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更新于：2026-04-02
Mezigdomide
美齐格米特
更新于：2026-04-02
概要
基本信息
原研机构 |
非在研机构- |
权益机构- |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)临床3期 |
特殊审评- |
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结构/序列
分子式C32H30FN5O4 |
InChIKeyYTINZZFBHWSAGL-NDEPHWFRSA-N |
CAS号2259648-80-9 |
关联
26
项与 美齐格米特 相关的临床试验NCT07355335
A Phase 1 Study of Menin-KMT2A Inhibitor Ziftomenib (KO-539) in Combination With Cereblon E3 Ligase Modulator Mezigdomide (CC-92480) in Adolescents and Adults With Relapsed or Refractory Acute Myeloid Leukemia (AML)
NCT07356154
A Phase 1/2 Study of the Menin Inhibitor Revumenib With the CELMod Mezigdomide in Relapsed/Refractory KMT2A-rearanged, NPM1-mutant, and NUP98-rearranged Acute Leukemias
NCT07032714
MAGENTA: Phase I Study of Mezigdomide and Talquetamab in Relapsed and Refractory Multiple Myeloma
100 项与 美齐格米特 相关的临床结果
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100 项与 美齐格米特 相关的转化医学
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100 项与 美齐格米特 相关的专利（医药）
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34
项与 美齐格米特 相关的文献（医药）2026-03-01CLINICAL PHARMACOLOGY & THERAPEUTICS
Application of Physiologically Based Pharmacokinetic Modeling to Inform Dose Selection of Mezigdomide in a Phase I Drug–Drug Interaction Study
Article
作者: Shahane, Aditi ; Lamba, Manisha ; Sychterz, Caroline ; Chen, Wencong ; Gaudy, Allison ; Silva, Jose ; Wang, Xiaomin ; Shakeel, Faisal ; Burnett, Joseph ; Katz, Jessica
Mezigdomide (MEZI) is an oral, highly potent CELMoD™ agent with promising antitumor and immune‐stimulatory activity, optimized for Aiolos and Ikaros degradation. Preclinical evidence suggests MEZI is primarily metabolized by cytochrome P450 (CYP) 3A4/5 and has the potential to inhibit efflux transporters P‐glycoprotein (P‐gp) and breast cancer resistance protein (BCRP)
in vitro
. To predict the magnitude of enzyme‐ and transporter‐mediated drug–drug interactions (DDI) and inform clinical study design, a physiologically based pharmacokinetic (PBPK) model was developed. A PBPK‐informed Phase I clinical DDI study was conducted that evaluated MEZI as an object of CYP3A induction (rifampin) and inhibition (itraconazole) and as a precipitant of transporter‐mediated interactions (digoxin and rosuvastatin). PBPK modeling predicted substantial interactions with strong and moderate CYP3A modulators, which informed a unique dose selection strategy, PK sampling time, and washout period. Clinical results confirmed reductions in MEZI exposure with rifampin (AUC reduced 93–95%) and increases with itraconazole (~14‐fold for dose normalized AUC). MEZI was well‐tolerated despite these changes in exposure. Additionally, coadministration of MEZI with P‐gp and BCRP substrates, digoxin and rosuvastatin, showed no clinically meaningful changes in substrate plasma PK, indicating a low likelihood of significant transporter‐mediated DDIs. The prospective PBPK model was refined with clinical data, improving predictions and supporting simulations for moderate/weak CYP3A modulators. This iterative “learn‐confirm” approach underscores the utility of PBPK modeling in optimizing clinical trial design, ensuring participant safety, and anticipating DDI risks. The findings support MEZI’s clinical development with informed dosing strategies, particularly for coadministration with CYP3A modulators.
2026-02-01Blood neoplasia
Mezigdomide combined with bortezomib disrupts the cell cycle and elicits superior antitumor effects in multiple myeloma
Article
作者: Singh, Ram Kumar ; Ghosh, Kaushik ; Subramanyam, Prakash ; Chiu, Hsiling ; Kang, Jian ; Wu, Lei ; Larrayoz, Marta ; Gandhi, Anita K ; Dudhgaonkar, Shailesh ; Chow, Tracy T ; Martinez-Climent, Jose A ; Sridhara, Sneha ; Thakurta, Anjan ; Zhao, Junfei ; Li, Shirong ; Hsu, Chih-Chao ; Bahlis, Nizar J ; Amatangelo, Michael ; Shtraizent, Natasha ; Wollerman, Krista ; Bjorklund, Chad C ; Hagner, Patrick R ; Richardson, Paul G
Triplet regimens that include an immunomodulatory agent, proteasome inhibitor, and dexamethasone are widely used in newly diagnosed and relapsed/refractory (R/R) multiple myeloma (MM). Mezigdomide (MEZI; CC-92480) is a cereblon E3 ubiquitin ligase modulator that is being clinically investigated in combination with bortezomib (BTZ) and low-dose dexamethasone (DEX) for safety and efficacy in pretreated R/RMM. The single-agent mechanism of action (MOA) of MEZI has been defined by the recruitment and degradation of essential MM transcription factors Ikaros and Aiolos, leading to cell autonomous antitumor effects and immune modulation. These effects were confirmed in patients based on pharmacodynamic measurements of Ikaros/Aiolos degradation in biomarker evaluations of immune subsets. However, the MOA of triplet regimens, including that of MEZI/BTZ/DEX remain poorly defined. To better understand the MOA of this triplet combination, we compared the mechanistic contributions of MEZI, BTZ, or DEX alone, or in combination, in preclinical MM models in vitro and in vivo. Additionally, we have compared these results with similar combinations with the immunomodulatory agent pomalidomide (POM). Our studies indicate that the MEZI/BTZ/DEX triplet is superior to all single agents and POM/BTZ/DEX in terms of potency of antiproliferative and proapoptotic activities, substrate degradation depth and kinetics in the presence of BTZ, and in vivo efficacy. We show that the combination of MEZI with BTZ increases cell death through disruption of multiple phases of the cell cycle and this thereby enhances the direct cytotoxic effects of the combination treatment.
2025-07-01JCO Oncology Practice
Novel Treatment Options for Multiple Myeloma
Review
作者: Portuguese, Andrew J. ; Banerjee, Rahul ; Reddi, Swetha ; Cowan, Andrew J. ; Chen, GuiZhen
Multiple myeloma (MM), the second most common hematologic malignancy in the United States, is characterized by repeated cycles of remission and relapse, with increasing resistance to treatment after each line of therapy. Despite the virtually incurable nature of MM, recent therapeutic breakthroughs have fundamentally reshaped its treatment landscape. This review explores evolving care paradigms, spanning from newly diagnosed MM to relapsed or refractory disease. In the frontline setting, treatment strategies have shifted beyond their traditional emphasis on autologous stem-cell transplant eligibility to a broader categorization of patients on the basis of their suitability for quadruplet therapy. In the relapsed/refractory setting, novel immunotherapies, including chimeric antigen receptor T-cell (CAR-T) therapies and bispecific antibodies, have revolutionized treatment, offering new hope for patients with previously limited options. Precision medicine is playing a growing role in MM treatment, with venetoclax showing significant efficacy in patients with t(11;14) translocation, advancing targeted therapy for this subgroup. On the horizon, investigational CAR-T products and cereblon E3 ligase modulators, such as mezigdomide and iberdomide, may provide faster, more durable responses compared with current therapies. In addition, belantamab mafodotin, an antibody-drug conjugate withdrawn from the US market in 2022, is on the verge of reapproval after positive results from recent randomized trials. While these therapies offer significant potential, challenges remain in managing toxicity, ensuring treatment accessibility, and optimizing sequencing strategies. As the therapeutic arsenal expands, the need for personalized MM treatment plans that balance efficacy with quality of life becomes even more essential.
100 项与 美齐格米特 相关的药物交易
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 多发性骨髓瘤 | 临床3期 | 比利时 | 2022-09-20 | |
| 多发性骨髓瘤 | 临床3期 | 捷克 | 2022-09-20 | |
| 多发性骨髓瘤 | 临床3期 | 芬兰 | 2022-09-20 | |
| 多发性骨髓瘤 | 临床3期 | 法国 | 2022-09-20 | |
| 多发性骨髓瘤 | 临床3期 | 爱尔兰 | 2022-09-20 | |
| 多发性骨髓瘤 | 临床3期 | 波兰 | 2022-09-20 | |
| 多发性骨髓瘤 | 临床3期 | 葡萄牙 | 2022-09-20 | |
| 多发性骨髓瘤 | 临床3期 | 土耳其 | 2022-09-20 | |
| 难治性多发性骨髓瘤 | 临床3期 | 比利时 | 2022-09-20 | |
| 难治性多发性骨髓瘤 | 临床3期 | 智利 | 2022-09-20 |
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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 | 11 | 鏇繭鹽齋憲醖觸壓醖願(壓糧窪製襯簾廠壓蓋鬱) = 範餘網襯蓋鏇糧網齋蓋 獵糧製淵構築鬱簾獵齋 (簾觸壓糧襯範獵衊壓鬱 ) 更多 | 积极 | 2025-12-06 | |||
临床1期 | 13 | 鬱鏇鹹選夢積遞艱範醖(醖餘獵製範鹹壓壓壓築) = As of July 8, 2025, no dose-limiting toxicities (DLTs) were encountered in cohorts 1 and 2. Two DLTs occurred in cohort 3. One pt experienced Grade (G) 2 constipation and proctitis considered possibly related despite being pre-existing and withdrew consent prior to completion of cycle 1, thus qualifying as DLT. Another pt experienced G4 neutropenia on C1D15 that did not resolve within 7 days of holding study medication; G4 neutropenia recovered by C2D15 after 2 doses of filgrastim (C1D15 and C1D22), and pt was able to continue with S reduced to 40 mg and M 0.6 mg. 夢簾顧簾築艱餘餘鬱製 (膚鬱顧糧艱淵鹽鹽觸糧 ) 更多 | 积极 | 2025-12-06 | |||
临床1/2期 | - | MEZI + dexamethasone (MEZId) + TAZ | 醖憲鑰遞鹽觸鑰製艱願(獵膚膚遞憲網鹹鹽鹽鏇) = 1 with 1.0mg MEZId+TAZ; 1 with 0.3mg, and 4 with 1.0mg MEZId+BMS-986158; 2 with 1.0mg MEZId+TRAM 願鬱餘餘醖蓋齋壓鹽膚 (糧壓淵糧衊糧糧簾壓膚 ) 更多 | 积极 | 2025-05-14 | ||
MEZI + dexamethasone (MEZId) + BMS-986158 | |||||||
临床1/2期 | 104 | Mezigdomide (Mezi) + Dexamethasone (Dex) + Bortezomib (Bort) | 範積顧鏇憲繭獵遞獵蓋(築選觸鹽獵築觸憲夢觸) = 17.9% with MeziVd; 33.3% with MeziKd 齋觸廠艱衊襯衊範簾廠 (夢餘鬱艱鹹築範壓淵網 ) 更多 | 积极 | 2025-05-14 | ||
N/A | - | MeziVd | 艱窪廠網夢壓範艱夢製(蓋選鏇窪鹹簾夢願網鑰) = The most common grade 3/4 TEAEs were neutropenia (35.7%), thrombocytopenia (21.4%), and infections (17.9%) with MeziVd; and neutropenia (44.4%) and infections (33.3%) with MeziKd 積製襯齋簾醖壓醖蓋積 (願憲鑰艱獵鹹構糧簾壓 ) 更多 | - | 2024-12-09 | ||
MeziKd | |||||||
N/A | - | 窪憲積廠餘鹹繭鏇選壓(淵獵蓋壓獵糧艱製艱構) = Three pts had dose-limiting toxicities (1 with 0.3 mg MEZId + BMS-986158, 1 with 1.0 mg MEZId + BMS-986158, and 1 with 1.0 mg MEZId + TRAM) 蓋壓廠選構醖構衊簾範 (憲網顧夢艱鏇廠餘積簾 ) 更多 | - | 2024-12-08 | |||
N/A | - | 簾願鹽簾製製網選淵鹽(鹽獵築鹹鑰夢糧齋顧壓) = 膚選繭顧夢鏇糧餘遞餘 齋積餘鑰膚網繭繭淵選 (膚糧鹹壓鏇糧糧範鏇觸, 0.03–0.13) 更多 | - | 2024-09-04 | |||
簾願鹽簾製製網選淵鹽(鹽獵築鹹鑰夢糧齋顧壓) = 憲顧顧網鏇鬱壓齋膚繭 齋積餘鑰膚網繭繭淵選 (膚糧鹹壓鏇糧糧範鏇觸, 0.03–0.13) 更多 | |||||||
N/A | - | Mezigdomide (MEZI) + Dexamethasone (DEX) + Bortezomib (BORT) | 壓構艱鬱廠淵壓醖範齋(蓋憲膚網醖網鏇遞積膚) = 繭鹽積窪範願夢壓觸膚 鏇廠齋顧鏇遞齋選艱壓 (積糧鬱構範製淵膚蓋壓 ) 更多 | - | 2024-09-04 | ||
Mezigdomide (MEZI) + Dexamethasone (DEX) + Carfilzomib (CFZ) | 壓構艱鬱廠淵壓醖範齋(蓋憲膚網醖網鏇遞積膚) = 窪觸齋積繭積製衊膚選 鏇廠齋顧鏇遞齋選艱壓 (積糧鬱構範製淵膚蓋壓 ) 更多 | ||||||
临床1/2期 | 101 | 簾膚願艱獵遞衊淵糧艱(獵構築齋觸製艱艱鬱鑰) = 鹽網窪顧鏇憲壓壓醖廠 獵觸廠餘觸簾糧齋鏇願 (積鬱網鬱遞齋夢餘廠繭 ) 更多 | 积极 | 2024-05-24 | |||
(No RI) | 簾膚願艱獵遞衊淵糧艱(獵構築齋觸製艱艱鬱鑰) = 簾獵構壓醖簾壓壓齋積 獵觸廠餘觸簾糧齋鏇願 (積鬱網鬱遞齋夢餘廠繭 ) 更多 | ||||||
临床1/2期 | 多发性骨髓瘤 PRC2 Loss of Function Mutation | EZH2 Overexpression | 10 | MEZI+TAZ+DEX 0.3mg | 衊醖艱蓋餘醖襯夢遞鏇(範廠願築艱遞壓夢製鏇) = 簾艱積膚選膚壓鑰選夢 衊艱衊積醖構遞範獵壓 (壓齋襯膚顧襯艱築蓋製 ) 更多 | 积极 | 2024-05-14 |
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