Background:
Proteus syndrome is a rare overgrowth disorder. Most people begin to have symptoms between 6 months and 2 years of age. There are very few living adults with this disease. There is also no known treatment for it. Researchers want to see if a new drug can slow down or stop overgrowth in people with Proteus syndrome.
Objective:
To learn if miransertib is a safe and effective treatment for Proteus syndrome.
Eligibility:
People ages 3 and older with Proteus syndrome.
Design:
Participants will be screened with a medical checkup. They will answer questions about their medical history and current health. They will have a physical exam with vital signs. They will have an electrocardiogram to measure their heartbeat. They will give blood and urine samples. They will repeat the screening tests during the study.
Participants will take a miransertib pill once a day. They will bring their empty pill bottles with them to the NIH when they visit. If they can t swallow a pill, researchers will try to find other ways for them to take the drug.
Participants will have X-rays, ultrasounds, and imaging scans. Photos may be taken of their feet and other parts of the body that have or develop signs of Proteus syndrome.
Participants will have lung function tests to measure how much and how fast air moves out of their lungs.
Participants will complete surveys about their levels of pain, physical functioning, and quality of life.
Participants may have additional tests performed to assess their individual disease. They may have consultations with other specialists.
Participation lasts about 4 years. Participants will have 20-30 visits at the NIH....

开始日期2022-05-20

申办/合作机构

National Human Genome Research Institute

NCT04980872

/ Active, not recruiting临床2期

A Multicenter, Open-label, Phase 2, Extension Trial to Study the Long-term Safety in Participants With PROS or Proteus Syndrome Who Are Currently Being Treated With Miransertib in Other Studies

This is a study of the safety and tolerability of oral miransertib (MK-7075) administered to participants at least 2 years of age with phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA)-related overgrowth spectrum (PROS) or Proteus Syndrome (PS). This is an extension of other miransertib studies (MK-7075-002 [NCT03094832] or ArQule CU/EAP [NCT03317366]), and may also enroll participants who are approved for MK-7075-002 but have not yet started miransertib therapy.

开始日期2021-11-02

申办/合作机构

Merck Sharp & Dohme Corp.

NCT03094832

/ Terminated临床1/2期

A Phase 1/2 Study of ARQ 092 (Miransertib) in Subjects With PIK3CA-related Overgrowth Spectrum and Proteus Syndrome

This is an open label, Phase 1/2 study of oral miransertib (MK-7075) administered to participants at least 2 years of age with phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (PIK3CA)-related Overgrowth Spectrum (PROS) and Proteus Syndrome (PS) (MOSAIC).

开始日期2017-05-16

申办/合作机构

ArQule, Inc.

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100 项与 Miransertib 相关的临床结果

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100 项与 Miransertib 相关的转化医学

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100 项与 Miransertib 相关的专利（医药）

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项与 Miransertib 相关的文献（医药）

2025-08-01·COMPUTATIONAL BIOLOGY AND CHEMISTRY

A computational journey in anticancer drug discovery: Exploring AKT1 inhibition by novel oxadiazoles using molecular docking, ADMET, density functional theory and molecular dynamic simulation

Article

作者: Kumar, Shubham ; Sharma, Vishnu ; Paradkar, Omkar ; Naik, Gauri Alias Pooja ; Wadhwa, Pankaj ; Gupta, Pawan

AKT, also called (PKB) Protein Kinase B, is critical for cell proliferation, metabolism, and survival, with its dysfunction linked to various diseases, including cancer. The oxadiazole nucleus has demonstrated significant anticancer activity in literature surveys. The motivation for conducting this study stems from the fact that, despite numerous investigations into novel therapeutic targets and lead compounds, the inhibition of AKT1 presents limited treatment options due to various adverse drug reactions and specificity issues, given that AKT1 exists in three isoforms. So, this study aimed to identify top-hit molecules with 1,3,4 oxadiazole scaffold targeting the AKT1 enzyme by ligand-based virtual screening to produce a dataset library from PubChem database, structure-based virtual screening followed by ADMET profiling, DFT, and molecular dynamic simulation study as an innovative approach, as there is a dearth of AKT1 inhibitors that comprise oxadiazole in the market and clinical trials. The study employs a combination of advanced computational methods, including virtual screening, molecular docking, molecular dynamics simulations, density functional theory calculations, and ADMET predictions. This comprehensive approach offers a thorough investigation of prospective drug candidates. A comprehensive pharmacoinformatic analysis was conducted on a library of compounds containing oxadiazole rings. A total of 1000 compounds were analyzed through virtual screening utilizing molecular docking and subsequent validation, aiming to identify inhibitors that exhibit a strong affinity for binding for AKT1 (PDB ID: 3O96). Thus, 24 compounds demonstrating binding affinities analogous to the standard emerged as the most promising medicinal prospects and underwent ADMET profiling, and DFT studies followed by a molecular dynamic study on the best 2 compounds. Moreover, these compounds found by ADMET profiling showed suitable pharmacokinetic and pharmacodynamic profiles and were non-toxic using DFT analysis determining ideal structural characteristics. Especially showing comparable stability to the reference molecule over 200 ns in MD simulations, the best top 2 hit compounds having binding affinity -10.7 kcal/mol for PCOS_ 133 (CID-164189) and -11.6 kcal/mol for PCOS3_42 (CID-158973) emerged as potential AKT1 inhibitors for cancer therapy in comparison to -11.6 kcal/mol and -14.7 kcal/mol binding affinity of Miransertib reference drug and IQO cocrystallized ligand of AKT1 protein PDB code 3O96. LEU-210, LEU-264, ASP-292, and TRP-80 are the important amino acid residues required for AKT1 inhibition. These results provide important new perspectives for the rational design and optimization of oxadiazole-based AKT1/PKB inhibitors, therefore laying a strong basis for experimental validation including further in-vitro and in vivo studies and PKB inhibitor development.

2025-07-25·Orphanet Journal of Rare Diseases

Safety findings from the phase 1/2 MOSAIC study of miransertib for patients with PIK3CA-related overgrowth spectrum or Proteus syndrome.

Article

作者: Perkins, Jonathan ; Hammill, Adrienne ; Buonuomo, Paola Sabrina ; Leoni, Chiara ; Liaw, Danny ; Huang, Mo ; Iacobas, Ionela ; Simonetti, Alessandra ; Eng, Whitney ; Goldmacher, Gregory ; Briones, Michael ; Zampino, Giuseppe ; Goel, Himanshu

BACKGROUND:

PIK3CA-related overgrowth spectrum (PROS) and Proteus syndrome are associated with mosaic tissue overgrowth of varying severity that commonly presents in childhood. The multicenter, open-label, phase 1/2 MOSAIC study (NCT03094832) was designed to evaluate the clinical efficacy and safety of the selective pan-AKT inhibitor miransertib for participants with PROS or Proteus syndrome.

METHODS:

Participants ≥ 2 years of age with PROS with documented somatic PIK3CA mutations or Proteus syndrome with documented somatic AKT1 mutations were enrolled to receive oral miransertib at a starting dose of 15 mg/m² every day for the first 3 cycles (1 cycle = 28 days) and miransertib 25 mg/m² every day thereafter, provided no clinically significant drug-related toxicities were observed. The initial primary objective of the study was to assess clinical response to miransertib. Due to study design and data collection limitations, evaluating efficacy was no longer considered feasible and the primary objective was updated in 2021 to evaluate the safety and tolerability of miransertib.

RESULTS:

Between May 16, 2017 and January 25, 2021, 49 participants were enrolled and received ≥ 1 dose of study drug, comprising the safety analysis population. Forty-five participants had a diagnosis of PROS and four had a diagnosis of Proteus syndrome. The median (range) age at enrollment was 7 years (2-41). Median (range) duration of treatment was 20.5 months (9.9-45.6). A total of 23 (46.9%) participants had a drug-related adverse event, most commonly decreased neutrophil count (n = 6, 12.2%), increased blood insulin (n = 5, 10.2%), and stomatitis (n = 5, 10.2%). One (2.0%) participant experienced a grade 3 drug-related adverse event (deep vein thrombosis). No drug-related adverse events led to early study discontinuation or death. Laboratory assessment values remained generally stable throughout the study.

CONCLUSION:

Miransertib was safe and tolerable in participants with a confirmed diagnosis of PROS or Proteus syndrome. Future investigations are needed to determine whether patients receive measurable clinical benefit from miransertib.

TRIAL REGISTRATION:

NCT03094832 registered Mar 28, 2017, https://clinicaltrials.gov/ct2/show/NCT03094832 .

2025-04-01·MOLECULAR DIVERSITY

An in silico approach to identify novel and potential Akt1 (protein kinase B-alpha) inhibitors as anticancer drugs

Article

作者: Etikyala, Umadevi ; Manga, Vijjulatha ; Dalimba, Udayakumar ; Reddyrajula, Rajkumar ; Kuchana, Vinutha ; Vani, T

Akt1 (protein kinase B) has become a major focus of attention due to its significant functionality in a variety of cellular processes and the inhibition of Akt1 could lead to a decrease in tumour growth effectively in cancer cells. In the present work, we discovered a set of novel Akt1 inhibitors by using multiple computational techniques, i.e. pharmacophore-based virtual screening, molecular docking, binding free energy calculations, and ADME properties. A five-point pharmacophore hypothesis was implemented and validated with AADRR38. The obtained R² and Q² values are in the acceptable region with the values of 0.90 and 0.64, respectively. The generated pharmacophore model was employed for virtual screening to find out the potential Akt1 inhibitors. Further, the selected hits were subjected to molecular docking, binding free energy analysis, and refined using ADME properties. Also, we designed a series of 6-methoxybenzo[b]oxazole analogues by comprising the structural characteristics of the hits acquired from the database. Molecules D1-D10 were found to have strong binding interactions and higher binding free energy values. In addition, Molecular dynamic simulation was performed to understand the conformational changes of protein-ligand complex.

项与 Miransertib 相关的新闻（医药）

2025-08-11

·精准药物

follow式创新，E17K选择性AKT1抑制剂为例

follow？创新？两者兼而有之。 AKT1 E17K突变选择性抑制剂，作为一个例子。两家公司，两个临床分子。 Alterome Therapeutics，ALTA-2618 Atavistik Bio，ATV-1601 两个分子都是allosteric，AKT1 E17K选择性，目前都处于临床一期阶段 (ALTA-2618更早进入)。两者之间也有差异性，ALTA-2618为共价分子，ATV-1601应为非共价分子 (二者结构都没有公布)。临床分子的结构虽然没有公布，但相关专利或会议信息是有的。为何两家结构会这么相似？是其中一家fast-follow另一家？真实情况应该是，二者都是follow更早之前已经公开报道的一类AKT1变构抑制剂。但之前这类AKT1变构抑制剂，并不具备E17K突变选择性。回顾一下之前报道的AKT1变构抑制剂结构，及其报道的时间。如下图，前两个分子的scaffold与上述Alterome及Atavistik两家公司的分子基本一模一样，而其发表时间却要早得多。并且，这里的时间是见刊的时间，相关分子首次公开的时间可能更早。但这两个分子 (其中第二个分子ARQ 092也上了临床)，虽然是allosteric，但并不是突变选择性分子；而第三个分子 (也是相同scaffold) 是E17K突变选择性，但发表时间已经是2024年。至于第四个分子，发表时间最早，结构上与其它分子scaffold不一样，但其实它们都结合在同一个allosteric口袋，并且结合模式也大略相似，可以说神似形不似。而且上图四个分子都随着文章的发表，报道有公开的晶体结构，结合相关的modeling计算，可以支撑后续基于SBDD的改造。至于如何做出突变选择性，也并不神秘。有经验的读者看了上述分子结构，再结合E17K突变的残基特性，可能已经能猜出大概。没错，从三维结构来看，突变位点离小分子结合口袋并不太远。下图是2012年发表的共晶结构，这个小分子距离突变位点最近大约5.8埃米，而突变后可能更近一些 (K比E略长)。所以在这类小分子基础上，引入一些与突变位点E17K特异性的相互作用，来达到提高选择性的目的，是比较水到渠成的。复盘来看，似乎这类E17K突变选择性AKT1变构抑制剂的发现比较简单，事实上也确实是取巧。但这种取巧，需要多方面信息的综合才能想得到 (另外有个问题，ArQule公司当年为什么没有进一步往E17K突变选择性做)。回到标题，这算不算follow式创新的一个典型例子？你对follow式创新的看法如何，有哪些可能的利弊？你身边有类似的follow式创新的例子吗？最后，Alterome及Atavistik两家公司都没有发表其分子发现的具体过程，其分子是否来源于对之前发表分子的follow，仅为推断，不代表真实情况。声明：发表/转载本文仅仅是出于传播信息的需要，并不意味着代表本公众号观点或证实其内容的真实性。据此内容作出的任何判断，后果自负。若有侵权，告知必删！长按关注本公众号粉丝群/投稿/授权/广告等请联系公众号助手觉得本文好看，请点这里↓

临床1期临床终止引进/卖出

2024-12-10

·药精通Bio

【Nature】AKT 激酶共价赖氨酸(Lys)抑制剂

AKT1 激酶是 PI3K 激酶信号转导通路的关键效应器，该通路驱动细胞增殖并在多种肿瘤中异常激活。近期，Nature 杂志上发表了基于结构的药物设计来开发基于 Lys 共价抑制剂，选择性地针对致癌 AKT1 突变体，并避免泛 AKT 抑制剂的剂量限制毒性（10.1038/d41573-024-00197-y）。蛋白激酶AKT也被称作蛋白激酶B（protein kinase B，PKB），属于丝氨酸/苏氨酸蛋白激酶，同时也是致癌基因。AKT位于PI3K-AKT-mTOR信号通路（PAM）的中心节点。PAM整合细胞外和细胞内信号，在细胞代谢、生长、增殖中发挥核心调控作用。正常细胞中AKT自身抑制，在癌症中因突变而发生信号上调，从而驱动细胞增殖，是药物开发的重要靶点。 AKT已发现三种亚型：AKT1、AKT2、AKT3，具有80%以上的同源性，仅在PH结构域和激酶结构域连接处存在较大差异，但是它们在体内分布和生理功能上并非完全相同。因此在药物开发过程中需要选择性靶向AKT不同亚型。 AKT抑制剂按照结合位点不同，可以分为PH结构域抑制剂、变构抑制剂和ATP竞争性抑制剂。大多数 ATP 竞争性和变构抑制剂都以所有三种 AKT 旁系同源物为目标。例如2023 年上市的Capivasertib 属于ATP竞争性抑制剂，同时抑制AKT三种亚型，与Faslodex（氟维司群）联用，治疗HR+/HER2-的晚期或转移性乳腺癌成年患者。然而，广谱AKT抑制剂的毒性为高血糖，导致Capivasertib用药窗口窄，进一步可能导致对AKT1的抑制不足。小鼠和人类基因组研究显示，高血糖副作用归因于对AKT2的抑制。加州大学研究人员开始寻找专门针对最常见的 AKT1 癌蛋白的抑制剂，特别是其中赖氨酸突变了的 PH 结构域中的 Glu17 (E17K)，从而导致组成型激酶激活。研究报道，AKT(E17K)的在肿瘤中突变率分别为乳腺癌 (8%，5/61) 、结肠直肠癌中 (6%,3/51) 和卵巢癌 (2%，5/50) 。为了共价结合突变体 Lys17，作者首先模拟了该残基对与变构抑制剂 (ARQ092) 结合的野生型 AKT1 晶体结构的影响，变构抑制剂占据 PH 和激酶结构域之间的口袋。该模型表明，Lys17 的反应性 ε-胺基团可能会被从结合在变构袋的基于 ARQ092 的支架延伸出来的亲电水杨醛基团(salicylaldehyde)捕获。 AKT 别构抑制剂ARQ092 基于这一策略，作者合成了一系列共价抑制剂，它们在体外和细胞内选择性结合 AKT1 (E17K) 而不是 AKT2 和野生型 AKT1。结合是可逆的，并且 Lys17 被质谱证实是主要的共价修饰位点，而不是 AKT 旁系同源物中保守的附近赖氨酸残基。与表达 WT AKT1 的细胞系（SKBR3）相比，优化的抑制剂“化合物 4”可诱导表达 AKT1 (E17K) (LAPC4-CR)的前列腺癌细胞系更有效的细胞杀伤。在携带表达 AKT1 (E17K) 的异种移植肿瘤的小鼠模型中，每天两次腹膜内施用化合物 4，持续三周，可抑制肿瘤生长；它在表达野生型 AKT1 的异种移植模型中效果较差。重要的是，化合物 4 不影响血糖，而 ARQ092 则会明显诱导高血糖。与抑制剂结合的 AKT1 (E17K) 的晶体结构鉴定出 Lys17 和水杨醛部分之间的亚胺键，并揭示该复合物通过与亚胺缀合物和激酶结构域中的两个半胱氨酸结合的内源 Zn 2+离子进一步稳定。总体来说，开发赖氨酸靶向共价抑制剂一直具有挑战性，作者提出，他们使用水杨醛部分并通过两个近端残基招募 Zn 2+的策略可以应用于其他靶点。这项研究报告了针对突变癌蛋白 AKT1 (E17K) 的共价抑制剂，由于极长的停留时间，其选择性优于 WT AKT 旁系同源物。E17K 改变持续激活 AKT1 激酶信号传导，并已在多种实体瘤类型中得到鉴定。尽管泛 AKT 抑制剂在 AKT1 (E17K) 突变肿瘤的一部分患者中显示出令人鼓舞的初步活性，但靶向毒性（例如高血糖）需要间歇和/或减少剂量，这可能会导致AKT1 (E17K) 接合度不理想。通过为靶向共价抑制剂创建独特的亲核试剂，E17K 改变提供了持续激酶抑制的潜力，并提高了相对 WT AKT 旁系同源物的选择性。然而，这一机遇伴随着赖氨酸靶向共价抑制剂的开发所固有的重大挑战，包括亲核性大大降低以及赖氨酸相对于半胱氨酸的普遍性更高。在这里，作者报告了“新型锌螯合物”的形成，该螯合物包含可逆共价抑制剂和不与 Zn 2+结合的蛋白质。此前有报道，一类非共价抑制剂可通过螯合增强结合，将外来 Zn 2+募集至胰蛋白酶样丝氨酸蛋白酶的催化位点。最近，内源性 Zn 2+螯合与乳酸与 SUMO 水解酶 SENP1 的结合有关，而 SUMO 水解酶 SENP1 不会与过渡金属结合。原则上，水杨醛部分的赖氨酸修饰与两个近端侧链（例如 Cys 或 His）招募 Zn 2+偶联的配体设计策略可以应用于除 AKT1 (E17K) 之外的其他蛋白质靶标，从而增强效力和选择性。该策略还可用于靶向功能性金属结合位点附近的赖氨酸，例如金属酶或什至结构或调节域（例如锌指），其中金属结合本质上较弱或受到致病突变的损害。锌离子、非共价抑制剂与蛋白酶（10.1038/35422）乳酸与 SENP1 活性位点的锌形成复合物，抑制 APC4 去 SUMO 化（10.1038/s41586-023-05939-3）。尽管需要进一步优化来开发口服生物可利用的 AKT1 (E17K) 水杨醛抑制剂，但最近批准的基于水杨醛的药物 voxelotor（其靶向血红蛋白的氨基末端胺）表明这是一个可以实现的目标。尽管存在这些挑战，该研究证明了共价靶向突变致癌赖氨酸并抑制 AKT1 (E17K) 驱动的恶性肿瘤生长而不抑制 AKT2 或诱导高血糖的可行性。 END 免责声明：本文仅作知识交流与分享及科普目的，不涉及商业宣传，不作为相关医疗指导或用药建议。文章如有侵权请联系删除。 OTC2024类器官前沿应用与3D细胞培养论坛圆满落幕，点击图片可查看会后报告，咨询OTC2025类器官论坛请联系：王晨 180 1628 8769

2023-04-27

·FierceBiotech

Merck reveals HIV combo trial is back in the running after FDA partial hold lifted

Merck executives said on a first-quarter earnings call that the company is restarting a phase 2 trial testing a combination of islatravir and Gilead’s lenacapavir. The middle of Merck & Co.’s clinical batting order took center stage on the company’s first-quarter earnings call, including a phase 2 HIV combo therapy that once again returned to the lineup. The Big Pharma has resumed a phase 2 study of MK-8591D, an oral regimen of islatravir and Gilead’s Sunlenca, executives said on a call with analysts Thursday. Gilead's drug was approved in December as a twice-yearly treatment for patients with multi-drug resistant HIV. The two companies decided to slam the brakes on the trial back in November 2021 after dosing was stopped in a related study testing a combo of islatravir and another drug called MK-8507. At the time, Merck disclosed that the islatravir-MK-8507 combo spurred a reduction in patients’ lymphocyte and CD4+ T-cell levels. But now islatravir is being revived, with an FDA hold on the trial having been lifted after an amended protocol using a lower dose of islatravir was agreed to, according to a Merck spokesperson. In addition, the company is launching multiple new phase 3 studies testing the med with its FDA-approved HIV drug Pifeltro. “We are committed to advancing the science to offer new treatment options for the treatment of HIV,” Dean Li, M.D., Ph.D., president of Merck Research Labs, said on the call. But elsewhere the company is reevaluating priorities. A spokesperson confirmed to Fierce Biotech that MK-7075, a treatment for overgrowth syndrome that did not appear in the company's earnings presentation, is "not currently active." The med is still in development but is being deprioritized, the spokesperson explained. The mid-stage pipeline updates come as Merck’s executives touted internal and external victories meant to assure investors that its post-Keytruda plans were materializing. Less than two weeks ago, the company announced it was buying Prometheus Biosciences for $10.8 billion, an immunology company with a promising lead asset developed to treat ulcerative colitis and Crone’s disease that recently posted a phase 2 victory. That med, PRA023, is set to do battle with a competitor from Roivant that's so far performed similarly. The deal echoes Merck’s $11.5 billion acquisition of Acceleron Pharma in September 2021, which handed the New Jersey pharma keys to cardiovascular med sotatercept, now a potential crown jewel. After diving deeper into the med’s phase 3 victory, Merck executives said today that they plan to file for U.S. approval in the third quarter for patients with pulmonary arterial hypertension. Chief Medical Officer Eliav Barr, M.D., previously told Fierce Biotech that he expects the drug to launch in early 2024. The sum of the Big Pharma’s recent deals and internal development had CEO Rob Davis sounding confident that Merck is well-situated to thrive beyond Keytruda’s expected loss of exclusivity in 2028. “I am no longer focusing on 2028,” he said on the call. “I am looking at 'how do we have sustainable growth well into the next decade.'"

临床2期并购临床3期上市批准

100 项与 Miransertib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11409	-	-	DB14982

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
生长障碍	临床2期	西班牙	Merck GmbH	2019-09-19
PIK3CA相关的过度生长现象	临床2期	西班牙	ArQule, Inc.	2017-05-16
Proteus综合征	临床2期	西班牙	ArQule, Inc.	2017-05-16
子宫内膜癌	临床1期	美国	ArQule, Inc.	2015-06-09
卵巢癌	临床1期	美国	ArQule, Inc.	2015-06-09
局部晚期恶性实体瘤	临床1期	美国	ArQule, Inc.	2011-11-01
复发性淋巴瘤	临床1期	美国	ArQule, Inc.	2011-11-01
先天性心脏缺损	临床前	美国	Merck GmbH	-
血管闭塞危机	临床前	美国	Merck GmbH	-

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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


NCT03094832 (MK-7075-002 \| 7075-002 \| MOSAIC, CTgov)	临床1/2期	PIK3CA相关的过度生长现象 \| Proteus综合征	50	Miransertib (Part A: Miransertib PROS/PS)	憲夢製蓋製製糧顧顧餘 = 築鹽簾繭築網齋繭選淵繭糧蓋窪願廠鹽醖鹽鹹 (醖顧製獵醖願齋願鏇製, 廠簾構遞構製憲鬱糧簾 ~ 襯蓋顧廠構繭製艱網觸) 更多	-	2023-03-31
NCT03094832 (MK-7075-002 \| 7075-002 \| MOSAIC, CTgov)	临床1/2期	PIK3CA相关的过度生长现象 \| Proteus综合征	50	Miransertib (Part B: Miransertib PROS (Cohort 1))	憲夢製蓋製製糧顧顧餘 = 構齋製鏇築齋願餘醖積繭糧蓋窪願廠鹽醖鹽鹹 (醖顧製獵醖願齋願鏇製, 夢壓鹽糧糧廠壓鏇夢餘 ~ 夢壓願醖壓顧構獵觸淵) 更多	-	2023-03-31
NCT03094832 (MK-7075-002 \| 7075-002 \| MOSAIC, Biospace) 人工标引	临床1/2期	PIK3CA相关的过度生长现象 \| Proteus综合征	-	Miransertib	繭餘築遞餘窪鏇糧築簾(網齋選醖觸醖顧窪鹹簾) = mostly Grade 1 or 2 AEs 廠網鏇憲鹹衊製鑰窪繭 (膚積選觸鬱鏇鹽淵襯範 ) 更多	积极	2019-06-17
NCT02594215 (Pubmed \| Adv Exp Med Biol) 人工标引	临床1期	Proteus综合征	6	Miransertib	製構鏇鹽鹽構製蓋齋醖(鬱鬱鑰餘窪憲淵餘築壓) = 50% reduction (5/6) 網網範構簾襯鬱餘選窪 (淵齋蓋鹽膚繭餘艱衊鏇 )	积极	2019-03-07
NCT02476955 (ASCO 12017 \| ASCO 22017) 人工标引	临床1期	实体瘤	13	carboplatin+paclitaxel+ARQ 092	鑰製鬱憲鬱鏇鬱繭廠鑰(積淵鹽廠廠蓋觸築餘餘) = diarrhea 69%, fatigue 54%, hyperglycemia 31%, maculopapular rash 31%, nausea 23%, mucosal inflammation 23%, anemia 15%, platelet count decreased 15% and hypokalemia 15% 夢願窪選鹽襯廠齋網糧 (網餘鹽憲範遞襯鬱壓顧 ) 更多	积极	2017-06-05
AACR2013	临床1期	HR阳性/HER2低表达实体瘤	22	ARQ 092	繭壓艱觸願襯簾艱鹽願(膚艱淵蓋繭艱願膚衊觸) = 艱鹽衊製蓋願構窪艱糧壓壓餘願鏇構艱廠繭鏇 (繭廠獵齋鑰夢糧鏇製衊 )	-	2013-04-15