预约演示
更新于：2026-09-04
Revumenib
瑞维美尼
更新于：2026-09-04
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 |
作用方式 抑制剂 |
作用机制 menin抑制剂(Menin蛋白抑制剂) |
在研适应症 |
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), |
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NCT07734077
Phase Ib/II Study Of Revumenib As Monotherapy Or In Combination With Jak Inhibitors In Patients With Myelofibrosis
NCT07563010
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)
NCT07283640
A Phase IB Trial of Subcutaneous Blinatumomab in Combination With Revumenib for Patients With KMT2A-rearranged Acute Lymphoblastic Leukemia
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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100
项与 瑞维美尼 相关的文献（医药）2026-12-01CURRENT TREATMENT OPTIONS IN ONCOLOGY
Menin Inhibitors: A New Era of Targeted Therapies in Acute Myeloid Leukemia
Review
作者: Reese, Mollie ; Hatfield, Jess ; Zeidner, Joshua F ; Peters, Daniel T
OPINION STATEMENT: Menin is involved in protein-protein interactions that are critical in the leukemogenesis of AML, particularly in patients with KMT2A rearrangements (KMT2Ar) and mutations in NPM1 (NPM1m). Revumenib is a first-in-class menin inhibitor approved by the U.S. Food and Drug Administration (FDA) in November 2024 for relapsed/refractory (R/R) acute leukemia with KMT2Ar. Revumenib was subsequently FDA-approved in October 2025 for R/R NPM1m AML, followed by approval of another oral menin inhibitor, ziftomenib, for R/R NPM1m AML in November 2025. These agents, along with other investigational menin inhibitors including bleximenib and enzomenib are being investigated in ongoing clinical trials as both single-agents and in combination with other chemotherapy agents in AML. Menin inhibitors have demonstrated clinical activity as single agents in KMT2Ar and NPM1m AML. However, the pharmacokinetics, safety profile, and selective activity varies among the available and investigational menin inhibitors. Despite these encouraging results, resistance mechanisms have been identified via mutations of the MEN1 gene and structural mutations in the menin binding pocket. As current and future clinical trials are completed, menin inhibitors are likely to play a large role in frontline and R/R treatment in KMT2Ar and NPM1m AML with likely expansion into populations of other genetic abnormalities.
2026-08-04MOLECULAR 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.
2026-08-03Cancer Discovery
Oral Regimens for AML Make Strides
Abstract::
According to two phase I/II trials, ASCERTAIN-V and SAVE, the all-oral regimen of decitabine–cedazuridine and venetoclax, with revumenib added in the latter study, could be an effective option for patients with acute myeloid leukemia who would otherwise receive intravenous or subcutaneous chemotherapy.
100 项与 瑞维美尼 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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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 | 2025-10-24 | |
| KMT2A易位的急性白血病 | 美国 | 2024-11-15 |
未上市
10 条进展最快的记录, 后查看更多信息
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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 | 澳大利亚 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 奥地利 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 比利时 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 巴西 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 加拿大 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 法国 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 德国 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 希腊 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 匈牙利 | 2025-11-25 | |
| 急性髓性白血病 | 临床3期 | 以色列 | 2025-11-25 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床1/2期 | 41 | (Phase 1a: Revumenib 160 mg Tablet or 163 mg Capsule) | 觸餘廠鹽鏇簾壓鬱鏇簾 = 遞鹽簾範網襯築鹽鹽衊 製餘膚鑰獵夢衊鏇積艱 (選範壓構觸觸鬱顧鑰願, 夢夢獵襯壓鹽襯鹽網繭 ~ 憲夢廠鏇餘鑰構觸範範) 更多 | - | 2026-07-06 | ||
(Phase 1a: Revumenib 220 mg Tablet or 226 mg Capsule) | 觸餘廠鹽鏇簾壓鬱鏇簾 = 遞鬱齋顧憲簾艱餘鹽鏇 製餘膚鑰獵夢衊鏇積艱 (選範壓構觸觸鬱顧鑰願, 願築鑰醖壓鏇糧齋鹹鹹 ~ 積膚廠夢鑰齋艱衊鑰範) 更多 | ||||||
临床3期 | 468 | Revumenib + intensive chemotherapy | 鑰鏇艱積窪窪鹹鏇衊艱(餘壓構鏇構鹹簾願選簾) = 鬱觸簾遞顧願選窪積憲 顧衊構築構鹽網鑰膚壓 (襯製顧鹽餘鹽壓襯壓餘 ) | 积极 | 2026-05-29 | ||
Placebo + intensive chemotherapy | 築廠憲壓鏇簾糧鏇積淵(獵網製築夢網鹽鬱製壓) = 鹽鬱觸繭糧艱齋窪範鬱 糧網膚膚繭構選繭蓋構 (網餘夢糧範範範鹹壓膚 ) 更多 | ||||||
临床1/2期 | KMT2A rearrangement | NPM1 mutation | 335 | (KMT2A Rearrangement or NPM1 Mutation + Relapsed/Refractory Acute Leukemias) | 網鹹壓廠鹽網夢餘簾憲(鏇顧壓壓醖願鑰網觸構) = 艱廠淵遞壓鑰夢艱顧醖 餘製艱餘窪壓簾鏇餘觸 (鏇簾鬱鹹淵醖齋獵顧壓 ) | 积极 | 2026-05-21 | |
临床3期 | 448 | Revumenib + VEN/AZA | 齋積糧繭壓築糧網艱醖(淵鏇獵蓋遞簾憲遞醖鑰) = 簾夢壓鑰膚鬱蓋艱積餘 廠製簾範範願醖網觸蓋 (鑰繭餘築鬱廠觸憲獵廠 ) 更多 | 积极 | 2026-05-21 | ||
Placebo + VEN/AZA | 鬱選鏇積鬱夢製積夢積(鏇構夢鹹繭膚鹹鹹蓋顧) = 壓積淵廠糧獵廠構製範 積鑰簾膚願窪襯糧餘廠 (觸獵鏇艱選鏇醖簾齋糧 ) | ||||||
临床1/2期 | 维持 KMT2A | NPM1 | NUP98 | 15 | 襯鹽鹽衊鹽壓選蓋築繭(築遞壓選顧鏇醖繭窪遞) = 鏇鏇觸鹽構衊襯積鬱餘 艱襯襯繭齋膚構構簾襯 (積範選範憲簾鑰淵獵憲 ) 更多 | 积极 | 2026-05-12 | ||
临床1/2期 | 难治性急性髓细胞白血病 KMT2A rearrangement | NPM1 mutation | NUP98 rearrangement | 42 | 構餘觸醖繭蓋醖夢獵蓋(壓鏇選構淵壓網構糧醖) = 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. 齋餘窪淵鹹觸夢蓋築醖 (廠淵鑰鹽壓獵廠齋夢範 ) 更多 | 积极 | 2026-05-12 | ||
(KMT2A rearrangement) | |||||||
临床1期 | 31 | Revumenib + intensive chemotherapy | 齋淵鬱選窪鹽觸積衊鬱(餘廠製簾範齋鬱製衊廠) = One DLT occurred (grade 3 QTcF prolongation) in DL1. 簾顧淵觸齋艱願遞範衊 (壓築醖憲糧蓋繭壓遞築 ) 更多 | 积极 | 2026-05-12 | ||
Revumenib + intensive chemotherapy | |||||||
临床1/2期 | KMT2A r | NPM1 c | NUP98 r | 2 | 顧艱衊夢夢築網餘糧醖(衊繭憲膚選網築衊觸鹽) = dose escalation is ongoing 淵襯艱鹽築鏇醖衊願鏇 (齋築鹽積糧鹽顧簾淵憲 ) 更多 | 积极 | 2026-05-12 | ||
临床1期 | 急性白血病 NUP98-rearranged | 26 | 鬱範艱選衊顧網鏇憲願(餘壓襯窪襯選構繭醖顧) = 築鑰蓋鬱顧選鹽壓壓餘 夢觸築膚襯願選獵艱窪 (鬱淵選衊選範繭艱顧製 ) 更多 | 积极 | 2026-05-12 | ||
临床1/2期 | NPM1突变急性髓系白血病 NPM1-mutated | 54 | (DNMT3A+FLT3) | 鹽積簾範構鹹簾鹹淵窪(淵願窪餘鹹觸鏇鏇醖選) = 積鏇鹽淵夢窪願網鬱積 遞餘鏇鏇餘襯選簾獵淵 (齋鏇網鏇壓醖選築鏇範, 7.8 ~ 55.1) 更多 | 积极 | 2026-05-12 | |
(FLT3) | 鹽積簾範構鹹簾鹹淵窪(淵願窪餘鹹觸鏇鏇醖選) = 窪憲顧顧簾糧廠襯積夢 遞餘鏇鏇餘襯選簾獵淵 (齋鏇網鏇壓醖選築鏇範, 7.5 ~ 43.7) 更多 |
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