Phase Ib Study on the Prevention of Graft-versus-host Disease (GVHD) in Children After Haploid Stem Cell Transplantation Using Cyclophosphamide (PTCy) Combined With Sirolimus and VIC-1911 Tablets

This study is a single arm, open label Phase Ib clinical trial, consisting of two parts: the first part is a safety introduction trial, and the second part is a dose escalation trial. In the first part, the tolerability, safety, PK characteristics, PD characteristics, and preliminary efficacy of VIC-1911 tablets in combination with PTCy and sirolimus will be explored. The first part will conduct safety introduction tests at the same dose as those already tested abroad to determine the dosage required for VIC-1911 tablets to meet safety and effective biological activity. The dose limiting toxicity (DLT) in Phase I study will be evaluated from the first administration of VIC-1911 tablets to 28 days after administration. On this basis, the second part of the experiment will be conducted to further explore the effectiveness and safety of VIC-1911 tablets combined with PTCy and sirolimus under RP2D for preventing GVHD in haplo HSCT patients after myeloablative pretreatment

开始日期2026-09-28

申办/合作机构

上海交通大学医学院

NCT06519721

/ Active, not recruitingN/AIIT

Safety and Efficacy Study of Lenvatinib Combined With VIC-1911 for the Treatment of Advanced Hepatocellular Carcinoma

This study is a single-arm, open-label trial to clarify the safety and efficacy of the combined treatment of lenvatinib and VIC-1911 in patients with advanced liver cancer.

开始日期2024-08-06

申办/合作机构-

NCT05718882

/ TerminatedN/AIIT

Safety and Efficacy of Lenvatinib Combined With VIC-1911 in the Treatment of Lenvatinib-unresponsive or Lenvatinib-resistant Hepatocellular Carcinoma

This is a prospective clinical study aiming to test the safety and efficacy of lenvatinib in combination with Aurora kinase A inhibitor VIC-1911 in participate with lenvatinib-unresponsive or lenvatinib-resistant hepatocellular carcinoma(HCC).

开始日期2023-08-30

申办/合作机构

上海交通大学医学院附属仁济医院

100 项与 TAS-119 相关的临床结果

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100 项与 TAS-119 相关的转化医学

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100 项与 TAS-119 相关的专利（医药）

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项与 TAS-119 相关的文献（医药）

2026-08-04·MOLECULAR CANCER THERAPEUTICS

NN-01-195, a Novel Conjugate of HSP90 and AURKA Inhibitors, Effectively Targets Solid Tumors

Article

作者: Akunuri, Ravikumar ; Nguyen, Theodore T. ; Pirestani, Shabnam ; Cai, Kathy Q. ; Golemis, Erica A. ; Burtness, Barbara A. ; Cassel, Joel ; Nandwana, Nitesh K. ; Chkhalo, Oleksandra ; Srikanth, Yellamelli V.V. ; Salvino, Joseph M. ; Lu, Lily ; Mehra, Manish Kumar ; Borghaei, Hossein ; Bagnyukova, Tetyana ; Lamperelli, Julia

Abstract:

Aurora kinase A (AURKA) regulates cell-cycle progression into and through mitosis. As overexpression of AURKA in cancer cells is common and associated with mitotic defects and aneuploidy, small-molecule inhibitors of AURKA have been developed as candidate therapies for cancer. However, these have typically low activity in clinical trials, with systemic toxicities limiting dose escalation. To concentrate an AURKA inhibitor in tumors, we exploited the fact that cancer cells in solid tumors selectively express high levels of the chaperone HSP90 to counteract intratumoral stresses, providing a potential targeting moiety. We developed NN-01-195 as a novel chimeric small molecule that combines an AURKA inhibitor related to TAS-119/VIC-1911 with an HSP90-binding moiety related to SNX2112 and evaluated its function. NN-01-195 tightly binds and inhibits both AURKA and HSP90 in biochemical assays. In cancer cells, NN-01-195 causes mitotic arrest and spindle abnormalities and a profile of signaling changes that closely resembles that of an AURKA inhibitor. ADME assessment indicates moderate metabolism in liver microsomes (T1/2 = 46.7 minutes) and sustained plasma exposure following single intraperitoneal injection. Maximum tolerated repeated dose testing over 5 days indicates no weight loss or toxicity at 80 mg/kg. Importantly, NN-01-195 accumulates in xenografted tumors at higher levels and for longer duration than does an AURKA inhibitor. Furthermore, in combination with an inhibitor of the G2/M checkpoint protein WEE1, NN-01-195 is more potent than VIC-1911 in limiting growth of xenograft tumors. These data support the exploration of NN-01-195 and improved analogs as promising new candidates for therapeutic evaluation.

2026-08-01·Cancer research communications

Combination AURKA and WEE1 Inhibition Exhibits Efficacy in EGFR or Pan-ERBB Inhibitor–Resistant Head and Neck Squamous Cell Carcinoma

Article

作者: Nguyen, Theodore T. ; Golemis, Erica A. ; Bagnyukova, Tetyana ; Burtness, Barbara A. ; Silva, Flaviane N. ; Goeckel, Fiona M. ; Borghaei, Hossein ; Lee, Jong Woo

Abstract:

More than 600,000 cases of head and neck squamous cell carcinoma (HNSCC) are diagnosed globally each year. Many HNSCCs overexpress the ERBB family member epidermal growth factor receptor (EGFR), and EGFR inhibitors (EGFRi) and pan-ERBB inhibitors (ERBBi) are clinically active in the treatment of locally advanced, metastatic, or recurrent HNSCC. However, resistance to these inhibitors typically develops, often associated with epithelial–mesenchymal transition (EMT). Aurora kinase A (AURKA), a mitotic regulator with expanded signaling functions in tumors, has been reported to reverse EGFR resistance in EGFR-mutated lung cancer. To identify strategies to overcome resistance in HNSCC, we developed HNSCC cell models that were treatment-naïve parental or selected for resistance to the EGFRi erlotinib or the ERBBi afatinib. The resistant HNSCC models had typically undergone partial EMT, consistent with clinical resistance, associated with upregulation of the AURKA partner protein NEDD9. Synergy of the AURKA inhibitor VIC-1911 with erlotinib or afatinib in parental models was reduced in resistant models in short-term growth assays. In longer-term clonogenic assays and in vivo, cells selected for EGFRi/ERBBi resistance showed heightened sensitivity to VIC-1911, contributing to reduced synergy. Based on increased AURKA dependence, we compared the combination of VIC-1911 with adavosertib, an inhibitor of the cell-cycle checkpoint regulator WEE1, in parental and resistant models. These showed a combination effect both in vitro and in vivo that was retained in ERBBi-resistant xenografts, suggesting the potential value of combined AURKA and WEE1 inhibitor use in patients with ERBBi-resistant HNSCC.

Significance::

Treatment resistance is a major source of mortality for HNSCC. This study investigates strategies to overcome resistance to inhibitors of the ERBB family, which are commonly used for the treatment of advanced HNSCC. The results suggest the value of the use of combined AURKA and WEE inhibition in the resistance setting.

2026-04-14·Blood Advances

Targeting Aurora kinase A to prevent GVHD and relapse after myeloablative allogeneic hematopoietic cell transplantation

Article

作者: Maakaron, Joseph E. ; Myers, Thomas J. ; Walton, Kelly ; El Jurdi, Najla ; Cao, Qing ; Terezakis, Stephanie ; Grover, Punita ; Quinones, Victoria ; Paradiso, Linda J. ; Betts, Brian C. ; Holtan, Shernan G. ; Juckett, Mark B. ; DeFor, Todd E. ; Bachanova, Veronika ; Hou, Joshua H.

Abstract:

The success of posttransplant cyclophosphamide (PTCy) for graft-versus-host disease (GVHD) prophylaxis has driven efforts to optimize partner therapies that balance GVHD and relapse prevention. We report phase 1 dose-finding results of PTCy, sirolimus (SIR), and VIC-1911, a selective oral Aurora kinase A (AURKA) inhibitor, after myeloablative allogeneic hematopoietic cell transplantation (allo-HCT). Results from murine and in vitro studies informed the development of the novel drug combination. In the phase 1 trial, patients aged 18 to 60 years received myeloablative conditioning, followed by PTCy (50 mg/kg; days +3/+4), SIR (from day +5; target 8-12 ng/mL), and VIC-1911 (25, 50, or 75 mg twice daily; days +5 to +45). The primary end point was achieving <54% phosphorylated histone H3 serine 10 expression in CD4+ T cells by day +21. Preclinical models show that combining SIR with AURKA inhibition suppresses signaling downstream of CD28, enhancing GVHD prevention while leveraging the antileukemia activity of AURKA inhibition. In the phase 1 trial, the optimal VIC-1911 dose achieving target pathway inhibition without dose-limiting toxicities was 75 mg twice daily. Clinical outcomes included no grade 3 to 4 acute GVHD through day 180 (0%) and low rates of moderate/severe chronic GVHD (6%) and relapse (0%) through 1 year (5/16 received maintenance). The 1-year overall survival for this cohort was 94%. VIC-1911 at 75 mg twice daily, combined with PTCy and SIR, effectively suppressed AURKA activity, offering promising GVHD and relapse prevention with a favorable safety profile and promising early clinical outcomes. The trial was registered at www.clinicaltrials.gov as NCT05120570.

项与 TAS-119 相关的新闻（医药）

2024-06-01

·同写意

捷思英达将在2024 ASCO公布Aurora A抑制剂VIC-1911治疗肺癌的I期临床研究数据

同写意20岁庆！中国医药创新未来之路！“意”同创新，穿越周期，赢得未来。7月中旬，苏州金鸡湖畔，让我们与“新药写意人”一起为中国医药创新“同写意”！捷思英达将在2024年美国临床肿瘤学会年会（ASCO）公布极光激酶A （Aurora A）抑制剂VIC-1911治疗肺癌的I期临床研究数据，本次报告的标题为【Phase I trial of aurora kinase A（AURKA）Inhibitor VIC-1911 plus Osimertinib for TKI-resistant, EGFR-mutant non-small cell lung cancer（NSCLC）】，编号：8077。此项研究共入组了24例患者，剂量递增阶段入组了7例患者（150mg 4例，200mg 3例），未观察到DLT，后选择200mg作为RP2D。与VIC-1911相关的最常见不良反应为腹泻（52.3%）、白细胞减少（38.1%）、中性粒细胞减少（3.3%）和血小板减少（28.6%）。剂量扩展阶段入组了17例受试者。在总体可评价疗效的23例患者中，10例患者为未使用奥希替尼（T790m阴性8例，T790m阳性2例），13例患者为奥希替尼耐药。未使用奥希替尼患者的客观缓解率（ORR）为50% （5PRs, T790m阴性=4,T790m阳性=1），疾病控制率(DCR)为80%（3SDs）。对于奥希替尼耐药患者，ORR为0%，DCR为53.8%（7SDs)）。在疾病控制的患者中，66.7%（10/15）的患者在数据截止时仍在治疗中，中位随访时间为5.5个月，未达到中位缓解持续时间（DOR），6个月DOR率为50%。未使用奥希替尼和奥希替尼耐药患者的中位无进展生存期（PFS）分别为4.6个月和2.1个月，6个月无进展生存率分别为70.0%和38.5%。总体结果显示VIC-1911联合奥希替尼在既往接受过治疗的EGFR突变的非小细胞肺癌患者中具有良好的耐受性。联合用药也显示出持续的抗肿瘤活性，这表明阻断极光激酶A/AURKA在延缓奥希替尼耐药出现方面具有潜力。VIC-1911是新一代高选择性、临床安全的细胞周期调节激酶Aurora A抑制剂，目前在中美处于临床1b研究阶段，具备国际首创新药潜力。VIC-1911在干细胞移植后预防移植物抗宿主病（GVHD）和白血病复发的临床研究中初步展示很好的疗效（参见2023年12月美国血液肿瘤年会ASH会议报告）。关于捷思英达捷思英达是一家聚焦新一代肿瘤精准治疗新药研发的生物医药企业，公司核心业务致力于解决肿瘤新药研究的两个痛点：（a）精准靶向，改善药物的临床安全性和潜在治疗窗口；（b）肿瘤耐药解决方案。捷思英达和国内外最权威的临床医生和研究机构合作，开展国际前沿水平的转化医学研究和临床研究，目前已经在干细胞移植后预防GVHD和白血病复发，非小细胞肺癌，乳腺癌，黑色素瘤及其脑转移，头颈癌以及小细胞肺癌等领域取得重要进展。捷思英达目前有3个国家一类新药产品分别处于临床1期和临床II期研究阶段。近期直播推荐:

临床结果ASCO会议临床1期临床2期

2024-06-01

·医药观澜

捷思英达公布2款小分子抗肿瘤新药临床试验数据 | ASCO

▎药明康德内容团队报道5月31日消息，捷思英达宣布将在2024年美国临床肿瘤学会年会（ASCO）上公布两款在研新药临床试验数据，分别为：Aurora A抑制剂VIC-1911治疗肺癌的1期临床研究数据；以及ERK抑制剂JSI-1187治疗实体瘤的1期临床研究数据。VIC-1911：Aurora A抑制剂适应症：非小细胞肺癌VIC-1911是新一代高选择性、临床安全的细胞周期调节激酶Aurora A抑制剂，目前在中美处于临床1b研究阶段。此前，VIC-1911在干细胞移植后预防移植物抗宿主病（GVHD）和白血病复发的临床研究中已初步展示良好的疗效。本次在ASCO大会上展示的是一项1期临床研究数据，旨在评估VIC-1911联合第三代EGFR-TKI奥希替尼治疗TKI耐药、EGFR突变的非小细胞肺癌（NSCLC）患者的效果。此项研究共入组了24例患者，剂量递增阶段入组了7例患者（150mg 4例，200mg 3例），未观察到剂量限制性毒性（DLT），后选择200mg作为2期推荐剂量（RP2D）。与VIC-1911相关的最常见不良反应为腹泻（52.3%）、白细胞减少（38.1%）、中性粒细胞减少（33.3%）和血小板减少（28.6%）。剂量扩展阶段入组了17例受试者。在总体可评价疗效的23例患者中，10例患者为未使用奥希替尼（T790m阴性8例，T790m阳性2例），13例患者为奥希替尼耐药。未使用奥希替尼患者的客观缓解率（ORR）为50%（5例部分缓解[PRs], T790m阴性=4，T790m阳性=1)，疾病控制率（DCR）为80%（3例病情稳定[SDs]）。对于奥希替尼耐药患者，ORR为0%，DCR为53.8%（7例SDs）。在疾病控制的患者中，66.7%（10/15）的患者在数据截止时仍在治疗中，中位随访时间为5.5个月，未达到中位缓解持续时间（DOR），6个月DOR率为50%。未使用奥希替尼和奥希替尼耐药患者的中位无进展生存期（PFS）分别为4.6个月和2.1个月，6个月无进展生存率分别为70.0%和38.5%。研究认为：VIC-1911联合奥希替尼在既往接受过治疗的EGFR突变的非小细胞肺癌患者中具有良好的耐受性，联合用药也显示出持续的抗肿瘤活性，这表明阻断极光激酶A/AURKA在延缓奥希替尼耐药出现方面具有潜力。JSI-1187：ERK抑制剂适应症：实体瘤JSI-1187是一款高选择性ERK激酶抑制剂，目前在中美处于临床1期研究阶段。本次在ASCO大会上展示的是JSI-1187治疗MAPK通路突变晚期实体瘤患者的1期临床研究数据。截至2023年12月23日，此研究共入组了26例患者，其中每日两次（BID）组23例，80mg每日一次（QD）组3例。QD组未发生DLT；BID 96和80 mg组分别发生1例DLT（1例黄斑水肿）和2例DLT（1例黄斑水肿和1例肺炎）。JSI-1187的16 mg ~96mg BID组最常见的不良反应为低白蛋白血症（69.6%）、皮疹（62.5%）和贫血（43.5%），而JSI-1187 80mg QD最常见的不良反应为皮疹（100%）、白细胞减少（100%）和中性粒细胞减少（66.7%）。JSI-1187的16 mg ~ 96mg BID组治疗最常见的3级相关不良反应为贫血（17.4%）和血小板减少（8.7%）。26例患者中有18例评估了肿瘤缓解情况，在16-96 mg BID组和80 mg QD组中的最佳的疗效均为SD，包括1例NRAS突变黑色素瘤患者在32mg BID治疗时肿瘤缩小29.8%和1例MEK1 K57N突变肺癌患者在72mg BID治疗时肿瘤缩小21.6%，其中一例肺癌患者治疗持续时间已达14个月。研究认为：总体来看，JSI-1187单药治疗晚期实体瘤患者耐受性良好，初步显示出抗肿瘤作用。目前的证据支持未来在MAPK突变肿瘤患者中探索JSI-1187单药或联合治疗的效果。本文由药明康德内容团队根据公开资料整理编辑，欢迎个人转发至朋友圈。转发授权请在「医药观澜」微信公众号留言联系我们。其他合作需求，请联系wuxi_media@wuxiapptec.com。免责声明：药明康德内容团队专注介绍全球生物医药健康研究进展。本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。

ASCO会议临床结果临床1期临床2期

2024-03-13

·BioBAY

研发动态丨捷思英达Aurora A激酶抑制剂VIC-1911片治疗乳腺癌获批中国临床

3月11日，BioBAY园内企业捷思英达宣布，其小分子创新药Aurora A抑制剂VIC-1911片通过国家药品监督管理局（NMPA）的新药临床研究申请审评，并收到临床批件（2024LP00592）。捷思英达本次获批开展Aurora A抑制剂VIC-1911单药/联合奥拉帕利治疗晚期乳腺癌的临床研究。据世卫组织旗下的国际癌症研究机构(IARC)发布的最新的癌症负担数据（GLOBOCAN 2022)显示，全球乳腺癌年新增病例超过229万，高据第二位，年死亡病例超过66万（第四位），临床需求高未满足。VIC-1911有望为乳腺癌患者提供更为持久、显著的治疗效果。在此之前，VIC-1911片已获得两项中国临床1期批件(2021LP02060及2022LP00790)，批准适应症分别为与紫杉醇联合治疗晚期卵巢癌、输卵管癌和原发性腹膜癌，以及与奥希替尼联用治疗晚期非小细胞肺癌。此次IND获批是NMPA批准的第三项VIC-1911临床研究，也是地产化产品首次获批中国临床。地产化的成功保证了药品供应链的稳定，为开展更广泛、深入的临床开发提供了有力的支持。VIC-1911是新一代、高选择性、细胞周期调节激酶Aurora A抑制剂，美国临床I/II期开发阶段。VIC-1911已经率先在临床上被证明没有明显的骨髓抑制毒副作用。目前临床开发处于国际领先位置，具备国际首创潜力。捷思英达是一家聚焦肿瘤精准治疗新药研发生物医药企业，以临床需求和最新转化医学研究成果为驱动，致力于原创新药研发。资深和国际化高管团队在职业生涯中已经在中美开发成功20多款上市新药。捷思英达和国内外最权威的临床医生和研究机构合作，开展国际前沿水平的转化医学研究和临床研究，主要临床开发方向包括RAS基因突变的抗癌新药研发；克服EGFR抑制剂和KRAS抑制剂等靶向药的耐药研究；预防异基因造血干细胞移植后GVHD和白血病复发的研究；合成致死和药物联用策略的研究，目前已有三个产品进入或者即将进入临床2期研究阶段。▌文章来源：捷思英达责编：赵家帅审核：任旭推荐阅读研发动态丨星锐医药：呼吸道合胞病毒RSV mRNA疫苗STR-V003获美国FDA临床试验许可研发动态丨创澜生物：随机式、高通量全自动分子诊断系统GenMax 16全新上市研发动态丨映恩生物：靶向HER2的ADC拟纳入突破性治疗品种，针对子宫内膜癌

临床1期临床2期疫苗临床申请AACR会议

100 项与 TAS-119 相关的药物交易

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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
急性白血病	临床2期	美国	University of Minnesota Masonic Cancer Center	2022-03-17
移植物抗宿主病	临床2期	美国	University of Minnesota Masonic Cancer Center	2022-03-17
骨髓增生异常综合征	临床2期	美国	University of Minnesota Masonic Cancer Center	2022-03-17
骨髓增生性疾病	临床2期	美国	University of Minnesota Masonic Cancer Center	2022-03-17
非霍奇金淋巴瘤	临床2期	美国	University of Minnesota Masonic Cancer Center	2022-03-17
晚期肝细胞癌	临床1期	中国	捷思英达医药技术（上海）有限公司	2023-12-18
KRAS G12C突变非小细胞肺癌	临床1期	美国	VITRAC Therapeutics, LLC	2022-11-09
晚期非小细胞肺癌	临床1期	中国	-	2022-09-21
EGFR突变的非小细胞肺癌	临床1期	中国	-	2022-09-21
乳腺癌	临床1期	美国	捷思英达医药技术（上海）有限公司	2022-01-30

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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


NCT05120570 (4925, CTgov)	临床1/2期	骨髓增生性疾病 \| 非霍奇金淋巴瘤 \| 急性白血病 ... 更多	16	VIC- 1911	醖鑰鏇艱膚簾鏇壓襯鏇 = 顧願積鏇簾淵艱願鏇餘襯製範繭選製艱齋夢夢 (壓鬱醖選餘願製艱鏇壓, 糧蓋齋蓋網觸遞願齋鏇 ~ 夢窪繭壓願鹽鬱夢鬱鏇)	-	2025-12-22
NCT05374538 (CTgov)	临床1期	KRAS G12C突变非小细胞肺癌	3	VIC-1911 (Dose Escalation Phase, Cohort 1a: VIC-1911 Monotherapy)	窪蓋蓋選繭願構蓋鹽糧 = 膚選鏇壓觸鏇構鏇構顧願淵壓窪衊網夢壓衊襯 (製衊築膚鬱夢齋膚艱獵, 鑰醖鹹齋衊壓糧遞衊艱 ~ 遞膚顧鏇襯獵繭選鏇積) 更多	-	2025-05-01
NCT05374538 (CTgov)	临床1期	KRAS G12C突变非小细胞肺癌	3	VIC-1911+sotorasib (Dose Escalation Phase, Cohort 1b: VIC-1911 Plus Sotorasib Combination Therapy)	窪蓋蓋選繭願構蓋鹽糧 = 膚淵餘繭窪淵膚憲艱廠願淵壓窪衊網夢壓衊襯 (製衊築膚鬱夢齋膚艱獵, 蓋艱鏇醖構網鹹繭鏇鬱 ~ 觸積願鹽製繭艱淵憲觸) 更多	-	2025-05-01
NCT05489731 (ASCO2024) 人工标引	临床1期	EGFR突变的非小细胞肺癌 EGFR Mutation	24	VIC-1911 150mgosimertinib	觸淵餘網衊鹹鏇壓齋衊(衊築築鬱鏇繭鹹構觸淵) = No observed 膚鹹範淵願廠鹹構醖淵 (構糧獵夢膚夢鏇簾鑰鏇 ) 更多	积极	2024-05-24
NCT05489731 (ASCO2024) 人工标引	临床1期	EGFR突变的非小细胞肺癌 EGFR Mutation	24	VIC-1911VIC-1911 150mgosimertinib0mg or 200mg BID + osimertinib 80 mg QD (osimertinib-naïve)		积极	2024-05-24
NCT02134067 (ASCO 12019 \| ASCO 22019) 人工标引	临床1期	HR阳性/HER2低表达实体瘤	26	paclitaxel+TAS-119	夢鑰簾製簾襯顧鹽鏇鏇(衊壓蓋窪築廠窪遞獵淵) = diarrhea, nausea, and fatigue (most ≤Gr2) 範願襯窪積憲糧獵鬱蓋 (窪積觸衊鬱選憲積膚顧 ) 更多	积极	2019-06-01
NCT02448589 (ASCO2019)	临床1期	HR阳性/HER2低表达实体瘤	74	TAS-119	憲衊遞範簾衊廠淵願蓋(選衊齋醖製範鏇蓋夢遞) = Grade 3 ocular toxicity in 1 pt (300 mg cohort) 夢選鹽鏇選範醖鹽淵繭 (糧鏇築衊壓簾憲淵構淵 ) 更多	不佳	2019-05-26