Eganelisib(Eganelisib) - 药物靶点：PAK1 x PI3Kγ_在研适应症：骨髓增生异常综合征，难治性急性髓细胞白血病，复发性急性髓细胞白血病_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Pi3k-gamma inhibitor ipi-549、IPI-549

靶点

PAK1 x PI3Kγ

作用方式

抑制剂

作用机制

PAK1 inhibitors(p21 (RAC1) activated kinase 1 inhibitors)、PI3Kγ抑制剂(磷脂酰肌醇-3激酶γ抑制剂)

治疗领域

肿瘤血液及淋巴系统疾病

在研适应症

骨髓增生异常综合征难治性急性髓细胞白血病复发性急性髓细胞白血病

非在研适应症

肾上腺皮质癌晚期癌症晚期头颈癌+ [14]

原研机构

Infinity Pharmaceuticals, Inc.

在研机构

Stelexis Therapeutics LLC

非在研机构

Infinity Pharmaceuticals, Inc.

University of California San Diego

Arcus Biosciences, Inc.

权益机构

Healthcare Partners

Lite Strategy, Inc.

Infinity Pharmaceuticals, Inc.

+ [1]

最高研发阶段临床1期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

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结构/序列

分子式C30H24N8O2

InChIKeyXUMALORDVCFWKV-IBGZPJMESA-N

CAS号1693758-51-8

关联

7

项与 Eganelisib 相关的临床试验

NCT07439211

/ Not yet recruiting临床1期IIT

Safety of Targeting PI3Kgamma Signaling With Azacitidine, Venetoclax and Eganelisib in Acute Myeloid Leukemia: A Phase 1 Study (GAVEL)

This study is to evaluate the safety and preliminary efficacy of adding the PI3K-gamma inhibitor, eganelisib, to a standard of care treatment option with combination venetoclax and azacitidine in participants with acute myeloid leukemia (AML).
The names of the study drugs involved in this research study are:
* Venetoclax (a type of BCL-2 inhibitor)
* Azacitidine (a type of Demethylating Agent)
* Eganelisib (a type of PI3K-gamma inhibitor)

开始日期2026-07-01

申办/合作机构

Dana-Farber Cancer Institute, Inc.

[+1]

NCT06533761

/ Recruiting临床1期

A Phase 1b Open-Label Study to Evaluate the Safety and Tolerability of Eganelisib as Monotherapy and in Combination With Cytarabine in Patients With Relapsed/Refractory Acute Myeloid Leukemia

This is a Phase 1b open-label, multicenter, dose-escalation and dose-optimization study designed to evaluate the safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and anti-tumor efficacy of eganelisib as monotherapy and in combination with cytarabine in patients with relapsed/refractory (r/r) acute myeloid leukemia (AML) or r/r higher-risk myelodysplastic syndromes (HR-MDS).
The study consists of 2 parts:
* Part 1: Dose Escalation (DE) in both monotherapy and in combination.
* Part 2: Dose Optimization

开始日期2025-04-28

申办/合作机构

Stelexis Therapeutics LLC

NCT03795610

/ Completed临床2期IIT

Phase 2 Window of Opportunity Study of IPI-549 in Patients With Locally Advanced HPV+ and HPV- Head and Neck Squamous Cell Carcinoma

The purpose of this study is to investigate how effective the study drug IPI-549 is against types of cancers. IPI-549 is considered experimental because it is not approved by the US Food and Drug Administration (FDA) for the treatment of cancer.
Patients will be treated with 2 weeks of IPI-549, a specific PI3K? inhibitor. Tumor tissue for research purposes through core biopsies will be obtained prior to initiation of IPI-549 and at surgery.

开始日期2020-03-06

申办/合作机构

University of California San Diego

[+1]

100 项与 Eganelisib 相关的临床结果

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100 项与 Eganelisib 相关的转化医学

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100 项与 Eganelisib 相关的专利（医药）

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59

项与 Eganelisib 相关的文献（医药）

2026-12-31·CANCER BIOLOGY & THERAPY

PI3Kγ inhibition drives M1 macrophage differentiation and synergizes with PD-L1 blockade to improve survival in poorly immunogenic head and neck squamous cell carcinoma

Article

作者: Oghumu, Steve ; Lamenza, Felipe F. ; Mo, Xiaokui ; Roth, Peyton ; Ryan, Nathan M. ; Anderson, Kelvin ; Jordanides, Pete P. ; Jagadeesha, Sushmitha ; Kehres, Reegan ; Siddiqui, Arham ; Pracha, Sherefuddin H. ; Bopp, Anna R. ; Shrestha, Suvekshya ; Upadhaya, Puja

BACKGROUND:

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer globally with high mortality rates, highlighting the urgent need for novel therapeutic strategies. We investigated the efficacy of combining phosphoinositide 3-kinase gamma (PI3Kγ) inhibition with programmed death-ligand 1 (PD-L1) blockade in a poorly immunogenic HNSCC model.

MATERIALS AND METHODS:

Mouse bone marrow-derived macrophages (BMDMs) were differentiated and polarized in the presence or absence of the PI3Kγ inhibitor IPI-549 or culture supernatants from MOC2 cells treated with or without IPI-549. MOC2 cells were orthotopically injected into C57BL/6 mice, and treated with anti-PD-L1, IPI-549, combined anti-PD-L1 and IPI-549 or vehicle control. Tumor burden, survival, and immunological responses were evaluated.

RESULTS AND CONCLUSION:

Dual inhibition of PI3Kγ (using IPI-549) and PD-L1 demonstrated nearly significant reduction in primary tumor burden and significantly increased survival compared to single or control treatments. PI3Kγ inhibition promoted macrophage differentiation toward an antitumoral M1 phenotype. In the bone marrow, dual therapy significantly increased MHC-II expression across various myeloid cell subsets and effectively normalized myelopoiesis. Notably, combination therapy increased CD8+ T-cell infiltration into tumors while decreasing T-cell exhaustion marker (LAG-3, CTLA-4, and TIM-3) and protumoral cytokine (IL-4). Combined PI3Kγ and PD-L1 inhibition offers a promising strategy for treating poorly immunogenic HNSCC by simultaneously targeting multiple immunosuppressive mechanisms. These findings provide a strong rationale for combining PI3Kγ and PD-L1 inhibitors as a therapeutic strategy for poorly immunogenic HNSCC, potentially improving clinical outcomes for patients.

2026-05-05·Current Computer-Aided Drug Design

From IPI-549 to Novel Compounds: A Novel Strategy Integrating 3D-QSAR, Scaffold Growth, Molecular Docking, and Molecular Dynamics Simulation in PI3Kγ Inhibitor Design

Article

作者: Jia, Lei ; Yu, Li ; Jin, Jian ; Xu, Lei ; Chen, Yun ; Yu, Xiaolian ; Zhu, Jingyu ; Cai, Yanfei

Introduction::

Phosphoinositide-3-kinase gamma (PI3Kγ) has emerged as a valuable therapeutic target for various diseases. However, there is a notable scarcity of inhibitors that have advanced to clinical studies, highlighting the urgent need for the development of novel PI3Kγ inhibitors.

Methods::

A three-dimensional quantitative structure-activity relationship (3D-QSAR) analysis was conducted to investigate the structure-activity relationships of PI3Kγ inhibitors. A scaffold growth strategy was employed to design novel compounds. Furthermore, a virtual screening workflow integrating drug-likeness filtering, 3D-QSAR predictions, and molecular docking was established.

Results::

An optimal CoMFA model was developed with q² = 0.752, r² = 0.995, and r²pred = 0.736, revealing key structural features and interactions crucial for selective PI3Kγ inhibition. Using the N-phenyl isoquinolinone core of IPI-549 as a template, new compounds were generated via a reaction-based scaffold growth approach. Following drug-likeness evaluation, 3DQSAR predictions, and molecular docking, nine compounds demonstrated superior predicted activity compared to IPI-549. Three top-ranked hits were subsequently subjected to molecular dynamics simulations and binding free energy calculations, providing insights into the PI3Kγ/Hit binding mechanism and identifying critical residues governing selectivity, including MET804, TRP812, ILE831, VAL882, and MET953.

Discussion::

Developing selective PI3Kγ inhibitors is challenging due to the high homology among kinase structures. IPI-549, the first PI3Kγ inhibitor to enter clinical trials, served as a suitable template for designing novel selective inhibitors. This study applied computer-aided drug design strategies to formulate promising new PI3Kγ inhibitors.

Conclusion::

The present workflow provides an effective and precise approach for identifying novel PI3Kγ inhibitors and offers valuable guidance for the rational design of selective PI3Kγ- targeted therapeutics.

2026-04-01·CHIRALITY

Enantioselective Chiral Separation and Quantitation of PI3Kγ Inhibitor Eganelisib in Rat Plasma Using UHPLC–MS/MS: Application to Evaluate Pharmacokinetic Study

Article

作者: Kandula, Jony Susanna ; Karkile, Dayasagar Rajiv ; Radhakrishnanand, P. ; Priyadharshni, A. R. ; Parmar, Keyur ; Shirishkumar, Kale Shyam

ABSTRACT:

Eganelisib (EGN, IPI‐549), an investigational new drug, is a potent first‐in‐class PI3Kγ inhibitor with high selectivity compared to other class I PI3K isoforms, with one asymmetric center. Enantiomers have similar physicochemical properties but differ in their biological characteristics, like absorption, distribution, metabolism, and excretion. Hence, a suitable analytical approach is required to investigate the enantioselective behavior in ADME‐Tox. In the current study, a sensitive, reliable, and precise chiral LC–MS/MS method has been developed for quantifying EGN enantiomers in rat plasma, in accordance with USFDA guidelines. Enantiomeric separation was achieved within 15 min on a Chiralpak‐IK‐3 (250 × 4.6 mm, 3 μm) immobilized polysaccharide column, containing 10 mM ammonium bicarbonate and a premixed mixture of acetonitrile and methanol (80:20 v/v) as the mobile phase in the ratio of 10:90 (v/v), with isocratic elution at a flow rate of 0.6 mL/min. Multiple reaction monitoring (MRM) mode was used to detect EGN and SOF in positive electrospray ionization (ESI) mode, characterized by their transitions at m/z 529.3→326.3, 161.1, and m/z 465.1→447.1, 270.2, 252.1. The method demonstrated a linear response in the range of 1–600 ng/mL for both enantiomers, with a lower limit of quantification of 1 ng/mL. The validated bioanalytical method was applied to evaluate the enantioselective pharmacokinetics of EGN enantiomers in rat plasma for the first time, utilizing a model‐independent approach. The ( R )‐enantiomer showed relative fold differences in Cmax , t1/2 , AUC 0‐ t , and AUC 0‐∞ when compared to the ( S )‐enantiomer, indicating the enantioselective behavior of EGN enantiomers.

54

项与 Eganelisib 相关的新闻（医药）

2026-06-05

·动脉网

Stelexis BioSciences宣布eganelisib治疗复发/难治性急性髓系白血病（AML）及高危骨髓增生异常综合征（MDS）的1期临床数据积极，相关结果将于2026年ASCO年会上作口头报告Stelexis BioSciences Announces Positive Phase 1 Data for Eganelisib in Relapsed/Refractory AML and Higher-Risk MDS in an Oral Presentation at ASCO 2026

Eganelisib induced complete remissions and hematologic improvements as a single-agent via myeloid differentiation in a Phase 1 study in relapsed/refractory patients with myeloid malignancies (MDS/AML) who show high expression of PI3K-gamma in bone marrow blasts. 在一项针对骨髓原始细胞PI3K-γ高表达的复发/难治性髓系恶性肿瘤（MDS/AML）患者的1期研究中，艾加列司布作为单药通过髓系分化诱导了完全缓解与血液学改善。The improved overall survival in patients with high expression of PI3K-gamma in this Phase 1 study is internally consistent with the observed responses and is externally validated by the TCGA database, which suggests a poor prognosis for patients with high expression of PI3K-gamma. 本项I期研究中，PI3K-γ高表达患者总生存期的改善与观察到的疗效在内部保持一致，并得到了TCGA数据库的外部验证，该数据库表明PI3K-γ高表达患者预后较差。Eganelisib generated a striking efficacy signal while demonstrating a favorable safety and tolerability profile in this Phase 1 study. 在这项1期研究中，Eganelisib显示出显著的疗效信号，同时展现出良好的安全性和耐受性。WALTHAM, Mass. 沃尔瑟姆，马萨诸塞州, ，June 2, 2026 2026年6月2日/PRNewswire/ -- Stelexis BioSciences, Inc. (Stelexis) today announced results from a Phase 1 clinical trial (NCT06533761) of eganelisib, an oral, first-in-class PI3K-gamma inhibitor, in 21 patients with relapsed/refractory (R/R) acute myeloid leukemia (AML) or higher-risk myelodysplastic syndrome (HR-MDS). /美通社/ -- Stelexis BioSciences公司（Stelexis）今日公布了eganelisib（一种口服、首创的PI3K-γ抑制剂）在一项针对21例复发/难治性（R/R）急性髓系白血病（AML）或高危骨髓增生异常综合征（HR-MDS）患者的1期临床试验（NCT06533761）中的结果。The data were presented in an oral session at the 2026 ASCO Annual Meeting by Mendel Goldfinger, M.D., of Montefiore Einstein Comprehensive Cancer Center.. 这些数据由来自蒙蒂菲奥里爱因斯坦综合癌症中心的门德尔·戈尔德芬格（Mendel Goldfinger）医学博士在2026年美国临床肿瘤学会（ASCO）年会口头报告环节中进行展示。Key Findings 主要发现The trial recruited a heavily pretreated patient population that was uniformly characterized by features that convey an unfavorable prognosis: 该试验招募的患者人群均接受过大量既往治疗，且均具有提示预后不良的特征：29% TP53-deleted or -mutated 29% TP53缺失或突变90% abnormal cytogenetics 90% 细胞遗传学异常76% received more than two prior therapies 76%接受过两种以上既往治疗。76% received prior venetoclax 76% 既往接受过维奈克拉治疗A modified objective response rate (defined as CR + Stable Disease with neutrophil count improvement) was achieved in: 改良客观缓解率（定义为CR+伴中性粒细胞计数改善的疾病稳定）在……中达到：50% (6/12) of patients with high PI3K-gamma expression vs. 50%（6/12）的PI3K-γ高表达患者与……相比0% (0/8) of patients with low PI3K-gamma expression (p<0.05, Fisher's exact test), using immunohistochemical staining of bone marrow biopsies 通过对骨髓活检标本进行免疫组织化学染色，0%（0/8）的患者呈低 PI3K-γ 表达（p<0.05，Fisher精确检验）。Responses included molecular and major cytogenetic remissions in two patients in CR 应答包括2例完全缓解（CR）患者达到分子学缓解和主要细胞遗传学缓解。Five of six responding patients had severe or life-threatening neutropenia at baseline, and all five patients demonstrated rapid neutrophil count improvements, including a rapid 六名有应答的患者中有五名在基线时患有重度或危及生命的中性粒细胞减少症，且这五名患者均表现出中性粒细胞计数的快速改善，包括快速的normalization 标准化（或归一化/规范化/正常化，视具体领域而定）of neutrophil counts in four patients, consistent with induction of myeloid differentiation ……四名患者的中性粒细胞计数，与诱导髓系分化一致Median overall survival (OS) was 27 weeks in PI3K-gamma-high patients vs. 9.9 weeks in low expressors (HR 0.22; 95% CI 0.07–0.75) PI3K-γ高表达患者的中位总生存期（OS）为27周，而低表达患者为9.9周（HR 0.22；95% CI 0.07–0.75）。Based on historical patient data from the publicly available TCGA database, PI3K-gamma-high expression is an adverse prognostic factor for OS in patients receiving conventional therapy, thereby supporting a substantial clinical benefit observed following treatment with eganelisib in this study. 基于公开的TCGA数据库历史患者数据，在接受常规治疗的患者中，PI3K-γ高表达是总生存期（OS）的不良预后因素，从而印证了本研究中观察到的eganelisib治疗所获得的显著临床获益。Eganelisib was well tolerated at both dose levels (45 mg and 60 mg, once daily) with no dose-limiting toxicities and no intrinsic hematologic toxicity. This is consistent with the myeloid-restricted expression of PI3K-gamma, and with the observation that PI3K-gamma is dispensable for normal hematopoiesis (Gu et al., Blood 2024).. Eganelisib在两种剂量水平（45 mg和60 mg，每日一次）下均表现出良好的耐受性，未出现剂量限制性毒性，亦无固有的血液学毒性。这与PI3K-γ的髓系限制性表达相符，并与PI3K-γ对正常造血非必需的观察结果一致（Gu等，《Blood》2024）。The majority of adverse events in this study were disease-related rather than treatment-related, consistent with the underlying patient population. Treatment-related AEs were predominantly low-grade with no Grade 5 related AEs. Of note, no eganelisib-related SAEs were observed and no patient discontinued treatment due to an eganelisib-related AE.. 本研究中大多数不良事件与疾病相关而非与治疗相关，这与该患者人群的特征相符。治疗相关不良事件主要为低级别，且无5级相关不良事件。值得注意的是，未观察到与伊加奈利西布（eganelisib）相关的严重不良事件，且无患者因伊加奈利西布相关不良事件而终止治疗。Published outcomes for patients with relapsed/refractory disease who failed frontline venetoclax and hypomethylating agent therapy have shown a median overall survival of approximately 2.4 months (Maiti et al., Haematologica 2021), underscoring the high unmet need in this population. 已发表的针对一线维奈克拉联合去甲基化药物治疗失败的复发/难治性疾病患者的数据显示，其中位总生存期约为2.4个月（Maiti等，《Haematologica》2021），这凸显了该人群巨大的未满足临床需求。'The preliminary data generated by eganelisib in patients with heavily pretreated AML and higher-risk MDS is encouraging,' said Konstantinos N. Aprilakis, M.D., Board Member at Stelexis and Partner at Deerfield Management. 'In addition to a favorable safety and tolerability profile, Stelexis has observed evidence of biologic and clinical activity for eganelisib in a particularly difficult-to-treat patient population. “eganelisib在经多线前期治疗的急性髓系白血病（AML）和高危骨髓增生异常综合征（MDS）患者中取得的初步数据令人鼓舞，”Stelexis董事会成员兼Deerfield Management合伙人康斯坦丁诺斯·N·阿普里拉基斯医学博士表示。“除具备良好的安全性和耐受性外，Stelexis还在这一治疗难度极高的患者群体中，观察到了eganelisib具有生物学和临床活性的证据。”I am especially delighted that Stelexis has identified a biomarker that may be used to identify patients most likely to benefit from treatment with eganelisib. These clinical data suggest that eganelisib has the potential to be effective across multiple hematologic malignancies of high unmet need.'. 我尤为欣喜的是，Stelexis 已发现一种生物标志物，可用于识别最有可能从 eganelisib 治疗中获益的患者。这些临床数据表明，eganelisib 有望在多种高度未满足临床需求的血液系统恶性肿瘤中展现疗效。'For nearly 20 years now, the field has been searching for therapies that offer a better prognosis to MDS-patients than hypomethylating agents alone. For far too long, clinicians had to primarily rely on classifying and selecting patients for investigational treatment based on prognostic scores or bone marrow blast counts, alone. 近20年来，该领域一直在寻求能为MDS患者提供优于单用去甲基化药物预后的治疗方案。长期以来，临床医生在分类和筛选患者接受试验性治疗时，往往只能单纯依赖预后评分或骨髓原始细胞计数。It is time we begin to classify patients based on disease-specific, functional, biological vulnerabilities and offer therapies that selectively target those biological vulnerabilities' said Manuel Aivado, MD, PhD, President and Chief Executive Officer of Stelexis BioSciences. 'We believe that myeloid malignancies may find in PI3K-gamma an analog to HER2 in breast cancer, and we are thrilled that the ground-breaking discoveries of our co-founders have paved Stelexis' way to this doorstep.'. Stelexis BioSciences 总裁兼首席执行官 Manuel Aivado 医学博士、哲学博士表示：“是时候开始根据疾病特异性、功能性和生物学脆弱性对患者进行分类，并提供能够选择性靶向这些生物学脆弱性的疗法了。我们认为，PI3K-γ 有望成为髓系恶性肿瘤中类似于乳腺癌 HER2 的靶点。我们深感振奋，联合创始人的突破性发现已为 Stelexis 铺平了通往这一目标的大门。”Based on these results, Stelexis plans to advance eganelisib into a randomized expansion cohort with hypomethylating agents in treatment-naïve, PI3K-gamma-high MDS patients with an IPSS-R category of intermediate, high, or very-high risk or with CMML-2. 基于上述结果，Stelexis计划将eganelisib推进至一项随机扩展队列研究，联合去甲基化药物，用于治疗初治、PI3Kγ高表达且IPSS-R风险分层为中危、高危或极高危的骨髓增生异常综合征（MDS）患者，或慢性粒单核细胞白血病2型（CMML-2）患者。About Eganelisib 关于艾加尼利西布Eganelisib is a first-in-class, oral, highly potent, and isoform-selective inhibitor of PI3K-gamma, the myeloid-restricted isoform of the PI3K kinase family. PI3K-gamma is dispensable in normal hematopoiesis and lymphocytes, differentiating it from delta-class PI3K inhibitors that have been associated with significant immune-mediated adverse events.. Eganelisib 是一种同类首创的口服、高效且具有亚型选择性的 PI3K-γ 抑制剂，PI3K-γ 为 PI3K 激酶家族中的髓系限制性亚型。PI3K-γ 在正常造血和淋巴细胞中并非必需，这一特性使其区别于已知会引发严重免疫介导不良反应的 PI3K-δ 抑制剂。In myeloid malignancies, PI3K-gamma signaling reinforces the differentiation block characteristic of AML and higher-risk MDS through PAK1, identifying PI3K-gamma as a therapeutic target whose inhibition can re-engage myeloid differentiation without imposing intrinsic myelosuppression or lymphoid toxicity.. 在髓系恶性肿瘤中，PI3K-γ信号通路通过PAK1强化了急性髓系白血病（AML）和较高危骨髓增生异常综合征（MDS）特征性的分化阻滞，表明PI3K-γ是一个治疗靶点，抑制该靶点可在不引起固有骨髓抑制或淋巴细胞毒性的情况下重新激活髓系分化。About Stelexis 关于 StelexisStelexis BioSciences, Inc. is a privately held clinical-stage biopharmaceutical company developing targeted therapies for myeloid malignancies. Stelexis was founded by Deerfield Management and is headquartered in Waltham, Massachusetts. Stelexis BioSciences, Inc. 是一家私营的临床阶段生物制药公司，致力于开发针对髓系恶性肿瘤的靶向疗法。Stelexis 由 Deerfield Management 创立，总部位于马萨诸塞州沃尔瑟姆。Stelexis' Co-Founders discovered that PAK1 is a key kinase maintaining the malignant stem cell phenotype responsible for the maturation block in patients with MDS or AML (Pandolfi et al., Blood 2015), later they identified PI3K-gamma as a core vulnerability in myeloid malignancies, and eventually showed that eganelisib-mediated inhibition of PI3K-gamma acts via inhibition of PAK1 to exert its therapeutic effects (Luo et al., Nature 2024).. Stelexis的联合创始人发现，PAK1是一种关键激酶，负责维持导致MDS或AML患者成熟阻滞的恶性干细胞表型（Pandolfi等，《Blood》2015）；随后，他们鉴定出PI3K-gamma是髓系恶性肿瘤的核心脆弱性，并最终证明，eganelisib介导的PI3K-gamma抑制是通过抑制PAK1来发挥治疗作用的（Luo等，《Nature》2024）。Stelexis is advancing eganelisib as a first-in-class treatment for HR-MDS and AML, and Stelexis is developing a potential best-in-class anti-IL-1RAP antibody for the treatment of Lower-Risk MDS, and other indications. Stelexis正在推进eganelisib作为治疗HR-MDS和AML的同类首创药物，同时Stelexis正在开发一种潜在的同类型最优抗IL-1RAP抗体，用于治疗低危MDS及其他适应症。For more information, please visit 如需更多信息，请访问www.stelexis.com www.stelexis.com. 。SOURCE Stelexis BioSciences, Inc. 来源：Stelexis BioSciences, Inc.21 二十一% 百分号more press release views with 通过……获得更多新闻稿浏览量Request a Demo 申请演示

2026-06-02

·PRNewswire

Stelexis BioSciences Announces Positive Phase 1 Data for Eganelisib in Relapsed/Refractory AML and Higher-Risk MDS in an Oral Presentation at ASCO 2026

Eganelisib induced complete remissions and hematologic improvements as a single-agent via myeloid differentiation in a Phase 1 study in relapsed/refractory patients with myeloid malignancies (MDS/AML) who show high expression of PI3K-gamma in bone marrow blasts. The improved overall survival in patients with high expression of PI3K-gamma in this Phase 1 study is internally consistent with the observed responses and is externally validated by the TCGA database, which suggests a poor prognosis for patients with high expression of PI3K-gamma. Eganelisib generated a striking efficacy signal while demonstrating a favorable safety and tolerability profile in this Phase 1 study. WALTHAM, Mass., June 2, 2026 /PRNewswire/ -- Stelexis BioSciences, Inc. (Stelexis) today announced results from a Phase 1 clinical trial (NCT06533761) of eganelisib, an oral, first-in-class PI3K-gamma inhibitor, in 21 patients with relapsed/refractory (R/R) acute myeloid leukemia (AML) or higher-risk myelodysplastic syndrome (HR-MDS). The data were presented in an oral session at the 2026 ASCO Annual Meeting by Mendel Goldfinger, M.D., of Montefiore Einstein Comprehensive Cancer Center. Key Findings The trial recruited a heavily pretreated patient population that was uniformly characterized by features that convey an unfavorable prognosis: 29% TP53-deleted or -mutated 90% abnormal cytogenetics 76% received more than two prior therapies 76% received prior venetoclax A modified objective response rate (defined as CR + Stable Disease with neutrophil count improvement) was achieved in: 50% (6/12) of patients with high PI3K-gamma expression vs. 0% (0/8) of patients with low PI3K-gamma expression (p<0.05, Fisher's exact test), using immunohistochemical staining of bone marrow biopsies Responses included molecular and major cytogenetic remissions in two patients in CR Five of six responding patients had severe or life-threatening neutropenia at baseline, and all five patients demonstrated rapid neutrophil count improvements, including a rapid normalization of neutrophil counts in four patients, consistent with induction of myeloid differentiation Median overall survival (OS) was 27 weeks in PI3K-gamma-high patients vs. 9.9 weeks in low expressors (HR 0.22; 95% CI 0.07–0.75) Based on historical patient data from the publicly available TCGA database, PI3K-gamma-high expression is an adverse prognostic factor for OS in patients receiving conventional therapy, thereby supporting a substantial clinical benefit observed following treatment with eganelisib in this study. Eganelisib was well tolerated at both dose levels (45 mg and 60 mg, once daily) with no dose-limiting toxicities and no intrinsic hematologic toxicity. This is consistent with the myeloid-restricted expression of PI3K-gamma, and with the observation that PI3K-gamma is dispensable for normal hematopoiesis (Gu et al., Blood 2024). The majority of adverse events in this study were disease-related rather than treatment-related, consistent with the underlying patient population. Treatment-related AEs were predominantly low-grade with no Grade 5 related AEs. Of note, no eganelisib-related SAEs were observed and no patient discontinued treatment due to an eganelisib-related AE. Published outcomes for patients with relapsed/refractory disease who failed frontline venetoclax and hypomethylating agent therapy have shown a median overall survival of approximately 2.4 months (Maiti et al., Haematologica 2021), underscoring the high unmet need in this population. "The preliminary data generated by eganelisib in patients with heavily pretreated AML and higher-risk MDS is encouraging," said Konstantinos N. Aprilakis, M.D., Board Member at Stelexis and Partner at Deerfield Management. "In addition to a favorable safety and tolerability profile, Stelexis has observed evidence of biologic and clinical activity for eganelisib in a particularly difficult-to-treat patient population. I am especially delighted that Stelexis has identified a biomarker that may be used to identify patients most likely to benefit from treatment with eganelisib. These clinical data suggest that eganelisib has the potential to be effective across multiple hematologic malignancies of high unmet need." "For nearly 20 years now, the field has been searching for therapies that offer a better prognosis to MDS-patients than hypomethylating agents alone. For far too long, clinicians had to primarily rely on classifying and selecting patients for investigational treatment based on prognostic scores or bone marrow blast counts, alone. It is time we begin to classify patients based on disease-specific, functional, biological vulnerabilities and offer therapies that selectively target those biological vulnerabilities" said Manuel Aivado, MD, PhD, President and Chief Executive Officer of Stelexis BioSciences. "We believe that myeloid malignancies may find in PI3K-gamma an analog to HER2 in breast cancer, and we are thrilled that the ground-breaking discoveries of our co-founders have paved Stelexis' way to this doorstep." Based on these results, Stelexis plans to advance eganelisib into a randomized expansion cohort with hypomethylating agents in treatment-naïve, PI3K-gamma-high MDS patients with an IPSS-R category of intermediate, high, or very-high risk or with CMML-2. About Eganelisib Eganelisib is a first-in-class, oral, highly potent, and isoform-selective inhibitor of PI3K-gamma, the myeloid-restricted isoform of the PI3K kinase family. PI3K-gamma is dispensable in normal hematopoiesis and lymphocytes, differentiating it from delta-class PI3K inhibitors that have been associated with significant immune-mediated adverse events. In myeloid malignancies, PI3K-gamma signaling reinforces the differentiation block characteristic of AML and higher-risk MDS through PAK1, identifying PI3K-gamma as a therapeutic target whose inhibition can re-engage myeloid differentiation without imposing intrinsic myelosuppression or lymphoid toxicity. About Stelexis Stelexis BioSciences, Inc. is a privately held clinical-stage biopharmaceutical company developing targeted therapies for myeloid malignancies. Stelexis was founded by Deerfield Management and is headquartered in Waltham, Massachusetts. Stelexis' Co-Founders discovered that PAK1 is a key kinase maintaining the malignant stem cell phenotype responsible for the maturation block in patients with MDS or AML (Pandolfi et al., Blood 2015), later they identified PI3K-gamma as a core vulnerability in myeloid malignancies, and eventually showed that eganelisib-mediated inhibition of PI3K-gamma acts via inhibition of PAK1 to exert its therapeutic effects (Luo et al., Nature 2024). Stelexis is advancing eganelisib as a first-in-class treatment for HR-MDS and AML, and Stelexis is developing a potential best-in-class anti-IL-1RAP antibody for the treatment of Lower-Risk MDS, and other indications. For more information, please visit . SOURCE Stelexis BioSciences, Inc. 21% more press release views with Request a Demo

临床结果临床1期ASCO会议

2026-05-14

·小药说药

利用髓系细胞可塑性进行癌症治疗

-01- 引言髓系细胞在癌症中扮演着多重角色，它们既通过血管生成、转移和免疫抑制促进肿瘤进展，又能刺激抗肿瘤免疫。传统上，这种双重功能被归因于细胞异质性，但越来越多的证据表明，髓系细胞可塑性才是癌症的一个更根本的特征。 -02- 一、髓系细胞可塑性的定义与类型髓系细胞是一个庞大且多样化的群体，包括红细胞、巨核细胞、粒细胞（中性粒细胞、嗜酸性粒细胞和嗜碱性粒细胞）、单核细胞、巨噬细胞、肥大细胞以及树突状细胞（DCs）的髓系亚群。在癌症中，巨噬细胞、单核细胞和粒细胞是免疫调节、肿瘤进展和治疗反应的核心。髓系分化具有高度适应性，这种特性被称为髓系可塑性。在癌症背景下，细胞可塑性在两个相互关联的层面上运作：分化可塑性和功能可塑性。 1. 分化可塑性分化可塑性是指髓系前体细胞及部分成熟细胞扩增并跨越谱系界限改变命运的能力。在实体瘤中，这表现为粒细胞-巨噬细胞前体（GMPs）的扩增和髓系生成的增加。例如，单核细胞根据微环境信号的不同，倾向于分化为巨噬细胞而非DCs；在病理条件下，淋巴样和单核细胞前体可分化为粒细胞；反之，在紧急髓系生成期间，中性粒细胞定向的前体细胞也可分化为单核细胞。 2. 功能可塑性功能可塑性是指髓系细胞在不发生谱系身份改变的情况下，其活性发生重大转变。在癌症中，经典的、具有宿主保护功能的细胞可以被重编程为一种病理状态，这种状态的细胞会抑制免疫、促进血管生成并协助肿瘤细胞侵袭。处于这种病理激活状态的细胞被称为髓源性抑制细胞，包括多形核MDSC（PMN-MDSC）和单核细胞MDSC（M-MDSC）亚群，它们具有独特的转录谱、表型特征和功能活性。 -03- 二、癌症中髓系可塑性的调控机制 1. 髓系生成的重编程在急性感染期间，病原体衍生的信号会触发强烈的髓系生成，以迅速扩增髓系细胞保护宿主。而在癌症中，肿瘤衍生的信号驱动适度但持久的髓系生成。这种持续的压力启动了PMN-MDSCs和M-MDSCs的生成，随后M-MDSCs分化为免疫抑制性的肿瘤相关巨噬细胞。近期研究表明，这种重编程始于造血干细胞（HSC）阶段的早期变化。在GMP阶段，正常的嗜中性粒细胞定向以IRF8下调、GFI1表达和C/EBPα上调为特征。GFI1抑制IRF8和EGR1，阻断单核细胞程序同时激活嗜中性粒细胞基因。在癌症中，GMPs中IRF8和视网膜母细胞瘤蛋白水平的降低使嗜中性粒细胞偏向PMN-MDSCs。IL-1家族细胞因子介导癌症相关的髓系生成并使前体细胞偏向免疫抑制命运。例如，IL-1β促进乳腺癌模型和患者中的粒细胞生成，而阻断IL-1β可部分逆转这种效应并减少小鼠模型中的转移。 2. 肿瘤微环境（TME）的塑造作用髓系细胞在癌症中的功能状态取决于TME中的许多因素，包括细胞因子环境、缺氧、肿瘤类型和分期。中性粒细胞是功能可塑性的典型例子。虽然PMN-MDSCs的功能状态通常与癌症患者的不良临床预后和对治疗的反应降低有关，但在特定条件下，中性粒细胞也可以促进抗肿瘤效应。例如，在小鼠肉瘤模型中，肿瘤诱导前消耗中性粒细胞与非常规T细胞缺乏激活有关，这对防止肉瘤发展至关重要。在大多数情况下，中性粒细胞的抗肿瘤效应是在治疗干预后观察到的。单核细胞和巨噬细胞也表现出功能二分法。虽然在癌症早期阶段存在促进抗肿瘤反应并是治疗反应所需的亚群，但也存在免疫抑制和促肿瘤的亚群。研究表明，巨噬细胞的功能比转录簇或基于生物标志物的亚群更具定义性，这意味着定位而非特定表型决定了巨噬细胞的功能。触发受体2（TREM2）已被确定为小鼠癌症模型和人类癌症中免疫抑制性TAMs的表型和功能标志物。 3. 对癌症治疗的反应髓系细胞可塑性不仅取决于肿瘤演变，还取决于治疗类型。这在分析免疫检查点抑制剂（ICIs）等免疫治疗药物后的肿瘤浸润髓系细胞时尤为明显。抗CD40或抗PD-1治疗可诱导表达高水平L-选择素（CD62L）的特定中性粒细胞亚群在小鼠体内积累。这些细胞刺激DCs产生IL-12，并在体外对癌细胞表现出细胞毒性活性。抗CTLA4和抗OX40治疗抗体的组合已被证明能诱导一种抗肿瘤中性粒细胞亚群，其特征是增强的激活特征，包括IL-1β和干扰素的产生及反应性。 DNA损伤反应（DDR）抑制剂对TME中髓系细胞的调节作用也日益明显。聚腺苷二磷酸核糖聚合酶（PARP）抑制剂奥拉帕利已被证明能重塑TME中的巨噬细胞浸润，主要促进促炎性巨噬细胞表型。耗竭免疫抑制性巨噬细胞可增强奥拉帕利在小鼠中的疗效。另一种DDR抑制剂——共济失调毛细血管扩张症和RAD3相关蛋白（ATR）抑制剂cerasertib，通过显著减少M-MDSCs和TAMs并消除PMN-MDSCs的免疫抑制活性，重塑了肿瘤内的髓系细胞区室。布鲁顿酪氨酸激酶（BTK）抑制剂依鲁替尼对单核细胞和TAM表型及功能产生细微影响，并在体内耗竭MDSCs，从而改善ICIs和CAR-T细胞疗法的疗效。 -04- 三、髓系细胞可塑性的治疗靶向策略 1. 巨噬细胞和M-MDSC的重编程针对M-MDSCs和TAMs关键调节因子的治疗药物已在多种癌症中进行了测试。靶向CSF1R–CSF1轴是研究最广泛的策略，包括小分子CSF1R抑制剂（如培西达替尼）和抗CSF1R抗体等。尽管这些治疗在CSF1驱动的疾病——腱鞘巨细胞瘤中产生了明确的临床疗效，但在实体瘤中的总体结果令人失望。CSF1R抑制在临床上减少了TAM/M-MDSC含量，耗竭了CSF1R依赖的库普弗细胞并调节了肝酶，表明靶点接合。有限的临床获益可能反映了多种因素，包括因肝毒性导致的剂量限制，这减少了通路抑制，PMN-MDSCs的代偿性扩增以及抗肿瘤TAM亚群的附带耗竭。靶向单核细胞趋化因子受体CCR2的早期研究也结果不一。在胰腺癌中，CCR2抑制剂PF-04136309与FOLFIRINOX联合是可耐受的并显示出令人鼓舞的活性，而与吉西他滨联合白蛋白紫杉醇联用则无益处且耐受性降低。TREM2阻断剂（如PY314抗体）正用于重编程肿瘤相关髓系表型。TREM2在胶质母细胞瘤中尤为相关，支持免疫抑制性髓系状态。然而，在三阴性乳腺癌和卵巢癌中的发现表明，TREM2表达可以标记抑制性和抗肿瘤髓系群，且叶酸受体2（FOLR2）阳性的髓系细胞在某些情况下可能代表更主要的抑制性亚群。 2. 中性粒细胞和PMN-MDSC的靶向靶向中性粒细胞和PMN-MDSCs面临独特的挑战，主要因为缺乏可操作的机制来直接调节这些群体。大多数临床努力使用CXCR2配体中和抗体和小分子拮抗剂。抗IL-8抗体（BMS-986253）与免疫疗法联合测试降低了血清IL-8水平，但未显示疗效信号。CXCR2小分子抑制剂已在多种联合方案中进行了探索。AZD5069在去势抵抗性前列腺癌患者亚群中产生了令人鼓舞的信号，但在胰腺癌或头颈癌中未显示明确的临床活性。SX-682在免疫治疗后转移性黑色素瘤的II期研究中显示出有希望的效果后，正在多项II期试验中研究。 3. 靶向细胞内通路 MDSC分化受多个信号节点影响，其中两个已从临床前研究进入临床试验：磷酸肌醇3-激酶γ（PI3Kγ）和JAK-STAT信号传导。PI3Kγ抑制剂eganelisib/IPI-549在头颈鳞状细胞癌、三阴性乳腺癌、肾细胞癌和非小细胞肺癌中进行了评估，主要与ICIs和化疗联合。转录特征表明，eganelisib-阿替利珠单抗联合重塑了TME，改变了表达CXCL9的TAMs与SPPI+TAMs的比例，并产生了更均匀的外周免疫细胞激活。 JAK抑制剂鲁索替尼在霍奇金淋巴瘤的I期试验中显示出有希望的活性，增强了ICI反应。除了T细胞调节外，该治疗还调整了外周中性粒细胞与淋巴细胞比率。另一种靶向JAK–STAT的方法使用STAT3反义寡核苷酸danvatirsen下调巨噬细胞和M-MDSCs中的STAT3。Danvatirsen主要被巨噬细胞、调节性T细胞和内皮细胞摄取，而非肿瘤细胞，提供了对抑制性巨噬细胞的选择性。 4. 靶向免疫抑制代谢物精氨酸酶在髓系细胞中过表达，其增强的精氨酸转化为尿素和鸟氨酸被认为限制T细胞和自然杀伤（NK）细胞功能。在一项Ib期试验中，精氨酸酶抑制剂INCB001158与帕博利珠单抗联合调节了外周精氨酸水平，但在头颈鳞状细胞癌和胆道癌中未观察到临床活性。吲哚胺2,3-双加氧酶（IDO）将色氨酸转化为犬尿氨酸。色氨酸耗竭损害T和NK细胞功能，而犬尿氨酸激活芳烃受体和一般控制非抑制性2（GCN2）激酶。多种IDO抑制剂试验结果为阴性，突显了通路冗余，这可能包括色氨酸2,3-双加氧酶（TDO）表达补偿IDO阻断。 -05- 三、面临的挑战与未来方向 1. 冗余性与毒性为什么多种针对髓系细胞的策略未能产生一致的临床获益？证据表明，广泛的细胞和信号冗余削弱了治疗效果。解决这一问题的方法包括同时靶向多个髓系细胞群体，如将CSF1R抑制剂与CXCR2拮抗剂联合靶向PMN-MDSCs，或在TAMs中上调C/EBPα并抑制PMN-MDSCs中的脂肪酸转运蛋白2（FATP2）。然而，这些方法带来相当大的靶向脱靶毒性风险，可能导致毒性并限制有效剂量。髓系定向疗法不太可能显示出有意义的单药活性，其最大益处预期来自与其他治疗的联合。 2. 选择性与精准治疗最有希望的策略是靶向选择性与病理性髓系细胞相关的分子和通路。这种方法可以减少毒性，同时保留抗肿瘤的、经典激活的TAMs、单核细胞和中性粒细胞。例如，病理性髓系细胞上内质网应激相关的DR5上调、PMN-MDSCs而非经典多形核中性粒细胞中FATP2的表达，以及PMN-MDSCs上CD300LD的表达。最终目标是将癌症中的髓系细胞从病理激活的促肿瘤细胞转变为抗肿瘤的经典激活细胞。 3. 疾病阶段与治疗时机髓系细胞在肿瘤演变的不同阶段具有不同的作用。在患有确定疾病的患者和携带肿瘤的小鼠中，髓系细胞主要是免疫抑制和促肿瘤的。然而，在肿瘤负荷非常低的情况下——特别是在有效的免疫治疗后——正常的髓系细胞可能是有益的，并可能发挥抗肿瘤活性。因此，临床试验中常用的连续给药模式可能忽略了髓系细胞反应的时间复杂性。阐明中性粒细胞和其他髓系亚群何时最相关将是优化治疗时机和完善患者选择的关键。参考资料： Harnessing myeloid cell plasticity for cancer therapy. Nat Cancer. 2026 May 12 公众号已建立“小药说药专业交流群”微信行业交流群以及读者交流群，扫描下方小编二维码加入，入行业群请主动告知姓名、工作单位和职务。

100 项与 Eganelisib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	Eganelisib	-	DB16296

研发状态

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
晚期头颈癌	临床2期	美国	University of California San Diego	2020-03-06
HPV相关鳞状细胞癌	临床2期	美国	University of California San Diego	2020-03-06
局部晚期头颈部鳞状细胞癌	临床2期	美国	University of California San Diego	2020-03-06
局部晚期透明细胞肾细胞癌	临床2期	美国	Infinity Pharmaceuticals, Inc.	2019-12-17
转移性透明细胞性肾细胞癌	临床2期	美国	Infinity Pharmaceuticals, Inc.	2019-12-17
三阴性乳腺癌	临床2期	美国	Infinity Pharmaceuticals, Inc.	2019-12-17
晚期癌症	临床2期	美国	Infinity Pharmaceuticals, Inc.	2019-09-25
晚期癌症	临床2期	捷克	Infinity Pharmaceuticals, Inc.	2019-09-25
晚期癌症	临床2期	法国	Infinity Pharmaceuticals, Inc.	2019-09-25
晚期癌症	临床2期	意大利	Infinity Pharmaceuticals, Inc.	2019-09-25

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临床结果

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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


NCT06533761 (ASCO2026)	临床1期	急性髓性白血病 \| 高危骨髓增生异常综合征 TP53 mutation	15	Eganelisib 45 mg	艱壓艱製選觸鑰鹽襯願(齋鏇選獵製窪積繭糧憲) = 網築憲夢獵鏇製願膚簾襯鹽艱醖鏇廠遞鏇憲鬱 (壓憲壓齋憲蓋糧範糧糧 )	积极	2026-05-29
NCT03795610 (CTgov)	临床2期	晚期头颈癌 \| HPV相关鳞状细胞癌 \| 局部晚期头颈部鳞状细胞癌	16	IPI-549	製網選築範構鬱襯獵鹽 = 積蓋鹽範醖襯觸淵築觸獵艱獵襯積餘夢繭顧積 (範顧製鏇遞鹹繭衊艱壓, 網遞鏇願蓋夢積憲遞鏇 ~ 築繭鑰獵範構獵艱壓醖) 更多	-	2025-07-25
MARIO-3 (SABCS2022)	临床2期	三阴性乳腺癌一线 PD-L1 positive	43	Eganelisib 30 mg + Atezolizumab + Nab-paclitaxel	鏇憲網蓋醖淵願選鑰窪(壓製憲廠鏇獵遞艱構蓋) = 築選蓋積製糧窪觸範鬱廠衊顧願糧鬱壓獵鑰遞 (窪廠構艱願蓋簾蓋顧餘 ) 更多	积极	2022-02-15
NCT03961698 (MARIO-3, Corporate Publications) 人工标引	临床2期	三阴性乳腺癌 \| 尿路上皮癌一线 Triple Negative	49	Atezolizumab+Albumin-Bound Paclitaxel+Eganelisib	衊觸鏇鬱蓋夢蓋膚齋淵(積遞鑰積顧網蓋鬱廠製) = 鹽艱鑰繭餘選壓繭襯鏇顧鑰築糧齋簾範膚窪鑰 (餘窪鬱範製積鑰鏇獵鏇 ) 更多	积极	2021-07-27
NCT03980041 (MARIO-275, Corporate Publications) 人工标引	临床2期	三阴性乳腺癌 \| 尿路上皮癌 Triple Negative	49	Nivolumab+Placebo	醖糧鑰鏇糧蓋觸選鑰觸(鏇願選襯網繭淵願艱製) = the most common ≥Grade 3 TEAEs across all doses, all causality, were disease progression (27.3%), anemia (12.1%), and hepatic AEs including hepatotoxicity (15.2%), increased ALT (12.1%) and increased AST (12.1%) with no Hy’s Law. 齋蓋壓夢鏇製觸壓願繭 (鏇鹹簾齋網衊糧獵艱蓋 ) 更多	积极	2021-07-27
NCT03980041 (MARIO-275, Corporate Publications) 人工标引	临床2期	三阴性乳腺癌 \| 尿路上皮癌 Triple Negative	49	Nivolumab+eganelisib		积极	2021-07-27
NCT03980041 (MARIO-275, ASCO_GU 12021 \| ASCO_GU 22021) 人工标引	临床2期	晚期尿路上皮癌	-	nivolumab+IPI 549	鬱鬱膚窪鹽餘簾範鏇夢(憲蓋鬱網壓範窪醖齋獵) = 淵壓鏇築齋鑰蓋艱網鬱範鹹膚築獵鬱蓋齋積淵 (餘觸廠醖醖壓淵廠觸簾 ) 更多	积极	2021-02-20
NCT03980041 (MARIO-275, ASCO_GU 12021 \| ASCO_GU 22021) 人工标引	临床2期	晚期尿路上皮癌	-	placebo+nivolumab	鬱鬱膚窪鹽餘簾範鏇夢(憲蓋鬱網壓範窪醖齋獵) = 觸選淵廠壓淵夢顧網淵範鹹膚築獵鬱蓋齋積淵 (餘觸廠醖醖壓淵廠觸簾, 1 ~ 91) 更多	积极	2021-02-20
NCT03719326 (ARC-2, AACR2021) 人工标引	临床1期	卵巢癌 \| 转移性三阴性乳腺癌	29	AB928 150 mg + pegylated liposomal doxorubicin (Doublet)	願範憲壓遞製範艱網願(夢膚繭積憲鏇簾遞鹹願) = Four pts reported 6 Gr ≥3 SAEs 廠鹹窪襯鑰選築觸願簾 (獵醖網範範窪鏇製繭製 ) 更多	积极	2021-02-15
NCT03719326 (ARC-2, AACR2021) 人工标引	临床1期	卵巢癌 \| 转移性三阴性乳腺癌	29	IPI-549 40 mg + AB928 150 mg + pegylated liposomal doxorubicin (Triplet)		积极	2021-02-15
NCT03961698 (Mario-3, SABCS2021)	临床2期	三阴性乳腺癌一线	6	Eganelisib 30 mg	襯鬱壓鹽簾範築窪憲網(蓋獵壓鹽鹹簾範顧願顧) = 簾憲顧淵窪觸齋廠艱衊齋鹽膚憲積構願餘窪壓 (醖糧遞築淵網鏇觸製醖 )	积极	2021-02-15
NCT02637531 (IPI-549-01, SITC2020)	临床1期	头颈部鳞状细胞癌	180	Eganelisib 40 mg QD PO + Nivolumab 240 mg Q2W IV	觸醖積構遞鏇觸簾構獵(構壓廠簾襯艱製鏇衊壓) = 22.8% of patients experienced anemia 觸艱願鏇齋蓋糧鏇窪鏇 (糧膚憲壓築夢範簾艱廠 ) 更多	积极	2020-12-10
NCT02637531 (IPI-549-01, SITC2020)	临床1期	黑色素瘤	180	Eganelisib 40 mg	鏇鏇壓醖夢獵廠簾夢範(繭構淵襯憲觸製醖糧糧) = 22.8% of patients treated with eganelisib + nivolumab experienced anemia 範範顧壓製淵齋襯網簾 (築餘蓋醖夢憲淵製蓋選 ) 更多	积极	2020-11-09