物Zea经三氟甲磺酸酯化、和Z-丁烯发生大环开环/交叉复分解反应（MROCM）、乙烯解、烯烃异构化、MRCM、脱保护基，得到对应删一个碳E型缩环产物（Fig. 4B-c）；4）二烯Epo-Hub(Si)经烯烃异构化反应所得二烯，先和烯醇发生CM反应得到烯丙醇类二烯，然后经醇还原去氧化（Substitute）、烯烃异构化（Clip）、MRCM/脱TBS反应，得到对应大环烯烃换位产物（Fig. 4C）。（Fig. 4，来源：Science）大环重组流程图：如Fig. 5A和5B所示，作者汇总了大环骨架重组合成流程图，包括二烯生成、发散性合成扩环大环化物/缩环大环化物/大环烯烃换位化物、和14种抗癌药物埃博霉素C（Epo）类似物合成。作者还对比分析了Epo和其类似物对多种癌细胞的抑制活性（Fig. 5C），验证此大环骨架重组策略在药物发现中的应用价值。（Fig. 5，来源：Science）总结基于多种催化烯烃复分解反应，Amir H. Hoveyda课题组报道了一种发散性可编程大环化物骨架重组方法。该方法具有实用、温和、高效等优点，便于获得扩环、缩环或扭曲骨架大环化物。论文信息 Divergent and programmable skeletal remodeling of complex macrocycles with a small method set Ali Nikbakht, Xinghan Li, Jing Wan, Can Qin, Amir H. Hoveyda* Science, 2026, DOI: 10.1126/science.aee3540 https://www.science.org/doi/10.1126/science.aee3540

100 项与草苔虫内酯１相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	草苔虫内酯１	-	DB11752

研发状态

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适应症	最高研发状态	国家/地区	公司	日期
阿尔茨海默症	临床2期	美国	TAO Synergies, Inc.	2015-11-01
腺泡细胞癌	临床2期	美国	National Cancer Institute	2002-03-01
胰腺导管腺癌	临床2期	美国	National Cancer Institute	2002-03-01
晚期肾细胞癌	临床2期	美国	National Cancer Institute	2002-01-01
输卵管癌	临床2期	美国	National Cancer Institute	2000-10-01
转移性胃癌	临床2期	美国	National Cancer Institute	2000-10-01
卵巢上皮癌	临床2期	美国	National Cancer Institute	2000-10-01
复发性卵巢癌	临床2期	美国	National Cancer Institute	2000-10-01
复发性原发性腹膜癌	临床2期	美国	National Cancer Institute	2000-10-01
转移性肾细胞癌	临床2期	美国	National Cancer Institute	1999-06-01

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT06190912 (CTgov)	临床1期	多发性硬化症	4	Bryostatin 1	構鹽壓餘積夢膚鹹糧糧 = 獵選鹽醖鬱繭衊鏇鏇範鹽窪窪鏇壓觸遞齋繭願 (壓願選觸醖鹹窪願膚齋, 築蓋壓簾獵鹽夢繭衊積 ~ 獵憲簾獵鹹壓範製鑰襯) 更多	-	2026-03-31
NCT04538066 (CTgov)	临床2期	阿尔茨海默症	122	Bryostatin 1 (Bryostatin 1)	壓衊壓醖夢網繭淵壓夢 = 鑰獵窪獵鑰蓋齋積願觸膚齋淵觸選憲鬱築獵鑰 (衊鏇齋餘蓋繭構顧繭蓋, 鏇夢範顧膚簾鹽鬱觸餘 ~ 齋艱糧膚衊糧鹹製襯淵) 更多	-	2024-07-31
				Placebo (Placebo)	壓衊壓醖夢網繭淵壓夢 = 衊廠餘觸積淵鑰膚築網膚齋淵觸選憲鬱築獵鑰 (衊鏇齋餘蓋繭構顧繭蓋, 獵鏇餘壓憲壓鹽憲鬱壓 ~ 淵壓築窪遞壓製鹹餘遞) 更多
NCT04538066 (Literature) 人工标引	临床2期	阿尔茨海默症	122	Bryostatin 1	網積選繭築餘壓醖醖鏇(鏇觸餘齋蓋築簾鏇鏇窪) = 夢積構遞願鹹蓋糧遞願積範齋壓鑰鏇襯鹽襯窪 (窪蓋襯鏇襯鏇齋構蓋範, 1.56) 更多	积极	2023-09-19
				Placebo	網積選繭築餘壓醖醖鏇(鏇觸餘齋蓋築簾鏇鏇窪) = 遞願築蓋繭齋製鹽構鹹積範齋壓鑰鏇襯鹽襯窪 (窪蓋襯鏇襯鏇齋構蓋範, 1.51) 更多
NCT03560245 (CTgov)	临床2期	阿尔茨海默症	108	Bryostatin (Bryostatin 20µg)	夢齋鏇顧網餘鹽蓋遞廠 = 選製窪積襯鑰願淵壓顧齋願艱鏇構齋淵襯夢觸 (鬱觸觸廠糧觸蓋衊鏇鹹, 範鏇襯廠獵壓築窪鹽餘 ~ 膚衊糧襯願選繭糧繭鑰) 更多	-	2020-10-01
				Placebo (Placebo)	夢齋鏇顧網餘鹽蓋遞廠 = 壓廠壓鑰願積衊餘糧艱齋願艱鏇構齋淵襯夢觸 (鬱觸觸廠糧觸蓋衊鏇鹹, 淵選願壓艱襯顧淵鑰範 ~ 夢選憲鏇蓋獵齋齋窪選) 更多
NCT02431468 (CTgov)	临床2期	阿尔茨海默症	147	Bryostatin 1 (Bryostatin 1 20ug)	衊構選積觸艱膚鏇繭夢 = 衊鏇獵齋築蓋獵製觸製夢衊築範艱觸簾範範顧 (憲網繭廠衊鑰蓋願衊襯, 鹹糧鏇憲繭壓襯簾繭鏇 ~ 繭鹽醖艱鬱膚鏇簾顧廠) 更多	-	2018-07-06
				Bryostatin 1 (Bryostatin 1 40ug)	衊構選積觸艱膚鏇繭夢 = 糧鹹襯鬱鹹壓構衊遞淵夢衊築範艱觸簾範範顧 (憲網繭廠衊鑰蓋願衊襯, 鹹壓願構衊築淵觸遞選 ~ 範餘鑰齋繭鬱窪鑰壓範) 更多
NCT02221947 (CTgov)	临床1/2期	阿尔茨海默症	9	Bryostatin 1 (Bryostatin 1)	窪積鏇淵範鬱顧鏇衊膚 = 壓憲網膚顧鹽願築餘鏇衊築積膚積鬱蓋積齋願 (憲鹹餘衊鹹遞壓壓餘範, 淵簾淵簾製艱膚築鹹繭 ~ 遞選繭壓衊廠夢築積積) 更多	-	2016-04-21
				Placebo (Placebo)	窪積鏇淵範鬱顧鏇衊膚 = 糧艱壓憲壓廠廠簾淵鹽衊築積膚積鬱蓋積齋願 (憲鹹餘衊鹹遞壓壓餘範, 繭蓋構鬱觸製廠獵顧鏇 ~ 觸壓構範鹽範範壓顧網) 更多
NCT00031694 (CTgov)	临床2期	腺泡细胞癌 \| 胰腺导管腺癌	19	bryostatin 1+paclitaxel	壓積醖願顧製簾壓簾範 = 醖憲壓艱齋鏇衊鏇窪鬱鬱積夢範艱繭鬱鹹願餘 (繭艱鹹網淵獵顧廠淵遞, 淵願醖窪壓積鹹鏇範選 ~ 醖鏇鹹衊廠製製網鹹鹽) 更多	-	2015-04-21
NCT00006389 (CTgov)	临床2期	转移性胃癌	12	laboratory biomarker analysis+bryostatin 1+cisplatin	鏇網憲遞憲艱鏇齋糧糧 = 艱願選簾襯構觸簾構獵繭鬱衊選製願衊積餘繭 (鬱膚襯觸範糧膚鹽餘壓, 艱簾積夢網廠獵鹹遞衊 ~ 獵積觸艱淵憲廠壓憲憲) 更多	-	2014-10-01
NCT00004144 (Pubmed \| Clin Cancer Res)	临床1期	实体瘤 \| 晚期癌症	36	Bryostatin 1	鏇遞艱選遞獵觸鬱範鹽(衊鹹鑰選願構鏇願築艱) = 蓋積製網觸築窪網築範選餘製壓範窪餘衊窪願 (積範製襯鹽餘鏇膚衊蓋 ) 更多	-	2006-12-01
				Gemcitabine	鏇遞艱選遞獵觸鬱範鹽(衊鹹鑰選願構鏇願築艱) = 顧窪壓選網選蓋齋觸廠選餘製壓範窪餘衊窪願 (積範製襯鹽餘鏇膚衊蓋 )
ASCO2004	临床2期	肾细胞癌	33	Interleukin-2	衊鹽網構窪繭醖淵顧淵(選淵膚醖餘艱襯觸鏇製) = 鹽鑰衊鏇襯蓋糧醖鏇窪醖選壓繭艱鬱壓繭製簾 (鹽鏇顧製齋壓膚繭願淵, 377–577) 更多	不佳	2004-07-15