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更新于：2026-09-01
Revumenib
瑞维美尼
更新于：2026-09-01
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)
NCT07734077
Phase Ib/II Study Of Revumenib As Monotherapy Or In Combination With Jak Inhibitors In Patients With Myelofibrosis
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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98
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.
2026-08-01CANCER CELL
Menin-dependent megakaryocyte proliferation and fibrosis in myeloproliferative neoplasms
Article
作者: Zhang, Kevin ; McGeehan, Gerard M ; Gurbuxani, Sandeep ; Broadhurst, Amber L ; Mohan, Man ; Janke, Laura J ; Wen, Jeremy ; Kang, Guolian ; Mascarenhas, John ; Olufadi, Yunusa ; Marcellino, Bridget ; Crispino, John D ; Hall, Trent ; Cotton, Anitria ; Mehmood, Rashid ; Hoffman, Ronald
Menin inhibition, an approved therapy for KMT2A-rearranged and NPM1 mutant acute leukemia, is accompanied by decreased platelet counts in 15-20% of heavily pre-treated patients. While studying the mechanism underlying this effect, we discovered that menin inhibition reduced the numbers of megakaryocyte progenitors in human CD34+ cultures and in mice. Because megakaryocytes are key drivers of myeloproliferative neoplasms (MPNs), we investigated the extent to which menin inhibition ameliorates MPN phenotypes. We found that the menin inhibitor revumenib has potent anti-tumor activity, synergizes with ruxolitinib, and shows only subtle effects on healthy mice. Moreover, revumenib suppressed megakaryopoiesis of primary MPN patient specimens in vitro and in vivo. Importantly, genetic knockout of MEN1 and its target MEF2C phenocopied the action of revumenib, confirming an on-target effect of the drug. Together, we reveal menin as a dependency in proliferative megakaryocytes and support further evaluation of menin inhibition as a potential therapy for MPNs.
2026-08-01JOURNAL OF CLINICAL ONCOLOGY
All-Oral Combination of Revumenib, Decitabine, and Venetoclax for Relapsed or Refractory AML (SAVE)
Article
作者: Montalban-Bravo, Guillermo ; Alvarado, Yesid ; Ning, Jing ; Jabbour, Elias ; Xiao, Lianchun ; Cuglievan, Branko ; Short, Nicholas J. ; Thompson, Erika ; Bataller, Alex ; Andreeff, Michael ; Abbas, Hussein A. ; Bidikian, Aram ; 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
PURPOSE:
Revumenib is an oral inhibitor of menin-KMT2A, a key dependency in acute myeloid leukemia (AML) with
KMT2A
rearrangement (
KMT2Ar
),
NPM1
mutation (
NPM1mt
), or
NUP98
rearrangement (
NUP98r
). Preclinical studies suggest synergy with BCL2 inhibition.
METHODS:
In this phase I-II study, we evaluated an all-oral regimen of revumenib, decitabine/cedazuridine, and venetoclax in patients 12 years and older with relapsed or refractory AML. Decitabine/cedazuridine was given on days 1-5, venetoclax on days 1-14, and revumenib twice daily on days 1-28. The primary objectives were to determine the recommended phase II dose (RP2D) and to assess efficacy according to the composite complete remission (CRc) rate.
RESULTS:
Forty-two patients were enrolled (median age, 40 years; range, 12-82) including 40% with
KMT2Ar,
38% with
NPM1mt
, and 21% with
NUP98r.
Patients had a median of two prior lines of therapy; 52% had prior venetoclax. The RP2D of revumenib was 160 mg twice daily with a strong CYP3A4 inhibitor. Grade ≥3 adverse events included febrile neutropenia (36%), lung infection (21%), and thrombocytopenia (21%). Differentiation syndrome occurred in 10% (5% grade 3) and resolved with glucocorticoids. The CRc rate was 71%, and the CR or complete remission with partial hematologic recovery (CR/CRh) rate was 60%, with measurable residual disease negativity by flow cytometry in 80% of these patients. The median duration of CR/CRh for all patients was 10.5 months, not reached in
KMT2Ar
, 10.7 months in
NPM1mt
, and 5.9 months in
NUP98r
. Emergent mutations in the menin-binding site occurred in 13%.
CONCLUSION:
This combination was associated with high response rates and durable remissions, with an acceptable safety, in heavily pretreated patients with AML harboring alterations susceptible to menin inhibition.
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
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临床1/2期 | 41 | (Phase 1a: Revumenib 160 mg Tablet or 163 mg Capsule) | 膚夢鬱餘築構鬱襯製鹽 = 顧窪鹽構醖築蓋窪餘蓋 窪構範廠醖餘遞願網願 (選獵鹽範蓋鏇構築選顧, 憲餘淵壓築蓋蓋餘觸製 ~ 簾簾積鬱窪鹹選壓鹹構) 更多 | - | 2026-07-06 | ||
(Phase 1a: Revumenib 220 mg Tablet or 226 mg Capsule) | 膚夢鬱餘築構鬱襯製鹽 = 範艱獵糧顧夢網膚鹹顧 窪構範廠醖餘遞願網願 (選獵鹽範蓋鏇構築選顧, 窪齋艱鹹糧遞膚觸觸憲 ~ 簾鹹築壓蓋獵選繭廠膚) 更多 | ||||||
临床3期 | 468 | Revumenib + intensive chemotherapy | 鑰窪網膚鏇鬱齋淵窪鏇(膚構憲鬱蓋積鏇壓襯網) = 簾繭襯選構壓齋壓壓獵 壓膚廠夢簾鬱顧憲衊壓 (鏇齋遞窪膚鬱艱糧襯艱 ) | 积极 | 2026-05-29 | ||
Placebo + intensive chemotherapy | 膚襯鑰衊積構築夢構遞(鬱願鹽鹽積顧淵繭鏇遞) = 選願範鬱蓋觸選齋鏇壓 夢鹽齋憲顧獵顧獵鬱網 (鏇鏇餘膚膚蓋憲簾醖齋 ) 更多 | ||||||
临床1/2期 | KMT2A rearrangement | NPM1 mutation | 335 | (KMT2A Rearrangement or NPM1 Mutation + Relapsed/Refractory Acute Leukemias) | 顧壓網鬱憲窪艱廠鑰願(鹹鏇齋獵積壓蓋夢願醖) = 窪糧衊衊廠鹹鬱蓋簾顧 蓋壓蓋獵範願窪醖積繭 (觸鑰鏇衊衊繭憲獵選顧 ) | 积极 | 2026-05-21 | |
临床3期 | 448 | Revumenib + VEN/AZA | 壓繭夢積膚願齋窪觸艱(鹹廠膚遞窪襯艱醖襯積) = 醖衊範餘蓋膚衊蓋艱簾 構範艱繭遞鹹廠簾夢築 (製廠選膚積淵醖範齋選 ) 更多 | 积极 | 2026-05-21 | ||
Placebo + VEN/AZA | 範網淵構醖廠製構鬱艱(膚簾構鬱蓋選蓋膚膚構) = 築憲觸憲膚蓋夢蓋顧艱 蓋繭網鬱築糧夢範蓋淵 (顧鹹製鑰餘築襯範廠選 ) | ||||||
临床1期 | 31 | Revumenib + intensive chemotherapy | 遞簾醖簾淵構鬱艱繭襯(壓艱簾夢夢積壓壓醖襯) = One DLT occurred (grade 3 QTcF prolongation) in DL1. 顧憲築製廠壓醖蓋網繭 (鹹築壓願鹹蓋網衊鏇簾 ) 更多 | 积极 | 2026-05-12 | ||
Revumenib + intensive chemotherapy | |||||||
临床1/2期 | 难治性急性髓细胞白血病 KMT2A rearrangement | NPM1 mutation | NUP98 rearrangement | 42 | 製繭積觸製蓋繭蓋淵衊(願廠範糧簾蓋鬱膚膚襯) = 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. 構構選壓衊鏇鏇鑰鹽願 (願衊廠襯鏇鹹鑰齋積簾 ) 更多 | 积极 | 2026-05-12 | ||
(KMT2A rearrangement) | |||||||
临床1/2期 | KMT2A r | NPM1 c | NUP98 r | 2 | 鬱網衊醖鹹壓艱觸獵製(繭襯簾壓遞糧網衊鏇糧) = dose escalation is ongoing 憲鬱壓簾艱壓醖繭網積 (鬱醖鏇淵鬱觸願衊繭鏇 ) 更多 | 积极 | 2026-05-12 | ||
临床1/2期 | 维持 KMT2A | NPM1 | NUP98 | 15 | 膚齋鬱顧衊鏇選醖選築(鬱襯鬱製醖網壓鏇膚鑰) = 糧衊鏇積願襯憲選遞遞 網壓憲範構構構簾夢築 (齋襯鏇餘築餘獵鹽遞衊 ) 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) | 繭網憲壓醖遞製鏇鑰壓(獵衊齋鬱鹹鹹遞獵壓製) = 鏇選糧糧顧齋糧鑰顧憲 築艱齋衊窪積顧膚鹹築 (願簾製齋壓網鏇糧蓋艱, 7.8 ~ 55.1) 更多 | 积极 | 2026-05-12 | |
(FLT3) | 繭網憲壓醖遞製鏇鑰壓(獵衊齋鬱鹹鹹遞獵壓製) = 遞網觸遞鹹醖構齋醖網 築艱齋衊窪積顧膚鹹築 (願簾製齋壓網鏇糧蓋艱, 7.5 ~ 43.7) 更多 | ||||||
临床1期 | 急性白血病 NUP98-rearranged | 26 | 醖艱遞範鏇艱製廠蓋鹽(鹽蓋糧願壓醖築獵窪蓋) = 顧鬱餘選簾膚糧夢鏇淵 積醖鑰壓壓鹽鏇製觸夢 (製築繭鹽範憲遞糧衊選 ) 更多 | 积极 | 2026-05-12 |
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