A Phase 2, Open-Label, Single-Arm, Multicenter Study to Evaluate the Efficacy of Cemsidomide + Dexamethasone in Subjects With Relapsed/Refractory Multiple Myeloma

This is a Phase 2, open-label, single-arm, multicenter study to assess the antimyeloma activity and further characterize the safety, tolerability, PK, and PD of cemsidomide in combination with dexamethasone in participants with relapsed/refractory multiple myeloma (r/r MM).

开始日期2026-02-18

申办/合作机构

C4 Therapeutics, Inc.

NCT07280013

/ Recruiting临床1期

A Phase 1B, Open-label, Multicenter Study to Evaluate the Safety and Preliminary Efficacy of Cemsidomide in Combination With Elranatamab in Relapsed/Refractory Multiple Myeloma Subjects

The main purpose of the study is to understand the safety and tolerability of cemsidomide when given along with elranatamab in subjects with relapsed or refractory multiple myeloma.
The first part of the study will evaluate different dose levels of cemsidomide in combination with elranatamab in a limited number of subjects. Approximately 3 different dose levels of cemsidomide in combination with elranatamab may be explored. Once a dose level is determined safe, additional subjects may be enrolled through expansion of the dose level. This expansion will provide further exploration of the safety and evaluation of preliminary antimyeloma activity.
Cemsidomide will be taken orally each cycle for 14 days on/14 days off (1 cycle=28 days). Elranatamab will be administered by subcutaneous injection twice a month. Dexamethasone will be administered weekly until a confirmed response but no longer than 4 cycles.

开始日期2026-02-06

申办/合作机构

C4 Therapeutics, Inc.

NCT04756726

/ Active, not recruiting临床1期

A Phase 1/2 Open-Label Multi-Center Study to Characterize the Safety and Tolerability of CFT7455 in Subjects With Relapsed/Refractory Non-Hodgkin's Lymphoma or Multiple Myeloma

The purpose of this study is to characterize the safety, tolerability, pharmacokinetics, pharmacodynamics, and antitumor activity of oral cemsidomide (also known as CFT7455) administered at different dosages in subjects with Relapsed/Refractory (r/r) Non-Hodgkin's Lymphoma (NHL) or Multiple Myeloma (MM). Cemsidomide may be administered as a single agent and, in MM only, in combination with oral dexamethasone.

开始日期2021-04-27

申办/合作机构

C4 Therapeutics, Inc.

100 项与 Cemsidomide 相关的临床结果

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100 项与 Cemsidomide 相关的转化医学

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100 项与 Cemsidomide 相关的专利（医药）

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项与 Cemsidomide 相关的文献（医药）

2023-01-01·Blood reviews

Targeting cereblon in hematologic malignancies

Review

作者: Ota Fuchs

The protein cereblon (CRBN) is a substrate receptor of the cullin 4-really interesting new gene (RING) E3 ubiquitin ligase complex CRL4^CRBN. Targeting CRBN mediates selective protein ubiquitination and subsequent degradation via the proteasome. This review describes novel thalidomide analogs, immunomodulatory drugs, also known as CRBN E3 ubiquitin ligase modulators or molecular glues (avadomide, iberdomide, CC-885, CC-90009, BTX-1188, CC-92480, CC-99282, CFT7455, and CC-91633), and CRBN-based proteolysis targeting chimeras (PROTACs) with increased efficacy and potent activity for application in hematologic malignancies. Both types of CRBN-binding drugs, molecular glues, and PROTACs stimulate the interaction between CRBN and its neosubstrates, recruiting target disease-promoting proteins and the E3 ubiquitin ligase CRL4^CRBN. Proteins that are traditionally difficult to target (transcription factors and oncoproteins) can be polyubiquitinated and degraded in this way. The competition of CRBN neosubstrates with endogenous CRBN-interacting proteins and the pharmacology and rational combination therapies of and mechanisms of resistance to CRL4^CRBN modulators or CRBN-based PROTACs are described.

CANCER JOURNAL

Beyond Immunomodulatory Drugs: Next-Generation Cereblon Modulators in Multiple Myeloma

Review

作者: Lonial, Sagar ; Cani, Lorenzo ; Mina, Roberto

Despite substantial improvements in survival over recent decades, multiple myeloma (MM) remains largely incurable, and most patients ultimately experience relapsed or refractory disease, highlighting the need for novel therapeutic strategies. Immunomodulatory drugs (IMiDs) have transformed MM treatment through direct antitumor and immune-enhancing effects mediated by cereblon modulation, while their ability to stimulate T-cell and NK-cell function has provided a strong rationale for combination with modern immunotherapies, including bispecific antibodies and chimeric antigen receptor (CAR) T-cell therapies. More recently, cereblon E3 ligase modulators (CELMoDs), such as iberdomide and mezigdomide, have emerged as next-generation cereblon-targeting agents with enhanced potency, deeper substrate degradation, and activity in lenalidomide- and pomalidomide-resistant settings. Clinical studies have demonstrated promising efficacy and manageable safety profiles across newly diagnosed and relapsed/refractory MM, including in heavily pretreated patients. In parallel, novel degraders such as cemsidomide have shown encouraging preliminary activity, further expanding the therapeutic potential of cereblon-directed approaches in MM. In this review, we aim to summarize the evolution of oral therapies in MM, focusing on the efficacy and safety of next-generation cereblon modulators and emerging cereblon-directed degraders.

EXPERT OPINION ON EMERGING DRUGS

PROTAC degraders for lymphoid malignancies — current status and future directions

Review

作者: Wolska-Washer, Anna ; Robak, Tadeusz

INTRODUCTION:

Despite remarkable advances in targeted therapy, some patients with lymphoid malignancies develop resistance to all available treatment modalities. Proteolysis-targeting chimeras (PROTACs), harness the ubiquitin-proteasome system to eliminate both catalytic and scaffolding protein functions of disease-causing proteins, offering a strategy to overcome this resistance.

AREAS COVERED:

This review discusses the mechanisms of PROTAC activity, current preclinical and clinical data across lymphoid malignancies, and challenges for this emerging therapeutic class. PubMed, Google Scholar, and major hematology conference proceedings (ASH, ASCO, EHA) from 2017 to April 2026 were reviewed. Search terms included combinations of: PROTAC, targeted protein degradation, cereblon, von Hippel-Lindau, combined with individual disease terms and target names.

EXPERT OPINION:

Among PROTACs, BTK degraders, tacabrutideg (BGB-16673) and bexobrutideg (NX-5948), have demonstrated overall response rates exceeding 75% in heavily pretreated relapsed/refractory CLL/SLL. The STAT3 degrader KT-333 and the IKZF1/3 degrader cemsidomide (the so-called molecular glue) have shown proof-of-concept clinical activity in T-cell and Hodgkin lymphomas. The durability of responses, long-term safety and predictive biomarkers have yet to be defined.The ongoing phase III trial of tacabrutideg will likely determine whether PROTACs become an established treatment option in lymphoid malignancies.

124

项与 Cemsidomide 相关的新闻（医药）

2026-10-29

·动脉网

C4 Therapeutics宣布扩展其发现平台能力，采用以靶点为中心的方法加速新型分子胶降解剂的识别C4 Therapeutics Unveils Expansion of Discovery Platform Capabilities Utilizing Target-Centric Approach to Accelerate the Identification of Novel Molecular Glue Degraders

DEL Technology Integrating C4T’s Cereblon Library Can Rapidly Advance Projects Into Hit-To-Lead Stage DEL技术整合C4T的Cereblon文库可快速推动项目进入从命中到先导阶段WATERTOWN, Mass., Oct. 29, 2026 (GLOBE NEWSWIRE) -- C4 Therapeutics, Inc. (C4T) (Nasdaq: CCCC), a clinical-stage biopharmaceutical company dedicated to advancing targeted protein degradation (TPD) science, today highlighted its novel DNA-encoded library (DEL) that leverages C4T’s large library of cereblon-binding ligands and screening capabilities in a presentation at the 9. 马萨诸塞州沃特敦，2026年10月29日（环球电讯社）——专注于推进靶向蛋白降解（TPD）科学的临床阶段生物制药公司C4 Therapeutics, Inc.（C4T）（纳斯达克股票代码：CCCC）今日在一次演讲中重点介绍了其新型DNA编码库（DEL），该库利用了C4T庞大的cereblon结合配体库及其筛选能力。th 泰国Annual Targeted Protein Degradation Summit in Boston titled “Target-First Discovery of Molecular Glue Degraders Using DNA-Encoded Libraries.” 在波士顿举行的年度靶向蛋白降解峰会，题为“利用DNA编码库进行分子胶降解剂的靶点优先发现”。“Our new DEL capability captures both our strong track record of investing in cereblon and driving innovation across targeted protein degradation science to create a differentiated engine for generating new drug discovery opportunities,” said Scott Boyle, chief business officer of C4 Therapeutics. “To date, this new technology has shown it can deliver attractive hits against high-value targets within four months and further enhances the speed and precision of our discovery efforts. C4 Therapeutics 首席商务官 Scott Boyle 表示：“我们全新的 DNA 编码库（DEL）能力，既彰显了我们在大脑蛋白（cereblon）领域的深厚投资积淀，也体现了我们在靶向蛋白降解科学领域推动创新的实力，从而打造出一个独具特色的引擎，以催生新的药物发现机会。迄今为止，这项新技术已展现出在四个月内针对高价值靶点提供具有吸引力的先导化合物的能力，并进一步提升了我们药物发现工作的速度与精准度。”We are eager to push the boundaries of this library and our rapid screening process with diverse and undruggable targets both for our own internal pipeline and alongside future partners.”. 我们渴望突破该库及快速筛选流程的边界，面向多样且难以成药的靶点，既服务于我们自身的内部研发管线，也与未来合作伙伴协同推进。Integrated within C4T’s TORPEDO 集成于 C4T 的 TORPEDO 系统中® ®platform, the addition of DEL creates a powerful hit-finding engine that enables the rapid development of targeted protein degraders. C4T has integrated the company’s cereblon-binding ligand libraries into its DEL capability, which has helped develop a diverse library unique to C4T. The target-first approach integrated into C4T’s DEL technology further enables rapid evaluation, validation, characterization and development of molecular glue degraders.. 在该平台上，DNA编码库（DEL）的引入构建了一个强大的先导化合物发现引擎，能够加速靶向蛋白降解剂的开发。C4T 已将其 cereblon 结合配体库整合到 DEL 技术平台中，从而建立起一个独具特色且多样化的 C4T 专属化合物库。C4T 的 DEL 技术所融合的“靶点优先”策略，进一步实现了对分子胶降解剂的快速评估、验证、表征和开发。C4T has validated this DEL capability by identifying both known and novel molecular glue degrader hits for VAV1, which C4T does not plan to advance without a partner. Led by its target-first approach, C4T has also screened a range of high-value targets where degradation turns undruggable to druggable or provides a therapeutic benefit relative to inhibitors; this has identified hits for additional undisclosed targets. C4T 通过鉴定出针对 VAV1 的已知和新型分子胶降解剂候选化合物，验证了其 DEL 平台的能力；若无合作伙伴，C4T 不计划推进这些候选化合物的进一步开发。在以靶点为先导的策略推动下，C4T 还对一系列高价值靶点进行了筛选，在这些靶点中，降解作用能够将“不可成药”转化为“可成药”，或相较于抑制剂提供治疗优势；该筛选已发现针对其他未公开靶点的候选化合物。C4T remains focused on advancing cemsidomide through clinical development and its discovery strategy centered around undisclosed targets that drive inflammation, neuroinflammation and neurodegenerative diseases.. C4T 仍专注于推进 cemsidomide 的临床开发，并实施以未公开靶点为核心的发现策略，这些靶点驱动炎症、神经炎症和神经退行性疾病。C4T will highlight this new capability and more information on the VAV1 target in a presentation at the 9 C4T将在第9届会议上通过演讲重点介绍这一新功能以及关于VAV1靶点的更多信息th 泰国Annual Targeted Protein Degradation Summit on October 29, 2026. The presentation is available on C4T’s 2026年10月29日举行的年度靶向蛋白降解峰会。演讲资料可在C4T上获取。website 网站, under Scientific Presentations and Publications. ，在科学报告与出版物部分。About the TORPEDO 关于TORPEDO® ®Platform 平台The proprietary TORPEDO 专有技术 TORPEDO® ®platform drives C4 Therapeutics’ (C4T) efforts to create a new generation of small molecule medicines centered around heterobivalent degraders (BiDAC 该平台推动了C4 Therapeutics（C4T）致力于开发以异双价降解剂（BiDAC）为中心的新一代小分子药物™ 商标degraders), molecular glue degraders (MonoDAC 降解剂），分子胶降解剂（MonoDAC® ®degraders) and degrader-antibody conjugates (DACs). A DNA-encoded library (DEL) that leverages C4T’s cereblon binder library alongside machine learning and artificial intelligence serves as a rapid hit-finding engine. Once a hit is identified, the TORPEDO platform utilizes diverse chemical libraries, degrader design assisted by structural biology, ternary complex models and proteomics, allowing C4T’s scientists to rapidly design degraders with properties that enhance catalytic degradation turnover and drug performance that directly impact disease.. 降解剂）以及降解剂-抗体偶联物（DACs）。一种DNA编码库（DEL）利用C4T的cereblon结合剂库，并结合机器学习和人工智能，作为快速发现先导化合物的引擎。一旦确定先导化合物，TORPEDO平台便利用多样化的化学库、结构生物学辅助的降解剂设计、三元复合物模型以及蛋白质组学技术，使C4T的科学家能够快速设计出具有增强催化降解周转率和药物性能的降解剂，从而直接对疾病产生影响。About C4 Therapeutics 关于 C4 TherapeuticsC4 Therapeutics (C4T) (Nasdaq: CCCC) is a clinical-stage biopharmaceutical company dedicated to delivering on the promise of targeted protein degradation science to create a new generation of medicines that transforms patients’ lives. C4T is progressing targeted oncology programs through clinical studies and leveraging its TORPEDO. C4 Therapeutics（C4T）（纳斯达克股票代码：CCCC）是一家处于临床阶段的生物制药公司，致力于实现靶向蛋白降解科学的潜力，打造变革患者生活的新一代药物。C4T 正通过临床研究推进其靶向肿瘤学项目，并利用其 TORPEDO 技术平台。® ®platform to efficiently design and optimize small-molecule medicines to address difficult-to-treat diseases. C4T’s degrader medicines are designed to harness the body’s natural protein recycling system to rapidly degrade disease-causing proteins, offering the potential to overcome drug resistance, drug undruggable targets and improve patient outcomes. 平台，用于高效设计和优化小分子药物，以应对难治性疾病。C4T的降解剂药物旨在利用人体天然的蛋白质回收系统，快速降解致病蛋白，从而有望克服耐药性、攻克不可成药靶点并改善患者预后。For more information, please visit . 更多信息，请访问。www.c4therapeutics.com www.c4therapeutics.com. 。Forward Looking Statement 前瞻性陈述This press release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements may include, but may not be limited to, express or implied statements regarding our ability to discover or develop potential therapies for patients; the capabilities and potential benefits of our DEL and its ability to accelerate drug discovery; the capabilities of the TORPEDO. 本新闻稿包含经1995年《私人证券诉讼改革法案》界定的“前瞻性陈述”。这些前瞻性陈述可能包括但不限于，关于我们为患者发现或开发潜在疗法的能力、我们的DEL（DNA编码库）的能力及其加速药物发现的潜力和益处、以及TORPEDO的能力的明示或暗示性陈述。® ®platform; the advancement, timing, progress and potential benefits of our discovery and clinical programs, including cemsidomide; the potential for future collaborations, partnerships, milestone or royalty payments; and our ability to fund its future operations. Any forward-looking statements in this press release are based on management’s current expectations and assumptions and are subject to risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. 平台；我们包括cemsidomide在内的发现和临床项目的进展、时间安排、进度及潜在益处；未来合作、伙伴关系、里程碑付款或特许权使用费支付的潜力；以及我们为未来运营提供资金的能力。本新闻稿中的任何前瞻性陈述均基于管理层当前的预期和假设，并受风险和不确定性的影响，这些风险和不确定性可能导致实际结果与上述前瞻性陈述中所述或暗示的结果产生重大且不利的差异。These risks and uncertainties include, but are not limited to: risks inherent in drug discovery and development; the risk that screening results or identified hits may not be reproducible, validated or successfully translated into product candidates; the risk that the results of preclinical studies and/or clinical trials will not be predictive of results from future studies or trials; the timing and outcome of regulatory submissions or interactions; and the risk that any one or more of our programs or product candidates will cost more to develop or may not be successfully developed and commercialized. 这些风险和不确定性包括但不限于：药物发现和开发中固有的风险；筛选结果或已识别的命中化合物可能无法重现、验证或成功转化为候选产品的风险；临床前研究和/或临床试验的结果可能无法预测未来研究或试验结果的风险；监管申报或互动的时间和结果的不确定性；以及我们的任何一项或多项计划或候选产品开发成本可能超出预期，或可能无法成功开发并商业化的风险。For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause our actual results to differ from those contained in the forward-looking statements, see the section entitled “Risk Factors” in C4 Therapeutics’ most recent Annual Report on Form 10-K and/or Quarterly Report on Form 10-Q, as filed with the Securities and Exchange Commission. 有关这些及其他风险与不确定性，以及其他重要因素的讨论（任何此类因素均可能导致我们的实际结果与前瞻性陈述中所载内容存在差异），请参阅 C4 Therapeutics 向美国证券交易委员会提交的最新 Form 10-K 年度报告和/或 Form 10-Q 季度报告中标题为“风险因素”的章节。All information in this press release is as of the date of the release, and C4 Therapeutics undertakes no duty to update this information unless required by law.. 本新闻稿中的所有信息均截至发布之日，除非法律另有要求，C4 Therapeutics 不承担更新该信息的义务。Contacts: 联系人：Investors: 投资者：Courtney Solberg 考特尼·索尔伯格Associate Director, Investor Relations 投资者关系副总监CSolberg@c4therapeutics.com CSolberg@c4therapeutics.comMedia: 媒体：Loraine Spreen 洛雷恩·斯普林Senior Director, Corporate Communications & Patient Advocacy 企业传播与患者倡导高级总监LSpreen@c4therapeutics.com LSpreen@c4therapeutics.com

2026-10-29

·BioSpace

C4 Therapeutics Unveils Expansion of Discovery Platform Capabilities Utilizing Target-Centric Approach to Accelerate the Identification of Novel Molecular Glue Degraders

DEL Technology Integrating C4T’s Cereblon Library Can Rapidly Advance Projects Into Hit-To-Lead Stage WATERTOWN, Mass., Oct. 29, 2026 (GLOBE NEWSWIRE) -- C4 Therapeutics, Inc. (C4T) (Nasdaq: CCCC), a clinical-stage biopharmaceutical company dedicated to advancing targeted protein degradation (TPD) science, today highlighted its novel DNA-encoded library (DEL) that leverages C4T’s large library of cereblon-binding ligands and screening capabilities in a presentation at the 9 th Annual Targeted Protein Degradation Summit in Boston titled “Target-First Discovery of Molecular Glue Degraders Using DNA-Encoded Libraries.” “Our new DEL capability captures both our strong track record of investing in cereblon and driving innovation across targeted protein degradation science to create a differentiated engine for generating new drug discovery opportunities,” said Scott Boyle, chief business officer of C4 Therapeutics. “To date, this new technology has shown it can deliver attractive hits against high-value targets within four months and further enhances the speed and precision of our discovery efforts. We are eager to push the boundaries of this library and our rapid screening process with diverse and undruggable targets both for our own internal pipeline and alongside future partners.” Integrated within C4T’s TORPEDO ® platform, the addition of DEL creates a powerful hit-finding engine that enables the rapid development of targeted protein degraders. C4T has integrated the company’s cereblon-binding ligand libraries into its DEL capability, which has helped develop a diverse library unique to C4T. The target-first approach integrated into C4T’s DEL technology further enables rapid evaluation, validation, characterization and development of molecular glue degraders. C4T has validated this DEL capability by identifying both known and novel molecular glue degrader hits for VAV1, which C4T does not plan to advance without a partner. Led by its target-first approach, C4T has also screened a range of high-value targets where degradation turns undruggable to druggable or provides a therapeutic benefit relative to inhibitors; this has identified hits for additional undisclosed targets. C4T remains focused on advancing cemsidomide through clinical development and its discovery strategy centered around undisclosed targets that drive inflammation, neuroinflammation and neurodegenerative diseases. C4T will highlight this new capability and more information on the VAV1 target in a presentation at the 9 th Annual Targeted Protein Degradation Summit on October 29, 2026. The presentation is available on C4T’s website , under Scientific Presentations and Publications. About the TORPEDO ® Platform The proprietary TORPEDO ® platform drives C4 Therapeutics’ (C4T) efforts to create a new generation of small molecule medicines centered around heterobivalent degraders (BiDAC ™ degraders), molecular glue degraders (MonoDAC ® degraders) and degrader-antibody conjugates (DACs). A DNA-encoded library (DEL) that leverages C4T’s cereblon binder library alongside machine learning and artificial intelligence serves as a rapid hit-finding engine. Once a hit is identified, the TORPEDO platform utilizes diverse chemical libraries, degrader design assisted by structural biology, ternary complex models and proteomics, allowing C4T’s scientists to rapidly design degraders with properties that enhance catalytic degradation turnover and drug performance that directly impact disease. About C4 Therapeutics C4 Therapeutics (C4T) (Nasdaq: CCCC) is a clinical-stage biopharmaceutical company dedicated to delivering on the promise of targeted protein degradation science to create a new generation of medicines that transforms patients’ lives. C4T is progressing targeted oncology programs through clinical studies and leveraging its TORPEDO ® platform to efficiently design and optimize small-molecule medicines to address difficult-to-treat diseases. C4T’s degrader medicines are designed to harness the body’s natural protein recycling system to rapidly degrade disease-causing proteins, offering the potential to overcome drug resistance, drug undruggable targets and improve patient outcomes. For more information, please visit . Forward Looking Statement This press release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements may include, but may not be limited to, express or implied statements regarding our ability to discover or develop potential therapies for patients; the capabilities and potential benefits of our DEL and its ability to accelerate drug discovery; the capabilities of the TORPEDO ® platform; the advancement, timing, progress and potential benefits of our discovery and clinical programs, including cemsidomide; the potential for future collaborations, partnerships, milestone or royalty payments; and our ability to fund its future operations. Any forward-looking statements in this press release are based on management’s current expectations and assumptions and are subject to risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to: risks inherent in drug discovery and development; the risk that screening results or identified hits may not be reproducible, validated or successfully translated into product candidates; the risk that the results of preclinical studies and/or clinical trials will not be predictive of results from future studies or trials; the timing and outcome of regulatory submissions or interactions; and the risk that any one or more of our programs or product candidates will cost more to develop or may not be successfully developed and commercialized. For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause our actual results to differ from those contained in the forward-looking statements, see the section entitled “Risk Factors” in C4 Therapeutics’ most recent Annual Report on Form 10-K and/or Quarterly Report on Form 10-Q, as filed with the Securities and Exchange Commission. All information in this press release is as of the date of the release, and C4 Therapeutics undertakes no duty to update this information unless required by law. Contacts: Investors: Courtney Solberg Associate Director, Investor Relations CSolberg@c4therapeutics.com Media: Loraine Spreen Senior Director, Corporate Communications & Patient Advocacy LSpreen@c4therapeutics.com

蛋白降解靶向嵌合体

2026-10-17

·Bunny MediTalk

Iberdomide获批之后：CELMoD能否重塑多发性骨髓瘤的治疗格局？

在多发性骨髓瘤领域，“新篇章”是一个使用频率很高的词。蛋白酶体抑制剂、免疫调节剂、CD38单抗、CAR-T和双特异性抗体先后进入临床时，人们都曾使用过类似表述。如今，Iberdomide获得FDA加速批准，成为首个获得FDA批准的CELMoD药物，“新篇章”再次成为行业讨论的关键词。这次确实有充分理由保持乐观，但也没有必要过早下结论。 Iberdomide的批准不仅验证了新一代CRBN调节剂的临床和监管可行性，也为MRD作为多发性骨髓瘤加速批准终点提供了一个重要案例。更关键的是，在批准之后，百时美施贵宝披露的EXCALIBER-RRMM最新PFS顶线结果进一步显示，MRD阴性完全缓解的改善已经转化为明确的无进展生存获益。但是，要判断CELMoD是否真正改变了多发性骨髓瘤的治疗格局，还需要回答三个问题： 1.它相对于传统IMiD究竟是药理升级，还是治疗范式改变？ 2.它将在CD38单抗、CAR-T和双抗已经高度竞争的市场中占据什么位置？ 3.除了Iberdomide本身，这一机制能否持续产生有差异化、可交易、可商业化的后续资产？答案可能比“新篇章”三个字更复杂，也更值得讨论。一、机制回顾：CELMoD是什么？ CELMoD的全称是Cereblon E3 Ligase Modulator，通常译为CRBN E3连接酶调节剂。这一概念由Celgene及后来的BMS体系主要推动，用于描述经过结构优化、能够更有效调节CRBN构象和底物招募的新一代小分子。从机制传承看，CELMoD与沙利度胺、来那度胺和泊马度胺等传统IMiD属于同一个药理谱系，但两者不宜简单画等号。 CRBN是CRL4-CRBN E3泛素连接酶复合物中的底物受体。药物结合CRBN后，可改变其底物识别界面，使IKZF1、IKZF3等原本不会被CRBN充分识别的蛋白成为药物诱导的新底物。随后形成“药物-CRBN-底物”三元复合物，底物被泛素化，并由蛋白酶体降解。对于Iberdomide、Mezigdomide和Golcadomide等经典CELMoD，主要药理仍然围绕IKZF1和IKZF3降解展开。IKZF1/3降解一方面可削弱骨髓瘤细胞依赖的生存和转录程序，另一方面可影响T细胞、NK细胞及相关免疫功能，因此兼具直接抗肿瘤和免疫调节作用。 CELMoD相对传统IMiD的潜在进步，除了与CRBN结合得更紧，还能通过药物设计更有效地驱动CRBN进入适合招募新底物的构象，从而实现更快、更深或更持久的底物降解。二、Iberdomide为什么获批：MRD和PFS给予的双重信心 FDA于2026年8月13日加速批准Iberdomide，商品名ZENBEXUS，与达雷妥尤单抗-透明质酸酶及地塞米松联合，用于既往至少接受过一线治疗，且既往方案包含蛋白酶体抑制剂和免疫调节剂的成人多发性骨髓瘤患者。批准依据来自Ⅲ期EXCALIBER-RRMM研究。研究比较Iberdomide、达雷妥尤单抗和地塞米松组成的ZDd方案，与达雷妥尤单抗、硼替佐米和地塞米松组成的DVd方案。在最初用于主要疗效分析的420例患者中： ·ZDd组任何时间达到MRD阴性完全缓解的比例为41.1%； ·DVd组为20.7%； ·OR为2.75； ·p<0.0001。这里的终点是“MRD阴性完全缓解率”，即患者需要同时达到完全缓解及MRD阴性。这一结果支持了Iberdomide的加速批准。MRD分析已经在国际骨髓瘤学会年会上公布，并发表于《柳叶刀·肿瘤学》。EXCALIBER-RRMM同行评议论文显示，该研究为开放标签、随机对照的Ⅲ期研究，在31个国家的211个医院和社区研究中心开展。新数据显示，PFS已经达到阳性批准之初，一个核心疑问是：MRD阴性完全缓解的改善，能否真正转化为更长的疾病控制时间？ 2026年10月8日，百时美施贵宝公布EXCALIBER-RRMM的PFS顶线结果： ·中位PFS：42个月 vs 20个月； ·HR：0.49； ·p<0.000001； ·中位随访时间：23个月。这意味着，与DVd相比，ZDd使疾病进展或死亡风险相对降低51%。 MRD结果证明了Iberdomide可以带来更深的缓解，而PFS结果则初步证明，这种深度缓解或许能进一步转化成为临床上更持久的疾病控制。 PFS阳性顶线数据是一个实质性进展，完整数据预计在进一步学术会议中公布，OS尚未报告成熟结果，但确实值得期待。三、疗效令人鼓舞，但存在安全性隐忧（友商医学部狂喜） FDA说明书包含两项黑框警告： ·胚胎-胎儿毒性； ·严重静脉和动脉血栓栓塞。说明书还提示中性粒细胞减少、感染和第二原发恶性肿瘤等风险。由于胚胎-胎儿毒性，Iberdomide需要通过受限分销的REMS项目进行管理。从公开的MRD分析看，中性粒细胞减少和感染是尤其值得关注的治疗窗限制。后续评价不应只看缓解率和PFS，还应关注： ·3级及以上中性粒细胞减少； ·发热性中性粒细胞减少； ·严重感染和机会性感染； ·减量、暂停和永久停药比例； ·血栓事件及预防性抗凝管理； ·第二原发恶性肿瘤； ·长期治疗依从性和生活质量。这对Iberdomide前移至维持治疗尤其关键。晚期肿瘤中可以接受的风险收益比，不一定能直接适用于长期无症状或低疾病负荷患者。目前，Iberdomide已经证明了“是不是有效”，接下来要持续回答的是“能否长期、安全、便利地有效”。四、CELMoD是升级还是革命？如果只看Iberdomide的核心底物，它仍然主要围绕IKZF1/3展开，与来那度胺和泊马度胺存在清晰的药理传承。因此，它更像是对成熟机制进行深度优化，而不是从无到有建立一条完全不同的治疗路径。但“不是全新机制”并不等于“临床价值有限”。药物创新并不只属于第一次发现某个机制的分子。一个药物如果能够： ·在既往药物经治或难治人群中保留活性； ·显著加深缓解； ·延长PFS； ·改善给药便利性； ·成为更有效的联合治疗骨架； ·向早线、维持或新适应症扩展；同样可能改变临床实践。因此，Iberdomide的更准确定位，或许在于重新定义IMiD体系的能力边界。如果把视野扩大到整个CRBN分子胶平台，情况则更接近真正的机制扩展。IKZF2、GSPT1、NEK7、CK1α、WIZ和其他新底物使CRBN药物的适应症从MM和淋巴瘤逐渐延伸至实体瘤、免疫炎症性疾病及其他领域。 CELMoD是已经跨过监管门槛的第一条路径，新底物分子胶才是未来平台价值能否继续扩大的关键。五、药企布局：BMS守住MM主场，其他玩家争夺新底物和新疾病1. BMS：从单一资产获批走向治疗骨架重建 BMS是经典CELMoD领域最具系统性布局的企业。其核心管线形成了相对清晰的分工： ·Iberdomide：以RRMM为商业化起点，并向更早线次、移植后维持、冒烟型多发性骨髓瘤及其他场景扩展； ·Mezigdomide：主要面向更难治的MM人群，并通过与硼替佐米、卡非佐米、地塞米松等方案联合，探索在IMiD、PI和抗CD38治疗后的定位； ·Golcadomide：主要向DLBCL、滤泡性淋巴瘤及其他B细胞或T细胞淋巴瘤延伸。 BMS还在探索Iberdomide联合伊沙妥昔单抗治疗中高危SMM，以及Golcadomide与纳武利尤单抗、阿扎胞苷等药物的联合开发。从战略上看，BMS当然不会只想推出一款“更强的来那度胺”，而是希望用CELMoD重新建立一个可以与CD38单抗、PI、双抗和细胞治疗协同的口服治疗骨架。这也与BMS在MM领域的整体位置有关。公司既拥有IMiD积累，也拥有BCMA CAR-T等资产，但双抗布局相对有限，因此口服CELMoD能否成为不同疗法之间的联合和序贯连接点，对其MM长期竞争力具有重要意义。个人认为，BMS在联合与序贯方案方面仍有继续加强的空间。2. Monte Rosa：从肿瘤新底物转向免疫炎症 Monte Rosa的布局代表了与CELMoD的另一条路线： ·MRT-2359针对GSPT1，重点探索神经内分泌表型肿瘤等实体瘤； ·MRT-8102针对NEK7，进入炎症和免疫疾病方向； ·其分子胶平台进一步向免疫相关新底物扩展。 Monte Rosa避免与Iberdomide直接竞争MM市场，转而证明CRBN或其他E3介导的分子胶能否进入更广泛的肿瘤和慢性免疫疾病。这一扩展也获得了MNC的BD关注。内部BD资料显示，诺华在2025年9月与Monte Rosa开展合作，涉及新型降解剂在免疫介导疾病中的开发，以及两项临床前免疫产品的许可选择权；披露的首付款为1.2亿美元，潜在总交易金额为57亿美元。 MNC愿意为具有可重复发现能力的平台、明确的新底物生物学，以及能够进入免疫等核心治疗领域的项目支付平台溢价，但首付比例可以进一步窥探他们具体愿意承担多少风险。3. C4 Therapeutics：经典IKZF药理之外，验证平台兑现能力 C4 Therapeutics的Cemsidomide已进入MM及淋巴瘤临床开发。与BMS相比，该资产还需要证明： ·相对Iberdomide、Mezigdomide是否存在底物谱、治疗窗或人群差异； ·公司能否在缺少成熟商业化血液瘤体系的情况下完成全球后期开发； ·单一项目价值能否上升为可持续的平台价值。对于中小型企业来说，平台价值最终仍需由临床资产兑现，而不能只靠筛选技术、结构平台或“可降解靶点数量”支撑。4. 诺华、吉利德及其他MNC：关注的重点正在从经典IKZF转向新底物和平台诺华在蛋白降解领域采取自研与合作并行策略，既关注分子胶和PROTAC，也重视AI驱动的新靶点筛选和平台合作。既往BD交易显示，其对分子胶的BD兴趣逐渐集中于平台能力、新底物和免疫领域，而不是简单复制BMS的MM产品组合。吉利德则通过与Plexium等公司的合作布局IKZF2/Helios降解，希望通过调控Treg增强肿瘤免疫治疗。IKZF2方向目前更多被视为免疫检查点治疗的潜在增效机制，其价值取决于能否实现足够高的IKZF2选择性，并避免IKZF1/3或其他底物相关毒性。因此，目前在这一领域已经出现初步分层： ·BMS重点守住MM和淋巴瘤； ·一部分企业通过新底物进入实体瘤； ·一部分企业通过VAV1、NEK7或其他底物进入免疫炎症； ·还有企业通过平台合作获取分子胶发现、蛋白质组筛选和AI设计能力。这意味着未来的行业竞争正在向着谁能持续发现并验证有临床治疗窗的新底物的方向发展。六、国内企业布局：临床主线集中于IKZF1/3，差异化窗口仍未关闭国内可查的临床阶段的经典CELMoD项目： ·上海超阳的CY001进入Ⅱ期，覆盖MM和NHL； ·标新生物的GT919进入Ⅱ期，布局POEMS、MM和NHL，GT929进入Ⅰ/Ⅱ期； ·诺诚健华的ICP-490进入Ⅰ/Ⅱ期，覆盖MM和NHL； ·康朴生物的KPG-818，同时布局SLE、IBD、ITP、MM和NHL； ·格博生物的GLB-002进入Ⅰ期，并布局CK1α、WIZ等新底物； ·恒瑞医药HRS-3738和正大天晴TQB3820处于临床Ⅰ期。从治疗领域看，国内公司大致形成四种策略。第一类：MM及淋巴瘤的经典跟随路径上海超阳、标新生物、诺诚健华、格博生物、恒瑞医药和正大天晴的临床阶段项目，主流仍然围绕IKZF1/3降解，并集中在MM及NHL。这一策略的优点是： ·靶点和疾病生物学已经得到验证； ·临床终点及联合治疗框架相对成熟； ·可以利用中国较大的患者资源推进临床； ·监管路径较新底物项目更加清晰。但问题也同样明确。Iberdomide已经建立监管和临床先发优势，后来者不能再只证明“具有IKZF1/3降解活性”或“在早期研究中有缓解”。还需要进一步回答： ·在来那度胺或泊马度胺难治患者中是否保留活性？ ·与Iberdomide相比，是否具有更宽的血液学安全窗口？ ·是否能减少严重中性粒细胞减少和感染？ ·是否能形成更便利的给药周期？ ·是否有更适合中国临床环境的联合方案和支付优势？ ·是否能够向更明确的细分人群或适应症拓展？第二类：以差异化适应症避开直接竞争标新生物的GT919布局POEMS，是一个值得关注的差异化方向。 POEMS与浆细胞疾病相关，但临床人群、证据生成路径和商业模型与典型MM并不完全相同。如果能够建立充分的疗效、安全性和疾病机制关联，较小适应症可能成为较快形成临床识别度和监管差异化的切入口。但小适应症并不会自动带来BD价值。其价值仍取决于： ·患者识别和诊断的可行性； ·临床终点是否可接受； ·是否能够从POEMS进一步回到更大的浆细胞疾病市场； ·除了换一个适应症，项目是否显示出分子层面的差异化。第三类：从肿瘤扩展到自身免疫康朴生物的KPG-818同时覆盖肿瘤和自身免疫，包括SLE、IBD和ITP。这一策略的商业天花板可能更高，但临床要求也更高。晚期肿瘤允许一定程度的骨髓抑制和感染风险，自身免疫慢病则需要： ·更长期、更稳定的安全性； ·更低的严重感染风险； ·更可控的血液学毒性； ·生殖安全和长期用药管理； ·相对现有生物制剂或小分子药物具有清晰优势。因此，自免CELMoD的关键不只是“低剂量也有效”，而是能否在长期治疗中建立足够宽的治疗窗。第四类：通过新底物离开经典红海格博生物同时布局IKZF、CK1α和WIZ；康朴的KPG-121涉及CK1α方向；开拓药业、明德新药和美志医药等布局GSPT1或相关新底物。这类项目避开了Iberdomide的正面竞争，但也进入了更高风险的开发区： ·底物生物学是否真正决定疾病依赖； ·降解是否具有足够的肿瘤选择性； ·正常组织中的底物降解是否限制剂量； ·非预期新底物是否造成血液、神经或其他系统毒性； ·是否存在可用于患者筛选的生物标志物。新底物带来更高的潜在BD溢价，也意味着更高的失败概率。七、MNC愿意买的不是又一个CELMoD Iberdomide获批会在有限范围内提高整个CRBN分子胶领域的关注度，但不会让所有同机制资产同步升值。 BD市场通常不会为“靶点相同、适应症相同、临床阶段更晚”的项目支付相同溢价。随着首个CELMoD获得批准，潜在买方对国内项目的要求反而可能提高。1. 经典IKZF型项目的BD门槛已经改变在Iberdomide获批前，一个Ⅰ期或Ⅱ期IKZF1/3项目可以凭借“新一代CRBN调节剂”的机制新颖性获得关注。在Iberdomide获批及PFS顶线阳性后，项目需要承担更明确的比较责任。2. 适应症差异化只有在证据链完整时才有价值 POEMS、自身免疫或特定淋巴瘤亚型都可能形成差异化，但不能只把适应症名称不同视为竞争壁垒。高质量的BD证据链还需要包括明确的疾病生物学依据、与底物降解相关的患者分层方法、具有临床意义的早期疗效、剂量、暴露、底物降解和疗效之间的关系、与现有标准治疗的可比较性等等。3. 新底物项目的BD核心是“可重复的平台能力” 包括诺华与Monte Rosa合作在内的交易显示，MNC愿意为新型降解剂和免疫疾病平台支付较高的潜在里程碑，但这类交易通常或许具备以下特点： ·不只是一个孤立分子； ·具有系统性的化合物发现和底物筛选能力； ·买方可以获得多个项目、选择权或平台访问权； ·项目能够补充买方的核心治疗领域； ·交易结构多采用首付款加开发里程碑，以分散早期风险。对国内企业而言，若希望获得平台型BD，而不是单资产授权，需要证明： ·能够持续产生新底物项目； ·候选底物不是仅由计算预测，而有细胞和体内验证； ·具备结构生物学、三元复合物、蛋白质组和药物化学的完整闭环； ·能够识别并排除非预期底物； ·能够把平台命中物推进为具有口服暴露、组织分布和安全窗口的候选药物。4. 最现实的交易结构未必是一次性全球授权对于尚未形成全球临床证据的国内CELMoD项目，可以考虑多种交易结构： ·中国或大中华区保留权益、海外授权； ·按适应症拆分肿瘤和自身免疫权益； ·以联合开发及成本分担降低买方前期风险； ·给予买方后续全球许可选择权； ·平台合作加单项目期权； ·通过NewCo承接海外权益和全球开发。但交易结构无法替代资产质量。低首付、高里程碑可以降低买方风险，却不能解决项目同质化。结语：门已经推开，但竞争才刚进入更严格的阶段那么，Iberdomide是否开启了多发性骨髓瘤治疗的新篇章？从监管层面看，答案是肯定的。首个CELMoD获得批准，意味着新一代CRBN调节剂已经跨过商业化门槛。从临床证据看，答案也比批准时更积极。MRD阴性完全缓解率从约21%提高至41%，随后PFS达到42个月对20个月，HR为0.49，说明更深缓解已经转化为明确的疾病控制获益。但从治疗格局看，现在仍然只是开始。 CELMoD需要证明，它能否在双抗、CAR-T和CD38单抗共同前移的时代，取代经典药物，成为一个疗效明确、安全可管理、能够长期使用并适合联合的治疗骨架。对国内企业而言，Iberdomide的成功既是验证，也是压力。赛道的科学风险下降了，但同质化项目的商业容忍度也随之下降。接下来真正具有价值的资产，不会只是“国内另一个CELMoD”，而应当能够回答至少一个明确的问题： ·更有效吗？ ·更安全吗？ ·更适合某类患者吗？ ·能进入新的疾病领域吗？ ·能产生新的底物和平台价值吗？ ·能成为MNC现有管线中不可替代的一块拼图吗？可以说，MM领域进入了一轮证据标准更高、竞争维度更多的长期赛程。想要留在牌桌上，光靠有CELMoD项目已经不够看啦，还需要有足够好的CELMoD+可持续的药物发现与临床开发能力。参考文献 1.U.S. Food and Drug Administration. FDA grants accelerated approval to iberdomide with daratumumab and hyaluronidase-fihj and dexamethasone for multiple myeloma. 2026-08-13. 2.U.S. Food and Drug Administration. ZENBEXUS（iberdomide）Prescribing Information. NDA 221075, 2026. 3.Lonial S, Dimopoulos MA, Gavriatopoulou M, et al. Iberdomide plus daratumumab and dexamethasone versus daratumumab, bortezomib, and dexamethasone in patients with relapsed or refractory multiple myeloma（EXCALIBER-RRMM）: an open-label, randomised, controlled, phase 3 trial. The Lancet Oncology. Published online September 25, 2026. 4.Bristol Myers Squibb. First presentation of results for ZENBEXUS（iberdomide）in combination with daratumumab from the Phase 3 EXCALIBER-RRMM trial. 2026-09-25. 5.Bristol Myers Squibb. ZENBEXUS（iberdomide）in combination with daratumumab and dexamethasone demonstrates superior progression-free survival in Phase 3 EXCALIBER-RRMM. 2026-10-08. 6.Watson RA, et al. Molecular glue CELMoD compounds are regulators of cereblon conformation. Science. 2022. 7.Mining the CRBN target space redefines rules for molecular glue-induced neosubstrate recognition. Science. 2025. DOI: 10.1126/science.adt6736. 8.Unveiling the hidden interactome of CRBN molecular glues. Nature Communications. 2025. 9.An engineered cereblon optimized for high-throughput screening and molecular glue discovery. Cell Chemical Biology. 2024/2025. 10.康朴生物. 研发管线. 11.康朴生物. KPG-818在复发/难治性血液系统恶性肿瘤Ⅰ期临床研究结果. 12.诺诚健华. ICP-490机制及IND申请相关公告. 13.诺诚健华. ICP-490在中国完成首例患者给药. 本文基于截至2026年10月12日可获得的监管文件、同行评议论文、企业公告、临床试验资料及行业研究信息撰写。EXCALIBER-RRMM的PFS结果目前为BMS于2026年10月8日披露的顶线数据，完整结果、成熟OS及监管审评结论仍待后续公布。国内项目阶段和企业权益可能随临床登记、监管及公司披露发生变化。本文仅用于科学研究与行业讨论，不构成临床诊疗、投资或交易建议。

100 项与 Cemsidomide 相关的药物交易

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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2期	美国	C4 Therapeutics, Inc.	2026-02-18
多发性骨髓瘤	临床2期	法国	C4 Therapeutics, Inc.	2026-02-18
多发性骨髓瘤	临床2期	意大利	C4 Therapeutics, Inc.	2026-02-18
多发性骨髓瘤	临床2期	波兰	C4 Therapeutics, Inc.	2026-02-18
多发性骨髓瘤	临床2期	西班牙	C4 Therapeutics, Inc.	2026-02-18
多发性骨髓瘤	临床2期	英国	C4 Therapeutics, Inc.	2026-02-18

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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


NCT04756726 (CFT7455-1101, EHA2026)	临床1期	多发性骨髓瘤	73	Cemsidomide plus Dexamethasone	壓壓窪範鑰觸願築願範(鹽鹹觸繭遞醖鬱蓋齋獵) = 選顧蓋醖積製鹽鹹衊顧醖鹽積鏇觸鹽壓簾襯獵 (鹽壓簾範鏇願築衊夢願 ) 更多	积极	2026-05-12
				Cemsidomide plus Dexamethasone (75 µg QD)	鏇製鹽鹽餘顧艱繭網壓(夢鹹蓋繭遞壓壓簾簾蓋) = 範選獵窪壓齋鬱齋衊夢遞艱積襯鑰積淵觸廠遞 (積鬱積夢淵膚製壓鬱艱 )
NCT07284758 (MOMENTUM, EHA2026)	临床2期	复发性多发性骨髓瘤	100	CEMSIDOMIDE 100 μg QD 14/14 + DEXAMETHASONE	齋積鏇繭膚醖繭壓鹹選(齋顧憲齋範鹽繭築遞壓) = 淵範鹹廠衊遞糧鏇鏇廠觸構糧範齋構鏇糧壓醖 (餘顧衊遞繭憲窪襯網廠 ) 更多	积极	2026-05-12
NCT04756726 (CFT7455-1101, IMS 12025 \| IMS 22025) 人工标引	临床1/2期	复发性多发性骨髓瘤	64	Cemsidomide + Dexamethasone (Cemsidomide 75 μg)	遞鹹鹽壓網鏇選衊鏇餘(築網製鹹窪獵構艱築齋) = 積艱衊襯築觸膚憲夢襯觸襯範製鏇艱簾顧蓋鑰 (簾築鹹餘鑰壓築積廠衊 )	积极	2025-09-17
				Cemsidomide + Dexamethasone (Cemsidomide 100 μg)	遞鹹鹽壓網鏇選衊鏇餘(築網製鹹窪獵構艱築齋) = 糧鏇繭範襯淵淵鹽艱鏇觸襯範製鏇艱簾顧蓋鑰 (簾築鹹餘鑰壓築積廠衊 ) 更多
NCT04756726 (CFT7455-1101, ASH2024 \| Company_Website) 人工标引	临床1期	外周T细胞淋巴瘤 \| B细胞淋巴瘤 \| 非霍奇金淋巴瘤	23	Cemsidomide	壓選糧繭選積艱蓋願鬱(窪選觸廠艱膚鑰網廠鏇) = 選簾顧顧壓選鬱鏇膚繭淵鹽鏇築獵襯齋顧網淵 (廠憲鹹襯構夢鬱選鹹鑰 ) 更多	积极	2024-12-08
				Cemsidomide (PTCL)	願製築襯範繭網壓鑰獵(憲網襯衊憲顧膚糧網鹹) = 糧鹹願壓願膚鹹構構積膚積糧願簾鹹壓衊憲觸 (範餘鹽糧醖淵憲繭壓觸 ) 更多
NCT04756726 (CFT7455-1101, ASH2024 \| Corporate Publications) 人工标引	临床1/2期	多发性骨髓瘤末线	47	Cemsidomide + Dexamethasone	願顧範鹹醖簾廠憲窪觸(糧網製襯窪繭壓獵鏇齋) = 獵鬱積製積壓蓋鹹醖範艱願壓壓範壓壓網鏇鑰 (構鏇糧鏇憲廠夢範製齋 ) 更多	积极	2024-12-08
				Cemsidomide 50 µg MWF + Dexamethasone	願顧範鹹醖簾廠憲窪觸(糧網製襯窪繭壓獵鏇齋) = 築衊積窪製夢獵憲顧夢艱願壓壓範壓壓網鏇鑰 (構鏇糧鏇憲廠夢範製齋 ) 更多
NCT04756726 (GlobeNewswire) 人工标引	临床1/2期	多发性骨髓瘤 \| 非霍奇金淋巴瘤	-	CFT7455	鹹糧顧夢築願淵憲鹹餘(廠蓋顧鹹願艱鏇積夢齋) = CFT7455 as a monotherapy for R/R MM patients, the most common adverse events (AEs) Grade 3 or above were neutropenia (n=11), anemia (n=4) and leukopenia (n=4). CFT7455 in Combination with Dexamethasone for R/R MM Patients, consistent with the monotherapy safety signal. 積憲鹹衊簾顧築壓壓淵 (鹹鏇鹽遞醖繭膚壓夢鹹 )	积极	2023-12-12
				CFT7455+dexamethasone
NCT04756726 (AACR2022)	临床1/2期	多发性骨髓瘤	5	CFT7455	構膚選衊醖製廠鏇窪遞(壓膚糧窪壓鏇衊網艱餘) = observed in 3/5 pts without coincident fever or infection 憲選糧糧鹽餘鑰餘獵繭 (窪膚鏇構壓鬱簾餘襯觸 ) 更多	-	2022-06-15
NCT04756726 (GlobeNewswire) 人工标引	临床1/2期	多发性骨髓瘤 \| 非霍奇金淋巴瘤	5	CFT7455	鏇齋壓廠淵憲鬱餘窪憲(鏇窪夢鑰廠壓襯鏇選鬱) = 獵齋獵鹽醖獵廠膚簾構醖構壓鑰夢網獵衊壓範 (憲構襯製廠積範窪夢憲 ) 更多	积极	2022-04-08