An Open Label Phase II Platform Modular Study Exploring the Efficacy and Safety of the Valemetostat (EZH1/2 Inhibitor) in Patients With Selected Solid Tumors

Rational, objective and design: Some cancer-protecting genes are inactivated when the EZH2 enzyme is too active or the SWI/SNF complex is less active. The EZH1/2 enzymes and the SWI/SNFs complex play opposing roles in gene expression: we hypothesize that valemetostat, an inhibitor of the EZH1/2 enzymes, will stop/slow down the growth of cancer cells by reactivating these genes. Numerous clinical trials are currently underway worldwide to optimize the development of valemetostat tosylate and potentially offer a new targeted therapeutic option for patients suffering from various cancer pathologies.
The aim of this research is to evaluate the efficacy of valemetostat on solid tumors, which have an alteration in certain genes: SMARC (B1/A4/A2/C1/C2), ARID (1A/1B), PBRM1, BAP1 and other SWI/SNF sub-units. The research will be conducted in two phases: 1) Pre-selection of patients with the desired alterations. 2) Treatment with valemetostat, 200mg/day, for a maximum of 2 years, with examinations every 28 days.
This is a multicenter, international, phase II open-label, multicenter modular study exploring the efficacy and safety of valemetostat. Module 1 will be the SWI/SNF basket monotherapy study describe below. Such design will allow the study to evolve considering signals for further monotherapy and/or combination modules.
The Primary endpoint of the study is Overall Response Rate at 24 weeks, defined as the proportion of patients with a confirmed best overall response.
Trial population: Adult patients with histologically/cytologically confirmed progressive metastatic or recurrent solid tumor, who have selected chromatin remodeling deficiency in at least one of the following genes: SMARCB1, SMARCA4, SMARCA2, SMARCC1, SMARCC2, ARID1A, ARID1B, PBRM1, BAP1and other SWI/SNF sub-units; or molecularly (Wildtype) and phenotypically-selected Clear cell endometrial or ovarian carcinoma cancers. Patients must be using an effective method of contraception and have signed the consent form. They must not participate in another clinical study with an investigational product during the last 3 weeks, during the study treatment and not have a contraindication to the study treatment (…) Intervention: After confirmation by IHC of the loss of expression in tumors cells of SMARCB1, SMARCA4, SMARCA2, SMARCC1, SMARCC2, ARID1A, ARID1B, PBRM1, BAP1and other SWI/SNF sub-units and validation of inclusion/exclusion criteria patients will included in different cohorts (refer to investigation scheme). All patients will receive Valemetostat (200 mg per day), divided into 28-day periods called treatment cycles, for a maximum of two years. The main interventions scheduled are blood samples (to evaluate biological parameters and for translational research), electrocardiogram, echocardiography and CTscan. For patients who have consented, sequential biopsies will be performed as follow: at baseline, on treatment and at progression.
Ethical consideration: This research will make it possible to collectively evaluate the interest of EZH1/2 inhibitor in solids tumors with SWI/SNF defect. Individually, by participating in this research, patients could benefit from these treatments based on cell-based results and in the treatment of relapsed/refractory peripheral T-cell lymphomas, with an improvement in symptoms and quality of life. As with any research, the investigational drug and other procedures that take place may involve risks, some of which are already known and others not yet described. The main risks (described in the consent form) are side effects of the valemetostat. If they agree, patients will also be monitored more closely with their safety assessed through patient-reported outcomes (PRO), the evaluation of their experience through qualitative interviews & assessment of quality of care and the evaluation of their biometric physiological via a wearable device.

开始日期2026-02-28

申办/合作机构

Gustave Roussy, Cancer Campus, Grand Paris

[+1]

CTIS2024-519788-16-00

/ Not yet recruiting临床2期IIT

An open label phase II platform modular study exploring the efficacy and safety of the Valemetostat (EZH1/2 inhibitor) in patients with selected solid tumors (EZHiSWITCH)

开始日期2026-02-28

申办/合作机构

Institut Gustave Roussy EURL

NCT07244341

/ Recruiting临床1期

A Phase 1, Multicenter Trial Evaluating the Safety, Tolerability, and Efficacy of Valemetostat (DS-3201) in Combination With Darolutamide in Metastatic Castration Resistant Prostate Cancer (mCRPC)

This study will assess the safety and tolerability of valemetostat in combination with darolutamide in participants with Metastatic Castration Resistant Prostate Cancer (mCRPC).

开始日期2025-12-03

申办/合作机构

Daiichi Sankyo Co., Ltd.

[+1]

100 项与伐美妥司他相关的临床结果

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100 项与伐美妥司他相关的转化医学

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100 项与伐美妥司他相关的专利（医药）

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项与伐美妥司他相关的文献（医药）

2025-12-01·FUNCTIONAL & INTEGRATIVE GENOMICS

Polycomb repressive complex 2 (PRC2) pathway’s role in cancer cell plasticity and drug resistance

Review

作者: Tabari, Mohammad Amin Khazeei ; Khan, Haroon ; Javan, Alireza ; Larsen, Danaé S ; Rezaee, Aryan ; Heidari, Mohammad Mahdi ; Sanaye, Pantea Majma ; Hadipour, Mahboube ; Daglia, Maria ; Goleij, Pouya

Polycomb Repressive Complex 2 (PRC2) is a central regulator of gene expression via the trimethylation of histone H3 on lysine 27. This epigenetic modification plays a crucial role in maintaining cell identity and controlling differentiation, while its dysregulation is closely linked to cancer progression. PRC2 silences tumor suppressor genes, promoting cell proliferation, metastasis, epithelial-mesenchymal transition, and cancer stem cell plasticity. Enhancement of zeste homolog 2 (EZH2) overexpression or gain-of-function mutations have been observed in several cancers, including lymphoma, breast, and prostate cancers, driving aggressive tumor behavior and drug resistance. In addition to EZH2, other PRC2 components, such as embryonic ectoderm development (EED) and suppressor of zeste 12, are essential for complex stability and function. EED, in particular, enhances EZH2 activity and has emerged as a therapeutic target. Inhibitors like MAK683 and EED226 disrupt EED's ability to maintain PRC2 activity, thereby reducing H3K27me3 levels and reactivating tumor suppressor genes. Valemetostat, a dual inhibitor of both EZH2 and EED, has shown promising results in aggressive cancers like diffuse large B-cell lymphoma and small-cell lung cancer, underlining the therapeutic potential of targeting multiple PRC2 components. PRC2's role extends beyond gene repression, as it contributes to metabolic reprogramming in tumors, regulating glycolysis and lipid synthesis to fuel cancer growth. Furthermore, PRC2 is implicated in chemoresistance, particularly by modulating DNA damage response and immune evasion. Tazemetostat, a selective EZH2 inhibitor, has demonstrated significant clinical efficacy in EZH2-mutant cancers, such as non-Hodgkin lymphomas and epithelioid sarcoma. However, the compensatory function of enhancer of zeste homolog 1 (EZH1) in some cancers requires dual inhibition strategies, as seen with agents like UNC1999 and Tulmimetostat, which target both EZH1 and EZH2. Given PRC2's multifaceted role in cancer biology, its inhibition represents a promising avenue for therapeutic intervention. The continued development of PRC2 inhibitors and exploration of their use in combination with standard chemotherapy or immunotherapy has great potential for improving patient outcomes in cancers driven by PRC2 dysregulation.

2025-12-01·CANCER CHEMOTHERAPY AND PHARMACOLOGY

Pharmacokinetics, metabolism, and excretion of [14C]-valemetostat in healthy male participants, and in vitro plasma protein binding

Article

作者: Siebers, Nicholas ; Inaba, Shinichi ; Craveiro, Thuy Vu ; Ikeda, Tomoko ; Kazui, Miho ; Shimizu, Takako ; Tachibana, Masaya ; Abutarif, Malaz A

INTRODUCTION:

Valemetostat tosylate (valemetostat) is an oral, selective, dual inhibitor of enhancer of zeste homolog (EZH)2 and EZH1. This article reports findings on the mass balance and pharmacokinetics of valemetostat in a phase I study; valemetostat metabolite identification in plasma, urine, and fecal samples; and plasma-protein-binding of valemetostat in vitro.

METHODS:

Eight healthy participants received a single 200-mg oral dose of [¹⁴C]-valemetostat under fasting conditions. Blood, urine, and feces samples were collected to determine total radioactivity and/or unchanged valemetostat, and for metabolite identification. The binding of valemetostat 600-10,000 ng/mL to plasma, 4% human serum albumin (HSA), and 0.1% alpha-1-acid glycoprotein (AAG) was assessed in vitro.

RESULTS:

Mean cumulative recovery of administered radioactivity was 95.3% by 360 h post-dose, with a mean recovery of 15.6% in urine and 79.8% in feces. Valemetostat accounted for the most radioactivity in the excreta, at 10% and 64.9% of the administered dose in the urine and feces, respectively. CALZ-1809a was the most abundant metabolite, present in all biological samples, and accounted for 5.6% of total radioactivity in the feces. Valemetostat was minimally associated with red blood cells, with a blood-to-plasma total radioactivity ratio of 0.54. In vitro, valemetostat was highly plasma-bound (> 94%) at clinically relevant concentrations, with a higher affinity to AAG than to HSA.

CONCLUSION:

Valemetostat was rapidly absorbed into the systemic circulation, mainly excreted via the biliary/fecal route, primarily metabolized by CYP3A enzymes to CALZ-1809a, and highly bound to plasma proteins, with a greater affinity to AAG than HSA in vitro.

2025-12-01·JOURNAL OF CLINICAL PHARMACOLOGY

Population Pharmacokinetics of Valemetostat and Exposure–Response Analyses of Efficacy and Safety in Patients with Relapsed/Refractory Peripheral T–Cell Lymphoma

Article

作者: Inoue, Hiroyuki ; Lau, Yvonne ; Yoo, YoungJun ; Chen, Yang ; Garcia, Ramon ; Wang, Xiaoning ; Reilly, Brian ; Tachibana, Masaya

Abstract:

Valemetostat is a dual inhibitor of EZH2/1 approved in Japan for the treatment of relapsed/refractory (R/R) adult T–cell lymphoma/leukemia (ATLL) and R/R peripheral T–cell lymphoma (PTCL). It is administered orally once daily (QD) at 200 mg. Here, we present comprehensive population pharmacokinetic (PPK) and exposure–response (ER) analyses of valemetostat. The PPK model included data from six clinical trials in patients with non–Hodgkin lymphoma, including ATLL/PTCL, or healthy participants. ER efficacy analyses were based on data from one phase 2 clinical trial in patients with PTCL; ER safety analyses used data from three trials in patients with ATLL or PTCL. Valemetostat unbound average concentration up to event was used as the exposure metric. ER analyses included overall response rates for efficacy and six safety endpoints (any Grade ≥3 treatment–emergent adverse event [TEAE]; Grade ≥3 thrombocytopenia, anemia, and neutropenia; and dose reduction and interruption due to TEAEs). Valemetostat pharmacokinetics were well described by a three–compartment model, with a sequential linked zero–/first–order absorption, a saturable binding component in the central compartment, and linear elimination of unbound valemetostat from the central compartment. Alpha‐1‐acid glycoprotein was the only identified covariate significantly affecting total valemetostat exposure but had no impact on unbound exposure. The ER relationship on efficacy was not significant, and positive relationships were identified for multiple safety endpoints. Safety simulations across different doses suggested an acceptable safety profile for 200 mg QD. Overall, these analyses support the favorable benefit–risk profile of valemetostat at 200 mg QD in patients with R/R PTCL.

项与伐美妥司他相关的新闻（医药）

2025-12-16

·百度百家

表观遗传学机遇与挑战：默沙东收购与赛道新发展

【默沙东收购Imago 】最近，默沙东宣布将通过其子公司以约13.5亿美元的现金收购表观遗传单管线公司Imago BioSciences。 Imago，这家总部位于美国加州旧金山湾区的创新药公司，专注于血液和骨髓肿瘤的研究，并于2021年7月在纳斯达克上市。其核心产品Bomedemstat（IMG-7289）是一款在研口服赖氨酸特异性脱甲基酶1（LSD1）抑制剂，该靶点LSD1作为一种表观遗传调节蛋白，在骨髓干细胞的成熟以及多种血液肿瘤的治疗中发挥着关键作用。这一收购引发了人们对表观遗传学领域的广泛关注。表观遗传学在新药研发中展现出潜力，多家跨国药企通过并购与合作加速在这个领域的布局。近年来，跨国药企如BMS、GSK、诺华、阿斯利康、罗氏等在表观遗传学领域的合作并购动作频繁，以期在这一新兴领域占据更有利的地位。【表观遗传的发展与布局】表观遗传学，作为近年来新兴的科研领域，正逐渐展现出其巨大的潜力。国内聚焦表观遗传研发的赛岚医药CEO吴海平博士指出，国际上，表观遗传学正迎来一系列突破性进展。回顾2022年，两款重磅新药Ezharmia（valemetostat, 第一三共）和Rezlidhia（Olutasidenib，Rigel Therapeutics）的获批上市，更是进一步证明了该领域的蓬勃发展。 2019年，Celgene以4000万美元首付款和9.4亿美元里程碑付款，引进了Triphase的临床前资产，其靶向WDR5。 2020年，GSK以1.2亿美元首付款、股权投资及额外里程碑付款，收购了IDEAYA的临床前资产，其靶向MAT2A。同年，阿斯利康与美国RNA表观遗传学药物开发公司Accent Therapeutics达成交易，包括5500万美元首付款和11亿美元里程碑，后者更荣获当年的“FIERCE 15” Biotech Companies。 2021年6月，MorphoSys以17亿美元收购了表观遗传学赛道上的biotech公司Constellation Pharmaceuticals。而到了2022年，默沙东更是通过其子公司以约13.5亿美元的现金收购了Imago BioSciences。这一连串的并购和合作事件，无疑彰显了表观遗传学在新药转化方面的巨大潜力和突破。吴海平博士认为，表观遗传学的风口即将到来，未来几年内，该领域将迎来更多的并购和合作消息，推动整个行业的发展。【国内企业赛岚医药的角色】赛岚医药专注于表观遗传治疗，拥有领先的EpigenPLUS技术平台，致力于推动药物研发。在国内，赛岚医药是专注于表观遗传治疗领域的新药研发公司之一。他们利用小分子药物等创新的表观遗传学技术，精准靶向肿瘤及其微环境的基因表达，实现对肿瘤等重大疾病的有效治疗。成立短短两年内，赛岚医药已打造出十余条针对临床迫切需求的产品管线，并推动多个候选治疗药物进入临床试验阶段。其主力管线产品在全球范围内均处于领先地位。赛岚医药的EpigenPLUS平台汇聚了表观基因组学、生物学、药物化学、毒理药理、结构生物学及转化医学等多领域的研发技术，实现了高效、集成且综合性的评估与转化。通过这一平台，赛岚能够系统地探索表观遗传学的新机理、新靶点及新技术，从而快速发现创新靶点和候选化合物。此外，EpigenPLUS技术平台还具备外延性，能够与外部的学术界、医学界及产业界进行对接合作，有望在未来进一步发展成为行业领先的技术平台。表观遗传学在新药研发中展现出潜力，多家跨国药企通过并购与合作加速在这个领域的布局。随着表观遗传学和表观遗传组学基础研究的进展，表观遗传调控在癌症发生机制和靶向治疗中的重要性日益凸显，成为新药研发领域的热点。

并购

2025-12-14

·小盖睡不着

治疗白血病的30种药物列表

以下是30种用于治疗白血病（包括急性淋巴细胞白血病ALL、急性髓细胞白血病AML、慢性淋巴细胞白血病CLL和慢性髓细胞白血病CML等类型）的药物列表。这些药物基于FDA批准和临床指南选取，信息来源于可靠医疗来源（如NCI、Drugs.com和CancerNetwork）。每个药物包括作用机制（mechanism of action）、用法用量（dosage and administration）、副作用（side effects）和注意事项（precautions）。请注意，实际使用需在医生指导下，根据患者具体情况调整。信息可能因最新研究更新而变化。 Cytarabine (阿糖胞苷) 作用机制：抗代谢物，抑制DNA聚合酶，干扰癌细胞DNA合成。用法用量：AML诱导治疗：100 mg/m²/d 静脉持续输注7天；复发ALL：3 g/m² 静脉注射，每12小时1次，4剂。副作用：骨髓抑制、恶心呕吐、腹泻、口腔炎、肝功能异常、发热、结膜炎、中枢神经毒性（如混乱、共济失调）。注意事项：监测骨髓功能，避免高剂量时神经毒性；孕妇禁用（D类）。 Daunorubicin (柔红霉素) 作用机制：蒽环类抗生素，嵌入DNA并抑制拓扑异构酶II，导致DNA断裂。用法用量：缓解诱导：30–45 mg/m²/d 静脉注射3天，总累积剂量不超过550 mg/m²。副作用：骨髓抑制、心毒性、脱发、恶心呕吐、腹泻、口腔炎、发热、皮肤炎。注意事项：监测心脏功能，避免累积剂量过高；孕妇禁用（D类）。 Cyclophosphamide (环磷酰胺) 作用机制：烷化剂，交联DNA链，抑制癌细胞增殖。用法用量：40–50 mg/kg 静脉分次注射2–5天，随后10–15 mg/kg 每7–10天1次。副作用：骨髓抑制、出血性膀胱炎、免疫抑制、脱发、口腔炎、SIADH综合征。注意事项：大量饮水预防膀胱毒性；孕妇禁用（D类）。 Methotrexate (甲氨蝶呤) 作用机制：抗叶酸药，抑制二氢叶酸还原酶，阻断DNA合成。用法用量：低剂量：2.5–5 mg 口服每日；高剂量：1–12 g/m² 静脉注射，每1–3周1次，伴叶酸救援；鞘内：5–10 mg/m² 每3–7天。副作用：黏膜炎、胃肠溃疡、骨髓抑制、肺纤维化、肝硬化、肾损伤、腹泻、皮肤红斑。注意事项：监测肾肝功能，避免与叶酸拮抗剂合用；孕妇禁用（X类）。 Mercaptopurine (巯基嘌呤) 作用机制：嘌呤类似物，干扰DNA和RNA合成。用法用量：1.5–2.5 mg/kg/d 口服，直至响应或毒性出现；与别嘌呤醇合用减量50%-75%。副作用：骨髓抑制、恶心呕吐、食欲不振、腹泻、胆汁淤积。注意事项：监测血细胞计数，避免与别嘌呤醇合用未调整剂量；孕妇禁用（D类）。 Imatinib (伊马替尼) 作用机制：BCR-ABL酪氨酸激酶抑制剂，阻断CML信号通路。用法用量：慢性期CML：400 mg/d 口服；加速期或爆裂危象：600 mg/d。副作用：恶心呕吐、水肿、肌痛、腹泻、骨髓抑制、转氨酶升高。注意事项：监测心脏和肝功能；孕妇禁用（D类）。 Dasatinib (达沙替尼) 作用机制：多靶点酪氨酸激酶抑制剂，针对BCR-ABL突变。用法用量：Ph+ CML或ALL：成人100 mg/d 口服；儿童根据体重调整。副作用：骨髓抑制、胸痛、腹泻、头痛、皮疹。注意事项：监测QT间期，避免葡萄柚汁；孕妇禁用（D类）。 Nilotinib (尼洛替尼) 作用机制：BCR-ABL酪氨酸激酶抑制剂，抑制CML细胞增殖。用法用量：新诊断慢性期CML：300 mg 口服每日2次；耐药期：400 mg 每日2次。副作用：骨髓抑制、高胆红素血症、皮疹、瘙痒、恶心、头痛、疲劳、QT延长。注意事项：空腹服用，避免食物干扰；监测心脏功能；孕妇禁用（D类）。 Bosutinib (博舒替尼) 作用机制：BCR-ABL酪氨酸激酶抑制剂，针对Ph+ CML。用法用量：成人Ph+ CML：400 mg/d 口服。副作用：腹泻、恶心、呕吐、皮疹、肝毒性。注意事项：监测肝功能，与食物同服；孕妇禁用（D类）。 Ponatinib (波尼替尼) 作用机制：多靶点酪氨酸激酶抑制剂，针对耐药BCR-ABL突变。用法用量：CML或Ph+ ALL：45 mg/d 口服，根据响应调整。副作用：动脉血栓、高血压、心衰、骨髓抑制。注意事项：监测血管事件风险；孕妇禁用（D类）。 Blinatumomab (布林妥昔单抗) 作用机制：双特异性T细胞衔接器，激活T细胞杀伤CD19+ B细胞。用法用量：第1周期：9 μg/d 持续输注1–7天，然后28 μg/d 8–28天；后续周期：28 μg/d 1–28天。副作用：细胞因子释放综合征、神经毒性、发热、头痛、水肿、中性粒细胞减少。注意事项：预处理预防CRS；监测神经症状；孕妇禁用（D类）。 Inotuzumab ozogamicin (伊诺妥珠单抗奥佐米星) 作用机制：抗CD22抗体-药物偶联物，靶向递送毒素破坏癌细胞。用法用量：复发/难治B-ALL：0.8 mg/m² 静脉注射第1天，0.5 mg/m² 第4、8天，每21–28天1周期。副作用：肝毒性、静脉闭塞性肝病、骨髓抑制、感染。注意事项：监测肝功能，避免与双重移植；孕妇禁用（D类）。 Azacitidine (阿扎胞苷) 作用机制：去甲基化剂，促进癌细胞分化并诱导凋亡。用法用量：AML维持：300 mg/d 口服，每周期28天。副作用：骨髓抑制、恶心、便秘、疲劳、注射部位反应。注意事项：监测血细胞计数；孕妇禁用（D类）。 Decitabine (地西他滨) 作用机制：DNA甲基转移酶抑制剂，诱导基因表达变化。用法用量：AML：20 mg/m²/d 静脉注射5天，每28天1周期。副作用：骨髓抑制、恶心、疲劳、发热。注意事项：用于老年或不耐受化疗患者；孕妇禁用（D类）。 Venetoclax (维奈托克) 作用机制：BCL-2抑制剂，诱导线粒体外膜通透化，促进凋亡。用法用量：CLL：剂量递增至400 mg/d 口服；AML：400 mg/d 与低强度化疗合用。副作用：中性粒细胞减少、恶心、腹泻、疲劳、肿瘤裂解综合征。注意事项：预防TLS，监测感染；孕妇禁用（D类）。 Midostaurin (米哌司他) 作用机制：多激酶抑制剂，针对FLT3突变AML。用法用量：新诊断FLT3+ AML：50 mg 口服每日2次，与化疗合用。副作用：恶心、呕吐、头痛、鼻出血、QT延长。注意事项：监测心脏功能；孕妇禁用（D类）。 Gilteritinib (吉特替尼) 作用机制：FLT3/AXL抑制剂，针对复发/难治FLT3+ AML。用法用量：120 mg/d 口服。副作用：骨髓抑制、疲劳、水肿、发热、QT延长。注意事项：监测眼部毒性和心脏；孕妇禁用（D类）。 Gemtuzumab ozogamicin (吉妥珠单抗奥佐米星) 作用机制：抗CD33抗体-药物偶联物，靶向AML细胞。用法用量：新诊断AML：3 mg/m² 静脉注射，第1、4、7天。副作用：肝毒性、静脉闭塞性肝病、骨髓抑制、出血。注意事项：监测肝功能；孕妇禁用（D类）。 Glasdegib (格拉度尼) 作用机制：Hedgehog通路抑制剂，阻断AML干细胞增殖。用法用量：100 mg/d 口服，与低强度化疗合用。副作用：肌肉痉挛、疲劳、恶心、QT延长。注意事项：监测心脏和胚胎毒性；孕妇禁用（D类）。 Enasidenib (依那西尼) 作用机制：IDH2抑制剂，针对IDH2突变AML，促进分化。用法用量：100 mg/d 口服。副作用：分化综合征、高胆红素血症、恶心、食欲不振。注意事项：管理分化综合征；孕妇禁用（D类）。 Ivosidenib (伊沃希尼) 作用机制：IDH1抑制剂，针对IDH1突变AML。用法用量：500 mg/d 口服。副作用：分化综合征、QT延长、疲劳、恶心。注意事项：监测ECG；孕妇禁用（D类）。 Olutasidenib (奥鲁他尼) 作用机制：IDH1抑制剂，诱导AML细胞分化。用法用量：150 mg 口服每日2次。副作用：肝毒性、恶心、疲劳、关节痛。注意事项：监测肝酶；孕妇禁用（D类）。 Arsenic Trioxide (三氧化二砷) 作用机制：诱导PML-RARα降解，促进APL分化与凋亡。用法用量：APL诱导：0.15 mg/kg/d 静脉注射。副作用：QT延长、心电异常、电解质紊乱、恶心。注意事项：监测心脏和电解质；孕妇禁用（D类）。 Fludarabine (氟达拉滨) 作用机制：嘌呤类似物，抑制DNA修复酶。用法用量：25 mg/m²/d 静脉注射5天，每28天1周期。副作用：骨髓抑制、恶心、发热、肺浸润、肿瘤裂解综合征。注意事项：监测肺功能；孕妇禁用（D类）。 Cladribine (克拉屈滨) 作用机制：嘌呤类似物，干扰DNA合成。用法用量：0.09 mg/kg/d 静脉持续输注7天。副作用：骨髓抑制、发热、皮疹、感染、败血症。注意事项：用于毛细胞白血病；孕妇禁用（D类）。 Pentostatin (喷司他丁) 作用机制：腺苷脱氨酶抑制剂，积累毒性核苷酸。用法用量：4 mg/m² 静脉注射，每2周1次。副作用：肾毒性、中枢神经抑制、骨髓抑制、恶心、结膜炎。注意事项：充分水化；孕妇禁用（D类）。 Hydroxyurea (羟基脲) 作用机制：核糖核苷酸还原酶抑制剂，阻断DNA合成。用法用量：间歇：80 mg/kg 口服每3天；连续：20–30 mg/kg/d。副作用：骨髓抑制、轻度恶心、皮肤疹、放射敏感性。注意事项：监测皮肤变化；孕妇禁用（D类）。 Busulfan (丁硫氮芥) 作用机制：烷化剂，交联DNA。用法用量：2–8 mg 口服每日诱导缓解，根据WBC调整。副作用：骨髓抑制、肺纤维化、再生障碍性贫血、闭经、男性乳房发育、皮肤色素沉着。注意事项：监测肺功能；孕妇禁用（D类）。 Idarubicin (伊达比星) 作用机制：蒽环类，抑制拓扑异构酶II。用法用量：12 mg/m²/d 静脉注射3天，每3周1次。副作用：骨髓抑制、恶心、口腔炎、脱发、心毒性。注意事项：监测心脏功能；孕妇禁用（D类）。 Vincristine (长春新碱) 作用机制：微管抑制剂，阻断有丝分裂。用法用量：ALL诱导：1.4 mg/m² 静脉注射，每周1次，总剂量不超过2 mg。副作用：神经毒性（周围神经病）、便秘、脱发、颌痛。注意事项：避免鞘内注射；孕妇禁用（D类）。 31.急性髓性白血病特效药他米巴罗汀(Tamibarotene)是由日本Nippon Shinyaku公司开发的一款视黄酸受体α (RARα)激动剂类小分子抗癌药物，2005年在日本被批准用于急性早幼粒细胞白血病的治疗。近来，该药物被用作急性髓性白血病、脊髓发育不良、小儿实体瘤等多种疾病的治疗药物已经进入临床研究阶段；除了对癌症的治疗效果，现有的研究也发现该药物对阿尔兹海默症、牙周炎等其他疾病的治疗也具有一定的药物开发潜力。因此，为满足不断增长的市场和研究需求，研究人员一直在开发该药物分子的高效合成方法。 32.伐美妥司他（Ezharmia、Valemetostat）是日本第一三共制药研发的新型口服高选择性EZH1/EZH2双重抑制剂，专为T细胞淋巴瘤治疗设计，通过双重抑制活性调控基因表达以阻断肿瘤细胞增殖，2022年3月在日本获批上市，成为全球首款针对复发或难治性成人T细胞白血病/淋巴瘤及外周T细胞淋巴瘤的靶向疗法，但目前未在中国上市，也未被纳入医保体系。如有意向了解更多信息，可添加文末微信详询。药物适应症：（恶性淋巴癌、胃癌、肝癌、白血病、肾盂肿瘤、乳腺癌、尿路上皮癌、膀胱癌、卵巢癌、尿管肿瘤）用法：1急性白血病时，1日1次5~7天静脉注射15mg(效价)/m2(体表面积)作为表柔比星盐酸盐，停药3周这个1个疗程必要时重复2~3个疗程2.恶性淋巴瘤：1日1次静脉注射40~60mg(效价)/m2(体表面积)作为表柔比星盐酸盐。停药3~4周，以此为1个疗程，重复3〜4个疗程3.乳腺癌、卵巢癌、胃癌、尿路上皮癌(膀胱癌、肾盂、输尿管肿瘤)的情况：表比西作为盐酸盐，每天静脉注射60mg(效价)/m2(体表面积)1次，停药3~4周，以此为1个疗程，重复3~4个疗程4.肝癌的情况：根据在肝动脉内插入60mg(效价)/m2(体表面积)作为盐酸盐的表皮霉素，每天在肝动脉内投药1次，停药3~4周。反复进行3~4个疗程5.膀胱癌(仅限于浅表性膀胱癌)的情况：作为盐酸盐，每天1天1次1次3天向膀胱腔内注入60mg(效价)停药4天以此为1个疗程，反复注入2-4个疗程，用内拉通导管导尿，充分膀胱腔内空出后，再注入该导管从勒开始注入盐酸表柔比星溶液，在膀胱腔内握住1~2小时。给药量根据年龄、症状、副作用，适当增减6.乳腺癌(可以手术的病例)术前或术后化疗)与其他抗恶性肿瘤药物的并用疗法：1).在与环磷酰胺水合物的联合使用中，标准表霉素盐酸盐的给药量及给药方法为，1次静脉注射100mg(效价)/m2(体表面积)作为盐酸表非他命盐酸盐后，停药20天，此给药量为1个剂量的盐酸盐(盐酸盐，盐酸盐)100mg/m2(体表面积)1次。重复4~6个疗程2).在与环磷酰胺水合物、氟尿嘧啶的联合使用中，使用标准盐酸表柔比星的量和给药量。方法：1天静脉注射100mg(效价)/m2(体表面积)，停药20天，停药20天，以此为1个疗程，重复4~6个疗程。文章仅用于参考和交流学习，用药谨遵医嘱免责声明：图片转自网络，不代表本平台立场，仅供读者阅读，著作权属归原创者所有。如有侵权，请在后台留言联系我们进行删除，谢谢感谢关注带图私信客服微信👇 推荐阅读⬇️ 科普常见50款日本处方药购买渠道和使用方法推荐家庭常备日本女性妇科用药，建议码住日本15款肠癌的药物帮助你一起抗击癌细胞《阳痿吃药=终身依赖？揭秘：他达拉非这样用，或实现"功能性治愈"》「全球首款外泌体ED修复霜-Exstem：临床实证改善勃起功能+男性更年期双重困扰」【建议收藏】日本常用护肝养肝处方药：东和肝胆、武田特效肝胆、 EPL护肝药、红保肝、田辺三菱戒酒药、最强保肝、小乙肝日本天地苁蓉，专为追求高品质生活的您而设计！让你和ta恩爱如初探秘日本汉方中的“脾胃守护者”：六君子汤、归脾汤、小建中汤使用方法膀胱守护者：尿失禁药物，咪达那新（‌Imidafenacin‌、Uritos、ウリトス錠）——精准控尿，缓解膀胱过度活动困扰

临床结果

2025-12-08

·Business Wire

Daiichi Sankyo Showcases Strength of Industry-Leading ADC Portfolio with Latest Research Updates from Five Landmark Breast Cancer Trials at SABCS

Additional data from DESTINY-Breast11, DESTINY-Breast05, DESTINY-Breast09, DESTINY-Breast03 and TROPION-Breast02 reinforce practice-changing results of ENHERTU ® and DATROWAY ® across a broad spectrum of patients with breast cancer Trials-in-progress across breast cancer portfolio of Daiichi Sankyo demonstrate company’s commitment to creating new standards of care Science & Technology Day to be held following SABCS to discuss R&D and oncology business updates TOKYO & BASKING RIDGE, N.J.--(BUSINESS WIRE)--Daiichi Sankyo (TSE: 4568) will present new breast cancer clinical research across its DXd antibody drug conjugate (ADC) portfolio from more than 30 abstracts at the 2025 San Antonio Breast Cancer Symposium (#SABCS25), which include four rapid fire mini-oral sessions and other presentations from five landmark trials of ENHERTU® (trastuzumab deruxtecan) and DATROWAY® (datopotamab deruxtecan) across a broad spectrum of breast cancer. Four rapid fire mini-oral sessions will feature ENHERTU data in the curative-intent and metastatic settings of HER2 positive breast cancer, including two presentations from the DESTINY-Breast11 phase 3 trial highlighting patient reported outcomes (RF6-06) and further safety analyses (RF6-02) of ENHERTU followed by paclitaxel, trastuzumab and pertuzumab (THP) compared to dose-dense doxorubicin and cyclophosphamide followed by THP (ddAC-THP) in the neoadjuvant setting (before surgery) in patients with high-risk, locally advanced HER2 positive early-stage breast cancer. Additional efficacy and safety data (RF6-01) from the DESTINY-Breast05 phase 3 trial comparing ENHERTU to trastuzumab emtansine (T-DM1) as a post-neoadjuvant (after surgery) therapy in patients with high-risk HER2 positive early breast cancer with residual invasive disease in the breast and/or axillary lymph nodes also will be highlighted. The fourth rapid fire presentation will feature patient reported outcomes (RF6-07) from the ENHERTU plus pertuzumab arm of the DESTINY-Breast09 phase 3 trial as a first-line treatment of HER2 positive metastatic breast cancer. Interim results from DESTINY-Breast09 were recently published in The New England Journal of Medicine, marking the eighth pivotal trial of ENHERTU to be published in the prestigious journal. Additional updates from two other landmark breast cancer trials include poster presentations featuring the final analysis and five-year follow-up of efficacy and safety data (PS5-01-30) from the DESTINY-Breast03 phase 3 trial comparing ENHERTU versus T-DM1 as a second-line treatment of HER2 positive metastatic breast cancer, and further safety analysis (PS5-03-05) from the TROPION-Breast02 phase 3 trial of DATROWAY, the first trial ever to demonstrate a significant improvement in overall survival compared to chemotherapy as first-line treatment for patients with locally recurrent inoperable or metastatic triple negative breast cancer (TNBC) for whom immunotherapy is not an option. “Our latest research across these five landmark trials demonstrate how the DXd antibody drug conjugate portfolio of Daiichi Sankyo continues to potentially transform standards of care for patients with breast cancer,” said Ken Takeshita, MD, Global Head, R&D, Daiichi Sankyo. “We remain committed to following the science and collaborating with the breast cancer community to create innovative medicines that advance the treatment of breast cancer.” Additional data from the DESTINY clinical trial program to be highlighted in poster presentations at SABCS include an exploratory post-hoc subgroup analysis by hormone receptor status from the DESTINY-Breast12 phase 3b/4 trial (PS5-01-27) of ENHERTU in patients with HER2 positive metastatic breast cancer and brain metastases; the final results from the ENHERTU monotherapy and ENHERTU plus pertuzumab arms of the DESTINY-Breast07 phase 1b/2 trial (PS5-01-14) in patients with previously untreated HER2 positive metastatic breast cancer; and, initial characteristics of first enrolled patients from the DESTINY Breast Respond HER2 Low Europe non-interventional study (PS5-08-14) of ENHERTU in HER2 low metastatic breast cancer. Collaborations Supporting Innovation in Breast Cancer Research Additional data presented at SABCS include results from four externally sponsored trials across the DXd ADC pipeline of Daiichi Sankyo. Two spotlight poster presentations will report interim results from the HALLOW prospective observational trial (PD13-11) evaluating the efficacy and safety of ENHERTU in patients with HER2 low (IHC 1+ or 2+/ISH-) metastatic breast cancer with and without active brain metastases in Japan, and a post-hoc pooled efficacy analysis (PD13-10) from the TUXEDO-3 phase 2 trial of patritumab deruxtecan (HER3-DXd) in patients with HER2 positive metastatic breast cancer and active brain metastases or leptomeningeal disease previously treated with ENHERTU. Results from cohorts 1 and cohorts 2 of the TUXEDO-3 trial were recently published in The Lancet Oncology and results from cohort 3 were published in Nature Medicine. Two poster presentations will report on the intracranial and/or extracranial activity of ENHERTU and DATROWAY. A translational ctDNA analysis of intracranial and extracranial activity (PS2-08-20) of ENHERTU from the DEBBRAH phase 2 trial in patients with HER2 positive and HER2 low breast cancer with leptomeningeal disease will be highlighted, as well as results of intracranial activity (PS1-09-02) of DATROWAY from the DATO-BASE phase 2 trial in patients with HER2 negative breast cancer with leptomeningeal disease. Trials-in-Progress Across Breast Cancer Portfolio of Daiichi Sankyo Several trials-in-progress poster presentations at SABCS further highlight research underway to address a broad spectrum of unmet needs for patients with breast cancer. Additional externally sponsored trials for ENHERTU and DATROWAY include the PONTIAC phase 2 trial (PS5-07-15) evaluating ENHERTU versus CDK4/6 inhibitor-based endocrine therapy as a first-line treatment of non-luminal HR positive, HER2 low and HER2 ultralow advanced breast cancer; a phase 1b trial (PS5-09-22) evaluating ENHERTU in combination with valemetostat, an EZH1/2 inhibitor, in patients with HER2 low, HER2 ultralow and HER2 null metastatic breast cancer; and the TROPION-Breast06 phase 3b trial (PS5-07-21) of DATROWAY in patients with HR positive, HER2 IHC 0 inoperable or metastatic breast cancer refractory to endocrine therapy. Three additional trials-in-progress from the HERTHENA clinical development program of patritumab deruxtecan (HER3-DXd) also will be highlighted. These include the HERTHENA-Breast04 phase 3 trial (PS5-07-22) evaluating patritumab deruxtecan versus physician’s choice of treatment in patients with HR positive, HER2 negative unresectable locally advanced or metastatic breast cancer; the HERTHENA-Breast03 phase 2 trial (PS5-12-21) evaluating neoadjuvant patritumab deruxtecan plus pembrolizumab before or after pembrolizumab plus chemotherapy in patients with high-risk early-stage TNBC or HR low positive/HER2 negative breast cancer; and, the HERTHENA-Breast01 phase 1b/2 trial (PS5-12-23) evaluating patritumab deruxtecan in combination with HER2 targeted agents in patients with HER2 positive unresectable locally advanced or metastatic breast cancer. Science & Technology Day Daiichi Sankyo will hold its annual Science & Technology Day for investors on Monday, December 15, 2025, from 5:30 to 7:30 pm ET / Tuesday, December 16, 2025, from 7:30 – 9:30 am JST. Executives from Daiichi Sankyo will provide an update on R&D, business and manufacturing developments across the portfolio. Daiichi Sankyo Presentation Highlights at SABCS Presentation Title Author Abstract Presentation (CST) ENHERTU (trastuzumab deruxtecan; T-DXd) Patient-reported outcomes in DESTINY-Breast11: neoadjuvant treatment with trastuzumab deruxtecan (T-DXd) alone or followed by paclitaxel + trastuzumab + pertuzumab (THP) vs dose-dense doxorubicin + cyclophosphamide followed by THP (ddAC-THP) in high-risk, HER2+ early-stage breast cancer S. Modi RF6-06 Rapid Fire 6 Mini-Oral Session Wednesday, December 10 1:00 – 2:00 pm DESTINY-Breast11 safety: neoadjuvant trastuzumab deruxtecan (T-DXd) alone or followed by paclitaxel + trastuzumab + pertuzumab (THP) vs dose-dense doxorubicin + cyclophosphamide followed by THP (ddAC-THP) in high-risk, HER2+ early-stage breast cancer G. Curigliano RF6-02 Rapid Fire 6 Mini-Oral Session Wednesday, December 10 1:00 – 2:00 pm Additional efficacy and safety from the DESTINY-Breast05 study of trastuzumab deruxtecan (T-DXd) vs trastuzumab emtansine (T‑DM1) in patients with high-risk human epidermal growth factor receptor 2–positive (HER2+) primary early breast cancer with residual invasive disease after neoadjuvant therapy S. Loibl RF6-01 Rapid Fire 6 Mini-Oral Session Wednesday, December 10 1:00 – 2:00 pm Trastuzumab deruxtecan (T-DXd) + pertuzumab vs taxane + trastuzumab + pertuzumab (THP) for first-line treatment of patients with HER2 positive (HER2+) advanced/metastatic breast cancer: patient-reported outcomes from the DESTINY-Breast09 study M. Rimawi RF6-07 Rapid Fire 6 Mini-Oral Session Wednesday, December 10 1:00 – 2:00 pm Trastuzumab deruxtecan (T-DXd) versus trastuzumab emtansine (T-DM1) in patients with human epidermal growth factor receptor 2-positive (HER2+) metastatic breast cancer: final analysis from DESTINY-Breast03 S. Im PS5-01-30 Poster Session 5 Friday, December 12 12:30 – 2:00 pm Trastuzumab deruxtecan (T-DXd) monotherapy and T-DXd + pertuzumab in patients with previously untreated HER2+ unresectable/metastatic breast cancer: final results from DESTINY-Breast07 F. Andre PS5-01-14 Poster Session 5 Friday, December 12 12:30 – 2:00 pm Outcomes by hormone receptor status in patients with HER2+ advanced/metastatic breast cancer with brain metastases treated with trastuzumab deruxtecan (T-DXd): a post-hoc subgroup analysis of DESTINY-Breast12 H. Wildiers PS5-01-27 Poster Session 5 Friday, December 12 12:30 – 2:00 pm DESTINY-Breast Respond HER2 low Europe: description of first enrolled patients in the non-interventional study of T-DXd in HER2 low metastatic breast cancer V. Guarneri PS5-08-14 Poster Session 5 Friday, December 12 12:30 – 2:00 pm Interim analysis results for the effectiveness and safety of trastuzumab deruxtecan in patients with HER2 low breast cancer and brain metastases: the HALLOW study N. Niikura PD13-11 Poster Spotlight 13 Friday, December 12 7:00 – 8:30 am Translational analysis of cerebrospinal fluid and plasma circulating tumor DNA from breast cancer patients with leptomeningeal disease treated with trastuzumab deruxtecan (T-DXd) in the DEBBRAH trial A. Fitzpatrick PS2-08-20 Poster Session 2 Wednesday, December 10 5:00 – 6:30 pm Trials-in-Progress A randomized phase 2 study to evaluate the efficacy and safety of trastuzumab deruxtecan (T-DXd) versus CDK4/6 inhibitor-based endocrine therapy as first-line therapy of hormone receptor-positive and HER2 low/ultralow advanced breast cancer patients classified as non-luminal subtype according to gene expression profiling: the PONTIAC study J. Cortes PS5-07-15 Poster Session 5 Friday, December 12 12:30 – 2:00 pm Phase 1b study of EZH1/2 inhibitor valemetostat in combination with trastuzumab deruxtecan in subjects with HER2 low/ultralow/null metastatic breast cancer S. Damodaran PS5-09-22 Poster Session 5 Friday, December 12 12:30 – 2:00 pm DATROWAY (datopotamab deruxtecan; Dato-DXd) First-line datopotamab deruxtecan (Dato-DXd) vs chemotherapy in patients with locally recurrent inoperable or metastatic triple negative breast cancer (TNBC) for whom immunotherapy was not an option: additional safety analyses from the TROPION-Breast02 study T. Traina PS5-03-05 Poster Session 5 Friday, December 12 12:30 – 2:00 pm Intracranial activity of datopotamab deruxtecan (Dato-DXd) for patients with HER2 negative breast cancer and leptomeningeal disease: results from cohort C of the DATO-Base phase 2 trial P. Tarantino PS1-09-02 Poster Session 1 Wednesday, December 10 12:30 – 2:00 pm Trials-in-Progress TROPION-Breast06: multicenter, multinational, open-label, single-arm, phase 3b study of datopotamab deruxtecan (Dato-DXd) in patients with locally advanced inoperable or metastatic HR+/HER2 IHC 0 breast cancer refractory to endocrine therapy K. Jhaveri PS5-07-21 Poster Session 5 Friday, December 12 12:30 – 2:30 pm Patritumab Deruxtecan (HER3-DXd) Outcome of patritumab deruxtecan (HER3-DXd) in patients with HER2 positive metastatic breast cancer and CNS involvement previously treated with T-DXd: a subanalysis of TUXEDO-3 R. Bartsch PD13-10 Poster Spotlight 13 Friday, December 12 7:00 – 8:30 am Trials-in-Progress HERTHENA-Breast04: a phase 3, randomized, open-label study evaluating the efficacy and safety of patritumab deruxtecan (HER3-DXd) versus treatment of physician’s choice in hormone receptor positive (HR+)/human epidermal growth factor receptor 2 negative (HER2-) unresectable locally advanced or metastatic breast cancer B. Pistilli PS5-07-22 Poster Session 5 Friday, December 12 12:30 – 2:00 pm HERTHENA-Breast03: a phase 2, randomized, open-label study evaluating neoadjuvant patritumab deruxtecan (HER3-DXd) + pembrolizumab before or after pembrolizumab + chemotherapy for early-stage TNBC or HR-low+/HER2− breast cancer J. O’Shaughnessy PS5-12-21 Poster Session 5 Friday, December 12 12:30 – 2:00 pm HERTHENA-Breast01: a phase 1b/2, multicenter, open-label, dose-finding study to evaluate the safety and antitumor activity of patritumab deruxtecan (HER3-DXd) in HER2+ unresectable locally advanced or metastatic breast cancer S. Tolaney PS5-12-23 Poster Session 5 Friday, December 12 12:30 – 2:00 pm About the ADC Portfolio of Daiichi Sankyo The Daiichi Sankyo ADC portfolio consists of eight ADCs in clinical development crafted from ADC technology discovered in-house by Daiichi Sankyo. The DXd ADC Technology platform of Daiichi Sankyo consists of six ADCs in clinical development where each ADC is comprised of a monoclonal antibody attached to a number of topoisomerase I inhibitor payloads (an exatecan derivative, DXd) via tetrapeptide-based cleavable linkers. The DXd ADCs include ENHERTU® and DATROWAY®, which are being jointly developed and commercialized globally with AstraZeneca, and ifinatamab deruxtecan (I-DXd), raludotatug deruxtecan (R-DXd) and patritumab deruxtecan (HER3-DXd), which are being jointly developed and commercialized globally with Merck & Co., Inc, Rahway, NJ, USA. DS-3939 is being developed by Daiichi Sankyo. Additional ADCs being developed by Daiichi Sankyo include DS-9606, which consists of a monoclonal antibody attached to a modified pyrrolobenzodiazepine (PBD) payload and DS3610, which consists of an antibody attached to a novel immunomodulatory payload that acts as an agonist of STING. Ifinatamab deruxtecan, raludotatug deruxtecan, patritumab deruxtecan, DS-3939, DS-9606 and DS3610 are investigational medicines that have not been approved for any indication in any country. Safety and efficacy have not been established. About Daiichi Sankyo Daiichi Sankyo is an innovative global healthcare company contributing to the sustainable development of society that discovers, develops and delivers new standards of care to enrich the quality of life around the world. With more than 120 years of experience, Daiichi Sankyo leverages its world-class science and technology to create new modalities and innovative medicines for people with cancer, cardiovascular and other diseases with high unmet medical needs. For more information, please visit www.daiichisankyo.com.

临床2期临床3期临床结果抗体药物偶联物临床1期

100 项与伐美妥司他相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11551 D16662	-	-	-

研发状态

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适应症	国家/地区	公司	日期
成人T细胞白血病/淋巴瘤	日本	Daiichi Sankyo Co., Ltd.	2022-09-26
外周T细胞淋巴瘤	日本	Daiichi Sankyo Co., Ltd.	2022-09-26

未上市

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适应症	最高研发状态	国家/地区	公司	日期
子宫内膜透明细胞癌	临床2期	法国	Daiichi Sankyo Co., Ltd.	2026-02-28
恶性实体肿瘤	临床2期	法国	Daiichi Sankyo Co., Ltd.	2026-02-28
卵巢癌	临床2期	法国	Daiichi Sankyo Co., Ltd.	2026-02-28
转移性非小细胞肺癌	临床2期	美国	Daiichi Sankyo Co., Ltd.	2024-10-30
转移性非小细胞肺癌	临床2期	中国	Daiichi Sankyo Co., Ltd.	2024-10-30
转移性非小细胞肺癌	临床2期	日本	Daiichi Sankyo Co., Ltd.	2024-10-30
转移性非小细胞肺癌	临床2期	阿根廷	Daiichi Sankyo Co., Ltd.	2024-10-30
转移性非小细胞肺癌	临床2期	巴西	Daiichi Sankyo Co., Ltd.	2024-10-30
转移性非小细胞肺癌	临床2期	韩国	Daiichi Sankyo Co., Ltd.	2024-10-30
鳞状非小细胞肺癌	临床2期	美国	Daiichi Sankyo Co., Ltd.	2024-10-30

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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


NCT04842877 (VALYM, ASH2025)	临床2期	难治性B细胞淋巴瘤 EZH2 \| EZH1	120	Valemetostat 200 mg QD	鬱鹽繭膚蓋網糧簾餘蓋(範醖艱積餘窪艱築選糧) = 21% 窪願壓壓顧鑰觸醖衊遞 (鹽餘糧餘鹽繭醖艱憲廠 )	积极	2025-12-06
NCT06244485 (ESMO2025)	临床1期	非鳞状非小细胞肺癌	22	Datopotamab deruxtecan 6.0 mg/kg + Datopotamab deruxtecan 6.0 mg/kg	鹹糧鏇繭網廠範願構壓(壓膚鏇餘鑰糧夢艱積鹹) = no Vale MTD has been identified up to 200 mg 鑰構憲憲糧艱鏇觸憲鹽 (夢築壓襯醖鏇鹹繭選鹽 )	积极	2025-10-17
NCT04388852 (ESMO2025)	临床1期	泌尿生殖系统肿瘤	65	DS3201 (200 mg/day) plus ipilimumab (metastatic clear cell renal cell carcinoma)	製網遞衊淵淵醖簾顧窪(蓋構襯製願齋鏇襯顧鏇) = 獵繭顧鏇齋鏇糧繭繭獵鬱鑰壓餘築憲廠選鬱衊 (醖遞鬱齋獵淵窪鹽範窪 ) 更多	积极	2025-10-17
				DS3201 (200 mg/day) plus ipilimumab (aggressive variant prostate cancer)	夢襯壓餘築窪憲鏇艱壓(壓願淵夢衊鹽選蓋範鏇) = 範鑰遞蓋淵壓憲糧積構餘願艱糧淵願選齋積鑰 (糧選艱衊願醖糧壓築壓 ) 更多
JPRN-jRCT2031190268 (NCCH1904, ASCO2025)	临床1期	实体瘤 INI1-negative	30	Valemetostat tosylate (DS-3201b) 150 mg/1.7 m^2	鑰衊憲積鏇醖鹹繭壓鬱(淵鏇蓋鬱壓醖網繭簾顧) = One patient with NB developed acute lymphocytic leukemia as a secondary malignancy 鏇願衊襯構遞鹹鬱壓觸 (憲獵壓鬱選醖艱餘鏇網 ) 更多	积极	2025-05-30
				Valemetostat tosylate (DS-3201b) 200 mg/1.7 m^2
Phase II clinical trial (AACR2025)	临床2期	成人T细胞白血病/淋巴瘤 HTLV-1	-	Valemetostat (VAL)	範獵壓簾衊艱簾憲壓鏇(廠糧齋鹹鏇鬱廠憲選蓋) = 窪齋範鏇艱簾鹹鬱獵構襯鹹壓憲獵鏇願觸窪範 (獵繭製鏇鏇願願壓憲選 )	-	2025-04-29
NCT04703192 (VALENTINE-PTCL01, Pubmed \| Lancet Oncol)	临床2期	外周T细胞淋巴瘤	-	Valemetostat tosylate (valemetostat) 200 mg per day	鏇餘鬱鑰窪觸鏇襯鹹構(襯製範觸齋鬱顧網遞築) = 襯衊鹽網廠衊餘獵範衊製鏇顧顧齋築顧憲顧製 (蓋遞繭醖簾簾鑰蓋壓鏇, 35 ~ 53)	积极	2024-12-01
NCT04703192 (VALENTINE-PTCL01, CTgov)	临床2期	成人T细胞白血病/淋巴瘤 \| 外周T细胞淋巴瘤 \| 成人T细胞淋巴瘤/难治性白血病	155	Valemetostat Tosylate	鹽顧獵選衊鑰醖鹽選醖 = 鹹淵襯鹹艱襯壓淵廠選願鬱齋壓艱築糧繭鹽鬱 (獵繭鹽鏇築獵構製鏇壓, 範餘廠憲願積衊壓艱積 ~ 顧鏇鹽鑰積簾願淵襯醖) 更多	-	2024-07-22
NCT04703192 (VALENTINE-PTCL01, EHA2024) 人工标引	临床2期	外周T细胞淋巴瘤	119	Valemetostat tosylate 200 mg/day (pts with 1 prior LOT)	窪淵夢鏇願壓廠鏇鹹繭(憲窪觸艱鬱觸糧築鏇鬱) = 選鹽艱鹹鬱鏇願齋鬱齋糧蓋糧願鹹顧窪蓋齋窪 (鏇壓鹹鹹遞繭憲廠鏇艱, 35.5 ~ 69.6)	积极	2024-05-14
				Valemetostat tosylate 200 mg/day (pts with 2 prior LOT)	窪淵夢鏇願壓廠鏇鹹繭(憲窪觸艱鬱觸糧築鏇鬱) = 夢獵糧鹹醖膚構齋憲簾糧蓋糧願鹹顧窪蓋齋窪 (鏇壓鹹鹹遞繭憲廠鏇艱, 28.3 ~ 65.7)
NCT02732275 (DS3201-A-J101, EHA2024) 人工标引	临床1期	非霍奇金淋巴瘤 EZH2 mutation	90	valemetostat tosylate 150-300 mg/d	鑰積網獵齋糧窪顧鏇齋(顧鏇糧淵膚鬱顧繭淵構) = 鑰鬱鹹壓餘積衊獵製選鏇鑰鏇餘糧夢廠願窪獵 (糧築淵膚衊積顧廠蓋簾 ) 更多	积极	2024-05-14
				valemetostat (ATLL)	鏇夢憲鏇齋齋糧糧膚糧(鹽壓網簾鬱糧簾觸鹹廠) = 獵製鏇膚獵窪窪醖繭鑰夢膚壓夢範觸糧夢鹹淵 (積簾鏇願製淵鬱壓蓋鏇, 1.4 ~ 38.7) 更多
NCT03110354 (CTgov)	临床1期	急性髓性白血病 \| 急性淋巴细胞白血病	28	DS-3201b (DS-3201b 150 mg)	構簾簾築衊夢鑰範憲簾 = 鏇顧鏇觸夢壓獵艱壓製衊襯醖範遞願齋糧衊製 (鑰壓獵壓淵網壓觸膚鬱, 夢鹽範糧夢願構蓋鏇獵 ~ 願淵觸夢艱鬱廠範艱獵) 更多	-	2024-01-30
				DS-3201b (DS-3201b 250 mg)	構簾簾築衊夢鑰範憲簾 = 簾艱艱顧遞範鹽製鏇壓衊襯醖範遞願齋糧衊製 (鑰壓獵壓淵網壓觸膚鬱, 窪衊觸醖窪願鑰壓獵憲 ~ 糧齋廠繭壓齋衊鹽憲膚) 更多