A Single Arm, Open Label, Multi-center Study of Mitoxantrone Hydrochloride Liposome With Cyclophosphamide, Vincristine, Etoposide and Prednisone (CMOEP) in Treatment-Naive Patients With Peripheral T-Cell Lymphoma

This is a prospective, single arm, multicenter study to evaluate the safety and efficacy of CMOEP in patients with untreated peripheral T-cell lymphoma.

开始日期2024-06-01

申办/合作机构

Tianjin Medical University Cancer Institute and Hospital

ChiCTR2300078813 / Suspended临床2期IIT

Mitoxantrone hydrochloride liposome injection, cyclophosphamide, vincristine, and prednisone with or without rituximab in the treatment of elderly patients with previously untreated aggressive non-Hodgkin lymphoma: a single-arm, multicenter, exploratory research

开始日期2023-12-20

申办/合作机构

中国医学科学院

NCT06224842 / Recruiting临床1/2期IIT

A Phase Ib/II Clinical Study of Mitoxantrone Liposome and Azacitidine in the Treatment of Relapsed/Refractory Angioimmunoblastic T-cell Lymphoma

This study is an open-label, single-arm Phase Ib/II clinical trial designed to evaluate the safety and efficacy of the combination therapy with mitoxantrone liposome and azacitidine in the treatment of relapsed/refractory angioimmunoblastic T-cell lymphoma(R/R AITL). The study includes two parts: a dose escalation phase and a dose expansion phase, each comprising screening, treatment, and follow-up periods. In the dose escalation phase, the mitoxantrone liposome injection will start at a dose of 16 mg/m^2 on day1, combined with subcutaneous injection of azacitidine at a dose of 75 mg/m^2 on days 1-7, with each cycle lasting 4 weeks (28 days). Three predetermined dose groups for mitoxantrone liposome are 16, 18, and 20 mg/m^2. In the dose expansion phase, 10-20 cases will be included with the mitoxantrone liposome injection at the recommended phase II dose (RP2D) based on the results of the dose escalation phase. After the treatment period, safety and survival information will be collected during the follow-up period. This study aims to comprehensively evaluate the safety and efficacy of mitoxantrone liposome in combination with azacitidine for the treatment of R/R AITL, exploring a combination therapy that offers higher survival benefits with limited adverse reactions and providing new therapeutic approaches for R/R AITL.

开始日期2023-12-12

申办/合作机构

湖北省肿瘤医院

[+1]

100 项与盐酸米托蒽醌脂质体相关的临床结果

登录后查看更多信息

100 项与盐酸米托蒽醌脂质体相关的转化医学

登录后查看更多信息

100 项与盐酸米托蒽醌脂质体相关的专利（医药）

登录后查看更多信息

5,715

项与盐酸米托蒽醌脂质体相关的文献（医药）

2024-12-01·Molecular biology reports

Transcription factor E2F3 activates CDC25B to regulate DNA damage and promote mitoxantrone resistance in stomach adenocarcinoma

Article

作者: Mei, Yijun ; Liu, Ming ; Pan, Xiaoming ; Chen, Zhengwei ; Xu, Chaobo ; Cheng, Guoxiong

BACKGROUND:

CDC25B, as a member of the cell cycle regulating protein family, is located in the cytoplasm and is involved in the transition of the cell cycle and mitosis. CDC25B is highly expressed in various tumors and is a newly discovered oncogene. This study aimed to investigate the impact of CDC25B on mitoxantrone resistance in stomach adenocarcinoma (STAD) and its possible mechanisms.

METHODS:

This study analyzed the expression of CDC25B and its potential transcription factor E2F3 in STAD, as well as the IC₅₀ values of tumor tissues by bioinformatics analysis. Expression levels of CDC25B and E2F3 in STAD cells were measured by qRT-PCR. MTT was utilized to evaluate cell viability and IC₅₀ values of STAD cells, and comet assay was utilized to analyze the level of DNA damage in STAD cells. Western blot was used to analyze the expression of DNA damage-related proteins. The targeting relationship between E2F3 and CDC25B was validated by dual-luciferase and ChIP assays.

RESULTS:

Bioinformatics analysis and molecular experiments showed that CDC25B and E2F3 were highly expressed in STAD, and CDC25B was enriched in the mismatch repair and nucleotide excision repair pathways. The IC₅₀ values of tumor tissues with high expression of CDC25B were relatively high. Dual-luciferase and ChIP assays confirmed that CDC25B could be transcriptionally activated by E2F3. Cell experiments revealed that CDC25B promoted mitoxantrone resistance in STAD cells by regulating DNA damage. Further research found that low expression of E2F3 inhibited mitoxantrone resistance in STAD cells by DNA damage, but overexpression of CDC25B reversed the impact of E2F3 knockdown on mitoxantrone resistance in STAD cells.

CONCLUSION:

This study confirmed a novel mechanism by which E2F3/CDC25B mediated DNA damage to promote mitoxantrone resistance in STAD cells, providing a new therapeutic target for STAD treatment.

2024-12-01·Molecular biology reports

Inhibition of mitochondrial calcium transporters alters adp-induced platelet responses

Article

作者: Barki, Saima ; Shehwar, Durre ; Bertaggia Calderara, Debora ; Aliotta, Alessandro ; Veuthey, Lucas ; Alam, Muhammad Rizwan ; Alberio, Lorenzo

INTRODUCTION:

ADP-stimulated elevation of cytosolic Ca²⁺ is an important effector mechanism for platelet activation. The rapidly elevating cytosolic Ca²⁺ is also transported to mitochondrial matrix via Mitochondrial Ca²⁺ Uniporter (MCU) and extruded via Na⁺/Ca²⁺/Li⁺ Exchanger (NCLX). However, the exact contribution of MCU and NCLX in ADP-mediated platelet responses remains incompletely understood.

METHODS AND RESULTS:

The present study aimed to elucidate the role of mitochondrial Ca²⁺ transport in ADP-stimulated platelet responses by inhibition of MCU and NCLX with mitoxantrone (MTX) and CGP37157 (CGP), respectively. As these inhibitory strategies are reported to cause distinct effects on matrix Ca²⁺ concentration, we hypothesized to observe opposite impact of MTX and CGP on ADP-induced platelet responses. Platelet aggregation profiling was performed by microplate-based spectrophotometery while p-selectin externalization and integrin αIIbβ3 activation were analyzed by fluorescent immunolabeling using flow cytometery. Our results confirmed the expression of both MCU and NCLX mRNAs with relatively low abundance of NCLX in human platelets. In line with our hypothesis, MTX caused a dose-dependent inhibition of ADP-induced platelet aggregation without displaying any cytotoxicity. Likewise, ADP-induced p-selectin externalization and integrin αIIbβ3 activation was also significantly attenuated in MTX-treated platelets. Concordantly, inhibition of NCLX with CGP yielded an accelerated ADP-stimulated platelet aggregation which was associated with an elevation of p-selectin surface expression and αIIbβ3 activation.

CONCLUSION:

Together, these findings uncover a vital and hitherto poorly characterized role of mitochondrial Ca²⁺ transporters in ADP-induced platelet activation.

2024-03-01·Current pharmaceutical biotechnology

Evaluation of New Folate Receptor-mediated Mitoxantrone Targeting Liposomes In Vitro

Article

作者: Shan, Bin ; Wen, Tianjiao ; Song, Cong ; Gao, Yuan ; Cui, Jingxia ; An, Yahui ; Zheng, Ying

Background:::

Ligand-mediated liposomes targeting folate receptors (FRs) that are overexpressed on the surface of tumor cells may improve drug delivery. However, the properties of liposomes also affect cellular uptake and drug release.

Objective:::

Mitoxantrone folate targeted liposomes were prepared to increase the enrichment of drugs in tumor cells and improve the therapeutic index of drugs by changing the route of drug administration.

Methods:::

Liposomes were prepared with optimized formulation, including mitoxantrone folatetargeted small unilamellar liposome (MIT-FSL), mitoxantrone folate-free small unilamellar liposome (MIT-SL), mitoxantrone folate-targeted large unilamellar liposome (MIT-FLL), mitoxantrone folate-free large unilamellar liposomes (MIT-LL). Cells with different levels of folate alpha receptor (FRα) expression were used to study the differences in the enrichment of liposomes, the killing effect on tumor cells, and their ability to overcome multidrug resistance.

Results:::

The results of the drug release experiment showed that the particle size of liposomes affected their release behavior. Large single-compartment liposomes could hardly be effectively released, while small single-compartment liposomes could be effectively released, MIT-FSL vs MIT-FLL and MIT-SL vs MIT-LL had significant differences in the drug release rate (P<0.0005). Cell uptake experiments results indicated that the ability of liposomes to enter folic acid receptor-expressing tumor cells could be improved after modification of folic acid ligands on the surface of liposomes and it was related to the expression of folate receptors on the cell surface. There were significant differences in cell uptake rates (p<0.0005) for cells with high FRα expression (SPC-A-1 cells), when MIT-FSL vs MIT-SL and MIT-FLL vs MIT-LL. For cells with low FRα expression (MCF-7 cells), their cell uptake rates were still different (p<0.05), but less pronounced than in SPC-A-1 cells. The results of the cell inhibition experiment suggest that MIT-FLL and MIT-LL had no inhibitory effect on cells, MIT-FSL had a significant inhibitory effect on cells and its IC50 value was calculated to be 4502.4 ng/mL, MIT-SL also had an inhibitory effect, and its IC50 value was 25092.1 ng/mL, there was a statistical difference (p<0.05), MIT-FSL had a higher inhibitory rate than MIT-SL at the same drug concentration. Afterward, we did an inhibitory experiment of different MIT-loaded nanoparticles on MCF-7 cells compared to the drug-resistant cells (ADR), Observing the cell growth inhibition curve, both MIT-FSL and MIT-SL can inhibit the growth of MCF-7 and MCF-7/ADR cells. For MCF- 7 cells, at the same concentration, there is little difference between the inhibition rate of MITFSL and MIT-SL, but for MCF-7/ADR, the inhibition rate of MIT-FSL was significantly higher than that of MIT-SL at the same concentration (P<0.05).

Conclusion:::

By modifying folic acid on the surface of liposomes, tumor cells with high expression of folic acid receptors can be effectively targeted, thereby increasing the enrichment of intracellular drugs and improving efficacy. It can also change the delivery pathway, increase the amount of drug entering resistant tumor cells, and overcome resistance.

项与盐酸米托蒽醌脂质体相关的新闻（医药）

2024-06-17

·药通社

中国药科大学杨劲教授：改良型高端制剂的开发-如何改？如何证明临床优势？

一键报名 · 见证合作！限量！扫描二维码抢免费门票高端制剂具有技术门槛相对较高、临床价值可以很大的特点。不少传统药企转型，定位在通过高端制剂CMC平台进行改良型新药的开发，但是往往存在以下痛点：第一，这类公司的知识背景是CMC的大规模生产的经验。他们的困境在于引进临床理念，对未被满足的临床需求进行改良开发。然而，如何选择合适的CMC平台去解决已有产品的不足？CMC改良和临床需求、临床优势如何关联？第二，如何证明临床优势？改良型新药立项、临床开发策略怎么做？基本逻辑是什么？业内对这一问题的认知仍然不足。许多申请人在与CDE交流遇到困难后，才开始寻求专业帮助。而且部分企业往往缺乏足够的知识背景，错误地认为，即使有重大改变，只要通过生物等效性试验就可以豁免临床风险，从而上市。但实际上，这种改变可能带来很多风险，需要提供更为充分的证据。图 | 2024年改良型新药申报情况图源 | 药融云数据库图源 | 杨劲教授课程 / 杨劲 / 中国药科大学教授中国药科大学药理系教授，从事临床药理和药品监管科学研究工作30余年，科研方向是建模仿真引导下的药物开发和监管科学研究。当前，“改良型新药”临床策略已然从一味想要BE/PK免确证性临床、追求“短平快”，迅速发展到追求“既有临床优势又有技术壁垒”。举几个成功案例：绿叶制药的注射用利培酮缓释微球改良了释放方式，通过改良药物释放方式，可以缩短初始的释药延滞期，注射给药后就能够直接获得药效作用所需的有效血药浓度，从而不再需要首次注射后的口服制剂补充。在保持临床有效血药浓度稳定的情况下，这个产品能提高临床治疗过程的便利性。从临床注册路径上，他们通过Ⅰ期临床试验豁免了Ⅱ期和Ⅲ期临床试验。石药集团中诺药业的盐酸米托蒽醌脂质体注射液通常用于既往至少经过一线标准治疗的复发或难治性外周 T 细胞淋巴瘤成人患者。盐酸米托蒽醌脂质体注射液是一种改良型新药，其在人体内的药代动力学特征和组织分布得到改良，能够选择性向肿瘤组织富集，在肿瘤微环境中以适合的释药速度持续释放药物，进而发挥抗肿瘤活性。同时，药物经脂质体包裹后，对正常组织的损伤减少，降低了蒽环类药物的心脏毒性；通过对粒径和形态改良，基本避免了手足综合征、口腔黏膜炎、药物输注相关反应等脂质体药物常见不良反应。该产品通过PK试验、 78 例患者的有效性试验和 13 项安全性试验，豁免了Ⅲ期临床试验。中国药科大学杨劲教授指出：做改良型新药，第一要了解原研，第二需要走三个步骤：“立、改、良”。立立项出发点奠定了筛寻项目来源，和临床治疗价值的基础。此时需要提出“五段论”的假说。现有产品当前面临什么样的不足？依从性不足？不良反应大？还是有效性不足？拟定适应症人群的关键指标和现有产品是否有显著改变？图源 | 杨劲教授课程确证性临床风险有多大？要花多少成本？是否可以豁免？如果不需要开展确证性临床试验，那此后如何推进？监管是否能批准上市？工业化是否可行？这些假说是整个改良型新药立项的根本逻辑，也决定了内部的投入成本，和对外体现的临床优势。图源 | 杨劲教授课程企业是否能在下述要点中体现优势？一是临床获益；二是安全性，耐受性是否更好？不良反应发生率是否能更低？但这里其实有一个悖论：降低有效性和提高安全性之间不能兼得。提供证据是一个很复杂的命题，每个项目、品种都不太一样。这其中还包含非劣效界值如何选择？安全性数据如何证明等等问题。三是依从性，依从性更多是减轻患者的治疗负担。比如把静脉改皮下注射，把皮下注射改为透皮贴剂，或者减少给药频次，这类肯定依从性更好。此处如果是非劣效临床试验，非劣效界值怎么算？用什么指标表示？依从性是否显而易见？这里都有很大的探讨空间。四就是其它。举个例子，如果针对脑卒中人群，由于这部分人群脑部受损，导致他们吞咽困难，此时就需要把药物碾碎或者做成溶液剂给药。针对普通片的不足，泡腾片或分散片的改良就是有价值，且有了具体场景。改 CMC平台如何进行改良？这对技术平台的要求很高。举个例子，口服给药由于首过效应代谢产物高，这对安全性有一定的影响。此时应该用什么平台改变口服代谢的不良反应？合适的技术平台非常重要，而不是自身有一个平台，再看能解决什么问题，这样的逻辑顺序是错误的。良改剂型的终极证据是什么？也就是临床优势如何证明？PK有三条路径，仿制药路径、临床优效性路径和临床非劣效路径。图源 | 杨劲教授课程通过PK改变来体现临床优势，如果是这个定位，是否要做确证性临床？是否可以用PK/PD代替有效性？是否可以用非统计学假设在内的安全性试验证明安全性？这相比传统的、以统计学为前提的RCT实验，风险对申请人来说就会小很多。如果针对优效性的改良，比如皮下埋置的长效注射液，肯定需要做确证性的临床；但如果只需要证明非劣效性，那就需要提供依从性的证据。案例很多，杨教授会在现场和大家进行分享。默沙东前任主席乔治·W·默克曾说：“我们应当永远铭记：药品是为人类而生产，而不是为追求利润而制造的。只要我们坚守这一信念，利润必将随之而来。” 改良型新药的发展是一个不断进步和创新的过程，未来，上市将不再是遥不可及的梦想。图源 | 杨劲教授课程杨教授将于8月15-16日参与CMC交流大会，并与大家探讨《一“立”二”改”三“良”，改良型新药上市的三个关键步骤》。届时，杨教授将与大家共同探讨业内改良型新药重要案例，我们诚挚邀请各位对改良型新药技术感兴趣的同仁参加这次论坛，与杨教授一起深入剖析行业深度内容。期待在苏州与大家相会。推荐阅读

临床3期临床2期

2024-06-14

·生物谷

革命性突破！Acta Pharm Sin B | 双聚乙二醇化胰岛素——一种长效胰岛素偶联物，在降低低血糖方面具有优越的安全性

胰岛素药物是最经典的血糖控制药物，全球超过900万的1型糖尿病患者和6000万的2型糖尿病患者定期服用胰岛素药物。然而，两个固有的缺点(即半衰期短和治疗指数窄)限制了其充分的治疗潜力。与许多其他蛋白质药物相似，胰岛素在血液中的半衰期很短，约为9分钟。为了达到血糖指标，糖尿病患者通常需要每天注射胰岛素数次，这严重影响患者的生活质量。更糟糕的是，胰岛素的治疗指数较窄，这意味着过量使用胰岛素可能会导致严重的副作用，即糖尿病的低血糖。低血糖症的症状包括头晕、颤抖和精神错乱，在最极端的情况下，这些症状会导致危及生命的低血糖昏迷。反复的低血糖发作会增加患脑血管疾病的风险，并最终损害认知功能。此外，针头恐惧症和对低血糖的恐惧常常导致胰岛素使用不足，从而导致血糖管理不善，最终导致严重的并发症，如心血管疾病、糖尿病足和糖尿病肾病。随着蛋白质工程技术的进步，越来越多的长效胰岛素类似物出现在市场上或临床试验中。其中，聚合物结合已被证明是通过降低肾脏清除率来延长胰岛素半衰期的有效途径。在这方面，聚乙二醇(PEG)由于其亲水性、生物相容性和成熟的合成工艺，仍然是最常用的蛋白质偶联聚合物。为了避免牺牲胰岛素的生物活性，PEG通常在Phe B1或Lys B29位置进行单修饰。因此，聚乙二醇化的胰岛素作为天然胰岛素能够与胰岛素受体结合。尽管聚乙二醇化胰岛素的药代动力学得到了适度改善，但对胰岛素的治疗指标没有改善，过量使用仍可引起低血糖。糖尿病患者仍需经常自我监测血糖，及时调整胰岛素剂量，避免低血糖的发生。因此，一种既能保证长效控糖的同时又显著提升安全性的创新药物是糖尿病患者急需的。图片来源：https://doi-org.libproxy1.nus.edu.sg/10.1016/j.apsb.2024.02.022 近日，来自中山大学第三附属医院的研究者们在Acta Pharm Sin B杂志上发表了题为“Di-PEGylated insulin: A long-acting insulin conjugate with superior safety in reducing hypoglycemic events”的文章，该研究表明长期大剂量双聚乙二醇化胰岛素可减轻糖尿病肾病，且无明显的系统毒性。双聚乙二醇化胰岛素对糖尿病小鼠的长期疗效在本研究中，本研究开发了一种方法来扩大胰岛素的治疗指数，降低使用期间低血糖的风险。研究者合成并鉴定了一种能同时降低肾脏清除率和受体介导清除率的双聚乙二醇化胰岛素，证实其聚乙二醇化位点为胰岛素的Lys B29和Gly A1(涉及受体结合区)，双聚乙二醇化显著降低了胰岛素的体外生物活性。与传统的单聚乙二醇化胰岛素相比，双聚乙二醇化胰岛素不仅能表现出更好的药代动力学，进一步延长胰岛素的半衰期，更重要的是，它成功拓宽了胰岛素的治疗指数，即便在高剂量使用下也能有效避免低血糖事件，这是现有长效胰岛素类似物尚未实现的里程碑。研究中，双聚乙二醇化胰岛素在动物模型中展现了卓越的安全性与有效性，不仅成功抑制了一种常见的糖尿病并发症-糖尿病肾病的进展，且未观察到显著的系统毒性，为糖尿病患者带来了长期血糖稳定管理的新希望。并且，在10 U/kg的高剂量测试中，双聚乙二醇化胰岛素展现出了防止低血糖的显著能力，与之相比，常规胰岛素和单聚乙二醇化胰岛素在相同剂量下导致了严重的低血糖反应。双聚乙二醇化胰岛素改善治疗指标和药代动力学的示意图这项成果标志着糖尿病治疗领域的一大飞跃，为克服胰岛素治疗的根本障碍提供了创新思路。它不仅预示着未来糖尿病患者可能拥有更加灵活、安全的胰岛素治疗选项，还为其他具有治疗指数限制的蛋白质药物开发打开了思路。综上所述，双聚乙二醇化胰岛素作为新一代长效胰岛素药物的代表，凭借其在扩大治疗窗、保障患者安全及改善长期疾病管理方面的卓越表现，正引领糖尿病治疗迈入一个兼顾高效与安全的新纪元。参考文献： Zhipeng Zeng et al. Di-PEGylated insulin: A long-acting insulin conjugate with superior safety in reducing hypoglycemic events. Acta Pharm Sin B. 2024 Jun;14(6):2761-2772. doi: 10.1016/j.apsb.2024.02.022. 本文仅用于学术分享，转载请注明出处。若有侵权，请联系微信：bioonSir 删除或修改！

临床结果

2024-06-11

·BioSpace

Actinium Announces Results of Actimab-A + CLAG-M Combination Trial Highlighted in Oral Presentation at the 2024 Society of Nuclear Medicine & Molecular Imaging Annual Meeting

- Novel targeted radiotherapy-based combination being studied as potential backbone therapy potential relapsed or refractory acute myeloid leukemia - Actimab-A + CLAG-M produced high rates of response, measurable residual disease negativity, bone marrow transplant access and improved survival outcomes in high-risk patients including TP53+ and venetoclax treated patients - SNMMI oral presentation highlighted dosimetry results and safety data supporting this novel radiotherapy combination NEW YORK, June 11, 2024 /PRNewswire/ --Actinium Pharmaceuticals, Inc., (NYSE AMERICAN: ATNM) (Actinium or the Company), a leader in the development of Antibody Radiation Conjugates (ARCs) and other targeted radiotherapies, today highlighted data from the completed Phase 1b combination trial of Actimab-A + CLAG-M in patients with relapsed or refractory acute myeloid leukemia (r/r AML) at the 2024 Society of Nuclear Medicine & Molecular Imaging (SNMMI) Annual Meeting held June 8 – 11, 2024, in Toronto, Canada. Actimab-A is an ARC comprised of a CD33 targeting monoclonal antibody conjugated with the alpha-particle emitter Actinium-225 isotope payload. Actimab-A has been studied as a single agent and in combination with chemotherapies and targeted therapies in Phase 1 and Phase 2 trials. Sandesh Seth, Actinium's Chairman and CEO, said, "These results demonstrate the immense potential of targeted radiotherapy via ARCs from both an efficacy and safety perspective. Through the use of dosimetry, we can estimate radiation doses to the target organ and non-targeted healthy organs and as observed in this trial, we saw no safety signals for the kidneys, liver or other major organs. Together with the potent efficacy, particularly in these high-risk relapse and refractory patients, we are highly excited by the building clinical pro We look forward to continuing to advance our Actimab-A program as a broad-based combination approach with targeted and non-targeted therapies in collaboration with the NCI for the benefit of AML patients who are eligible for targeted radiotherapy." The Phase 1b Actimab-A + CLAG-M combination trial enrolled patients with high-risk r/r AML with the following features: Median age of 62 with patients up to 73 years old 91% of patients had intermediate (n=3, 13%) or adverse cytogenetics (n=18, 78%) Over 50% of patients had a TP53 mutation Median of 2 lines of prior therapy (range:1-5) including: Prior bone marrow transplant: 57% Prior venetoclax treatment: 57% Despite the high-risk pro the patients on the study, the combination of Actimab-A + CLAG-M produced high rates of response and measurable residual disease negativity and improved survival outcomes across all patient subsets: 64% of eligible patients proceeded to bone marrow transplant with these patients having a median overall of 24 months. Dosimetry and Safety: A validated pharmacokinetic model was used to estimate the biodistribution of Actimab-A based on the distribution of CD33+ AML blast cells based on data derived from patients in the Phase 1b study Across all dose levels including 0.75 µCi/kg, which was determined to be the optimal dose, and 1.0 µCi/kg (the highest dose in the Phase 1b study) radiation doses for key organs were well below known tolerance levels with external beam radiation therapy (EBRT) No safety signals for major organs such as liver, heart, kidneys, lungs and intestines were observed and a safety pro with that expected in heavily pre-treated r/r AML patients given salvage therapy A single 30-minute administration of Actimab-A results in rapid radiation delivery and clearance with peak concentration reached around 0.6 hours and undetectable in the blood by 48 hours after administration The dose of 0.75 µCi/kg was identified as optimal for this combination therapy and will be further evaluated in the next stage of clinical development About the SNMMI Annual Meeting The SNMMI Annual Meeting is recognized as the premier educational, scientific, research, and networking event in nuclear medicine and molecular imaging. The four-day event, taking place each June, provides physicians, technologists, pharmacists, laboratory professionals, and scientists with an in-depth view of the latest research and development in the field as well as providing insights into practical applications for the clinic. About Actinium Pharmaceuticals, Inc. Actinium develops targeted radiotherapies to meaningfully improve survival for people who have failed existing oncology therapies. Advanced pipeline candidates Iomab-B (pre-BLA & MAA (EU)), an induction and conditioning agent prior to bone marrow transplant, and Actimab-A (National Cancer Institute CRADA pivotal development path), a therapeutic agent, have demonstrated potential to extend survival outcomes for people with relapsed and refractory acute myeloid leukemia. Actinium plans to advance Iomab-B for other blood cancers and next generation conditioning candidate Iomab-ACT to improve cell and gene therapy outcomes. Actinium holds more than 230 patents and patent applications including several patents related to the manufacture of the isotope Ac-225 in a cyclotron. For more information, please visit: Forward-Looking Statements This press release may contain projections or other "forward-looking statements" within the meaning of the "safe-harbor" provisions of the private securities litigation reform act of 1995 regarding future events or the future financial performance of the Company which the Company undertakes no obligation to update. These statements are based on management's current expectations and are subject to risks and uncertainties that may cause actual results to differ materially from the anticipated or estimated future results, including the risks and uncertainties associated with preliminary study results varying from final results, estimates of potential markets for drugs under development, clinical trials, actions by the FDA and other governmental agencies, regulatory clearances, responses to regulatory matters, the market demand for and acceptance of Actinium's products and services, performance of clinical research organizations and other risks detailed from time to time in Actinium's filings with the Securities and Exchange Commission (the "SEC"), including without limitation its most recent annual report on form 10-K, subsequent quarterly reports on Forms 10-Q and Forms 8-K, each as amended and supplemented from time to time. Investors: investorrelations@actiniumpharma.com Company Codes: AMEX:ATNM

临床结果临床1期放射疗法

100 项与盐酸米托蒽醌脂质体相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB01204

研发状态

批准上市

10 条最早获批的记录,

后查看更多信息

适应症	国家/地区	公司	日期
外周T细胞淋巴瘤	中国	石药集团有限公司	2021-06-01

未上市

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
多发性硬化症	申请上市	美国	Immunex Corp.	2000-02-01
鼻咽癌	临床3期	中国	石药集团中诺药业（石家庄）有限公司合并	2023-02-15
难治性外周T细胞不明淋巴瘤	临床3期	中国	石药集团中奇制药技术（石家庄）有限公司	2021-04-14
复发性弥漫性大B细胞淋巴瘤	临床2期	中国	石药集团中奇制药技术（石家庄）有限公司	2023-07-27
难治性弥漫性大 B 细胞淋巴瘤	临床2期	中国	石药集团中奇制药技术（石家庄）有限公司	2023-07-27
复发性多发性硬化	临床2期	中国	石药集团中诺药业（石家庄）有限公司合并	2022-11-08
视神经脊髓炎	临床2期	中国	石药集团中诺药业（石家庄）有限公司	2022-10-31
难治性急性髓细胞白血病	临床2期	中国	石药集团欧意药业有限公司	2022-07-21
复发性急性髓细胞白血病	临床2期	中国	石药集团欧意药业有限公司	2022-07-21
晚期癌症	临床2期	中国	石药集团中奇制药技术（石家庄）有限公司	2022-04-25

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT03794778 (ASCO2023) 人工标引	临床4期	卵巢癌一线	391	carboplatin+Pegylated liposomal doxorubicin (CD group)	獵觸糧齋願壓鹽獵鹹糧(壓齋艱築淵艱憲壓衊範) = 積鑰艱憲鏇鹽壓艱網選製鹽積顧觸憲遞餘糧顧 (築獵遞鑰製網糧襯構網 ) 更多	相似	2023-05-31
				carboplatin+paclitaxel (CP group)	獵觸糧齋願壓鹽獵鹹糧(壓齋艱築淵艱憲壓衊範) = 壓衊觸憲齋願顧夢糧醖製鹽積顧觸憲遞餘糧顧 (築獵遞鑰製網糧襯構網 ) 更多
ASCO2023 人工标引	临床1期	肉瘤	23	Pegylated liposomal doxorubicin+ifosfamide	襯淵選衊網積願製簾範(繭衊網獵範壓餘壓窪鬱) = 蓋醖願觸蓋艱鬱範餘夢製製積築淵簾廠憲鹹窪 (範餘鹽淵膚積醖窪鏇夢 ) 更多	积极	2023-05-26
P013 (EBMT2023)	N/A	急性髓性白血病	20	FLAG-MITOXANTRONE (M)	積糧築鹽範膚蓋選艱選(憲廠淵憲選繭鹹選餘構) = 遞觸蓋窪築製遞築構廠繭選築願構齋餘夢憲廠 (網遞鏇網遞淵願構憲鬱 ) 更多	-	2023-04-23
NCT04509466 (ESMO2022)	临床1/2期	结外NK-T细胞淋巴瘤	31	Mitoxantrone hydrochloride liposome	壓齋夢獵鹽鏇衊簾簾鹽(衊憲鏇鬱鹽艱醖齋壓廠) = 淵夢廠簾壓範顧鏇餘齋構構構選餘獵壓壓鑰醖 (構夢觸醖選簾襯構淵淵, 70.2% ~ 96.4%) 更多	-	2022-09-12
ChiCTR1900028433 (ESMO2022)	临床2期	HER2阳性乳腺癌新辅助	78	PLD + C + HP	積鹽餘鬱鹽繭糧糧艱積(餘憲鹽遞憲獵繭鏇構願) = 淵願網築鑰憲繭齋窪艱壓壓夢觸齋糧積壓艱糧 (艱範糧蓋觸築膚鑰膚顧 )	-	2022-09-10
				Taxanes + HP	築糧壓範繭衊壓積壓廠(糧鹹襯憲憲餘糧憲鬱顧) = 構顧鬱襯襯鑰襯鏇範餘壓齋鏇艱繭蓋醖願膚網 (範築選蓋鏇衊衊繭憲鹽 )
NCT04718376 (ASCO2022) 人工标引	临床1期	铂耐药性卵巢癌末线	47	PLM60 20 mg/m2	遞積獵選衊願鹹簾壓鑰(獵鏇構觸窪壓襯窪餘蓋) = The most common ≥ grade 3 TRAEs (incidence ≥10%) were leucopenia (51.1%), neutropenia (40.4%), anemia (19.1%), lymphocytopenia (17.0%) and thrombocytopenia (17.0%) 構餘顧製鏇艱夢願積鏇 (遞構網壓構蓋鹹鹽膚壓 )	积极	2022-06-02
				PLM60 20 mg/m2 (platinum-resistant patients with ≥3 prior lines)
NCT04902027 (ASCO2022)	临床1期	头颈癌转移	34	Mitoxantrone hydrochloride liposome	鹹積鹹齋夢構觸壓簾製(築衊構齋獵獵襯顧範膚) = 41.2% 築構鏇夢醖窪觸遞顧艱 (願鑰鏇遞選鏇壓繭顧簾 ) 更多	积极	2022-06-02
NCT02596373 (Pubmed \| Invest New Drugs)	临床2期	晚期乳腺癌	-	Lipo-MIT	夢醖窪夢觸獵窪顧觸選(簾獵餘範廠醖淵網簾膚) = 淵蓋選衊製憲鏇鑰夢齋鑰淵餘願窪窪齋鹽獵顧 (遞膚繭醖願積鹹糧遞鹹, 3.8 ~ 30.7) 更多	-	2021-10-11
				MIT	夢醖窪夢觸獵窪顧觸選(簾獵餘範廠醖淵網簾膚) = 範築艱膚願鹽膚鹽艱膚鑰淵餘願窪窪齋鹽獵顧 (遞膚繭醖願積鹹糧遞鹹, 0.8 ~ 22.1) 更多
NCT03776279 (CSCO2021)	临床2期	外周T细胞淋巴瘤 \| 结外NK-T细胞淋巴瘤	108	Mitoxantrone Hydrochloride Liposome	衊觸構糧製糧窪艱簾襯(窪構願壓選網衊艱構襯) = 蓋醖衊範糧鏇鹽齋願顧餘艱鹹鹹鏇壓範構蓋糧 (蓋鏇積夢膚淵窪顧淵積, 32.3 ~ 51.5) 更多	积极	2021-09-25
NCT01483690 (CTgov)	临床1/2期	复发性成人急性淋巴细胞白血病 \| 前体T淋巴细胞白血病淋巴瘤 \| 前体B细胞成淋巴细胞白血病淋巴瘤	23	Vorinostat+Pegaspargase+Decitabine+dexamethasone+Methotrexate+Vincristine+mitoxantrone (Initial Dose Level)	餘觸醖蓋淵構醖觸襯網(選構遞艱壓繭憲憲鹹齋) = 膚築積淵齋醖襯蓋襯製鏇衊醖鹹艱憲網蓋醖鹹 (選範網繭憲夢蓋觸鹽積, 觸製鏇壓壓糧顧艱範構 ~ 窪選願選鏇構構築鑰簾) 更多	-	2020-10-27
				Vorinostat+Pegaspargase+Decitabine+dexamethasone+Methotrexate+Vincristine+mitoxantrone (Modified Dose Level)	餘觸醖蓋淵構醖觸襯網(選構遞艱壓繭憲憲鹹齋) = 齋鏇簾製觸膚窪醖鹽鏇鏇衊醖鹹艱憲網蓋醖鹹 (選範網繭憲夢蓋觸鹽積, 蓋廠膚網齋築憲鏇鹽願 ~ 簾淵窪憲鑰積遞壓鏇蓋) 更多