瑞维美尼(Revumenib) - 药物靶点：menin_在研适应症：NPM1突变急性髓系白血病，KMT2A易位的急性白血病，急性髓性白血病_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Revumenib Citrate、SNDX 5613、SNDX-50613 FREE BASE

+ [3]

靶点

menin

作用方式

抑制剂

作用机制

menin抑制剂(Menin蛋白抑制剂)

治疗领域

肿瘤血液及淋巴系统疾病免疫系统疾病+ [1]

在研适应症

NPM1突变急性髓系白血病KMT2A易位的急性白血病急性髓性白血病+ [10]

非在研适应症

转移性结直肠癌复发性儿童急性淋巴细胞白血病难治性急性未分化白血病

原研机构

Syndax Pharmaceuticals, Inc.

在研机构

Syndax Pharmaceuticals, Inc.

The Children's Oncology Group Foundation, Inc.

Astex Pharmaceuticals, Inc.

+ [1]

非在研机构-

权益机构-

最高研发阶段批准上市

首次获批日期

美国 (2024-11-15),

KMT2A易位的急性白血病

最高研发阶段(中国)临床申请批准

特殊审评快速通道 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、优先审评 (美国)、突破性疗法 (美国)

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结构/序列

分子式C32H47FN6O4S

InChIKeyFRVSRBKUQZKTOW-YOCNBXQISA-N

CAS号2169919-21-3

关联

30

项与瑞维美尼相关的临床试验

NCT07563010

/ Not yet recruiting临床2期IIT

Phase 2 Randomized Controlled Study of Revumenib as Maintenance Therapy After Allogeneic Hematopoietic Stem Cell Transplantation in Patients With KMT2Ar, NPM1m, or NUP98r Acute Myeloid Leukemia (AML)

Revumenib is a first in class oral menin inhibitor that targets a central oncogenic dependency shared across KMT2Ar, NPM1m, and NUP98r AML. In addition to suppressing leukemogenic transcriptional programs and promoting leukemic differentiation, menin inhibition has been shown to modulate epigenetic states linked to antigen presentation and immune recognition. These properties provide a strong biological rationale for evaluating revumenib as maintenance therapy following alloHCT, with the goal of suppressing residual leukemic clones while preserving or enhancing GVL activity during immune reconstitution.

开始日期2026-12-01

申办/合作机构

Center for International Blood & Marrow Transplant Research

[+2]

NCT07734077

/ Not yet recruiting临床1/2期IIT

Phase Ib/II Study Of Revumenib As Monotherapy Or In Combination With Jak Inhibitors In Patients With Myelofibrosis

This is a Phase Ib/II 2 study investigating the safety and efficacy of revumenib in two cohorts of participants with myelofibrosis. COHORT-1 will investigate the safety of revumenib as monotherapy in participants with myelofibrosis previously treated with a JAK inhibitor. Following confirmation of safety in COHORT-1, the study will proceed with enrollment in COHORT-2, which will evaluate the efficacy and safety of revumenib in combination with a JAK inhibitor.

开始日期2026-12-01

申办/合作机构

Icahn School of Medicine at Mount Sinai

[+2]

NCT07283640

/ Not yet recruiting临床1期IIT

A Phase IB Trial of Subcutaneous Blinatumomab in Combination With Revumenib for Patients With KMT2A-rearranged Acute Lymphoblastic Leukemia

To learn about the safety and effects of revumenib in combination with blinatumomab in patients with newly diagnosed or relapsed/refractory Ph-negative ALL with a KMT2A rearrangement.

开始日期2026-11-18

申办/合作机构

The University of Texas MD Anderson Cancer Center

[+2]

100 项与瑞维美尼相关的临床结果

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100 项与瑞维美尼相关的转化医学

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100 项与瑞维美尼相关的专利（医药）

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98

项与瑞维美尼相关的文献（医药）

2026-08-20·JOURNAL OF CLINICAL ONCOLOGY

Erratum: All-Oral Combination of Revumenib, Decitabine, and Venetoclax for Relapsed or Refractory AML (SAVE)

Article

作者: Montalban-Bravo, Guillermo ; Ning, Jing ; Alvarado, Yesid ; Jabbour, Elias ; Xiao, Lianchun ; Cuglievan, Branko ; Short, Nicholas J. ; Thompson, Erika ; Bataller, Alex ; Andreeff, Michael ; Bidikian, Aram ; Abbas, Hussein A. ; DiNardo, Courtney D. ; Issa, Ghayas C. ; Mouhayar, Elie ; El Hajjar, Georgina ; Tan, Sheila ; Daver, Naval ; Bazinet, Alexandre ; Zhang, Baili ; Garcia-Manero, Guillermo ; Duose, Dzifa Yawa ; Jen, Wei Ying ; Furudate, Ken ; Pinto, Alessandro ; Ravandi, Farhad ; Kantarjian, Hagop M. ; Kadia, Tapan M. ; Farhat, Aziz ; Takahashi, Koichi ; McCall, David ; Loghavi, Sanam

2026-08-06·BLOOD

Discovery and preclinical activity of the menin-KMT2A inhibitor ziftomenib in acute leukemia models

Article

作者: Grembecka, Jolanta ; Klossowski, Szymon ; Park, SeRa ; Stevens, Rhiannon ; Miao, Hongzhi ; Clegg, Bradley ; Mody, Rajen ; Kim, EunGi ; Purohit, Trupta ; Sun, Duxin ; Wu, Tao ; Ray, Joshua ; Li, Lian-Sheng ; Kempinska, Katarzyna ; Wang, Yi ; Sulis, Maria-Luisa ; Borkin, Dmitry ; Cierpicki, Tomasz ; He, Miao ; Ren, Pingda ; Ding, Chao ; Goldman, Joshua W. ; Agrusa, Jennifer ; Kim, Annette S. ; Kessler, Linda ; Liu, Yi ; Wen, Bo ; Burrows, Francis ; Chen, Dong

Abstract:

The protein-protein interaction between menin and KMT2A (histone lysine methyltransferase 2A) plays a critical role in acute leukemia with KMT2A rearrangements, nucleophosmin 1 (NPM1) mutations, and nucleoporin 98 rearrangements and represents an emerging opportunity for therapeutic intervention. Here, we report the development and comprehensive evaluation of the activity of ziftomenib as an orally bioavailable, highly potent, and selective small-molecule inhibitor of the menin-KMT2A interaction. In leukemia cells and primary patient samples with the menin-KMT2A dependency, ziftomenib profoundly inhibited proliferation, reduced clonogenic potential, and induced differentiation, which was associated with strong downregulation of the menin-KMT2A target genes, including MEIS1, HOXA9, and HOXB2. In xenografts and patient-derived xenograft models of KMT2A-rearranged leukemia, ziftomenib induced leukemia regression or reduced leukemia burden, accompanied by a pronounced reduction in the menin-KMT2A target genes. We next assessed ziftomenib against 4 MEN1 (gene encoding menin) mutants (T349M, M327I, G331R, G331D) associated with clinical resistance to another menin inhibitor, revumenib. Ziftomenib retained antileukemic activity against T349M mutant cells and demonstrated low nanomolar potency (50% growth inhibition ≤ 25nM) against G331R cells, despite several-fold reduced potency relative to MEN1 wild-type cells, whereas the M327I and G331D mutants were resistant. The crystal structures of ziftomenib in complex with menin wild-type, T349M, or G331R mutants revealed a similar binding mode of ziftomenib to these menin variants, rationalizing the potent inhibitory activity toward these mutants. Ziftomenib has recently received US Food and Drug Administration approval for adult patients with NPM1-mutated acute myeloid leukemia and continues to be evaluated clinically in leukemias with NPM1 or KMT2A alterations, both as monotherapy and in combinations.

2026-08-04·MOLECULAR CANCER THERAPEUTICS

Targeting Menin in T-lineage Acute Lymphoblastic Leukemia

Article

作者: Odenike, Olatoyosi ; DuVall, Adam S. ; Thirman, Michael J. ; Patel, Anand A. ; Karaoglu, Diren Arda ; Kessler, Linda ; Arnold, Olivia ; Cheng, Jason X. ; Youshanlouei, Hamed R. ; Dhar, Arjun ; Saygin, Caner ; Chan, Zachary ; Shimamoto, Kathryn ; Burrows, Francis ; Drazer, Michael W. ; Stock, Wendy ; Giordano, Giorgia

Abstract:

T-lineage acute lymphoblastic leukemia (T-ALL) lacks effective targeted therapies, with poor outcomes in relapsed/refractory (R/R) disease. HOXAhigh T-ALL is biologically aggressive and often resistant to standard therapy. Menin inhibitors, recently approved for KMT2A-rearranged leukemias, may be effective in T-ALL, but biomarkers of response remain undefined. This study aims to evaluate the efficacy of menin inhibition in T-ALL and identify molecular predictors of sensitivity. We tested menin inhibitors (ziftomenib, revumenib, and VTP50469) in 14 primary T-ALL samples and 8 cell lines, representing HOXAhigh and HOXAlow genotypes. In vitro sensitivity assays, xenograft mouse models, transcriptomics, proteomics, and phosphoproteomics were used to characterize drug response. MEF2C modulation experiments and combination studies with cyclin-dependent kinase (CDK) 1/2 and ERK1/2 inhibitors were performed in vitro and in vivo. Menin inhibitors suppressed leukemic growth in a subset of HOXAhigh and HOXAlow primary human T-ALL samples. Similarly, ziftomenib was effective in reducing tumor burden in xenografts without major toxicity. Upon treatment, we observed downregulation of canonical menin targets (HOXA, MEIS1, and MEF2C) and upregulation of T-cell differentiation programs. Phosphoproteomic studies identified MEF2C S222 phosphorylation—mediated by CDK1/2 and ERK1/2—as a predictor of ziftomenib sensitivity in T-ALL. MEF2C overexpression promoted proliferation and ziftomenib resistance, whereas its knockdown impaired growth. Ziftomenib synergized with CDK1/2 and ERK1/2 inhibitors in vitro and improved survival in xenografted mice. In conclusion, a subset of T-ALL, defined by high p-MEF2C S222, is sensitive to menin inhibition. Combining ziftomenib with CDK or ERK inhibition offers synergistic efficacy, supporting biomarker-driven clinical trials of this strategy in R/R T-ALL.

377

项与瑞维美尼相关的新闻（医药）

2026-09-11

·盈德健康

瑞维美尼（Revuforj）获FDA优先审评资格，NPM1突变型AML有望迎来新靶向疗法！

盈德健康(lndian-Med)是少数获得印度政府授权的印度本土正规跨境药房。盈德健康属于印度最大的医药供应链集团Medikabazaar，全球员工超1500人，全印度各地设有42个分公司。盈德健康为病友们提供印度老挝孟加拉等多国仿制药和原研药合法跨境购买服务，所有药品均可提供印度源头采购文件，杜绝假药风险。盈德健康所有药品均通过印度药监局(CDSCO)认证，支持处方审核+跨境直邮，确保患者安全用药。中国人保产品责任险承保盈德健康跨境药房全线产品，央企为您的药品质量做全面保障，盈德健康药品质量值得信赖!①联系邮箱：china01@indianmed.cn ②联系方式：19926578359 ③微信号:IDM2026 美国FDA已受理Revuforj（revumenib，瑞维美尼）针对NPM1突变型AML的补充新药申请，并给予优先审查资格。本文梳理监管进展、作用机制、临床试验设计及疗效安全性数据。 1. 监管审查与既往获批情况 2. NPM1突变型AML及药物机制 3. AUGMENT-101试验设计 4. 疗效与微小残留病灶结果 5. 安全性与常见不良事件 6. 热门用户问答 7. 总结与参考来源 01 一、监管审查与既往获批情况 2025年6月24日，Syndax制药公司宣布，FDA已对Revuforj的补充新药申请授予优先审查资格。该申请拟用于治疗复发或难治性、伴核磷蛋白1（NPM1）突变的急性髓性白血病（AML）。按照处方药使用者费用法案，FDA当时预计在2025年10月25日前完成最终审查。优先审查意味着监管机构会缩短审评目标时间，但并不代表药物已经获得新的适应证批准。 Revuforj此前已于2024年11月获得FDA批准。当时的适应证为部分KMT2A基因重排急性白血病。此次申请能否获批，仍取决于FDA对补充申请资料的完整审评。若申请获批，revumenib将成为首个同时用于NPM1突变型AML和KMT2A基因重排急性白血病的menin抑制剂。该结果还需以FDA最终决定为准。 02 二、NPM1突变型AML与药物机制 NPM1基因突变是成人AML中较常见的基因改变，约占30%。 NPM1突变型AML属于复发风险较高的恶性血液肿瘤，复发或难治患者通常预后较差，临床上仍存在治疗需求。 NPM1突变型AML与KMT2A基因重排急性白血病都依赖menin-KMT2A相互作用。研究显示，破坏这一相互作用后，部分白血病相关基因的表达会下降。 NPM1突变通常可以借助现有筛查技术识别。截至原文所述阶段，尚无获批疗法能够选择性靶向驱动突变型NPM1 AML的潜在疾病机制，因此相关患者仍需要更多治疗选择。 Revumenib是一种口服menin抑制剂，通过阻断menin与KMT2A融合蛋白之间的相互作用，抑制白血病细胞增殖，并促进细胞分化，从而减慢或阻止肿瘤生长。Menin是人体细胞内的一种蛋白质。 Revumenib是首个获批的口服menin抑制剂。对于复发或难治性NPM1突变型AML患者，既往治疗主要包括化疗或FLT3抑制剂等方案，复发后的缓解率和预后仍可能受到限制。在原文所述研究中，revumenib显示出较高的缓解率和一定的缓解持续时间。口服给药减少了输注环节，但具体方案仍需由血液科医生结合患者病情、合并用药和实验室检查制定。 03 三、AUGMENT-101试验设计 2期AUGMENT-101试验（NCT04065399）评估了revumenib治疗复发或难治性NPM1突变型AML的疗效和安全性。相关结果已于2025年欧洲血液学协会（EHA）大会公布。每个治疗周期为28天。合并强CYP3A4抑制剂的患者，每12小时服用160 mg revumenib；未合并强CYP3A4抑制剂的患者，每12小时服用270 mg。治疗通常持续至出现无法耐受的毒性、疾病进展，或完成至少4个周期后仍未达到缓解。剂量和疗程不能脱离试验条件直接套用于个人治疗，临床用药需遵循医生处方。至少接受过1剂revumenib的患者纳入安全性分析。经研究中心确认存在NPM1突变的患者纳入疗效评估。研究共评估84例患者，其中74例符合疗效分析标准。主要终点为完全缓解加伴部分血液学恢复的完全缓解（CR+CRh）率。研究同时评估安全性和耐受性，次要终点包括客观缓解率（ORR）及缓解持续时间。可测量残留病灶（MRD）检测由研究者决定，检测方法包括当地聚合酶链式反应（PCR）或流式细胞术。不同检测方法的结果需要结合具体技术条件解读。 04 四、疗效与MRD结果在既往接受多线治疗的NPM1突变型AML患者中，revumenib持续观察到具有临床意义的缓解。 CR+CRh率为26.0%，95%置信区间为16.6%至37.2%。客观缓解率为48.1%，95%置信区间为36.5%至59.7%。这些数据反映了研究人群中的总体结果，不能直接等同于每位患者的个体获益。 CR+CRh的中位持续时间为4.7个月。其95%置信区间为2.1至8.2个月。患者首次达到CR+CRh的中位时间为2.76个月，范围为0.9至8.8个月。在19例达到CR+CRh且获得MRD状态结果的患者中，12例达到MRD阴性，占63.2%。其中6例通过PCR检测确认，另6例通过流式细胞术检测确认。首次达到MRD阴性的中位时间为2.78个月。个体达到MRD阴性的时间范围为1.8至4.7个月，实际判断仍需结合检测方法和临床病情。 05 五、安全性结果安全性结果与既往报告总体一致。在安全性分析人群中，66例患者发生治疗相关不良事件，占78.6%；其中50例发生3级或以上治疗相关不良事件，占59.5%。最常见的3级或以上治疗相关不良事件包括QTc间期延长18例（21.4%）、贫血12例（14.3%），以及发热性中性粒细胞减少症11例（13.1%）。分化综合征发生于11例患者，占13.1%。其中3级事件9例，占10.7%；4级事件2例，占2.4%。分化综合征可能需要及时识别和处理，出现相关症状应立即联系治疗团队。血小板计数减少发生于9例患者，占10.7%。对于发热、呼吸困难、明显乏力、出血倾向或其他快速加重的不适，应尽快就医，由医生判断是否需要检查或调整治疗。治疗相关不良事件导致4例患者停止治疗，占4.8%。另有1例患者因治疗相关不良事件死亡，占1.2%。研究数据提示，用药期间需要持续进行血液学、心电图及临床症状监测。 06 六、热门用户问答1. Revumenib目前获批用于哪些疾病？原文提到，Revuforj已获FDA批准用于部分KMT2A基因重排急性白血病。针对NPM1突变型AML的补充申请当时处于FDA优先审查阶段，是否获批需以监管机构最终决定为准。 2. NPM1突变型AML为什么受到关注？ NPM1突变约占成人AML基因改变的30%，相关患者存在复发风险。复发或难治患者的治疗效果和预后往往较差，因此针对其潜在疾病机制的药物研发具有临床需求。 3. Revumenib是如何发挥作用的？ Revumenib通过阻断menin与KMT2A融合蛋白之间的相互作用发挥作用。该过程可抑制白血病细胞增殖，并促进细胞分化，从而减慢或阻止肿瘤生长。 4. AUGMENT-101研究观察到哪些疗效结果？研究中CR+CRh率为26.0%，客观缓解率为48.1%。达到CR+CRh患者的中位缓解持续时间为4.7个月，部分患者还达到MRD阴性。 5. 使用Revumenib需要关注哪些安全性问题？研究中较常见的严重治疗相关不良事件包括QTc间期延长、贫血、发热性中性粒细胞减少症和分化综合征。治疗期间应按医生安排进行检查，出现明显不适需及时报告。 ▍扫码咨询专业顾问 | 在线一对一精准解读检查报告，同步海外药品前沿动态 07 七、总结 Revumenib针对menin相关通路，为复发或难治性NPM1突变型AML提供了新的研究方向。 AUGMENT-101研究显示，该药在既往接受多线治疗的患者中观察到缓解，但疗效和风险仍需结合个体情况判断。目前，NPM1突变型AML适应证的监管状态应以FDA最新公告为准。患者不应根据新闻或研究数据自行开始、停用或调整药物，治疗方案需要由专业医疗团队评估。 08 八、参考来源 Syndax Announces FDA Priority Review of sNDA for Revuforj® (revumenib) in Relapsed or Refractory mNPM1 Acute Myeloid Leukemia，Syndax Pharmaceuticals，新闻稿，2025年6月24日。 Syndax Announces Publication of Revumenib Data from the BEAT AML Trial in the Journal of Clinical Oncology and Simultaneous Presentation at EHA 2025，Syndax Pharmaceuticals，新闻稿，2025年6月12日。 Revumenib在NPM1突变型急性髓性白血病患者中的研究结果，Blood期刊，原文未提供具体文献题名及发表日期。本文仅供健康科普参考，不构成诊疗或用药建议；具体治疗与用药请遵循医生指导。声明：本文内容仅为科普，不构成任何医疗建议。具体用药方案请以主治医生的诊断为准。购买仿制药需通过正规渠道，避免购买来源不明的药品。▍跨境购买印度抗癌药，添加客服交流，获取更多健康信息--盈德健康是印度本土最大的持牌线上跨境药房 * 本文所涉及药械建议通过合法跨境贸易方式凭处方购买* 个体治疗效果存在差异，用药需遵医嘱，本文药械信息，仅供参考，不构成用药指引.* 资料来源：药品说明书. #什么是仿制药#哪里买印度靶向药好#印度药房需要处方吗点击下方阅读原文直接进入盈德健康印度线上药房获取你需要的印度药品更多药品相关问题，欢迎评论区留言讨论

优先审批申请上市

2026-09-09

·FierceBiotech

Kura creates Lilly-backed spinout armed with $50M to advance next-gen diabetes therapy

Kura Oncology has spun out a biotech armed with $50 million in fresh funding to take forward a next-generation diabetes treatment. The new entity, Caspian Therapeutics, will focus on KO-7246, a highly selective menin inhibitor that Kura has billed as being “purpose-designed for chronic metabolic diseases.” To fund KO-7246 through preclinical development and into a first-in-human study, Kura has secured $50 million in funding. The financing round was led by BVF Partners and included Eli Lilly—a major player in the diabetes space—alongside the diabetes-focused venture philanthropy fund T1D Fund, Invus, Montanova, members of Kura’s leadership team and “several successful biotech entrepreneurs,” according to a Sept. 9 release . A portion of the funding has also been earmarked to support development of another menin inhibitor aimed at diabetes and other cardiometabolic diseases. Kura will own half of Caspian and the biopharma has supplied the spinout with the relevant “intellectual property and know-how” to make KO-7246 a success. Kura has been busy rolling out Komzifti in the U.S. this year after securing FDA approval for the menin inhibitor to treat acute myeloid leukemia at the tail end of 2025. That approval came just weeks after Syndax Pharmaceuticals secured the first-ever approval for a menin inhibitor in the form of its own leukemia therapy Revuforj. So far, menin inhibitors have been used to block the interaction between the menin protein and specific mutant proteins that drive aggressive forms of leukemia. However, Kura has been exploring the ability of menin to selectively stimulate pancreatic β-cells to increase insulin production. “Our preclinical findings have strengthened our conviction that menin inhibition has the potential to address the underlying loss of functional β-cell capacity, rather than simply managing its consequences,” Kura’s Chief Scientific Officer Francis Burrows, Ph.D., said in the release. “The consistency of the findings across Type 1 and Type 2 diabetes models, together with their translation into human islet systems, provides a strong rationale to advance KO-7246 into clinical development,” Burrows added. Kura plans to unveil preclinical data supporting this thesis at the European Association for the Study of Diabetes Annual Meeting in Milan, Italy, at the end of the month. “Menin inhibition is a core area of Kura’s scientific and drug-development expertise, and the emerging biology in diabetes represents an exciting opportunity to extend that expertise beyond oncology,” Kura CEO Troy Wilson, Ph.D., added in this morning’s release. “By establishing Caspian with dedicated leadership and external capital, Caspian can pursue the potential of KO-7246 while Kura remains focused on executing its oncology strategy,” explained Wilson, who will take up the role of executive chairman of the spinout’s board of directors.

2026-09-09

·BioPharmaDive

Kura spins diabetes work into a Lilly-backed biotech startup

Dive Brief:Kura Oncology is spinning out a new company that intends to develop medicines known as menin inhibitors on diabetes and other cardiometabolic diseases.Called Caspian Therapeutics, the startup is initially focusing on a drug codenamed KO-7246. Preclinical testing has suggested the treatment might help the body regenerate pancreatic beta cells and produce more insulin in people with diabetes. That strategy represents a potentially new use for menin inhibitors, two of which have been approved in the U.S. to treat leukemia.Caspian has raised $50 million in financing to get going. While far smaller than the $100 million-plus megarounds that have become commonplace in biotech, Caspian can get by with less because it shares operational teams with Kura, according to Kura CEO and Caspian executive chairman Troy Wilson. Kura participated in the funding and will retain about a 50% stake in the fledgling firm, which is also backed by BVF Partners, Eli Lilly, the T1D Fund and other investors.Dive Insight:Kura had already started testing menin inhibition outside of oncology before it decided to spin out Caspian. But it wasnt until this past spring that Wilson and his team realized KO-7246 needed a separate home.As a company at our size and stage, you cannot be all things to all people, Wilson said in an interview. We needed to bring in dedicated expertise and capital. We needed to infuse it with the assets, the people and the capital to make a difference.Kura and another company, Syndax Pharmaceuticals, have already proven that blocking menin a protein that controls gene expression and cell signaling is an effective tool in treating acute myeloid leukemia. In AML, stifling an interaction between menin and another protein called KMT2A prevents leukemia cells from rapidly reproducing. Syndaxs therapy, Revuforj, was approved last October. Kuras, called Komzifti and co-developed with Kyowa Kirin, got to market shortly afterwards. It generated nearly $15 million in sales in the first half of 2026.Troy Wilson, CEO of Kura Oncology, is also the executive chairman of Caspian Therapeutics board.Permission granted by Kura OncologyIn diabetes, blocking menin can take the brakes off pancreatic beta islet cells, which is necessary for restoring normal levels of glucose and insulin production, Wilson said. KO-7246 is being tested in both Type 1 and Type 2 diabetes.Caspian has one direct competitor in Biomea Fusion, which is also making a menin inhibitor thats currently in mid-stage testing. But while Biomea has a time advantage, Caspians drug could have a superior safety profile, Wilson said.Importantly, preclinical research has shown Caspians drug doesnt appear to spur abnormal growth in other cell types. Additional data will be presented at a medical meeting later this month. The company has not disclosed when it plans to begin human testing.Caspian is also exploring the possibility of using menin inhibitors in conjunction with GLP-1 drugs to help patients who cannot control their diabetes with existing treatments.Once you have a drug that has good safety and clinical activity, give it to talented scientists and clinicians, and they'll help you learn how to use it, Wilson said.Kuras stock price dipped slightly on Wednesday morning, though TD Cowen analyst Phil Nadeau wrote in a note to clients that the spinout appeared to offer shareholders opportunity for upside while reducing the downside risk.The deal enables the efficient development of KO-7246 while Kuras resources remain focused on oncology, Nadeau wrote. '

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100 项与瑞维美尼相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
D12728 D12729	-	-	-

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适应症	国家/地区	公司	日期
NPM1突变急性髓系白血病	美国	Syndax Pharmaceuticals, Inc.	2025-10-24
KMT2A易位的急性白血病	美国	Syndax Pharmaceuticals, Inc.	2024-11-15

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适应症	最高研发状态	国家/地区	公司	日期
急性髓性白血病	临床3期	阿根廷	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	澳大利亚	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	奥地利	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	比利时	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	巴西	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	加拿大	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	法国	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	德国	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	希腊	Syndax Pharmaceuticals, Inc.	2025-11-25
急性髓性白血病	临床3期	匈牙利	Syndax Pharmaceuticals, Inc.	2025-11-25

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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


NCT05731947 (CTgov)	临床1/2期	结直肠癌 \| 转移性结直肠癌	41	Revumenib (Phase 1a: Revumenib 160 mg Tablet or 163 mg Capsule)	鹽簾積構壓鏇壓糧顧鑰 = 齋鹽廠觸顧襯壓淵淵淵廠壓鬱鹽衊餘鹹網淵願 (憲廠鹹糧願積選醖範蓋, 範窪遞憲網顧構範獵遞 ~ 獵齋夢選膚壓醖選構鏇) 更多	-	2026-07-06
				Revumenib (Phase 1a: Revumenib 220 mg Tablet or 226 mg Capsule)	鹽簾積構壓鏇壓糧顧鑰 = 淵顧積遞築繭鏇網艱餘廠壓鬱鹽衊餘鹹網淵願 (憲廠鹹糧願積選醖範蓋, 憲鏇壓憲積願艱遞選顧 ~ 顧壓醖鑰醖窪衊製衊構) 更多
NCT07211958 (REVEAL-ND NPM1, ASCO2026 \| EHA2026)	临床3期	NPM1突变急性髓系白血病一线 NPM1 mutation	468	Revumenib + intensive chemotherapy	廠鏇觸蓋鏇衊鬱鑰夢齋(憲獵築齋積夢齋醖簾網) = 鹹廠鬱顧積製鏇憲構窪繭觸襯簾構網鏇齋構繭 (鏇鏇襯壓齋齋壓鹽簾糧 )	积极	2026-05-29
				Placebo + intensive chemotherapy	鏇蓋窪憲夢艱憲顧積鹹(簾鹽網觸窪觸鬱鏇鹽蓋) = 鬱積鏇廠齋築艱獵壓網簾鬱窪餘齋觸醖構遞艱 (築衊壓淵餘範廠窪襯蓋 ) 更多
NCT06652438 (EVOLVE-2, EHA2026)	临床3期	急性白血病一线 NPM1 mutation \| KMT2A rearrangement	448	Revumenib + VEN/AZA	鹽衊簾構顧顧糧夢餘範(遞鹽壓鹽築糧築製願鬱) = 鏇衊製鬱遞觸淵壓範範願鏇鬱艱範衊簾襯鹹衊 (廠顧構簾構憲醖憲蓋遞 ) 更多	积极	2026-05-21
				Placebo + VEN/AZA	夢範醖艱醖醖簾鹹蓋齋(製鑰淵築醖鏇夢鹹構夢) = 淵鑰繭願糧鹽鑰獵簾憲夢糧網壓壓築窪窪鬱遞 (網壓廠鑰簾觸積簾醖蓋 )
NCT04065399 (AUGMENT-101, EHA2026)	临床1/2期	KMT2A rearrangement \| NPM1 mutation	335	Revumenib (KMT2A Rearrangement or NPM1 Mutation + Relapsed/Refractory Acute Leukemias)	願鏇構蓋簾餘醖夢齋選(築糧網衊衊鬱膚繭構鏇) = 網選鑰醖襯製憲蓋憲製餘顧遞願窪範壓膚壓蓋 (艱獵繭廠構鬱願憲淵壓 )	积极	2026-05-21
NCT04065399 (AUGMENT-101, EHA2026)	临床1期	急性白血病 NUP98-rearranged	26	Revumenib	艱醖鏇遞窪蓋壓醖選鑰(鹹鬱憲範繭鹽積選鑰鹽) = 衊衊獵壓衊蓋獵繭網獵築蓋鏇願築積鬱淵鑰選 (廠積觸繭醖齋選製遞鑰 ) 更多	积极	2026-05-12
NCT04065399 (AUGMENT-101, EHA2026)	临床1/2期	NPM1突变急性髓系白血病 NPM1-mutated	54	Revumenib (DNMT3A+FLT3)	齋糧鏇遞鹽醖艱鏇積構(鑰鏇窪艱遞窪糧範遞觸) = 構鏇蓋餘艱獵壓獵醖觸積蓋鑰鹽製觸鑰鹹簾衊 (鏇鏇顧鏇簾衊糧憲製醖, 7.8 ~ 55.1) 更多	积极	2026-05-12
				Revumenib (FLT3)	齋糧鏇遞鹽醖艱鏇積構(鑰鏇窪艱遞窪糧範遞觸) = 觸構積構鬱糧顧觸鏇顧積蓋鑰鹽製觸鑰鹹簾衊 (鏇鏇顧鏇簾衊糧憲製醖, 7.5 ~ 43.7) 更多
NCT04065399 (AUGMENT-101, EHA2026)	临床1/2期	维持 KMT2A \| NPM1 \| NUP98	15	Revumenib	簾廠積廠艱醖鏇鹹壓淵(蓋構艱鹽糧鹽夢鑰餘網) = 製積蓋範構夢構壓獵網獵艱鹹築顧顧願齋願製 (壓淵鹽鹹衊網淵膚鑰憲 ) 更多	积极	2026-05-12
NCT07356154 (EHA2026)	临床1/2期	KMT2A r \| NPM1 c \| NUP98 r	2	RevumenibMezigdomide + RevumenibMezigdomide	鏇衊鏇鑰獵艱簾醖網鏇(網襯鬱壓鑰艱築構構窪) = dose escalation is ongoing 鏇獵顧選鹽夢觸鹹獵艱 (構鏇餘淵廠遞艱製窪襯 ) 更多	积极	2026-05-12
NCT06226571 (SNDX-5613-0708, EHA2026)	临床1期	急性髓性白血病一线 KMT2A rearrangements \| NPM1 mutation \| NUP98 rearrangements	31	Revumenib + intensive chemotherapy	鬱顧鏇廠鏇糧齋餘繭網(繭齋壓憲構鹽鏇鬱醖網) = One DLT occurred (grade 3 QTcF prolongation) in DL1. 淵膚繭遞膚襯積壓鬱築 (廠襯願蓋觸鑰艱觸選艱 ) 更多	积极	2026-05-12
				Revumenib + intensive chemotherapy
NCT05360160 (EHA2026)	临床1/2期	难治性急性髓细胞白血病 KMT2A rearrangement \| NPM1 mutation \| NUP98 rearrangement	42	Revumenib+ASTX727+Venetoclax	廠襯築鹽範鏇簾網醖製(憲蓋獵鹽廠顧艱襯網簾) = The most common all-grade adverse events were nausea (60%), vomiting (52%), QTc prolongation (50%), and hypokalemia (45%), mostly grade 1-2. Grade ≥3 events were most frequently febrile neutropenia (35%), thrombocytopenia (22%), lung infection (20%), and respiratory failure (15%). QTc prolongation grade ≥3 occurred in 2 pts (5%). Differentiation syndrome occurred in 4 pts (10%) [grade ≥3, in 5%], all resolved with steroids. 鬱鹽醖窪艱壓製憲醖鹹 (簾廠壓襯鹽鬱鹽淵築繭 ) 更多	积极	2026-05-12
				Revumenib+ASTX727+Venetoclax (KMT2A rearrangement)