This phase II trial compares standard consolidation with daratumumab, carfilzomib, lenalidomide, and dexamethasone to consolidation with teclistamab following standard induction therapy and autologous hematopoietic stem cell transplant for improving overall survival of patients with plasma cell leukemia. Consolidation therapy is treatment given after initial therapy to kill any cancer cells that may remain in the body. Daratumumab is in a class of medications called monoclonal antibodies. It binds to a protein called CD38, which is found on some types of immune cells and cancer cells, including myeloma cells. Daratumumab may block CD38 and help the immune system kill cancer cells. Carfilzomib inhibits protein complexes called proteasomes, which inhibits cancer cell growth and leads to cancer cell death. Lenalidomide may help kill cancer cells and prevents the growth of blood vessels that cancer cells need to survive. Dexamethasone is in a class of medications called corticosteroids. It is used to reduce inflammation and lower the body's immune response to help lessen the side effects of chemotherapy drugs. Teclistamab is a monoclonal antibody that may interfere with the ability of cancer cells to grow and spread. A monoclonal antibody is a type of protein that can bind to certain targets in the body, such as molecules that cause the body to make an immune response (antigens). Giving teclistamab as consolidation therapy after induction and autologous hematopoietic stem cell transplant may improve survival outcomes in patients with plasma cell leukemia, compared to standard consolidation with daratumumab, carfilzomib, lenalidomide, and dexamethasone.

开始日期2026-07-29

申办/合作机构

National Cancer Institute

NCT07479979

/ Recruiting临床1/2期IIT

Phase Ib/II Study of Selinexor in Combination With Carfilzomib, Subcutaneous Isatuximab Administered Via Investigational Device and Dexamethasone (SCID) for Patients With Relapsed and/or Relapsed Refractory Multiple Myeloma

The primary objective of this Phase Ib/II trial is to study the safety and tolerability of the combination of selinexor, carfilzomib, isatuximab-OBDS (on body delivery system) and dexamethasone in patients with relapsed or relapsed/refractory multiple myeloma, who have received at least one line of therapy. The phase Ib portion comprises the safety run-in with 6-12 patients, with the option to reduce the selinexor dose from 40 mg to 20 mg if the higher dose reaches the prescribed toxicity threshold. The Phase II portion of the trial will test the Recommended Phase 2 Dose (RP2D) in an expansion cohort of up to 50 patients.

开始日期2026-07-01

申办/合作机构

Hoosier Cancer Research Network

[+3]

NCT07652879

/ Recruiting临床2期IIT

A Single-center, Prospective, Open-label Investigation of the KCD (Carfilzomib/Cyclophosphamide/Dexamethasone) Regimen for the Treatment of Newly Diagnosed POEMS Syndrome

This study is a single-center, prospective, open-label clinical study to evaluate the efficacy and safety of KCD(Carfilzomib/Cyclophosphamide/Dexamethasone) regimen in subjects with newly diagnosed POEMS Syndrome.

开始日期2026-06-15

申办/合作机构

上海长征医院

100 项与卡非佐米相关的临床结果

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100 项与卡非佐米相关的转化医学

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100 项与卡非佐米相关的专利（医药）

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2,400

项与卡非佐米相关的文献（医药）

2026-12-01·JOURNAL OF MOLECULAR MEDICINE-JMM

Anti-myeloma activity of the CXCR4 antagonist WZ811

Article

作者: Suroviakova, Katarina ; Sedlak, Jan ; Jakubikova, Jana ; Valuskova, Zuzana ; Strizova, Anna ; Marinkovicova, Maria Elisabeth ; Csicsatkova, Nikoleta ; Cholujova, Danka

Abstract:

The CXCR4-CXCL12 axis is crucial for the interaction between malignant plasma cells (PC) and their microenvironment in multiple myeloma (MM). Here, we show that CXCR4 expression is upregulated in MM cell lines and PCs during both premalignant and active stages of MM, compared to normal PCs from healthy donors. The CXCR4 antagonist WZ811 reduced the viability of MM PCs and cell lines, while tumor microenvironment cells from both MM patients and healthy donors exhibited significant resistance. In vivo, WZ811 significantly reduced tumor burden and improved survival. WZ811-mediated MM cell death involved disruption of mitochondrial transmembrane potential, externalization of transmembrane phosphatidylserine, activation of caspases, increased levels of autophagic proteins, and an increase in G 0 /G 1 phase of the cell cycle. WZ811 also eliminated the MM stem cell-like side population, though slight resistance was observed with stromal cells. Additionally, WZ811 increased levels of CXCL12 and extracellular matrix molecules collagen IV and laminin in MM cells. Combining WZ811 with anti-MM agents showed synergism with doxorubicin, dexamethasone, bortezomib, lenalidomide, and pomalidomide, while antagonism was observed with carfilzomib, supporting the clinical assessment of WZ811 in MM.

Key messages:

WZ811 reduced the viability of myeloma primary cells and cell lines.WZ811 reduced tumor burden and improved survival in vivo xenograft model.WZ811 mechanisms involved apoptotic and autophagic cell death.WZ811 eliminated the MM stem cell-like side population.WZ811 synergized with DOX, DEX, BTZ, LEN, and POM.

2026-09-01·BIOCHEMICAL PHARMACOLOGY

Nanoparticle-Based delivery of proteasome inhibitors for glioblastoma Therapy: Strategies to overcome Blood-Brain barrier and therapeutic resistance

Review

作者: Ali, Meser M ; Apu, Ehsanul Hoque ; Yadab, Mahesh Kumar ; Rahman, Md Ataur

Glioblastoma (GBM), the most malignant primary brain tumor, has a poor prognosis despite surgical resection, radiation, and temozolomide-based chemotherapy. GBM's strong infiltrativeness, intratumoral heterogeneity, activation of compensatory survival mechanisms, and the tight blood-brain barrier (BBB) prevent medication delivery to tumor regions, causing therapeutic failure. Dysregulation of the ubiquitin-proteasome system (UPS), which regulates proteostasis, apoptosis, cell cycle progression, and stress responses, contributes to glioblastoma progression and therapeutic resistance. Thus, proteasome inhibitors (PIs) such bortezomib (BTZ), carfilzomib, ixazomib, and marizomib are promising treatments. However, low BBB penetration, systemic toxicity, and drug resistance mechanisms have hampered its GBM clinical usefulness. Nanoparticle-based therapeutic delivery technologies improve drug solubility, pharmacokinetics, and brain tumor targeting to address these issues. Liposomes, polymeric nanoparticles, dendrimers, inorganic nanoparticles, and exosome-derived vesicles can improve PI bioavailability and treatment efficacy in preclinical GBM models. Surface functionalization with targeted ligands, peptides, and antibodies improves BBB transport and tumor uptake. Stimuli-responsive nanocarriers and multi-modal nanoparticle systems allow regulated drug release and combinatorial delivery of chemotherapeutics, genetic materials, and radiosensitizers. To improve glioblastoma clinical outcomes with nanomedicine and proteasome inhibition, we also explore translational difficulties and prospects. This review provides the UPS's biological role in GBM, proteasome inhibitors and their limitations, and nanoparticle-enabled delivery techniques to bypass BBB barriers and treatment resistance.

2026-09-01·DRUG RESISTANCE UPDATES

NHE6-driven endosome-autophagy axis confers proteasome inhibitor resistance in multiple myeloma

Article

作者: Yang, Jing ; He, Jin ; Fan, Yihui ; Wang, Yutong ; Wang, Zhiming ; Bao, Li ; Huang, Yung-Hsing ; Liu, Jiaqi ; Chen, Liuting ; Yi, Qing ; Lin, Pei ; Cheng, Feifei

AIMS:

Proteasome inhibitors (PIs) play a central role in multiple myeloma (MM) therapy; however, a substantial proportion of patients fail to achieve durable responses, resulting in early disease progression and limited long-term clinical benefit. This paper aims to understand the molecular mechanisms that constrain PI efficacy and drive resistance and explore a novel strategy for improving therapeutic outcomes in MM.

METHODS:

By integrative analysis of multiple publicly available transcriptomic datasets from large MM patient cohorts, we identified sodium-hydrogen exchanger 6 (NHE6), encoded by SLC9A6. This gene emerged as a candidate gene associated with resistance to PI-based therapy. Functional studies were performed using patient-derived primary MM cells, PI-resistant MM cell lines, and preclinical mouse models.

RESULTS:

NHE6 is highly expressed in MM cells with further upregulation in PI-nonresponsive disease. Elevated NHE6 expression is associated with reduced progression-free and overall survival. We demonstrate that NHE6 promotes acidification in the endosomal lumen, thereby facilitating early-to-late endosomal maturation and enhancing autophagic flux in MM cells. This process in turn attenuates PI-induced tumor cell apoptotic death. Consistent with this mechanism, genetic ablation or pharmacologic inhibition of NHE6 disrupted endosomal maturation, impaired autophagy, and markedly increased sensitivity to bortezomib and carfilzomib in vitro and in vivo PI-resistant models.

CONCLUSIONS:

These findings identify an NHE6-mediated endosomal-autophagy axis as a previously unrecognized mechanism of PI resistance in MM. Targeting NHE6 represents a promising upstream strategy to restore apoptotic responses to PI-based therapies and improve therapeutic outcomes in refractory MM.

819

项与卡非佐米相关的新闻（医药）

2026-07-13

·PMLiVE

Bristol Myers Squibb’s New Drug Application for mezigdomide accepted by FDA

Bristol Myers Squibb’s New Drug Application (NDA) for mezigdomide has been accepted by the US FDA. Mezigdomide is an oral cereblon E3 ligase modulator, or CELMoD, that leads to higher multiple myeloma cell killing and immune stimulation than traditional immunomodulatory agents. The application is based on results from the phase 3 SUCCESSOR-2 trial showing oral CELMoD mezigdomide, in combination with carfilzomib and dexamethasone (MeziKd), significantly improves progression-free survival in patients with relapsed or refractory multiple myeloma (RRMM) vs standard of care. The phase 3 trial of MeziKd showed a 52% reduction in the risk of disease progression or death compared with Kd in patients with RRMM, including those at first relapse after prior treatment with an anti-CD38 monoclonal antibody and lenalidomide. Pre-clinical data suggests the drug enhances T-cell function and reinvigorates patients’ exhausted immune systems. It is also being evaluated in the ongoing phase 3 SUCCESSOR-1 trial vs. standard of care regimen in relapsed or refractory multiple myeloma. “The FDA’s acceptance of our application for mezigdomide highlights the continued momentum of our targeted protein degradation programmes, as we now have two distinct agents under review in relapsed or refractory multiple myeloma, which remains a persistent disease,” said Cristian Massacesi, executive vice president, chief medical officer and head of development, Bristol Myers Squibb. “We’re rapidly progressing the development of our CELMoD pipeline and are committed to leveraging this platform to bring the next wave of advances for patients in both hematologic malignancies and solid tumours.” Results were recently presented at the 2026 American Society of Clinical Oncology (ASCO) Annual Meeting as a late-breaking oral presentation and published in The Lancet. The US FDA has assigned a target action date of 13 May 2027 for this New Drug Application.

临床3期临床结果ASCO会议申请上市

2026-07-13

·BioSpace

U.S. Food and Drug Administration Accepts Bristol Myers Squibb’s New Drug Application for Mezigdomide in Patients with Relapsed or Refractory Multiple Myeloma

Application based on results from SUCCESSOR-2 trial showing oral CELMoD mezigdomide in combination with carfilzomib and dexamethasone significantly improved progression-free survival vs. standard of care in this patient population The U.S. FDA has assigned a target action date of May 13, 2027 PRINCETON, N.J.--(BUSINESS WIRE)-- $BMY #BMS -- Bristol Myers Squibb (NYSE: BMY) today announced that the U.S. Food and Drug Administration (FDA) has accepted a New Drug Application (NDA) for mezigdomide in combination with carfilzomib and dexamethasone (MeziKd) in patients with relapsed or refractory multiple myeloma (RRMM). Mezigdomide is an oral cereblon E3 ligase modulator, or CELMoD, for the treatment of multiple myeloma. The FDA has granted a Prescription Drug User Fee Act (PDUFA) date of May 13, 2027 for this indication. “The FDA’s acceptance of our application for mezigdomide highlights the continued momentum of our targeted protein degradation programs, as we now have two distinct agents under review in relapsed or refractory multiple myeloma, which remains a persistent disease,” said Cristian Massacesi, MD, executive vice president, chief medical officer and head of development, Bristol Myers Squibb. “We’re rapidly progressing the development of our CELMoD pipeline and are committed to leveraging this platform to bring the next wave of advances for patients in both hematologic malignancies and solid tumors.” The filing was based on positive results from the Phase 3 SUCCESSOR-2 trial (NCT05552976) showing MeziKd demonstrated a clinically meaningful and statistically significant improvement in progression-free survival (PFS) (95% CI: 18.0 months vs. 8.3 months [HR:0.48; p<0.0001]), representing a 52% reduction in the risk of disease progression or death compared with Kd in patients with relapsed or refractory multiple myeloma, including those at first relapse after prior treatment with an anti-CD38 monoclonal antibody and lenalidomide. The safety pro MeziKd was consistent with that observed in prior studies of mezigdomide, as well as with the known safety profiles of the individual agents in the regimen. Results were recently presented at the 2026 American Society of Clinical Oncology (ASCO ® ) Annual Meeting as a late-breaking oral presentation and published in The Lancet . Bristol Myers Squibb thanks the patients and investigators involved with the Phase 3 SUCCESSOR-2 study. About mezigdomide Mezigdomide is an oral CELMoD specifically optimized to modulate cereblon for maximal and rapid degradation of Ikaros and Aiolos target proteins, leading to higher multiple myeloma cell killing and immune stimulation than traditional immunomodulatory agents. Pre-clinical data suggest mezigdomide enhances T cell function and prevents and reinvigorates an exhausted immune system. Mezigdomide is also being evaluated in the ongoing Phase 3 SUCCESSOR-1 trial vs. standard of care regimen in relapsed or refractory multiple myeloma. About SUCCESSOR-2 There is a growing number of patients exposed and/or refractory to lenalidomide and anti-CD38 antibodies from first relapse. The SUCCESSOR-2 trial addressed this growing need. SUCCESSOR-2 (NCT05552976) is an inferential, seamless Phase 3, multicenter, randomized, open-label study evaluating the efficacy and safety of mezigdomide in combination with carfilzomib and dexamethasone (MeziKd) versus carfilzomib and dexamethasone (Kd) in patients with relapsed or refractory multiple myeloma (RRMM). The primary endpoint of the Phase 3 study is progression-free survival. Key secondary endpoints include overall survival, overall response rate, duration of response, time to progression, time to next treatment, minimal residual disease negativity, and health-related quality of life. Dose optimization for mezigdomide occurred in stage 1. The mezigdomide dose selected for stage 2 of the study was 1.0 mg. In total, 479 patients (288 MeziKd at 1.0 mg of mezigdomide; 191 Kd) were included in the analysis. Across both arms, median age was 68 with 25.1% of patients ≥75 years old; median number of prior therapies was 2; 92.1% of patients were triple-class-exposed, with 85.8% refractory to an anti-CD38 monoclonal antibody and 75.8% to lenalidomide; 37.2% were exposed to pomalidomide and 7.3% to anti-BCMA treatment. At data cutoff, median follow-up was 10.6 months with 52.4% (MeziKd) and 31.4% (Kd) of patients still on treatment. About Targeted Protein Degradation and CELMoD Targeted protein degradation (TPD) is a differentiated research platform at Bristol Myers Squibb built on more than two decades of scientific expertise, providing new avenues to degrade therapeutically relevant proteins that were previously considered difficult to address. BMS is the only company that has successfully developed and commercialized protein degrader agents for the treatment of multiple myeloma. These agents, known as immunomodulatory drugs (IMiDs), helped establish the current standard of care in the treatment of this disease, which remains without a cure. BMS is building on this foundation with several investigational protein degraders in clinical trials, leveraging three different modalities including CELMoD, ligand-directed degraders (LDDs), and degrader antibody conjugates (DACs). This three-pronged approach enables matching the right therapeutic modality to a molecular mechanism of action to modulate targets most effectively and ultimately provides more opportunities for potential breakthroughs that may offer meaningful new options for patients across a broad range of diseases, in and beyond hematology and oncology. Learn more about the science behind TPD at Bristol Myers Squibb here . About Bristol Myers Squibb: Transforming Patients’ Lives Through Science At Bristol Myers Squibb, our mission is to discover, develop and deliver innovative medicines that help patients prevail over serious diseases. We are pursuing bold science to define what’s possible for the future of medicine and the patients we serve. For more information, visit us at BMS.com and follow us on LinkedIn , X , YouTube , Facebook and Instagram . Cautionary Statement Regarding Forward-Looking Statements This press release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 regarding, among other things, the research, development and commercialization of pharmaceutical products. All statements that are not statements of historical facts are, or may be deemed to be, forward-looking statements. Such forward-looking statements are based on current expectations and projections about our future financial results, goals, plans and objectives and involve inherent risks, assumptions and uncertainties, including internal or external factors that could delay, divert or change any of them in the next several years, that are difficult to predict, may be beyond our control and could cause our future financial results, goals, plans and objectives to differ materially from those expressed in, or implied by, the statements. These risks, assumptions, uncertainties and other factors include, among others, that future study results may not be consistent with the results to date, that mezigdomide in combination with carfilzomib and dexamethasone (MeziKd) may not receive regulatory approval for the indication described in this release in the currently anticipated timeline or at all, any marketing approvals, if granted, may have significant limitations on their use, and, if approved, whether such combination treatment for such indication will be commercially successful. No forward-looking statement can be guaranteed. It should also be noted that acceptance of the New Drug Application does not change the standards for FDA approval. Forward-looking statements in this press release should be evaluated together with the many risks and uncertainties that affect Bristol Myers Squibb’s business and market, particularly those identified in the cautionary statement and risk factors discussion in Bristol Myers Squibb’s Annual Report on Form 10-K for the year ended December 31, 2025, as updated by our subsequent Quarterly Reports on Form 10-Q, Current Reports on Form 8-K and other filings with the Securities and Exchange Commission. The forward-looking statements included in this document are made only as of the date of this document and except as otherwise required by applicable law, Bristol Myers Squibb undertakes no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events, changed circumstances or otherwise. corporatefinancial-news Contacts Bristol Myers Squibb Media Inquiries: media@bms.com Investors: investor.relations@bms.com

临床结果临床3期ASCO会议申请上市

2026-07-12

·谈医说药

2026年07月10日药品临床试验默示许可

序号受理号药品名称申请人名称适应症注册分类 1 JXHL2600165 Olomorasib胶囊 Eli Lilly and Company Olomorasib 联合西妥昔单抗和奥沙利铂+亚叶酸钙+氟尿嘧啶（mFOLFOX6）用于KRAS G12C突变的局部晚期不可切除或转移性结直肠癌CRC患者的治疗。化学药品:1类 2 JXHL2600164 Olomorasib胶囊 Eli Lilly and Company Olomorasib 联合西妥昔单抗和奥沙利铂+亚叶酸钙+氟尿嘧啶（mFOLFOX6）用于KRAS G12C突变的局部晚期不可切除或转移性结直肠癌CRC患者的治疗。化学药品:1类 3 CXHL2600555 GW5282片格物生物技术（江苏）有限公司;迪哲（江苏）医药股份有限公司 GW5282联合比瑞替尼或其他抗肿瘤治疗用于恶性肿瘤患者，包括但不限于：1）联合比瑞替尼治疗B细胞非霍奇金淋巴瘤（B-NHL）（如弥漫大B细胞淋巴瘤（DLBCL）和滤泡性淋巴瘤（FL））；2）联合含靶向CD20免疫疗法的方案治疗B-NHL；3）联合雄激素受体通路抑制剂（ARPI）或多西他赛治疗转移性去势抵抗前列腺癌（mCRPC）。 1 4 CXHL2600553 GW5282片格物生物技术（江苏）有限公司;迪哲（江苏）医药股份有限公司 GW5282联合比瑞替尼或其他抗肿瘤治疗用于恶性肿瘤患者，包括但不限于：1）联合比瑞替尼治疗B细胞非霍奇金淋巴瘤（B-NHL）（如弥漫大B细胞淋巴瘤（DLBCL）和滤泡性淋巴瘤（FL））；2）联合含靶向CD20免疫疗法的方案治疗B-NHL；3）联合雄激素受体通路抑制剂（ARPI）或多西他赛治疗转移性去势抵抗前列腺癌（mCRPC）。 1 5 JXSL2600112 注射用替奈普酶 Boehringer Ingelheim International GmbH 治疗距最后表现正常4.5-24小时（包括发病时间已知或不明的卒中，涵盖醒后卒中）的AIS患者，这些患者需要通过脑部影像学证实存在可挽救的脑组织。 2.2 6 CXHL2600538 注射用HHK001 珠海市华海康医药科技有限责任公司子宫腺肌病 2.2;2.4 7 CXHL2600537 注射用HHK001 珠海市华海康医药科技有限责任公司子宫内膜异位症 2.2 8 JXHL2600157 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 9 JXHL2600156 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 10 JXHL2600155 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 11 JXHL2600154 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 12 JXHL2600153 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 13 JXHL2600152 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 14 JXHL2600151 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 15 JXHL2600150 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 16 CXSL2600475 DR10624 注射液浙江道尔生物科技有限公司拟用于治疗射血分数保留/射血分数轻度降低的心力衰竭成人患者。 1 17 CXSL2600474 DR10624 注射液浙江道尔生物科技有限公司拟用于治疗射血分数保留／射血分数轻度降低的心力衰竭成人患者。 1 18 CXSL2600473 DR10624 注射液浙江道尔生物科技有限公司拟用于治疗射血分数保留／射血分数轻度降低的心力衰竭成人患者。 1 19 CXSL2600472 DR10624 注射液浙江道尔生物科技有限公司拟用于治疗射血分数保留/射血分数轻度降低的心力衰竭成人患者。 1 20 JXSL2600111 注射用Belantamab mafodotin GlaxoSmithKline Trading Services Limited 本品联合泊马度胺和地塞米松（BPd）或联合硼替佐米和地塞米松（BVd）用于治疗既往接受过1-2线治疗的复发/难治多发性骨髓瘤成人患者 3.1 21 JXSL2600110 注射用Belantamab mafodotin GlaxoSmithKline Trading Services Limited 本品联合卡非佐米和地塞米松（BKd）用于治疗既往接受过1-2线治疗的复发/难治多发性骨髓瘤成人患者 2.2 22 CXSL2600478 IBI3003 信达生物制药（苏州）有限公司本品拟用于IBI3003联合抗CD38单抗治疗新诊断多发性骨髓瘤成人患者 1 23 CXHL2600536 注射用莱古比星上海亲合力生物医药科技股份有限公司联合化疗治疗围手术期骨肉瘤化学药品:1类 24 JXHL2600149 LY4337713注射液 Eli Lilly and Company 单药用于治疗FAP阳性实体瘤。 1 25 JXHL2600148 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 26 JXHL2600147 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 27 JXHL2600146 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 28 JXHL2600145 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 29 JXHL2600144 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 30 JXHL2600143 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 31 JXHL2600142 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 32 JXHL2600141 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 33 JXSL2600109 注射用BMS-986525 Bristol-Myers Squibb Company 复发/难治性小细胞肺癌 1 34 CXHL2600533 TT-00973-MS片药捷安康（南京）科技股份有限公司 TT-00973-MS片联合伏美替尼治疗EGFR敏感突变局部晚期或转移性非小细胞肺癌患者 1 35 CXSL2600470 注射用SHR-1501 苏州盛迪亚生物医药有限公司本品±SHR-2005注射液±阿得贝利单抗注射液±BCG用于膀胱癌患者。 1 36 CXSB2600080 CM512注射液康诺亚生物医药科技有限公司;成都康诺行生物医药科技有限公司特应性皮炎、慢性鼻窦炎伴鼻息肉、慢性阻塞性肺疾病（COPD）、哮喘、支气管扩张、慢性自发性荨麻疹、过敏性鼻炎、拟适用于治疗未控制的慢性鼻窦炎不伴鼻息肉（CRSsNP）患者 1 37 CXSL2600471 阿得贝利单抗注射液上海盛迪医药有限公司;苏州盛迪亚生物医药有限公司本品联合注射用SHR-1501±SHR-2005注射液±BCG用于膀胱癌患者。 2.2 38 CXSL2600469 SHR-2005注射液上海恒瑞医药有限公司本品联合注射用SHR-1501±阿得贝利单抗注射液±BCG用于膀胱癌患者。 1 39 CXHL2600529 CB549 杭州成邦医药科技有限公司精神分裂症 2.2 40 JXSL2600108 注射用Dapirolizumab Pegol单抗 UCB Biopharma SRL 本品用于治疗成人中至重度活动性系统性红斑狼疮（SLE）。 1 41 CXSL2600468 注射用HLX43 上海复宏汉霖生物技术股份有限公司;上海复宏汉霖生物医药有限公司注射用HLX43联合HLX37注射液治疗晚期/转移性实体瘤治疗用生物制品:1类 42 CXSL2600467 HLX37注射液上海复宏瑞霖生物技术有限公司;上海复宏汉霖生物医药有限公司晚期/转移性实体瘤治疗用生物制品:1类 43 CXSL2600465 注射用芦康沙妥珠单抗四川科伦博泰生物医药股份有限公司芦康沙妥珠单抗联用SKB118用于表皮生长因子受体（EGFR）敏感突变阴性和间变性淋巴瘤激酶（ALK）融合基因阴性非小细胞肺癌的治疗。 2.2 44 CXSL2600464 注射用芦康沙妥珠单抗四川科伦博泰生物医药股份有限公司芦康沙妥珠单抗联用SKB118用于表皮生长因子受体（EGFR）敏感突变阴性和间变性淋巴瘤激酶（ALK）融合基因阴性非小细胞肺癌的治疗。 2.2 45 CXSB2600079 MRG004A 乐普生物科技股份有限公司晚期或转移性实体瘤。 1 46 CXHL2600525 醋酸奥曲肽片三迭纪（上海）医药科技有限公司肢端肥大症 2.2 47 CXHL2600522 GLR2038片甘李药业股份有限公司晚期乳腺癌 1 48 CXHL2600521 GLR2038片甘李药业股份有限公司晚期乳腺癌 1 49 CXSL2600463 SKB118注射液四川科伦博泰生物医药股份有限公司 SKB118联用芦康沙妥珠单抗用于表皮生长因子受体（EGFR）敏感突变阴性和间变性淋巴瘤激酶（ALK）融合基因阴性非小细胞肺癌的治疗。 1 50 CXHB2600120 HSK46575片海思科医药集团股份有限公司用于前列腺癌的治疗；本品联合奥拉帕利或联合多西他赛和泼尼松片用于前列腺癌的治疗 1 序号受理号药品名称申请人名称适应症注册分类 51 JXHL2600134 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于肥胖或超重并至少一种体重相关合并症的成人体重管理（包括减重和体重维持）。 1 52 JXHL2600133 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于肥胖或超重并至少一种体重相关合并症的成人体重管理（包括减重和体重维持）。 1 53 JXHL2600132 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于肥胖或超重并至少一种体重相关合并症的成人体重管理（包括减重和体重维持）。 1 54 JXHL2600131 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于肥胖或超重并至少一种体重相关合并症的成人体重管理（包括减重和体重维持）。 1 55 JXHL2600122 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 56 JXHL2600121 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 57 JXHL2600120 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 58 JXHL2600119 Elecoglipron薄膜包衣片 AstraZeneca AB 在饮食控制和运动的基础上，用于成人 2 型糖尿病的治疗。 1 59 CXZL2600037 清润养目颗粒上海医药集团中药研究所有限公司养阴润目，清热祛风。用于干眼中医辨证属肝肾阴虚证，症见眼干涩、视疲劳、异物感、畏光。 1.1

免疫疗法

100 项与卡非佐米相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D08880	卡非佐米	L01XX45	DB08889

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
多发性骨髓瘤	美国	Onyx Pharmaceuticals, Inc.	2012-07-20

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
难治性多发性骨髓瘤	临床3期	美国	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	日本	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	奥地利	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	保加利亚	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	捷克	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	芬兰	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	法国	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	德国	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	希腊	Amgen, Inc.	2019-05-08
难治性多发性骨髓瘤	临床3期	立陶宛	Amgen, Inc.	2019-05-08

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临床结果

适应症

分期

评价

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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


NCT05552976 (SUCCESSOR-2, EHA2026)	临床3期	复发性多发性骨髓瘤	479	Mezigdomide 1.0 mg + Kd	衊憲積範鏇築齋選壓憲(醖蓋簾蓋齋衊膚製鑰鑰) = 鏇顧網築襯製憲鹽構鹽糧鬱築鹽膚餘蓋範獵糧 (遞廠鑰鏇鏇襯壓網膚顧 ) 更多	积极	2026-06-02
				Kd	衊憲積範鏇築齋選壓憲(醖蓋簾蓋齋衊膚製鑰鑰) = 齋糧醖鹽廠簾膚獵艱膚糧鬱築鹽膚餘蓋範獵糧 (遞廠鑰鏇鏇襯壓網膚顧 ) 更多
ASCO2026	N/A	巨球蛋白血症 MYD88 p.L265P	43	Carfilzomib	膚廠願積願築選範簾願(鏇鬱願製網製繭廠範願) = 1 patient developed atrial fibrillation and 1 developed heart failure that resolved after carfilzomib withdrawal. 3 patients developed PN attributed to carfilzomib, 6 with pretreatment PN were diagnosed with IgM-associated neuropathy, 2 had anti myelin associated glycoprotein neuropathy and 1 developed PN after switching from carfilzomib to bortezomib. 2 patients stopped treatment due to toxicity, 1 cardiac and 1 non-cardiac. 簾艱繭簾繭襯艱製窪淵 (夢蓋鹽範蓋簾網顧築鹹 )	积极	2026-05-29
NCT01665794 (ASCO2026)	临床2期	复发性多发性骨髓瘤	28	Daratumumab+Carfilzomib+Pomalidomide+Dexamethasone	鹹廠餘壓觸蓋遞簾獵襯(夢觸鑰構構鏇繭襯鬱齋) = 膚餘積壓糧鬱壓壓網窪願選壓餘顧壓糧遞醖餘 (鹹顧餘淵網網鬱夢鏇積, 22 ~ 59) 更多	积极	2026-05-29
				Daratumumab+Carfilzomib+Pomalidomide+Dexamethasone (high risk group)	願簾蓋觸衊鑰網艱膚構(膚憲壓鹽鑰鏇積壓繭醖) = 醖蓋鹹願鹹積壓窪糧選構鏇艱廠窪壓觸鏇鹽網 (獵夢憲顧選簾獵蓋蓋糧 ) 更多
NCT05552976 (SUCCESSOR-2, ASCO2026)	临床3期	复发性多发性骨髓瘤	479	Mezigdomide 1.0 mg + Carfilzomib + Dexamethasone	鏇膚遞鬱鹹繭繭鬱艱網(襯艱衊壓窪夢鏇鏇夢繭) = 鑰衊艱顧鹹觸範糧膚壓築衊繭淵艱窪衊遞選選 (構衊鬱艱鏇壓遞選壓鑰 ) 更多	积极	2026-05-29
				Carfilzomib + Dexamethasone	鏇膚遞鬱鹹繭繭鬱艱網(襯艱衊壓窪夢鏇鏇夢繭) = 廠鹽願夢繭憲簾積觸膚築衊繭淵艱窪衊遞選選 (構衊鬱艱鏇壓遞選壓鑰 ) 更多
NCT03290950 (CTgov)	临床2期	多发性骨髓瘤 \| 浆细胞白血病	69	Lenalidomide+Carfilzomib+Daratumumab+dexamethasone (Cohort 1)	觸鑰艱廠觸艱顧積獵衊 = 鹽膚壓鑰餘遞願憲窪繭選齋醖築選艱壓簾壓憲 (襯積鏇艱淵膚觸糧廠艱, 艱獵簾壓餘糧網壓鏇壓 ~ 築憲膚壓艱觸壓繭鬱衊) 更多	-	2026-05-29
				Lenalidomide+Carfilzomib+Daratumumab+dexamethasone (Cohort 2)	觸鑰艱廠觸艱顧積獵衊 = 餘構夢壓獵鬱鹽獵淵窪選齋醖築選艱壓簾壓憲 (襯積鏇艱淵膚觸糧廠艱, 選窪構繭鬱範遞醖鑰艱 ~ 糧襯顧醖積鑰壓獵艱憲) 更多
NCT05675449 (MAGNETISMM-20, EHA2026)	临床1期	难治性多发性骨髓瘤	21	Elranatamab + Carfilzomib + Dexamethasone	糧網衊鏇繭衊顧艱壓觸(願積構蓋醖網繭獵願遞) = 廠築艱膚齋壓獵衊窪獵夢艱壓夢範顧糧鑰構築 (糧膚簾衊窪積衊廠襯膚, 43.0 ~ 85.4) 更多	积极	2026-05-12
EHA2026	N/A	多发性骨髓瘤	120	Carfilzomib-based combination regimens	繭構構構廠鏇觸鹽憲齋(選衊壓製顧鹽鹽繭願獵) = 襯遞鑰顧簾遞膚鬱艱鹹製蓋齋構夢蓋願鏇鑰製 (繭淵窪廠餘積壓鹽憲繭 ) 更多	积极	2026-05-12
EHA2026	N/A	多发性骨髓瘤	15	Carfilzomib+Dexamethasone+Cyclophosphamide+Etoposide+Cisplatin	繭遞廠築鏇鹽鑰膚壓簾(獵蓋衊觸醖鑰觸選淵糧) = dyspnea (20%), AKI (6.7%), AST/ALT elevation (6.7%), and 40% infection (n = 3 bacteremia, 2 viral pneumonia, and 1 with shingles) 夢鏇襯繭艱遞壓夢艱淵 (鹹艱鬱窪鏇網簾襯遞鏇 )	积极	2026-05-12
EHA2026	N/A	巨球蛋白血症一线	54	KCD-R	積餘鹹糧構簾窪積遞廠(製構齋鏇襯構鬱齋鑰壓) = 構顧鏇積壓淵淵糧艱廠餘繭範襯窪膚積蓋顧選 (衊獵壓鏇齋遞糧簾糧蓋 ) 更多	积极	2026-05-12
				Bendamustine-Rituximab	積餘鹹糧構簾窪積遞廠(製構齋鏇襯構鬱齋鑰壓) = 鹽鹽壓觸壓鏇壓齋築鑰餘繭範襯窪膚積蓋顧選 (衊獵壓鏇齋遞糧簾糧蓋 ) 更多
NCT02659293 (ATLAS, Pubmed \| Lancet Haematol)	临床3期	多发性骨髓瘤一线	180	Carfilzomib+Lenalidomide+Dexamethasone	窪醖顧壓鹹壓鬱艱鏇積(構餘淵範顧積觸艱壓襯) = 餘壓遞齋鏇網壓膚餘構選顧獵構繭獵蓋鑰構糧 (顧淵艱構淵膚繭齋獵廠 ) 更多	积极	2026-04-01
				Lenalidomide	淵醖襯積範糧蓋遞醖夢(選淵艱願簾淵鏇衊選觸) = 積獵齋廠構壓顧窪膚積積製築選餘鹹淵簾範淵 (簾顧願簾醖選鏇顧獵獵, 27.6 ~ 48.2) 更多