A Phase 1/1b Study of AOH1996 Alone or in Combination With the BCL-2 Inhibitor Venetoclax +/- Azacitidine in Patients With Relapsed/Refractory Acute Myeloid Leukemia

This phase I trial tests safety, side effects, and best dose of AOH1996 alone or in combination with venetoclax with or without azacitidine for the treatment of patients with acute myeloid leukemia (AML) that has come back after a period of improvement (relapsed) or AML that has not responded to previous treatment (refractory). AOH1996 is in a class of medications called PCNA inhibitors. It inhibits cancer growth and induces deoxyribonucleic acid (DNA) damage. This may help keep cancer cells from growing and damage cancer cell DNA. Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. It may stop the growth of cancer cells by blocking BCL-2, a protein needed for cancer cell survival. Azacitidine is in a class of medications called demethylation agents. It works by helping the bone marrow to produce normal blood cells and by killing abnormal cells in the bone marrow. Giving AOH1996 alone or in combination with venetoclax with or without azacitidine may be safe, tolerable and/or effective in treating patients with AML.

开始日期2025-08-16

申办/合作机构

City of Hope National Medical Center

[+1]

NCT06311227

/ Recruiting临床2期IIT

A Phase 2 Study of Venetoclax in Relapsed Classic or Variant Hairy Cell Leukemia

This phase II trial tests how well venetoclax works in treating patients with hairy cell leukemia that has come back after a period of improvement (relapsed). Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. It may stop the growth of cancer cells by blocking Bcl-2, a protein needed for cancer cell survival.

开始日期2025-05-15

申办/合作机构

National Cancer Institute

NCT06852222

/ Not yet recruiting临床3期

A Phase 3 Randomized, Double-Blind, Placebo-Controlled, Study of Bleximenib, Venetoclax and Azacitidine for the Treatment of Participants With Newly Diagnosed Acute Myeloid Leukemia Harboring KMT2A Rearrangements or NPM1 Mutations Who Are Ineligible for Intensive Chemotherapy

The purpose of this study is to assess how bleximenib and Venetoclax (VEN)+ Azacitidine (AZA) works as compared to placebo and VEN+AZA alone for the treatment of participants with Acute Myeloid Leukemia (AML).

开始日期2025-05-02

申办/合作机构

Janssen Research & Development LLC

100 项与维奈克拉相关的临床结果

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100 项与维奈克拉相关的转化医学

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100 项与维奈克拉相关的专利（医药）

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4,861

项与维奈克拉相关的文献（医药）

2025-12-31·Hematology

Identification of t(X;1)(q28;q21) generating a novel GATAD2B::MTCP1 gene fusion in CMML and its persistence during progression to AML

Article

作者: Chen, Yu ; Zhu, Yi-yan ; Liu, Yi-zi ; Hou, Chun-xiao ; Zhang, Zhi-yu ; Chen, Su-ning ; Wang, Qian ; Zhang, Feng-hong

OBJECTIVE:

Hematological malignancies often involve chromosomal translocations and fusion genes that drive disease progression. While MTCP1 is well-known in T-cell prolymphocytic leukemia (T-PLL), its role in myeloid neoplasms is less understood. This report presents the first identification of the t(X;1)(q28;q21) translocation leading to the GATAD2B::MTCP1 fusion in acute myeloid leukemia (AML) transformed from chronic myelomonocytic leukemia (CMML).

METHODS:

The karyotypes were described according to the International System for Human Cytogenetic Nomenclature 2009. We performed targeted next-generation sequencing (NGS) on a panel of 172 genes commonly mutated in hematological malignancies (Supplemental Table 1), using an Illumina platform. RNA sequencing was conducted on total RNA extracted from bone marrow, also using the Illumina platform. The GATAD2B::MTCP1 fusion gene was confirmed by reverse transcription-polymerase chain reaction (RT-PCR) and Sanger sequencing, with specific primers for the fusion transcript (GATAD2B-F: CCTCTTTTTTTCGACGCC; MTCP1-R: ACTGAGCACAACACTTACGC).

RESULTS:

The GATAD2B::MTCP1 fusion results from a breakpoint on 1q21 within GATAD2B exon 1 and Xq28 within MTCP1 exon 2. The patient with the GATAD2B::MTCP1 fusion exhibited disease progression from CMML to AML. Despite achieving initial remission with venetoclax-based therapy and allo-HSCT, the patient relapsed and died.

CONCLUSIONS:

We propose that the GATAD2B::MTCP1 fusion upregulates MTCP1 expression rather than generating a fusion protein, thereby contributing to transformation and relapse in AML. Further investigations are needed to elucidate the precise role of this fusion event in myeloid malignancies.

2025-12-31·CANCER BIOLOGY & THERAPY

Targeting the IKZF1/BCL-2 axis as a novel therapeutic strategy for treating acute T-cell lymphoblastic leukemia

Article

作者: Li, Jun ; Ye, Chunmei ; Li, Hui ; Li, Juan

OBJECTIVES:

Acute T-cell lymphoblastic leukemia (T-ALL) is a severe hematologic malignancy with limited treatment options and poor long-term survival. This study explores the role of IKZF1 in regulating BCL-2 expression in T-ALL.

METHODS:

CUT&Tag and CUT&Run assays were employed to assess IKZF1 binding to the BCL-2 promoter. IKZF1 overexpression and knockdown experiments were performed in T-ALL cell lines. The effects of CX-4945 and venetoclax, alone and in combination, were evaluated in vitro and in vivo T-ALL models.

RESULTS:

CUT&Tag sequencing identified IKZF1 binding to the BCL-2 promoter, establishing it as a transcriptional repressor. Functional assays demonstrated that IKZF1 overexpression reduced BCL-2 mRNA levels and increased repressive histone marks at the BCL-2 promoter, while IKZF1 knockdown led to elevated BCL-2 expression. CX-4945, a CK2 inhibitor, could reduced BCL-2 levels in T-ALL cells. Notably, knockdown of IKZF1 partially rescued the CX-4945-induced repression of BCL-2. These results underscore the CK2-IKZF1 signaling axis as a key regulator of BCL-2 expression. In vitro, CX-4945 enhanced the cytotoxicity of venetoclax, with the combination showing significant synergistic effects and increased apoptosis in T-ALL cell lines. In vivo studies with cell line-derived xenograft (CDX) and patient-derived xenograft (PDX) models demonstrated that CX-4945 and venetoclax combined therapy provided superior therapeutic efficacy, reducing tumor burden and prolonging survival compared to single-agent treatments.

CONCLUSIONS:

IKZF1 represses BCL-2 in T-ALL, and targeting the CK2-IKZF1 axis with CX-4945 and venetoclax offers a promising therapeutic strategy, showing enhanced efficacy and potential as a novel treatment approach for T-ALL.

2025-12-01·Blood Research

Relative efficacy of systemic treatments for patients with relapsed/refractory chronic lymphocytic leukemia: a network meta-analysis according to 17p deletion/TP53 mutations

Article

作者: Lim, Joo Han ; Kim, Jinchul ; Lee, Moon Hee ; Cho, Jinhyun

Abstract:

Purpose:

This network meta-analysis aimed to evaluate the relative efficacy of systemic treatments in patients with relapsed/refractory chronic lymphocytic leukemia (R/R CLL), focusing on key genetic mutations, specifically the 17p deletion and TP53 mutations.

Methods:

We conducted a systematic literature review to identify all publicly available randomized controlled trials (RCTs) using PubMed, EMBASE, the Cochrane database, and meeting abstracts published through December 2023. A Bayesian network meta-analysis was performed to estimate the hazard ratios (HRs) for progression-free survival (PFS) with 95% confidence intervals (CIs) and to determine the ranking of the included regimens.

Results:

Twelve trials involving 4,437 patients and 13 treatment options were included in the meta-analysis. Venetoclax plus rituximab and zanubrutinib emerged as the most effective treatments for the overall R/R CLL population, showing the lowest PFS HR (HR 0.62, 95% CI 0.32–1.20 and HR 0.65, 95% CI 0.49–0.86, respectively) versus ibrutinib, and were ranked as the best agent (surface under the cumulative ranking curve [SUCRA] value of both 90%, respectively) among the included drugs. In the 17p deletion/TP53 mutation subgroup, zanubrutinib demonstrated the most favorable efficacy (HR 0.52, 95% CI 0.31–0.88 versus ibrutinib) with the highest SUCRA value (97%). In patients without these mutations, venetoclax plus rituximab was the most effective (HR 0.49, 95% CI 0.26–0.94 versus ibrutinib) with a SUCRA value of 94%.

Conclusion:

Our findings highlight the superior efficacy of venetoclax plus rituximab and zanubrutinib for treating R/R CLL and confirm that the role of each regimen may vary depending on the clinically significant mutations.

1,346

项与维奈克拉相关的新闻（医药）

10 小时之前

·ioncology

Blood Advances丨慢性淋巴细胞白血病/小淋巴细胞淋巴瘤治疗共识：全球需求不容忽视

点击蓝字关注我们在最新一期的Blood Advances中，Soumerai等研究者发布了慢性淋巴细胞白血病/小淋巴细胞淋巴瘤（CLL/SLL）的专家共识治疗指南，这是淋巴瘤研究基金会（LRF）首次召集专家小组制定的系统性内容，标志着治疗领域的重要里程碑。点击文末“阅读原文”获取完整共识尽管“范式转变”一词在肿瘤学领域常被使用，但唯有在描述靶向药物引入后CLL治疗格局的变革时，这一表述才显得恰如其分。过去十年间，CLL治疗迈入新纪元：单臂研究逐步发展为随机对照试验，一致证实靶向药物（无论是单药还是联合方案）相比传统化疗免疫治疗的显著优势。基于此，CLL领域已批准多种新型靶向疗法，每种疗法均被证实“优于化疗”。 CLL领域研究者应获得认可——他们设计并执行了多项新型方案的头对头试验。然而，这些研究的结果仍需数年才能揭晓。当前，我们已拥有多种有效治疗方案，其疗程（持续用药 vs 限时治疗）和安全性特征各异。在与患者沟通时，需深入讨论不同方案的差异、优势与风险，通过共享决策综合考虑疾病相关因素（分子和细胞遗传学标志物）、治疗相关因素（疗程、不良反应）及患者相关因素（年龄、合并症、社会支持及患者偏好）。共识指南通过整合长期随访数据及安全性信息，为细化这类复杂对话提供了重要框架。本次共识的专家小组提出了具体且实用的建议，部分建议在其他实践指南中鲜有体现。作为共识指南的固有特性，专家组在保持包容性、无偏倚和循证原则的同时，对缺乏数据或证据模糊的领域给出了专业见解，堪称典范。 CLL领域正迫切期待多项可能改变或指导实践的试验结果：针对无症状患者，SWOG S1925（NCT04269902）研究将评估限时维奈克拉联合奥妥珠单抗是否可改善高危CLL患者的生存；德国CLL研究组的CLL17研究（NCT04608318）将比较伊布替尼（持续用药）、维奈克拉联合奥妥珠单抗（固定疗程）及伊布替尼联合维奈克拉（固定疗程）的疗效； MAJIC试验（NCT05057494）将评估全口服方案（二代BTK抑制剂阿卡替尼联合维奈克拉）对比维奈克拉联合奥妥珠单抗方案的效果； CELESTIAL TNCLL研究（NCT06073821）将探索另一种新型全口服组合（泽布替尼联合sonrotoclax）的潜力； BRUIN-CLL-314（NCT05254743）和BELLWAVE-011（NCT06136559）试验将部分解答共价（伊布替尼）与非共价（匹妥布替尼）BTK抑制剂的差异问题；针对经治患者，BRUIN-CLL-322（NCT04965493）将探索匹妥布替尼联合维奈克拉和利妥昔单抗的增效作用； BELLWAVE-010（NCT05947851）将比较维奈克拉联合nemtabrutinib与维奈克拉联合利妥昔单抗的疗效。此外，还有更多研究正在复发患者中探索新型作用机制药物，如BTK降解剂、T细胞衔接器、新型细胞免疫疗法及靶向药物。未来共识版本可能纳入更多组合及序贯策略，并进一步明确微小残留病检测在临床实践中的应用。此外，BTK抑制剂或BCL-2抑制剂耐药突变信息的整合，也可能影响未来治疗策略。尽管这些共识是临床实践的重要资源，但其制定基于所有药物和诊断手段均可充分获取的假设。遗憾的是，这一前提仅在少数国家成立，全球范围内非化疗CLL疗法的可及性仍极其有限。即便在可获得的情况下，许多地区的患者仅能选择有限方案，且药物高昂成本构成障碍。亟需系统研究以理解全球实践差异，包括因成本和可及性问题导致的治疗方案调整。遗憾的是，低资源地区往往并非行业合作的优先方向。多数共识基于资源充足国家的现实优化策略，这意味着全球共识可能缺乏前瞻性试验支持。总体而言，亟需制定适应本地资源分级的CLL实践共识，需同时考虑诊断局限性和治疗药物的可用性。例如，仅伊布替尼可用的地区，其推荐方案应与诊断手段和治疗选择更丰富的地区存在差异。多个平台可为此项工作提供支持，这为美国血液学会、美国临床肿瘤学会或LRF等专业机构与国际CLL工作组合作提供了契机，可通过全球伙伴子委员会组建多元包容的专家小组，有助于组建涵盖不同资源层级地区代表的多元化专家小组。最后，这份周全、详尽且均衡的CLL治疗共识的发布不仅为全球CLL患者和医疗团队提供了宝贵的指导，也为推动CLL治疗领域的持续进步奠定了坚实的基础。诊疗“疼痛”是全球性的挑战，但“止痛”手段的可及性却存在显著地域差异。在CLL治疗快速演变的背景下，衷心希望领域共识能够定期更新，平衡"可及性"与"过度治疗"问题。在共同推动全球新型诊疗资源普及的同时，呼吁CLL专家群体和专业组织行动起来，制定因时因地而异的实践共识，以确保所有CLL患者都能获得最佳治疗，消除地理带来的健康不平等。 CLL/SLL治疗流程建议（1）治疗方法遵循2018年国际慢性淋巴细胞白血病工作组（iwCLL）关于CLL/SLL启动治疗的指南；（2）对于因不耐受而停止治疗的CLL/SLL患者，可以考虑治疗间歇期；（3）当对CLL/SLL进行初始治疗时，推荐使用靶向药物，如维奈克拉联合奥妥珠单抗、阿卡替尼（±奥妥珠单抗）或泽布替尼；（4）对于既往接受维奈克拉联合抗CD20单抗治疗、随后疾病进展且需要治疗的患者，如果维奈克拉耐受良好且停药1年内疾病未进展，可考虑再次使用维奈克拉（±抗CD20单抗）治疗；（5）对于一线使用维奈克拉联合奥妥珠单抗后需二线治疗者，如果不倾向于再次使用维奈克拉（±抗CD20单抗），推荐二代共价BTK抑制剂（cBTKi，（阿卡替尼或泽布替尼）；（6）因不耐受停用cBTKi且需要进一步治疗的患者，除非不耐受的原因是危及生命或器官的状况，否则可以考虑另一种第二代cBTKi；（7）对于接受过2种先前治疗（包括cBTKi和维奈克拉）的CLL/SLL患者，如果不倾向于再次使用维奈克拉（±抗CD20单抗）或转换为另一种cBTKi，大多数情况下推荐使用匹妥布替尼。符合条件者，也应考虑将liso-cel用于此治疗线或更后线。（8）对3线治疗（含维奈克拉、cBTKi和匹妥布替尼）耐药者，若无法参与临床试验或使用liso-cel，可考虑PI3Kδ抑制剂；（9）对至少2线治疗（含维奈克拉和cBTKi）耐药且后续治疗获得缓解者，可转诊至CLL专家组讨论异基因干细胞移植的可行性；（10）当临床试验参与可行且研究目标与患者优先级高度契合时，应考虑让所有CLL/SLL患者参加临床试验；（11）尽管在一线治疗CLL/SLL时，奥妥珠单抗联合阿卡替尼一线治疗可能延长无进展生存期（PFS），但专家组因潜在毒性及静脉输注需求，通常不常规联用奥妥珠单抗。当前主要联用指征为无法控制的自身免疫性血细胞减少症；（12）尽管利妥昔单抗联合维奈克拉获批用于复发/难治CLL/SLL，但专家组在此情况更推荐奥妥珠单抗联合维奈克拉； END （来源：《肿瘤瞭望–血液时讯》编辑部）声明凡署名原创的文章版权属《肿瘤瞭望》所有，欢迎分享、转载。本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。

临床结果免疫疗法

23 小时之前

·药渡

全覆盖！阿斯利康「阿可替尼」新适应症在中国获批，BTK抑制剂市场格局生变

来源：药渡撰文：Pharmadeep 编辑：活力哈哈 2025年3月21日，中国国家药品监督管理局（NMPA）正式批准阿斯利康第二代BTK抑制剂阿可替尼（商品名：康可期）一线治疗慢性淋巴细胞白血病（CLL）的新适应症。该批准基于中国主导的全球3期ChangE临床试验数据，标志着中国CLL治疗进入靶向药物全覆盖的新阶段。 01 CLL治疗现状：从化疗到精准靶向的跨越 CLL是成人最常见的白血病类型，传统化疗联合免疫治疗（如苯丁酸氮芥+利妥昔单抗）存在缓解率低、毒性大等局限。近年来，BTK抑制剂逐步成为核心治疗药物。截至2025年，国内已上市的BTK抑制剂包括：伊布替尼（强生/艾伯维）：一代BTK抑制剂，但脱靶效应导致房颤、出血风险较高；泽布替尼（百济神州）：二代药物，选择性更优，2020年国内获批CLL；奥布替尼（诺诚健华）：2021年获批CLL和套细胞淋巴瘤（MCL）适应症。阿可替尼此次获批一线治疗，成为国内首个覆盖CLL全病程（一线至后线）的BTK抑制剂，直接改写治疗指南。 02 阿可替尼的临床优势：疗效与安全性双突破此次获批的关键依据为ChangE试验数据。该试验由中国研究者主导，纳入66%中国患者，结果显示：与苯丁酸氮芥联合利妥昔单抗相比，阿可替尼单药显著延长初治CLL患者的无进展生存期（PFS），且总体生存期（OS）呈现改善趋势。其核心优势包括：高靶点选择性：减少对EGFR、ITK等非靶点作用，房颤和出血风险显著低于一代药物；长期生存数据：全球ASCEND研究中，复发/难治CLL患者接受阿可替尼治疗的4年PFS率达62%；剂型迭代：2024年在美国获批的片剂剂型已提交国内申请，有望提升用药便利性。 03 市场前景：百亿赛道竞争加剧根据阿斯利康2024年财报，其全球总收入达540.73亿美元，同比增长21%，其中肿瘤业务收入223.53亿美元，同比增长24%，占总收入的41%，继续成为公司核心增长引擎。作为肿瘤领域的重要产品，阿可替尼（Calquence）在2024年实现销售额31.29亿美元，同比增长显著，其中国市场表现尤其值得关注。中国市场增长与挑战并存 2024年阿斯利康中国区营收64.13亿美元，同比增长11%，占全球收入的12%，但第四季度收入同比下降3%，主要受呼吸道药物需求下降及医院预算调整影响。尽管面临调查风波（如涉嫌偷逃税款最高或面临450万美元罚金），公司仍强调对中国市场的长期承诺，全年共有8个新药及新适应症在中国获批，并计划加大研发与生产投资。 BTK抑制剂竞争焦点阿可替尼新适应症获批后需加速医保准入以扩大市场份额。阿可替尼与BCL-2抑制剂（如维奈克拉）联用的临床试验持续推进，有望巩固其疗效优势。肿瘤领域多维布局除BTK抑制剂外，阿斯利康在ADC（抗体偶联药物）和细胞治疗领域动作频繁：2024年德曲妥珠单抗（Enhertu）销售额增长58%至19.82亿美元，适应症扩展至HER2+乳腺癌、胃癌等5类肿瘤；2025年3月，阿斯利康又以10亿美元收购EsoBiotec，加码体内CAR-T疗法（如ESO-T01），进一步强化实体瘤治疗布局（10亿美元！这家MNC再出手！用“体内魔法”改写癌症治疗规则？）。未来增长驱动力 2024年阿斯利康完成9项III期临床研究，2025年计划发布7款新药的III期数据，包括Enhertu在乳腺癌一线治疗的DESTINY-Breast09研究。2025年资本支出预计增长50%，重点投向美国、新加坡、中国无锡等地生产基地，提升供应链韧性。结语阿可替尼的获批与阿斯利康在肿瘤领域的多维度布局，凸显了其“靶向+免疫+细胞治疗”的战略野心。然而，中国市场面临的合规风险与集采压力，以及全球细胞疗法赛道的激烈竞争，将考验其长期增长韧性。未来，能否在疗效、合规与成本控制间取得平衡，将是阿斯利康守住百亿市场的关键。数据来源： 1.阿斯利康2024年财报及公开声明 2.中国国家药品监督管理局（NMPA）批准公告 3.阿斯利康全球收购及合作公告（本文基于官方发布信息综述，不构成医疗建议。）

财报临床3期上市批准

2025-03-24

·PRNewswire

Actinium Pharmaceuticals Announces Supply Agreement with Eckert & Ziegler for Ac-225 Radioisotope to Support Comprehensive Development Activities

NEW YORK, March 24, 2025 /PRNewswire/ -- Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, today announced it has entered into an agreement for the supply of Actinium-225 (Ac-225) with Eckert & Ziegler. Under this agreement, Actinium Pharmaceuticals will have access to Eckert & Ziegler's high-quality Actinium-225 to further develop its lead product Actimab-A as well as additional early and late-stage development candidates for both U.S. and international clinical trials. Targeted radiotherapies using Ac-225 have shown great promise in the treatment of cancer. The radioisotope releases powerful alpha particles with high energy and low penetration depth, enabling precise targeting of tumor cells, including hard-to-reach micrometastases, while minimizing effects on surrounding healthy tissue. Actimab-A is an Ac-225 based radiotherapy agent, directed against CD33, a receptor overexpressed in patients with acute myeloid leukemia (AML) and other myeloid indications. Sandesh Seth, Chairman and CEO at Actium Pharmaceuticals, Inc. commented: "We believe that targeted radiation therapy with Actinium-225 is one of the most promising approaches for treating patients with myeloid malignancies and solid tumors. As we have highlighted recently, we are advancing our lead targeted radiotherapy Actimab-A into a pivotal Phase 2/3 trial for patients with relapsed or refractory acute myeloid leukemia and in the frontline setting in a Phase 1 trial under our CRADA with the NCI. Additionally, we have launched our Actimab-A solid tumor program to combine with PD-1 checkpoint inhibitors KEYTRUDA and OPDIVO for patients with head and neck squamous carcinoma and non-small cell lung cancer in multiple trials. As a pioneer in the development of target radiotherapies, we have aggressive plans to expand our clinical pipeline to address indications with high unmet needs. With this supply agreement with Eckert & Ziegler, we will have access to reliable and constant supply of Ac-225 to advance our product development both in the U.S. as well as internationally." "We are happy to contribute to the continuous expansion of indications for Actinium-225, which is significantly being advanced by Actinium Pharmaceuticals," explained Dr. Harald Hasselmann, CEO of Eckert & Ziegler SE. "The progress we have made in our Ac-225 project over the past year marks only the start of our program to address the global shortage of this vital radionuclide." Eckert & Ziegler reliably supplies high-quality Gallium-68, Lutetium-177, Yttrium-90, and Actinium-225 to leading pharmaceutical companies, and research institutions worldwide. With expertise in radioisotope production and global logistics, the company is committed to continuously support the development and delivery of innovative radiopharmaceuticals. About Eckert & Ziegler Eckert & Ziegler SE, with more than 1,000 employees, is a leading specialist in isotope-related components for nuclear medicine and radiation therapy. The company offers a broad range of services and products for the radiopharmaceutical industry, from early development work to contract manufacturing and distribution. Eckert & Ziegler shares (ISIN DE0005659700) are listed in the TecDAX index of Deutsche Börse. Contributing to saving lives. About Actinium Pharmaceuticals, Inc. Actinium is a pioneer in the development of targeted radiotherapies intended to meaningfully improve patient outcomes. Actinium is advancing its lead product candidate Actimab-A, a CD33 targeting therapeutic, as potential backbone therapy in acute myeloid leukemia (AML) and other myeloid malignancies leveraging the mutation agnostic alpha-emitter radioisotope payload Actinium-225 (Ac-225). Actimab-A has demonstrated potential activity in relapsed and refractory acute myeloid leukemia (r/r AML) patients in combination with the chemotherapy CLAG-M including high rates of Complete Remissions (CR) and measurable residual disease (MRD) negativity leading to improved survival outcomes and is being advanced to a pivotal Phase 2/3 trial. In addition, Actinium is engaged with the National Cancer Institute (NCI) under the Cooperative Research and Development Agreement (CRADA) for development of Actimab-A in AML and other myeloid malignancies. The first clinical trial under the CRADA will evaluate the triplet combination comprised of Actimab-A, Venetoclax (Abbvie/Roche) an oral Bcl-2 inhibitor and ASTX-727 (Taiho Oncology, an Otsuka holdings company) a novel oral hypomethylating agent (HMA) in frontline acute myeloid leukemia (AML) patients. Additionally, Actinium is developing Actimab-A as a potential pan tumor therapy in combination with PD-1 checkpoint inhibitors including KEYTRUDA® and OPDIVO® by depleting myeloid derived suppressor cells (MDSCs), which represents a potential multi-billion-dollar addressable market. Iomab-ACT, Actinium's next generation conditioning candidate, is being developed with the goal of improving patient access and outcomes for potentially curative cell and gene therapies. Iomab-B is an induction and conditioning agent prior to bone marrow transplant in patients with r/r AML, which Actinium is seeking a potential strategic partner for the U.S. In addition, the company's R&D efforts are primarily focused on advancing several preclinical programs for solid tumor indications. Actinium holds 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: [email protected] SOURCE Actinium Pharmaceuticals, Inc. 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放射疗法

100 项与维奈克拉相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10679	维奈克拉	L01XX52	DB11581

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
难治性慢性淋巴细胞白血病	日本	AbbVie LLC	2019-09-20
复发性慢性淋巴细胞白血病	日本	AbbVie LLC	2019-09-20
小淋巴细胞淋巴瘤	美国	AbbVie, Inc.	2018-06-08
成人急性髓性白血病	欧盟	AbbVie Deutschland GmbH & Co. KG	2016-12-04
成人急性髓性白血病	冰岛	AbbVie Deutschland GmbH & Co. KG	2016-12-04
成人急性髓性白血病	列支敦士登	AbbVie Deutschland GmbH & Co. KG	2016-12-04
成人急性髓性白血病	挪威	AbbVie Deutschland GmbH & Co. KG	2016-12-04
急性髓性白血病	加拿大	AbbVie AS	2016-10-31
慢性淋巴细胞白血病	美国	AbbVie, Inc.	2016-04-11

未上市

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
肿瘤溶解综合征	临床3期	美国	AbbVie, Inc.	2024-08-05
肿瘤溶解综合征	临床3期	澳大利亚	AbbVie, Inc.	2024-08-05
肿瘤溶解综合征	临床3期	法国	AbbVie, Inc.	2024-08-05
肿瘤溶解综合征	临床3期	希腊	AbbVie, Inc.	2024-08-05
肿瘤溶解综合征	临床3期	波多黎各	AbbVie, Inc.	2024-08-05
肿瘤溶解综合征	临床3期	塞尔维亚	AbbVie, Inc.	2024-08-05
肿瘤溶解综合征	临床3期	西班牙	AbbVie, Inc.	2024-08-05
肿瘤溶解综合征	临床3期	中国台湾	AbbVie, Inc.	2024-08-05
肿瘤溶解综合征	临床3期	英国	AbbVie, Inc.	2024-08-05
复发性急性髓细胞白血病	临床3期	美国	AbbVie, Inc.	2022-10-01

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临床结果

适应症

分期

评价

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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


NCT03214562 (Pubmed \| Leukemia)	临床1/2期	难治性急性髓细胞白血病 wild-type TP53 status	138	FLAG-IDA + Venetoclax	壓窪鑰蓋繭鑰繭鹹衊膚(觸鹹鹽餘簾鹽選觸觸獵) = low 齋選遞鹹網壓夢壓鏇衊 (繭範製糧醖願願顧顧襯 ) 更多	积极	2025-02-25
NCT03836261 (NEWS \| Pubmed) 人工标引	临床3期	慢性淋巴细胞白血病一线	867	Acalabrutinib-Venetoclax	鏇襯鑰觸蓋憲齋範築積(夢窪齋遞製製鏇淵夢願) = 糧襯蓋糧夢餘鏇選衊艱窪糧鹽窪衊餘網顧構糧 (構膚選範膚膚糧鹽繭壓 ) 更多	积极	2025-02-21
NCT03836261 (NEWS \| Pubmed) 人工标引	临床3期	慢性淋巴细胞白血病一线	867	Acalabrutinib-Venetoclax-Obinutuzumab	鏇襯鑰觸蓋憲齋範築積(夢窪齋遞製製鏇淵夢願) = 構顧遞積鑰鹽鑰窪衊齋窪糧鹽窪衊餘網顧構糧 (構膚選範膚膚糧鹽繭壓 ) 更多	积极	2025-02-21
NCT03319901 (Pubmed \| Blood Adv)	临床1期	急性淋巴细胞白血病 hypodiploid TP53-mutated	19	Venetoclax + Mini-HCVD	憲窪淵選繭顧遞廠襯壓(網網鹽構窪艱選淵憲製) = 壓構遞艱餘廠夢簾鑰餘積獵鏇鹽襯構選獵繭膚 (鹽遞壓製淵廠鹽築選範, 71 ~ 100) 更多	积极	2025-02-11
NCT04599634 (CTgov)	临床1期	滤泡性淋巴瘤 \| 套细胞淋巴瘤 \| 慢性淋巴细胞白血病 ... 更多	11	magrolimab+venetoclax (Arm 1, Cohort 1 Follicular Lymphoma Level 1)	遞蓋顧網鏇壓艱膚淵膚 = 壓膚糧夢鏇壓齋壓襯淵範製淵壓鑰醖廠鏇鑰淵 (淵築積鹹膚廠繭簾積憲, 壓鏇醖構糧構衊窪簾艱 ~ 製願鏇繭襯範積糧觸夢) 更多	-	2025-02-04
NCT04599634 (CTgov)	临床1期	滤泡性淋巴瘤 \| 套细胞淋巴瘤 \| 慢性淋巴细胞白血病 ... 更多	11	magrolimab+venetoclax (Arm 2, Cohort 2 Marginal Zone Lymphoma, Mantle Cell Lymphoma, & Chronic Lymphocytic Leukemia Level 1)	遞蓋顧網鏇壓艱膚淵膚 = 醖構築糧鑰齋夢壓淵製範製淵壓鑰醖廠鏇鑰淵 (淵築積鹹膚廠繭簾積憲, 觸糧糧醖廠鬱鬱築鏇糧 ~ 鏇淵壓網積鬱壓製鏇簾) 更多	-	2025-02-04
NCT04477486 (CTgov)	临床2期	套细胞淋巴瘤	13	Ibrutinib+Venetoclax	糧廠餘觸蓋顧遞糧廠齋 = 壓願衊鏇範選憲遞製襯築淵願範繭艱願鏇蓋鹹 (繭網獵廠艱製壓觸窪餘, 鏇醖蓋壓願窪顧鑰窪築 ~ 壓繭鑰網襯鑰淵齋獵積)	-	2025-01-14
NCT05996406 (ASH2024) 人工标引	临床2期	免疫球蛋白轻链淀粉样变性一线 t(11;14)	29	Venetoclax + Dexamethasone	顧構膚醖鹹遞獵醖餘觸(顧遞願繭壓遞憲鏇衊鹽) = 壓淵淵範餘顧繭醖蓋衊淵憲觸網製願顧壓齋鏇 (衊蓋觸醖顧壓醖繭夢鹽 ) 更多	积极	2024-12-09
NCT03709758 (ASH2024) 人工标引	临床1期	急性髓性白血病一线	44	Venetoclax + Daunorubicin + Cytarabine	築獵窪醖衊衊齋製簾艱(窪獵淵壓選構選遞齋壓) = 100 mg/d venetoclax was the MTD for pts treated with consol ara-C at 3 gm/m2. 壓艱齋鬱窪範蓋襯遞膚 (鏇窪衊築繭廠憲築襯顧 ) 更多	积极	2024-12-09
ASH2024 人工标引	临床1期	非霍奇金淋巴瘤	13	Loncastuximab tesirine + Venetoclax	齋餘鏇積壓襯齋壓顧範(醖積遞餘構艱襯蓋網範) = 膚衊壓顧鹹夢積膚襯鹹簾觸製願選鑰鏇鏇襯觸 (壓衊夢選鬱製築繭構糧 ) 更多	积极	2024-12-09
NCT03836261 (AMPLIFY, ASH2024) 人工标引	临床3期	慢性淋巴细胞白血病一线	867	Acalabrutinib + Venetoclax	淵選蓋鹽窪築淵窪鹹繭(鹽夢齋鹹衊憲遞鬱襯廠) = 網製鹹夢膚鹹糧繭繭襯鏇選襯糧廠糧構獵膚蓋 (範獵製壓鏇廠顧壓願觸 ) 更多	积极	2024-12-09
NCT03836261 (AMPLIFY, ASH2024) 人工标引	临床3期	慢性淋巴细胞白血病一线	867	Acalabrutinib + Venetoclax + Obinutuzumab	淵選蓋鹽窪築淵窪鹹繭(鹽夢齋鹹衊憲遞鬱襯廠) = 顧觸積築憲選製鹹窪築鏇選襯糧廠糧構獵膚蓋 (範獵製壓鏇廠顧壓願觸 ) 更多	积极	2024-12-09
ASH2024 人工标引	N/A	慢性淋巴细胞白血病一线	-	Venetoclax + obinutuzumab (VO)	鹽鏇醖壓艱淵鏇觸窪鹹(憲膚網餘齋膚衊壓觸鏇) = 廠鏇蓋蓋鏇壓蓋鏇鏇蓋繭鬱蓋夢憲鹹餘窪繭窪 (構簾鏇鑰膚願憲顧醖願 ) 更多	积极	2024-12-09
ASH2024 人工标引	N/A	慢性淋巴细胞白血病一线	-	Bruton tyrosine kinase inhibitor (BTKi)	鹽鏇醖壓艱淵鏇觸窪鹹(憲膚網餘齋膚衊壓觸鏇) = 選窪憲鬱網簾製壓觸範繭鬱蓋夢憲鹹餘窪繭窪 (構簾鏇鑰膚願憲顧醖願 ) 更多	积极	2024-12-09