A Phase II, Open-Label Randomized Study of Intravenous Tambiciclib in Combination with the Standard of care Venetoclax and Azacitidine in Patients with Newly Diagnosed AML Who Failed to Achieve at Least MLFS After the First Two Cycles of Treatment with Venetoclax and Azacitidine Alone

开始日期2026-06-01

申办/合作机构

IIS La Fe

NCT06375733

/ Recruiting临床1/2期

A Phase Ib/II, Multicenter, Open-label, Single-arm Study to Assess the Safety and Efficacy of GFH009 in Combination With Zanubrutinib in Patients With Relapsed or Refractory Diffuse Large B-cell Lymphoma (DLBCL)

This is a multicentre, open-label phase Ib/II study. The purpose of the study is to assess the safety and efficacy of GFH009 in combination with Zanubrutinib in patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL)

开始日期2024-03-20

申办/合作机构

劲方医药科技（上海）股份有限公司

NCT05934513

/ Recruiting临床1/2期

A Phase Ib/II, Multicentre, Open-label Study to Assess the Efficacy, Safety/ Tolerability and Pharmacokinetic of GFH009 Monotherapy in Patients with Relapsed or Refractory Peripheral T-cell Lymphoma (PTCL)

This is a multicentre, open-label phase Ib/II study. The purpose of the study is to assess the efficacy, safety/ tolerability and pharmacokinetic of GFH009 monotherapy in patients with relapsed or refractory peripheral T-cell lymphoma

开始日期2023-09-06

申办/合作机构

劲方医药科技（上海）股份有限公司

100 项与 Tambiciclib 相关的临床结果

登录后查看更多信息

100 项与 Tambiciclib 相关的转化医学

登录后查看更多信息

100 项与 Tambiciclib 相关的专利（医药）

登录后查看更多信息

项与 Tambiciclib 相关的文献（医药）

2024-11-25·XENOBIOTICA

Preclinical metabolism and disposition of [ ¹⁴ C]GFH009, a novel selective CDK9 inhibitor

Article

作者: Zhao, Jin-Zhu ; Lan, Jiong ; Wang, Li ; Lu, Qiang ; Zhou, Fu-Sheng ; Ren, Hong-Can

GFH009 is a potent and highly selective cyclin-dependent kinase 9 (CDK9) inhibitor currently under phase II clinical trials. In this study, we investigated the metabolism and disposition of GFH009 in Sprague-Dawley (SD) rats, as well as in vitro metabolism of CD-1 mouse, SD rat, beagle dog, cynomolgus monkey, and human.A radiolabelled study indicated that [¹⁴C]GFH009 was quickly and widely distributed throughout the body, but presented low levels in brain, testis, and epididymis after a single intravenous dose of 6 mg (100 µCi)/kg to SD rats.GFH009 undergoes systemic metabolic changes, primarily through O-demethylation, oxidation to carboxylic acid and N-dealkylation, cleavage off the methoxyisopropyl moiety being a minor pathway. These metabolic pathways were found to be mainly consistent both in vitro and in vivo.In SD rats, GFH009 was rapidly and completely eliminated, with faeces serving as the major excretion pathway and urine serving as the minor one. Besides, the major clearance pathway for GFH009 was excretion and the minor one was metabolism.GFH009 exhibits favourable drug metabolism and pharmacokinetics (DMPK) properties, which provides valuable insights into the disposition of GFH009 and can be used to guide future clinical studies.

2024-02-01·Biomedical chromatography : BMC

Development and validation of a sensitive UPLC–MS/MS analytical method for GFH009 in rat plasma and its application to toxicokinetics studies

Article

作者: Zhou, Fu‐Sheng ; Ren, Hong‐Can ; Lan, Jiong ; Zhao, Jin‐Zhu ; Lu, Qiang ; Liu, Qiang

Abstract:

GFH009 is a potent, highly selective, small molecule that targets and inhibits the activity of the CDK9/cyclin T1 regulatory complex of P‐TEFb. This study aimed to develop and validate a highly selective and sensitive ultrahigh‐performance liquid chromatography–tandem mass spectrometry (UHPLC–MS/MS) method for precise quantification of GFH009 in rat plasma. This method was subsequently employed for conducting toxicokinetic studies of GFH009 in rats. Plasma was prepared using a simple protein precipitation method by acetonitrile. Chromatographic separation of the analytes was achieved on a BEH C18 analytical column with a rapid 3.0 min run time and a flow rate of 0.5 ml/min. The calibration curves for plasma samples exhibited excellent linearity over a wide concentration range of 1.0–1,000 ng/ml for GFH009. Intra‐ and inter‐day accuracies were within 92.7–105.7%, and precisions were no more than 6.7%. Furthermore, the analyte demonstrated stability under four different storage conditions, with variations of <15.0%. This study pioneers a methodological innovation by introducing a highly reliable, specific and sensitive analytical method for GFH009 in rat plasma. The successful application of this method in toxicokinetic studies further underscores its significance, offering valuable insights for the methodology of clinical pharmacokinetic research.

2023-12-20·Oncotarget

The pharmacodynamic and mechanistic foundation for the antineoplastic effects of GFH009, a potent and highly selective CDK9 inhibitor for the treatment of hematologic malignancies

Article

作者: Zhou, Fusheng ; Ge, Mei ; Ren, Jinmin ; Tang, Lili ; Lan, Jiong ; Xie, Fubo ; Cicic, Dragan ; Lu, Qiang ; Le, Siyuan

To evade cell cycle controls, malignant cells rely upon rapid expression of select proteins to mitigate proapoptotic signals resulting from damage caused by both cancer treatments and unchecked over-proliferation. Cyclin-dependent kinase 9 (CDK9)-dependent signaling induces transcription of downstream oncogenes promoting tumor growth, especially in hyperproliferative 'oncogene-addicted' cancers, such as human hematological malignancies (HHMs). GFH009, a potent, highly selective CDK9 small molecule inhibitor, demonstrated antiproliferative activity in assorted HHM-derived cell lines, inducing apoptosis at IC50 values below 0.2 μM in 7/10 lines tested. GFH009 inhibited tumor growth at all doses compared to controls and induced apoptosis in a dose-dependent manner. Twice-weekly injections of GFH009 maleate at 10 mg/kg significantly prolonged the survival of MV-4-11 xenograft-bearing rodents, while their body weight remained stable. There was marked reduction of MCL-1 and c-MYC protein expression post-drug exposure both in vitro and in vivo. Through rapid 'on-off' CDK9 inhibition, GFH009 exerts a proapoptotic effect on HHM preclinical models triggered by dynamic deprivation of crucial cell survival signals. Our results mechanistically establish CDK9 as a targetable vulnerability in assorted HHMs and, along with the previously shown superior class kinome selectivity of GFH009 vs other CDK9 inhibitors, strongly support the rationale for currently ongoing clinical studies with this agent in acute myeloid leukemia and other HHMs.

183

项与 Tambiciclib 相关的新闻（医药）

2026-05-14

·BioSpace

SELLAS Life Sciences to Participate in Upcoming Investor Conferences

NEW YORK, May 14, 2026 (GLOBE NEWSWIRE) -- SELLAS Life Sciences Group, Inc. (NASDAQ: SLS) (“SELLAS” or the “Company”), a late-stage clinical biopharmaceutical company focused on the development of novel therapies for a broad range of cancer indications, today announced that Angelos Stergiou, MD, ScD h.c., President and Chief Executive Officer of SELLAS, will participate in the following upcoming investor conferences: 2026 Stifel Virtual Targeted Oncology Forum Format: Corporate Presentation and Fireside Chat Date and Time: Tuesday, May 19, 2026, at 2:00 PM ET Location: New York, NY Webcast Link: Click here A.G.P.'s Annual Virtual Healthcare Conference Format: Fireside Chat Date: Wednesday, May 20, 2026, at 11:00 AM ET Location: Virtual Webcast Link: Click here TD Cowen’s 7th Annual Oncology Innovation Summit: Insights for ASCO & EHA Format: Fireside Chat Date: Wednesday, May 27, 2026, at 9:00 AM ET Location: Virtual About SELLAS Life Sciences Group, Inc. SELLAS is a late-stage clinical biopharmaceutical company focused on the development of novel therapeutics for a broad range of cancer indications. SELLAS’ lead product candidate, GPS, is licensed from Memorial Sloan Kettering Cancer Center and targets the WT1 protein, which is present in an array of tumor types. GPS has the potential as a monotherapy and combination with other therapies to address a broad spectrum of hematologic malignancies and solid tumor indications. The Company is also developing SLS009 (tambiciclib) - potentially the first and best-in-class differentiated small molecule CDK9 inhibitor with reduced toxicity and increased potency compared to other CDK9 inhibitors. Data suggests that SLS009 demonstrated a high response rate in AML patients with unfavorable prognostic factors including ASXL1 mutation, commonly associated with poor prognosis in various myeloid diseases. For more information on SELLAS, please visit . Forward-Looking Statements This press release contains forward-looking statements. All statements other than statements of historical facts are “forward-looking statements,” including those relating to future events. In some cases, forward-looking statements can be identified by terminology such as “plan,” “expect,” “anticipate,” “may,” “might,” “will,” “should,” “project,” “believe,” “estimate,” “predict,” “potential,” “intend,” or “continue” and other words or terms of similar meaning. These statements include, without limitation, statements related to the GPS clinical development program, including the REGAL study and the timing of future milestones related thereto. These forward-looking statements are based on current plans, objectives, estimates, expectations, and intentions, and inherently involve significant risks and uncertainties. Actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties, which include, without limitation, risks and uncertainties with oncology product development and clinical success thereof, the uncertainty of regulatory approval, and other risks and uncertainties affecting SELLAS and its development programs as set forth under the caption “Risk Factors” in SELLAS’ Annual Report on Form 10-K filed on March 19, 2026 and in its other SEC filings. Other risks and uncertainties of which SELLAS is not currently aware may also affect SELLAS’ forward-looking statements and may cause actual results and the timing of events to differ materially from those anticipated. The forward-looking statements herein are made only as of the date hereof. SELLAS undertakes no obligation to update or supplement any forward-looking statements to reflect actual results, new information, future events, changes in its expectations, or other circumstances that exist after the date as of which the forward-looking statements were made. Investor Contact John Fraunces Managing Director LifeSci Advisors, LLC jfraunces@lifesciadvisors.com

2026-05-12

·ir.sellaslifesciences.com

SELLAS Life Sciences Reports First Quarter 2026 Financial Results and Provides Corporate Update

– Contract Research Organization for the Pivotal Phase 3 REGAL Trial of Galinpepimut-S (GPS) in Acute Myeloid Leukemia (AML) Informed the Company that 78 Events have Occurred in the Trial as of May 11, 2026; SELLAS Remains Blinded to Trial Outcomes – – Final Analysis of REGAL Trial of GPS in AML to be Conducted Following the 80th Event – – Ongoing Dosing of Patients in Phase 2 Trial of SLS009 in Newly Diagnosed First Line AML – – $107.1 Million in Cash and Cash Equivalents as of March 31, 2026; Additional $7.5 Million in Proceeds Received in Q2 2026 to Date through Warrant Exercises – NEW YORK, May 12, 2026 (GLOBE NEWSWIRE) -- SELLAS Life Sciences Group, Inc. (NASDAQ: SLS) (“SELLAS’’ or the “Company”), a late-stage clinical biopharmaceutical company focused on the development of novel therapies for a broad range of cancer indications, today reported financial results for the first quarter ended March 31, 2026, and provided a corporate update. “The first quarter of 2026 marked an important period for SELLAS as we continued to execute across our clinical programs while preparing for the anticipated pivotal Phase 3 REGAL trial data readout,” said Angelos Stergiou, MD, ScD h.c., President and Chief Executive Officer of SELLAS. “We are grateful for the ongoing commitment of the patients, caregivers, and investigators participating in the pivotal Phase 3 REGAL trial and we believe that the upcoming results, triggered by reaching the pre-specified 80th event, will be an important milestone for the Company.” “In parallel, we are generating increasingly compelling data with SLS009, including recent preclinical findings presented at AACR demonstrating potent, mechanistically driven activity in AML through suppression of key survival pathways such as MCL-1 and induction of apoptosis, including in high-risk genetic subtypes like TP53 and ASXL1 mutations. Importantly, we have begun dosing patients in our Phase 2 study of SLS009 in newly diagnosed, first-line AML, targeting high-risk populations unlikely to benefit from standard therapies, including venetoclax. With REGAL approaching its critical readout and SLS009 advancing across clinical and translational fronts, we believe that SELLAS is entering an exciting time with multiple, high-value potential catalysts that could transform the AML treatment landscape.” Recent Corporate Highlights: Phase 3 REGAL Trial of GPS: Ongoing Phase 3 REGAL trial evaluating GPS in AML patients who have achieved complete remission following second-line salvage therapy. Reaching the required pre-specified 80th event (death) will trigger the customary database lock, blinded data review procedures prior to statistical analysis, unblinding, and disclosure of topline results. As of May 11, 2026, 78 events have occurred and SELLAS will provide an update and announce when the 80th event has been reached. Ongoing dosing of SLS009 in earlier-line AML: SELLAS has initiated an 80-patient Phase 2 trial in newly diagnosed AML patients, including those who become refractory early to AZA/VEN treatment identified through extensive transcriptomics, genomics, and proteomics models. The topline data are expected in Q4 2026. Additional information about the trial can be found at clinicaltrials.gov (NCT04588922). Preclinical Data on SLS009 in AML Presented at the 2026 American Association for Cancer Research (AACR): The data show that SLS009 induces apoptosis in AML cell lines, including those harboring high-risk ASXL1 and TP53 mutations. Pharmacodynamic changes were observed as early as 8 hours after treatment and became more pronounced over time, with reductions in MCL-1 and survivin levels that correlated with increased apoptosis. The poster, entitled “Tambiciclib (SLS009), a CDK9 inhibitor, promotes apoptosis and suppresses MCL-1 levels in AML cell lines,” can be viewed here. At-the-Market (ATM) Offering: SELLAS established an ATM equity offering under its S-3ASR shelf registration, providing the Company with the ability to raise up to $150 million in capital over time. The facility, to be utilized through TD Cowen, enables flexible and opportunistic access to the equity markets. The Company has not sold any shares of common stock through its ATM to date. Financial Results for the First Quarter 2026: Research and Development Expenses: Research and development expenses for the quarter ended March 31, 2026, were $5.1 million, compared to $3.2 million for the same period in 2025. The increase was primarily due to increases in manufacturing costs, clinical and regulatory consulting, and clinical trial expenses in preparation for a potential Biologics License Application for GPS following the final analysis of the REGAL study. General and Administrative Expenses: General and administrative expenses for the first quarter of 2026 were $4.1 million, as compared to $2.9 million for the same period in 2025. The increase was primarily due to increases in professional fees, consulting and public company costs, and non-cash stock-based compensation. Net Loss: The net loss was $8.4 million for the first quarter of 2026, or a basic and diluted loss per share of $0.05, as compared to a net loss of $5.8 million for the first quarter of 2025, or a basic and diluted loss per share of $0.07. Cash Position: As of March 31, 2026, cash and cash equivalents totaled approximately $107.1 million. Subsequent to March 31, 2026, the Company received an additional $7.5 million in proceeds from the exercise of previously outstanding warrants. About SELLAS Life Sciences Group, Inc. SELLAS is a late-stage clinical biopharmaceutical company focused on the development of novel therapeutics for a broad range of cancer indications. SELLAS’ lead product candidate, GPS, is licensed from Memorial Sloan Kettering Cancer Center and targets the WT1 protein, which is present in an array of tumor types. GPS has the potential as a monotherapy and combination with other therapies to address a broad spectrum of hematologic malignancies and solid tumor indications. The Company is also developing SLS009 (tambiciclib) - potentially the first and best-in-class differentiated small molecule CDK9 inhibitor with reduced toxicity and increased potency compared to other CDK9 inhibitors. Data suggests that SLS009 demonstrated a high response rate in AML patients with unfavorable prognostic factors including ASXL1 mutation, commonly associated with poor prognosis in various myeloid diseases. For more information on SELLAS, please visit www.sellaslifesciences.com. Forward-Looking Statements This press release contains forward-looking statements. All statements other than statements of historical facts are “forward-looking statements,” including those relating to future events. In some cases, forward-looking statements can be identified by terminology such as “plan,” “expect,” “anticipate,” “may,” “might,” “will,” “should,” “project,” “believe,” “estimate,” “predict,” “potential,” “intend,” or “continue” and other words or terms of similar meaning. These statements include, without limitation, statements related to the GPS clinical development program, including the REGAL study and the timing of future milestones related thereto. These forward-looking statements are based on current plans, objectives, estimates, expectations, and intentions, and inherently involve significant risks and uncertainties. Actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties, which include, without limitation, risks and uncertainties with oncology product development and clinical success thereof, the uncertainty of regulatory approval, and other risks and uncertainties affecting SELLAS and its development programs as set forth under the caption “Risk Factors” in SELLAS’ Annual Report on Form 10-K filed on March 19, 2026 and in its other SEC filings. Other risks and uncertainties of which SELLAS is not currently aware may also affect SELLAS’ forward-looking statements and may cause actual results and the timing of events to differ materially from those anticipated. The forward-looking statements herein are made only as of the date hereof. SELLAS undertakes no obligation to update or supplement any forward-looking statements to reflect actual results, new information, future events, changes in its expectations, or other circumstances that exist after the date as of which the forward-looking statements were made. Investor Contact John Fraunces Managing Director LifeSci Advisors, LLC jfraunces@lifesciadvisors.com

财报临床2期临床3期

2026-04-26

·优亿美康

2026AACR年会原版PPT合集分享

点击上方"蓝字" 关注我们吧！ 2026年4月17日至22日，2026年美国癌症研究协会大会（AACR）在美国圣地亚哥如期举行。AACR是全球肿瘤学领域历史最悠久、规模最大、覆盖最全面、最具源头创新力的顶级学术组织，堪称癌症科研的 “源头与风向标”。小优特地收集整理了该会议的口头报告及海报，共131份原版PPT（可编辑），为了方便阅读已将标题翻译为中文，省时又省力。从2025ESMO AISA、2025ASH、2025SABCS到2026ASCO GI、2026ELCC、2026AACR，小优已经收集整理了2025年底到当前的9个大型肿瘤会议近2000份原版PPT及解读，获取更多最新国外肿瘤会议资料，敬请关注我们。以下是内容目录，星球内已列出摘要号和中英文标题，搜索查找很方便 1.利用双特异性和三特异性抗体解锁新型生物学机制：抗体构型的重要性 2.【摘要25】采用超灵敏肿瘤信息结构变异检测法对转移性乳腺癌进行连续循环肿瘤DNA监测 3.【摘要114】从血浆来源的cfRNA中解析肿瘤与组织特异性基因表达模式 4.【摘要299】从工厂到患者：体内表达生物制剂作为免疫疗法生产新范式 5.【摘要300】细胞命运图谱：从代谢动力学到DNA损伤反应 6.【摘要410】CGT4255的临床前特性研究：一种保留EGFR活性、针对泛突变HER2的临床开发候选药物，具备潜在最佳脑部渗透能力 7.【摘要445】人类内源性逆转录病毒K作为非典型癌症治疗靶点的评估 8.【摘要796】数字空间分析揭示肝细胞癌肿瘤与基质区间的免疫异质性 9.【摘要1056】非小细胞肺癌Ⅲ期结局的综合多组学特征与人工智能驱动的生物标志物发现 10.【摘要1061】基于肿瘤信息的循环肿瘤DNA检测技术可识别高级别浆液性卵巢癌患者中，即使经过初次肉眼完全切除并接受最佳一线治疗后仍具有最高复发风险的群体 11.【摘要1386】非小细胞肺癌患者来源类器官可重现组织信号传导及浸润免疫细胞活化受损情况，以此预测患者对治疗的反应 12.【摘要1451】可视化基因型-表型关联：基于RNA的扩散模型预测药物诱导的组织动态 13.【摘要1622】亲和力优化的双特异性T细胞衔接器W308051能以有限细胞因子分泌选择性杀伤PSMA表达肿瘤细胞 14.【摘要1642】具有高抗RAS突变癌症活性的泛RAS抑制剂抗体偶联药物平台 15.【摘要1672】新型抗体药物偶联物PF-08052667在非肌层浸润性膀胱癌治疗中的递送与活性增强 16.【摘要1685】DAR12是一种靶向HER2的双载荷抗体药物偶联物，其结合拓扑异构酶I抑制剂与微管抑制剂的双重作用机制，在异种移植模型中展现出卓越疗效，并能克服单载荷抗体药物偶联物的耐药性问题 17.【摘要1737】使用sSTRIDE-NER直接测量NER活性 18.【摘要1750】构建DNA损伤药物研发的集成化平台 19.【摘要1769】LY4170156（Sofetabart mipitecan）是一种靶向叶酸受体α的抗体偶联药物，在临床前卵巢癌模型中与标准治疗方案联用展现出增强的抗肿瘤活性 20.【摘要1770】埃万妥单抗、西妥昔单抗和帕尼单抗对EGFR ECD耐药突变的体外活性差异 21.【摘要1862】ZW191——一种差异化的FRα靶向拓扑异构酶 I 抗体药物偶联物，在与标准治疗药物联合使用时具有活性 22.【摘要1873】Atebimetinib对MEK的深度循环抑制限制了RAS突变肿瘤患者中MAPK轴的适应性和获得性改变 23.【摘要2062】用于抗体药物偶联物有效载荷的mRNA翻译抑制剂的设计与评估 24.【摘要2113】光学成像与数字病理学评估提升患者来源转移性乳腺癌模型的转化价值与稳健性 25.【摘要2141】利用对比增强MRI研究原位胶质瘤SRG大鼠模型中血脑屏障渗漏的进展 26.【摘要2175】迈向伦理与稳健的药物研发：无动物基质用于体内肿瘤模型的全面验证 27.【摘要2437】BCMA、GPRC5D与CD38靶向疗法在多发性骨髓瘤中的比较评分框架 28.【摘要2439】RAS：PI3Kα抑制剂BBO-10203通过阻断非经典RAS信号通路，抑制HER2扩增模型中的PI3Kα／AKT活性 29.【摘要2606】液体活检检测雌激素受体活性可预测ER+／HER2−晚期乳腺癌对吉雷司群的治疗反应 30.【摘要2669】靶向B7-H3的抗体偶联药物Risvutatug Rezetecan（GSK5764227；HS-20093）在实体瘤转化模型中展现出广泛且多样化的抗肿瘤活性 31.【摘要2848】STRO-227的临床前特性研究：一种搭载拓扑异构酶1与微管蛋白抑制剂的双载荷靶向PTK7抗体偶联药物 32.【摘要2926】Sonrotoclax（BGB-11417），一种选择性BCL-2抑制剂，在血液癌细胞、异种移植模型和人血样本中显示出优于维奈克拉和利沙托克拉（APG-2575）的疗效 33.【摘要3231】染色质谱分析揭示氟维司群对乳腺癌细胞中雌激素受体驱动的染色质动态的影响 34.【摘要3299】STRO-006：靶向整合素β6的抗体偶联药物在临床前实体瘤模型中展现良好安全性及强效抗肿瘤活性 35.【摘要3372】预测性体外检测与外周血单核细胞供体库：降低人源化小鼠研究中的变异性 36.【摘要3414】PDO作为非小细胞肺癌生物标志物发现的转化研究模型 37.【摘要3420】基于实验设计法优化Harbor-IN系统转座子基因插入技术 38.【摘要3521】研究B7-H3抗体药物偶联物Risvutatug Rezetecan（GSK5764227）在患者来源癌症类器官中的作用机制及旁观者效应 39.【摘要3524】探索Risvutatug Rezetecan（GSK5764227）抗体偶联药物在患者来源肿瘤外植体中的靶向与非靶向（旁观者）效应 40.【摘要3710】适应与验证一种人源化小鼠模型，用于测试治疗性细胞中免疫屏蔽基因修饰 41.【摘要3803】人源化FcγR／FcRn小鼠模型表现出与野生型小鼠相当的免疫应答反应 42.【摘要3835】用于评估靶向cGAS-STING轴免疫疗法的新型临床前免疫健全小鼠模型 43.【摘要3877】Lymphly整合应用揭示B细胞淋巴瘤共享分子图谱 44.【摘要3881】子宫内膜癌不同错配修复亚型的肿瘤微环境异质性：基于ENGOT-EN6-NSGO／GOG-3031／RUBY试验的分析 45.【摘要3901】BGB-58067，一种具有脑渗透性的MTA协同PRMT5抑制剂，在MTAP缺失的肿瘤中展现出良好的抗肿瘤活性和有利的选择性 46.【摘要4164】基于扩散模型的色卡在组织学图像批量校正中的实施 47.【摘要4181】通过虚拟实验室机制驱动模拟实现靶点发现 48.【摘要4185】模块化虚拟筛选流程：跨适应症表面蛋白靶点的多组学评估 49.【摘要4309】PROTAC HPK1降解剂ARV-6723与免疫检查点抑制剂的临床前抗肿瘤及免疫调节活性对比研究 50.【摘要4364】新一代RNA疫苗技术实现高保真抗原发现与T细胞免疫原性筛选 51.【摘要4395】一款具有高效低毒设计、最大化抗体功能性的同类最佳HER2xHER2新型双表位抗体药物偶联物 52.【摘要4418】靶向ADAM金属肽酶结构域9的潜在同类最优喜树碱类抗体偶联药物的临床前特性研究 53.【摘要4419】开发首款靶向ALPP／ALPPL2的喜树碱类抗体偶联药物，具有强效抗肿瘤活性与优异耐受性 54.【摘要4436】Sutro定点双载荷抗体偶联药物：结合TOPO1抑制剂与DNA损伤反应抑制剂，提升疗效、克服耐药性并改善安全性 55.【摘要4556】ZW439：一种靶向CLDN18.2的新型泛RAS抑制剂抗体偶联药物，用于治疗RAS突变型胰腺癌 56.【摘要4575】Mocertatug Rezetecan（GSK5733584／HS-20089）的非临床特性研究：一种新型B7-H4靶向抗体偶联药物 57.【摘要4594】新型BCL6分子胶LY4584180在B细胞非霍奇金淋巴瘤临床前模型中展现抗肿瘤疗效 58.【摘要4604】PROTAC泛KRAS降解剂在KRAS G12D同基因小鼠模型中的临床前疗效及同步免疫肿瘤微环境变化 59.【摘要4608】GSK5471713：一种具有同类最优潜力的新型选择性口服雄激素受体降解剂，用于前列腺癌治疗 60.【摘要4617】口服生物可利用、中枢神经系统渗透性泛突变BRAF降解剂NRX-0305在黑色素瘤脑转移及原发性胶质瘤颅内模型中展现显著疗效 61.【摘要4663】新一代Bcl-2抑制剂BGB-21447在血液系统恶性肿瘤临床前模型中显示出卓越效力并克服维奈克拉耐药性 62.【摘要4874】利用肿瘤与胃肠道类器官模型评估HER2 CAR-T细胞的临床前治疗窗口界定 63.【摘要4944】ZW418的开发：一种双特异性靶向PTK7的抗体药物偶联物，整合新型泛RAS抑制剂有效载荷，用于治疗非小细胞肺癌 64.【摘要4963】跨平台空间域识别验证揭示非小细胞肺癌中肿瘤微环境结构的一致性——基于整合空间转录组学与多重免疫荧光技术 65.【摘要4969】自动化多组学检测技术：通过100余种生物标志物实现对多种癌症类型肿瘤微环境的深度空间分析 66.【摘要5068】PF‑08046033：一种具有改善耐受性和强效抗肿瘤活性的首创GPNMB靶向奥瑞他汀S抗体偶联药物 67.【摘要5166】选择性口服Aurora激酶A降解剂NRX-4972在小细胞肺癌模型中展现增强疗效，其体外协同作用优于AURKA抑制剂 68.【摘要5251】利用NGS精确描述代谢组状态揭示ccRCC对TKI治疗反应的新潜在生物标志物 69.【摘要5397】一种新型抗CD3xCD28xSTEAP1三特异性T细胞衔接器（HLX3902）在前列腺癌中展现出增强且持久的抗肿瘤反应 70.【摘要5421】综合分子检测在晚期癌症中的获益评估：BostonGene与Exigent基因组深度解析（BEGIN）研究 71.【摘要5529】LY4336619（一种新型ALPPL2xCD3双特异性抗体）用于治疗卵巢癌和子宫内膜癌的临床前特性研究 72.【摘要5534】INCA036873：一种用于治疗CD70阳性恶性肿瘤的首创CD70×CD3 T细胞重定向双特异性抗体 73.【摘要5541】PF-08634404（SSGJ-707）——一种用于癌症治疗的四价PD-1 x VEGF双特异性抗体的表征与功能评估 74.【摘要5628】Prifetrastat（KAT6i）联合PI3Kα通路抑制剂可增强对PIK3CA突变ER+／HER2-乳腺癌模型的抗肿瘤疗效 75.【摘要5666】Tambiciclib (SLS009)作为一种CDK9抑制剂，能够促进细胞凋亡并在急性髓系白血病细胞系中抑制MCL-1水平 76.【摘要5704】临床前研究揭示蛋白酶介导的载荷释放与免疫肿瘤学／免疫调节效应共同促进HLX43的抗肿瘤活性 77.【摘要5801】NRX-0305是一种口服生物可利用的泛突变BRAF降解剂，在1／2／3类BRAF突变癌症中单药或与MEK抑制剂或抗EGFR药物联用均显示出疗效 78.【摘要5824】ATNM-400 的临床前开发：一种具有泛实体瘤疗效的首创性锕-225放射性偶联药物 79.【摘要5827】Actimab-A：一种靶向CD33的锕-225放射性偶联药物，通过转录重编程驱动突变非依赖性抗白血病活性，并与AML标准疗法产生协同作用 80.【摘要5856】Hanjugator喜树碱平台：高效低毒设计，最大化抗体功能，提供潜在同类最优的cMet／EGFR双特异性抗体药物偶联物 81.【摘要5864】他雷替尼，一种新一代选择性ROS1抑制剂，可抑制TRKB信号通路诱导的肺癌细胞侵袭潜能 82.【摘要5869】CGT4255的临床前特性研究：一种保留EGFR活性、针对泛突变HER2的临床开发候选药物，具备潜在最佳脑部渗透能力 83.【摘要5869】解锁IL-18在癌症免疫治疗潜力的新型临床前工具：genO-hIL-18-hIL-18R小鼠 84.【摘要5870】莫洛替尼：治疗骨髓纤维化及其他疾病的独特多靶点药理学特性与创新联合方案 85.【摘要6284】genO-BRGSF-HIS小鼠：用于评估靶向Treg疗法的免疫系统人源化小鼠模型 86.【摘要6358】项目CoMMunity：一个旨在解决两个社区多发性骨髓瘤诊疗差距的本地学习网络 87.【摘要6416】DEL-化学组学方法用于癌症治疗中靶向蛋白质降解剂（TPDs）的发现 88.【摘要6423】DNA编码化合物库筛选用于肿瘤靶点分子胶发现 89.【摘要6550】全人源拮抗性抗BTLA单克隆抗体的体外特性研究 90.【摘要6665】验证两种黑色素瘤生物标志物及两种新型即用型多重免疫荧光检测组合，用于肿瘤微环境中基质与血管区室的空间分析 91.【摘要6680】利用三重组学解码肿瘤微环境：在同一组织切片上自动化分析蛋白质-蛋白质相互作用、RNA及蛋白质标志物的空间分布 92.【摘要6778】利用分子胶降解剂选择性靶向CCNE1基因治疗CCNE1扩增型癌症 93.【摘要7097】Risvutatug Rezetecan（GSK5764227／HS-20093）的非临床特性研究：一种新型B7-H3靶向抗体偶联药物 94.【摘要7104】BBO-11818：一种口服生物可利用、高效且选择性的非共价泛KRAS(ON)与(OFF)抑制剂，在KRAS突变临床前模型中展现出强大的抗肿瘤活性 95.【摘要7186】新型镥-177标记GRPR拮抗剂LY4257496的特性研究 96.【摘要7202】225Ac-PSMA-Trillium与其他225Ac-PSMA-SMOL制剂在前列腺癌异种移植模型中的临床前比较评估 97.【摘要7203】基于铅的CEA预靶向放射免疫疗法在免疫缺陷和人源化小鼠模型中展现出肿瘤靶向性和强效的肿瘤生长抑制作用，为转移性结直肠癌的首例人体研究提供了依据 98.【摘要7266】通过综合多组学分析推进对非肌层浸润性膀胱癌疾病生物学的深入理解 99.【摘要7541】用于理性候选药物遴选的综合性临床前体内肿瘤学平台 100.【摘要7715】ZW427，一种靶向Ly6E的抗体药物偶联物，搭载新型泛RAS抑制剂有效载荷，用于治疗RAS突变癌症 101.【摘要7747】接受瑞弗利单抗联合抗LAG3／抗TIM3治疗与单用瑞弗利单抗患者T细胞活化状态的比较 102.【摘要7775】TGFβR2xPD-1双特异性抗体INCA33890在MSS转移性结直肠癌（mCRC）患者中的药效学生物标志物研究 103.【摘要7899】临床前研究表明，BCL-2抑制剂BGB-21447在BCL-2过表达的B细胞非霍奇金淋巴瘤（NHL）中展现出高潜力 104.【摘要7940】TNX-1700在非人灵长类动物及人源FcRn／血清白蛋白转基因小鼠中的药代动力学研究 105.【摘要9950】STRO-004 ST1：一项评估组织靶向抗体药物偶联物STRO-004在难治性／复发性转移性实体瘤成人患者中的安全性、药代动力学及初步抗肿瘤活性的1期开放标签研究 106.【摘要CT001】CBL-B分子内胶水抑制剂的发现与特性研究：增强T细胞活性并抑制肿瘤生长 107.【摘要CT002】PLN-101095首次人体I期研究：评估这一首创性双重αvβ8／αvβ1整合素抑制剂单药及联合帕博利珠单抗治疗免疫检查点抑制剂（ICI）难治性晚期实体瘤患者 108.【摘要CT007】替雷利珠单抗（TIS）联合研究药物作为复发性及／或转移性头颈部鳞状细胞癌（R／M HNSCC）一线（1L）治疗的2期研究 109.【摘要CT029】新一代组织因子（TF）靶向DAR8-依喜替康ADC药物STRO-004，在综合性单鼠PDX试验中展现对TF表达实体瘤的卓越疗效 110.【摘要CT038】ARTEMIS-101研究：Risvutatug Rezetecan联合阿得贝利单抗治疗无可干预基因组改变的晚期非鳞状非小细胞肺癌患者的1期临床试验 111.【摘要CT073】FiREBOLT：一项评估LY4337713放射性配体疗法在特定FAP+实体瘤成人患者中的1期研究（进行中试验） 112.【摘要CT120】BGB-24714（一种第二线粒体衍生的半胱天冬酶激活剂[SMAC]模拟物）单药或联合化疗或同步放化疗治疗实体瘤的1期研究 113.【摘要CT121】BGB-24714（一种第二线粒体衍生的半胱天冬酶激活剂[SMAC]模拟物）在实体瘤首次人体研究中的药效学（PD）特征分析 114.【摘要CT131】BAY2862789（一种二酰甘油激酶α（DGKα）选择性细胞内T细胞检查点抑制剂）在实体瘤中的全球首次人体（FiH）单药剂量递增试验 115.【摘要CT132】BAY2965501首次人体试验：该药物为细胞内T细胞检查点二酰甘油激酶Zeta（DGKζ）选择性抑制剂，研究其单药疗法及与抗PD-1联合疗法的效果 116.【摘要CT154】新型BRAF抑制剂Plixorafenib（FORE8394）在BRAF V600突变晚期结直肠癌中的临床活性与安全性研究 117.【摘要CT174】破解内分泌耐药：Prifetrastat（PF-07248144）联合氟维司群共靶向KAT6与ER驱动ER+／HER2−转移性乳腺癌的肿瘤及ctDNA应答 118.【摘要CT175】循环肿瘤DNA清除作为广泛期小细胞肺癌预后生物标志物：来自LUMINANCE Ⅲb期研究的启示.pptx 119.【摘要CT197】ERY974在磷脂酰肌醇蛋白聚糖-3（GPC-3）阳性晚期实体瘤患者中的Ⅰ期研究 120.【摘要CT206】拉罗替尼治疗NTRK／2／3基因扩增实体瘤患者：靶向药物与基因分析应用注册研究（TAPUR）结果报告 121.【摘要CT232】抗CCR8抗体Denikitug在晚期实体瘤患者中的首次人体剂量递增Ⅰ期研究初步结果 122.【摘要CT244】他雷替尼在TKI经治ROS1阳性非小细胞肺癌患者中的应用：TRUST-Ⅰ和TRUST-Ⅱ 研究最新数据 123.【摘要CT268】ARV-393（一种PROTAC BCL6降解剂）单药治疗晚期非霍奇金淋巴瘤患者或联合格菲妥单抗治疗弥漫性大B细胞淋巴瘤患者的1期研究 124.【摘要CT273】FORTE：一项评估Plixorafenib治疗BRAF突变癌症的Ⅱ期总研究方案 125.【摘要CT300】阳性非小细胞肺癌初治患者中的应用：TRUST-和TRUST-Ⅱ研究最新数据 126.【摘要CT306】ZW191（一种靶向叶酸受体α（FRα）的抗体偶联药物（ADC））在晚期实体瘤患者中开展的首次人体Ⅰ期多中心开放标签研究：第1部分剂量递增结果 127.【摘要LB011】3期RATIONALE 305试验探索性生物标志物分析：替雷利珠单抗（TIS）联合化疗（CT）对比安慰剂（PBO）联合化疗一线治疗晚期胃癌／胃食管结合部腺癌（GC／GEJC） 128.【摘要LB461】单链DNA断裂处PARP1活性与捕获的原位测量 129.【摘要LB467】PF08634404（一种研究性抗PD-1和抗VEGF双特异性抗体）的剂量优化与暴露-反应分析 130.【摘要LB473】JNJ-95437446：基于埃万妥单抗的EGFR／MET抗体偶联药物在实体瘤适应症中的发现与临床前特性研究 131.【摘要LB474】一线挨万妥单抗-拉泽替尼对比奥希替尼对二线无进展生存期的影响小伙伴们扫描上方二维码加入知识星球，就可以获得这些全部内容。星球内已含20000+肿瘤资料，分类清晰，覆盖全面，每日持续更新中！（以上内容仅供专业人员交流及学习之用，如有侵权，请联系我们删除）近期国外肿瘤会议合集汇总 2025ESMO Asia原版PPT合集 2025ASH原版PPT及解读合集 2025SABCS原版PPT及解读合集 2026ASCO GI原版PPT及解读合集 2026ASCO GU原版PPT及解读合集 2026ESMO SRC原版PPT合集 2026ESMO TAT原版PPT合集 2026ELCC原版PPT合集常用及重点内容推荐 500+丨2025WCLC原版PPT及解读合集 1000+丨2025ASCO原版PPT及解读合集 900+丨2025ESMO原版PPT及解读合集 264份丨2025ESMO Asia原版PPT合集 351份丨2025CSCO学术年会PPT合集 1681份丨2024年肿瘤学术会议PPT合集 1510份丨最新肺癌学术会议PPT合集最新NCCN指南及中文版、解读合集附下载丨2025CACA指南合集（全29册） 140+丨肿瘤及放疗实用电子书合集优亿瘤研【20000+肿瘤知识库】 ✓共识指南：2025CSCO丨NCCN丨CACA丨官方指南丨专家共识等； ✓最新资料：肺癌丨乳腺癌丨胃癌丨肝癌丨食管癌丨结直肠癌丨妇科肿瘤丨泌尿肿瘤丨血液肿瘤丨骨与软组织肿瘤丨头颈部肿瘤丨放化疗丨影像诊断丨营养康复丨前沿研究等； ✓学术会议：CSCO丨CACA丨ASCO丨ESMO丨WCLC丨ELCC丨AACR等国内外会议视频及PPT； ✓相关书籍：内科学丨影像诊断丨放化疗丨基础科学丨免疫靶向等； ✓多端通用：微信小程序丨知识星球APP丨电脑网页版丨微信登录就能任意使用；点击阅读原文，获取资料

100 项与 Tambiciclib 相关的药物交易

登录后查看更多信息

研发状态

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
复发性弥漫性大B细胞淋巴瘤	临床2期	中国	劲方医药科技（上海）股份有限公司	2024-03-20
难治性弥漫性大 B 细胞淋巴瘤	临床2期	中国	劲方医药科技（上海）股份有限公司	2024-03-20
外周T细胞淋巴瘤	临床2期	中国	劲方医药科技（上海）股份有限公司	2023-09-06
伴有骨髓发育不良相关变化的急性髓系白血病	临床2期	美国	SELLAS Life Sciences Group, Inc.	2021-05-10
伴有骨髓发育不良相关变化的急性髓系白血病	临床2期	中国	SELLAS Life Sciences Group, Inc.	2021-05-10
急性髓单核细胞白血病	临床2期	美国	SELLAS Life Sciences Group, Inc.	2021-05-10
急性髓单核细胞白血病	临床2期	中国	SELLAS Life Sciences Group, Inc.	2021-05-10
淋巴母细胞淋巴瘤	临床2期	美国	SELLAS Life Sciences Group, Inc.	2021-05-10
淋巴母细胞淋巴瘤	临床2期	中国	SELLAS Life Sciences Group, Inc.	2021-05-10
伯基特淋巴瘤	临床2期	美国	SELLAS Life Sciences Group, Inc.	2021-05-10

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04588922 (GlobeNewswire) 人工标引	临床2期	急性髓性白血病	-	SLS009 + Venetoclax + Azacitidine	衊鹹衊蓋淵廠製鑰獵廠(觸艱鏇網範憲餘淵製簾) = 艱憲糧糧齋醖鏇範衊艱觸願鑰網鏇簾鏇醖衊構 (壓鏇襯獵構鏇範蓋鹹蓋 ) 更多	积极	2025-07-15
				SLS009 30mg BIW + Venetoclax + Azacitidine	衊鹹衊蓋淵廠製鑰獵廠(觸艱鏇網範憲餘淵製簾) = 網顧願選廠膚憲衊構繭觸願鑰網鏇簾鏇醖衊構 (壓鏇襯獵構鏇範蓋鹹蓋 ) 更多
NCT04588922 (GlobeNewswire) 人工标引	临床2期	急性髓性白血病 \| 伴有骨髓发育不良相关变化的急性髓系白血病	14	SLS009 + venetoclax/azacitidine (r/r AML)	艱廠選襯糧選築齋襯鑰(顧淵夢積願壓鑰獵鏇繭) = 齋膚鹹鬱齋鹹願選鹹鏇醖廠鑰齋觸網構膚遞糧 (夢積醖繭鏇網廠簾獵鹽 ) 更多	积极	2025-04-08
				SLS009 + venetoclax/azacitidine (AML MRC)	艱廠選襯糧選築齋襯鑰(顧淵夢積願壓鑰獵鏇繭) = 糧選糧觸鹹艱艱遞顧觸醖廠鑰齋觸網構膚遞糧 (夢積醖繭鏇網廠簾獵鹽 ) 更多
NCT06375733 (Company_Website) 人工标引	临床2期	弥漫性大B细胞淋巴瘤	9	SLS009 (tambiciclib) in combination with Zanubrutinib	鹹醖繭遞範遞艱窪襯餘(廠襯鏇壓淵憲糧鏇艱憲) = 築憲鹽構廠襯淵積築鬱鹹鏇窪膚夢簾鏇壓製觸 (廠顧淵觸蓋膚簾觸範製 ) 更多	积极	2025-02-20
				SLS009 (tambiciclib) in combination with Zanubrutinib (Difficult-to-Treat Non-GCB)	鹽範範範膚鹽鏇鏇積簾(齋鏇淵襯築夢廠積餘鹹) = 鹹觸齋憲築獵夢網憲憲鏇築鑰憲齋夢憲獵鏇遞 (醖鹽壓獵壓築夢糧觸顧 )
NCT04588922 (GlobeNewswire) 人工标引	临床2期	急性髓性白血病 ASXL1 Mutation	-	SLS009 30 mg BIW	鏇網艱窪鏇遞網憲窪鏇(獵壓糧繭製願廠鏇鑰廠) = 壓憲醖簾夢獵餘艱醖獵淵襯鏇艱壓憲壓範夢淵 (餘膚壓衊夢艱餘積簾簾 )	积极	2024-12-09
				SLS009 (AML MRC)	艱艱簾選夢齋膚築鹽願(獵顧簾獵範鏇膚憲鹹蓋) = 夢網糧淵醖壓製網積構醖糧鑰壓簾繭構製鏇醖 (憲鑰遞築淵鹽觸構憲餘 )
ASH2024	N/A	急性髓性白血病	-	SLS009 45 mg QW	選醖構築窪遞憲膚壓鏇(襯構憲鑰鏇醖膚製餘襯) = Drug related toxicities of any grade occurring in more than one patient across all cohorts were nausea (23%), diarrhea (13%), hyperphosphatemia (10%), pyrexia (7%) and white blood cell count decreased (7%) 壓範選積糧鑰積積構夢 (網鹹遞觸製餘窪蓋鏇鏇 ) 更多	-	2024-12-08
				SLS009 60 mg QW
NCT04588922 (GlobeNewswire) 人工标引	临床2期	急性髓性白血病	30	SLS009 30 mg BIW	壓鹽鬱襯繭醖構選膚鬱(膚範願齋襯廠築鹹醖鹹) = none 選壓積鬱夢齋選壓鹽範 (築觸簾鑰廠憲襯膚窪積 )	积极	2024-06-10
				SLS009 45 mg QW
NCT04588922 (GlobeNewswire) 人工标引	临床1/2期	急性髓性白血病 ASXL1 Mutation	-	GFH009+venetoclax+azacitidine	願夢夢構積顧鏇壓襯網(蓋艱憲鹹構衊齋襯餘築) = 築鏇獵醖憲獵遞積鹽衊膚鏇廠膚衊顧鹹鏇網壓 (淵夢衊製繭醖顧糧鏇網 ) 更多	积极	2024-05-01
NCT04588922 (GlobeNewswire) 人工标引	临床2期	急性髓性白血病	21	SLS009 45 mg+azacitidine+venetoclax	壓繭糧積選鬱襯願築醖(糧衊鹹齋齋糧膚獵蓋艱) = 範鏇醖願膚願膚鏇製憲獵醖艱窪糧夢選遞簾鑰 (醖鹽醖衊構顧窪蓋鑰願 )	积极	2024-03-26
				SLS009 60 mg QW+azacitidine+venetoclax	壓繭糧積選鬱襯願築醖(糧衊鹹齋齋糧膚獵蓋艱) = 窪憲衊選鏇鑰構襯鑰襯獵醖艱窪糧夢選遞簾鑰 (醖鹽醖衊構顧窪蓋鑰願 )
CTR20210356 (Biospace) 人工标引	临床1期	外周T细胞淋巴瘤	-	SLS009	憲齋繭夢鹽壓衊襯遞繭(淵醖鏇糧蓋製構積鬱夢) = 範糧夢獵積衊醖顧顧鑰艱餘積顧齋糧蓋窪顧製 (鹽繭選遞構膚鑰觸夢鹹 )	积极	2023-12-21
				belinostat	憲齋繭夢鹽壓衊襯遞繭(淵醖鏇糧蓋製構積鬱夢) = 淵鏇醖鑰繭膚簾願構網艱餘積顧齋糧蓋窪顧製 (鹽繭選遞構膚鑰觸夢鹹 )
NCT04588922 (Biospace) 人工标引	临床1期	血液肿瘤	11	SLS009	遞顧衊願遞獵製鏇鹹壓(齋範齋願網願獵餘鏇鬱) = 憲鏇鑰膚鏇襯餘膚鹽艱糧襯構範遞醖廠網廠膚 (淵鏇壓鑰憲鹹獵繭觸網 )	积极	2023-10-30