A Phase II, Open-Label, Multicenter Clinical Study to Evaluate the Safety, Efficacy, and Pharmacokinetics of TT-00420 (Tinengotinib) Tablets Combined With Fulvestrant Injection in Patients With Hormone Receptor-Positive (HR+) and Human Epidermal Growth Factor Receptor 2 (HER-2) Negative or Low-Expressing Recurrent or Metastatic Breast Cancer Who Have Failed Prior Treatment

The goal of this clinical trial is to learn if tinengotinib combined with fulvestrant works to treat patients with HR-Positive and HER-2-Negative or low-expressing advanced breast cancer. It will also learn about the safety of combination therapy. The main questions it aims to answer are:
1. Does tinengotinib combined with fulvestrant reduce the tumor burden in participants?
2. What medical problems do participants have when taking the combination therapy?
Participants will:
Take tinengotinib and fulvestrant to find the optimal dose of tinengotinib for the combination therapy in Part A.
In Part B, will take tinengotinib at the optimal dose with fulvestrant or tinengotinib alone to see if the combination therapy works better than tinengotinib monotherapy.

开始日期2026-03-17

申办/合作机构

药捷安康（南京）科技股份有限公司

NCT07328919

/ Not yet recruiting临床3期

A Phase III, Randomized Controlled, Open-Label, Multicenter Clinical Study Evaluating the Efficacy and Safety of TT-00420 Tablets Versus Chemotherapy in Patients With Surgically Unresectable Advanced or Metastatic Intrahepatic Cholangiocarcinoma Harboring FGFR2 Fusions/Rearrangements or Mutations, Who Have Progressed or Relapsed After Prior First-Line Systemic Therapy

This is an open-label, randomized, controlled, multicenter, phase III clinical study designed to evaluate the efficacy and safety of TT-00420 tablets as monotherapy versus chemotherapy in subjects with unresectable advanced or metastatic intrahepatic cholangiocarcinoma harboring FGFR2 gene fusions/rearrangements or mutations, who have experienced recurrence or progression after prior first-line systemic chemotherapy.

开始日期2026-01-01

申办/合作机构

药捷安康（南京）科技股份有限公司

100 项与替恩戈替尼相关的临床结果

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100 项与替恩戈替尼相关的转化医学

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100 项与替恩戈替尼相关的专利（医药）

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项与替恩戈替尼相关的文献（医药）

2026-02-01·The Lancet Gastroenterology & Hepatology

Tinengotinib for adults with advanced or metastatic cholangiocarcinoma: a multicentre, open-label, phase 2 trial

Article

作者: Sahai, Vaibhav ; Richards, Donald ; Peng, Peng ; Cohn, Allen ; Javle, Milind ; Ni, Shumao ; Fountzilas, Christos ; Sun, Caixia ; Fonkoua, Lionel Kankeu ; Pelster, Meredith ; Wang, Hui ; Li, Daneng ; Kingsley, Edwin ; Fan, Jean ; Liao, Chih-Yi ; Deming, Dustin ; Hennessy, Katie ; Mahipal, Amit ; Wu, Frank ; Mantry, Parvez

BACKGROUND:

Cholangiocarcinoma is a rare, aggressive cancer often driven by FGFR2 fusions, which are targetable with inhibitors such as pemigatinib and futibatinib. However, resistance frequently develops due to acquired FGFR2 mutations. In this study, we aimed to evaluate the efficacy and safety of tinengotinib in previously treated patients with advanced cholangiocarcinoma.

METHODS:

This open-label, multicentre, phase 2 trial was done at 32 medical centres in the USA. Eligible patients were aged 18 years or older with advanced or metastatic cholangiocarcinoma, who had previous systemic chemotherapy, and an Eastern Cooperative Oncology Group score of 0-1. Patients were assigned to one of four cohorts on the basis of FGFR status: cohort A1, FGFR2 fusions with primary FGFR inhibitor resistance; cohort A2, FGFR2 fusions with acquired FGFR inhibitor resistance; cohort B, other FGFR alterations; or cohort C, FGFR wild-type. Patints orally self-administered tinengotinib 10 mg daily in 28-day cycles in 28-day treatment cycles until documented disease progression, unacceptable toxicity, or withdrawal of consent. The primary endpoint was objective response rate as per investigator assessment, defined as the proportion of patients with confirmed tumour response (complete response or partial response) that was redocumented 4 weeks or after initial assessment based on RECIST (version 1.1), as assessed by the investigator. The primary endpoint was assessed in the in the efficacy evaluable population, which included all patients who received at least one dose of tinengotinib, had measurable disease at baseline, and had at least one post-baseline tumour assessment. Safety assessed in all patients who received at least one dose of tinengotinib. This trial is registered with ClinicalTrials.gov, NCT04919642, and enrolment is complete.

FINDINGS:

Between Nov 19, 2021, and March 5, 2024, 55 patients were enrolled and assigned to one of four cohorts (cohort A1 [n=18], cohort A2 [n=11], cohort B [n=13], and cohort C [n=13]); all received tinengotinib. Patients had a median age of 61 years (IQR 56-68); 31 (56%) patients were female. All patients had received at least one previous systemic therapy. Median follow-up was 11·3 months (IQR 6·5-17·3). Among 51 patients included in the efficacy evaluable set, the objective response rate was 6·3% (95% CI 0·2-30·2; one confirmed partial response) in cohort A1, 30·0% (6·7-65·3; three confirmed partial responses) in cohort A2, 23·1% (5·0-53·8; three confirmed partial responses) in cohort B, and 0% in cohort C. Grade 3 treatment-related adverse events included hypertension in 17 (31%) of 55 patients, palmar-plantar erythrodysesthesia syndrome in seven (13%) patients, and stomatitis in six (11%) patients. Grade 4 treatment-related adverse events occurred in two (4%) of 55 patients (increased lipase [n=1] and posterior reversible encephalopathy syndrome [n=1]); no grade 5 treatment-related adverse events were reported.

INTERPRETATION:

These findings suggest that tinengotinib might have activity in patients with cholangiocarcinoma with FGFR2 fusions that progressed following FGFR inhibitor therapy. Anti-tumour activity was also observed in patients with other FGFR alterations. The data from this phase 2 study supported the initiation of a phase 3 registration trial.

FUNDING:

TransThera Sciences.

2025-04-01·CANCER SCIENCE

Multiple Kinase Small Molecule Inhibitor Tinengotinib (TT‐00420) Alone or With Chemotherapy Inhibit the Growth of SCLC

Article

作者: Yuanhua Lu ; Peng Peng ; Rui Zhong ; Chenchen Tang ; Ying Cheng ; Hui Li ; Shaowei Lan ; Xiaoyan Qiang ; Yan Liu ; Chunjiao Wu ; Peiyan Zhao ; Ying Liu ; Frank Wu ; Rixin Li

ABSTRACT:

There is an urgent need to develop new targeted treatment agents for small cell lung cancer (SCLC). Tinengotinib (TT‐00420) is a novel, multi‐targeted, and spectrally selective small‐molecule kinase inhibitor that has shown significant inhibitory effects on certain solid tumors in preclinical studies. However, its role and mechanism of action in SCLC remain unclear. In this study, we demonstrated that tinengotinib effectively inhibited SCLC cell proliferation, especially highly expressing NeuroD1 (SCLC‐N), in the SCLC cell line‐derived xenograft (CDX) model and the malignant pleural effusion cell model of patients with SCLC. When combined with etoposide/cisplatin, it synergistically inhibited SCLC growth. Tinengotinib regulates proliferation, apoptosis, migration, cell cycle and angiogenesis in SCLC cells. Mechanistic studies revealed that c‐Myc expression may be a key factor influencing the effect of tinengotinib in SCLC‐N. This study provides reliable preclinical data and a new direction for tinengotinib as a promising therapy for SCLC, either alone or in combination with chemotherapy.

2025-04-01·ANNALS OF ONCOLOGY

A model for decoding resistance in precision oncology: acquired resistance to FGFR inhibitors in cholangiocarcinoma

Article

作者: Qiang, X ; Borad, M ; Kambadakone, A R ; Shroff, R T ; Danysh, B P ; Flaherty, K T ; Leshchiner, I ; Martin, E E ; DiToro, D ; Lennerz, J K ; Saha, S K ; Lin, B ; Javle, M ; Chen, C T ; Iyer, R ; Sun, C ; Friboulet, L ; Harris, T ; Wang, H ; Reyes, S ; Li, L ; Cleary, J M ; Stone, J R ; Fan, J ; Gordan, J D ; Karasic, T ; Bensen, D C ; Iyer, S ; Kelley, R K ; Hoffman, I D ; Berchuck, J E ; Sootome, H ; Maurer, J ; Damjanov, N ; Baiev, I ; Goyal, L ; Peng, P ; Uboha, N V ; Wehrenberg-Klee, E ; Mody, K ; Parida, L ; Getz, G ; Walmsley, C ; Hollebecque, A ; Juric, D ; Nelson, K J ; Harris, W ; Majeed, U ; Zhang, K ; Zhu, A X ; Wu, F ; Facchinetti, F ; Hirai, H ; Vasseur, D ; Pinto, C

BACKGROUND:

Fibroblast growth factor receptor (FGFR) inhibitors have significantly improved outcomes for patients with FGFR-altered cholangiocarcinoma, leading to their regulatory approval in multiple countries. As with many targeted therapies, however, acquired resistance limits their efficacy. A comprehensive, multimodal approach is crucial to characterizing resistance patterns to FGFR inhibitors.

PATIENTS AND METHODS:

This study integrated data from six investigative strategies: cell-free DNA, tissue biopsy, rapid autopsy, statistical genomics, in vitro and in vivo studies, and pharmacology. We characterized the diversity, clonality, frequency, and mechanisms of acquired resistance to FGFR inhibitors in patients with FGFR-altered cholangiocarcinoma. Clinical samples were analyzed longitudinally as part of routine care across 10 institutions.

RESULTS:

Among 138 patients evaluated, 77 met eligibility, yielding a total of 486 clinical samples. Patients with clinical benefit exhibited a significantly higher rate of FGFR2 kinase domain mutations compared with those without clinical benefit (65% versus 10%, P < 0.0001). We identified 26 distinct FGFR2 kinase domain mutations, with 63% of patients harboring multiple. While IC50 assessments indicated strong potency of pan-FGFR inhibitors against common resistance mutations, pharmacokinetic studies revealed that low clinically achievable drug concentrations may underly polyclonal resistance. Molecular brake and gatekeeper mutations predominated, with 94% of patients with FGFR2 mutations exhibiting one or both, whereas mutations at the cysteine residue targeted by covalent inhibitors were rare. Statistical genomics and functional studies demonstrated that mutation frequencies were driven by their combined effects on drug binding and kinase activity rather than intrinsic mutational processes.

CONCLUSION:

Our multimodal analysis led to a model characterizing the biology of acquired resistance, informing the rational design of next-generation FGFR inhibitors. FGFR inhibitors should be small, high-affinity, and selective for specific FGFR family members. Tinengotinib, a novel small molecule inhibitor with these characteristics, exhibited preclinical and clinical activity against key resistance mutations. This integrated approach offers a blueprint for advancing drug resistance research across cancer types.

310

项与替恩戈替尼相关的新闻（医药）

2026-08-04

·歆医荟OncoTalk

[Mini Review]多靶点TKI不是越广越好：替恩戈替尼把FGFR、Aurora和JAK信号重新绑到精准治疗里

作者导语在精准肿瘤学的发展史上，药物设计曾经历过两次剧烈的钟摆运动。早期的多靶点酪氨酸激酶抑制剂由于缺乏特异性，其作用靶点如同“散弹枪”，虽然覆盖面广，但往往因非选择性的强毒性令临床医生望而却步。随后，医学界走向了另一个极端，倾力研发针对单一基因突变的“神枪手”型单靶点药物。然而，癌细胞远比想象中狡猾，它们极易通过靶点激酶域的继发突变，或是快速激活旁路代偿通路，轻而易举地让那些高选择性的单靶点药物折戟沙场。如何在“广度”与“精准”之间找到完美的黄金分割点？光谱选择性（Spectrum-Selective）多靶点激酶抑制剂替恩戈替尼（TT-00420）的出现，为这一临床博弈提供了极具启发性的全新范式。它摒弃了无差别的广谱抑制，而是基于肿瘤演进与耐药的内在逻辑，精巧地将FGFRs 1-3、Aurora A/B以及JAK1/2这三大维度的核心通路重新“绑定”在一起。这种设计既保留了多靶点联合绞杀的深度，又避免了无谓的脱靶毒性，精准地掐断了肿瘤细胞的代偿退路。本文将结合国际学术期刊上的最新临床与机制研究，层层剥茧这一款“光谱选择性”抑制剂的独特设计哲学，探讨它如何为胆管癌及三阴性乳腺癌等难治性实体瘤患者带来生命的转机。从“地毯式轰炸”到“多维合围”：多靶点药物研发的终极进化长期以来，多靶点酪氨酸激酶抑制剂的设计常被贴上“ dirty drug（脏药）”的标签。这类药物通常过度聚焦于血管生成通路，在抑制肿瘤血管的同时，也带来了顽固的高血压和手足综合征等全身毒性，且往往对肿瘤细胞本身的驱动基因打击力度不足。相比之下，替恩戈替尼的靶点绑定机制则体现了深思熟虑的药理学进化，它将核心靶点牢牢锁定在肿瘤增殖、有丝分裂和免疫微环境三个最具威胁的维度上。具体而言，FGFR2融合与突变是胆管癌等实体瘤的经典驱动突变，但单一FGFR抑制剂极易诱发突变耐药；而Aurora A/B激酶则是细胞有丝分裂中染色体分配的“指挥官”，控制着肿瘤的异常增殖；JAK1/2则介导了肿瘤内部的炎性逃逸。替恩戈替尼通过将这三者进行光谱选择性的共同抑制，构筑了一张密不透风的“多维合围网”。它不再是单纯地和肿瘤的单一突变进行“猫鼠游戏”，而是从细胞分裂的物理阻断、生长因子的通路拦截，到微环境生存信号的切断等多路径协同发力。这种精密的协同作用，从机制上彻底封锁了肿瘤细胞通过旁路代偿产生耐药的可能性，展现出了超越传统TKI的抗肿瘤深度。直击有丝分裂与基因突变死角： Lancet子刊研究见证耐药胆管癌的强势“逆转” 这种全新的靶点绑定哲学在胆管癌的治疗中率先得到了震撼性的临床实证。对于那些携带FGFR2融合的晚期胆管癌患者，虽然初代选择性FGFR抑制剂在起初能带来显著缓解，但患者在后续治疗中几乎不可避免地会遭遇靶区突变引起的继发性耐药，临床上长期处于“耐药即无药”的被动绝境。发表在《The Lancet Gastroenterology & Hepatology》上的多中心、开放标签、II期临床研究，直接将替恩戈替尼推向了这一临床最难攻克的堡垒。研究结果表明，在那些既往接受过选择性FGFR抑制剂治疗且已经发生耐药进展的晚期胆管癌患者中，替恩戈替尼单药治疗展现出了极为亮眼的抗肿瘤活性。这种卓越的逆转耐药能力，直接得益于替恩戈替尼的“双重打击”机制：一方面，它对FGFR2的多种继发耐药突变依然保持了强劲的抑制活性；另一方面，即使肿瘤试图通过非FGFR依赖的通路实现增殖，替恩戈替尼对Aurora激酶的强效阻断也会将癌细胞牢牢锁死在有丝分裂阻滞阶段，迫使其走向凋亡。更令临床医生欣喜的是，在显示出优异抗肿瘤效能的同时，替恩戈替尼的安全谱表现良好，其非特异性毒性极低，患者耐受性优异。这一突破性临床进展，有力地证明了光谱选择性多靶点设计在克服肿瘤耐药性方面的巨大优势。图1：FGFR 基因异常胆管癌患者靶病灶相对于基线的最佳百分比变化跨越单一靶向壁垒：点燃三阴性乳腺癌与晚期实体瘤的“免疫与靶向”双重引擎除了在耐药胆管癌中的突破性表现，替恩戈替尼其精密的机制设计也展现出了极佳的广谱实体瘤应用前景。在《Clinical Cancer Research》上发表的一项针对晚期实体瘤的Phase Ib/II临床研究中，替恩戈替尼不仅在安全性与药代动力学（PK）特征上表现卓越，在多种难治性晚期实体瘤患者中也观察到了明确的客观缓解信号。这种多维度阻断的独特优势，在三阴性乳腺癌的临床前研究中同样得到了充分的印证。由于三阴性乳腺癌具有高度的异质性，且临床上极度缺乏单一的基因驱动靶点，传统靶向药常在此折戟。机制研究表明，替恩戈替尼能精准锁定三阴性乳腺癌最依赖的生长引擎——Aurora A/B激酶活性，同时通过对FGFR和JAK信号通路的辅助切断，特异性地抑制各亚型乳腺癌细胞的增殖。更为惊艳的是，替恩戈替尼对JAK通路的抑制，赋予了其调控肿瘤微环境并协同免疫治疗的特殊属性。通过调节炎性通路，替恩戈替尼能够促使肿瘤局部释放趋化因子，吸引更多活性免疫细胞浸润，将冷肿瘤“煮热”。这种集“靶向杀伤、抑制耐药、微环境重塑”于一体的多重机制，为替恩戈替尼未来与免疫检查点抑制剂开展联合疗法、进一步拓宽患者获益边界打开了全新的想象空间。拓展阅读：传统的多靶点激酶抑制剂在设计之初，其靶点筛选多带有被动的偶然性，药物设计者为了追求广谱效应，常将血管内皮生长因子受体（VEGFR）作为主攻靶点。这导致临床在使用此类药物时，肿瘤细胞虽然被断了“粮草”（血管生成），但其内部复杂的促分裂与耐药信号并未受到根本性遏制，反而极易在短时间内重塑微环境并产生耐药。与之形成鲜明对比的是，替恩戈替尼的“光谱选择性”设计则是一次主动的、极具靶向科学美学的机制整合。当患者遭遇选择性FGFR抑制剂耐药时，最根本的瓶颈在于突变体蛋白空间的微小位移阻碍了原有药物的结合。而替恩戈替尼凭借其独特的空间分子构象，不仅能够灵活地规避这种位阻，维持对FGFR突变体的超强亲和力，更关键的是引入了对细胞有丝分裂至关重要的Aurora A/B激酶的强效抑制。从细胞生物学角度看，Aurora激酶在有丝分裂前期的纺锤体组装及中后期的染色体分离中扮演着不可替代的角色。通过将FGFR和Aurora激酶信号重绑定，替恩戈替尼在分子靶向阻断的同时，还在物理层面给肿瘤细胞的正常分裂装上了“减速带”和“阻车钉”。一旦癌细胞在FGFR通路上寻找逃生出口，就会由于Aurora激酶受抑而导致有丝分裂着丝点异常，直接触发纺锤体装配检查点（SAC）报警，引导癌细胞走向有丝分裂灾难（Mitotic Catastrophe）并迅速自我毁灭。这种在分子信号转导和细胞物理分裂两个维度上同时落锁的设计，也让JAK1/2调控的代偿信号无处施展，真正实现了靶向药物对复杂耐药网络的完美合围。观点评述替恩戈替尼的研发与临床成功，无疑是对肿瘤靶向药设计哲学的一次深刻反思。它用扎实的数据向临床及科研界证明：靶向药物的靶点设计不应当是单一靶点的独角戏，也不应该是无差别多靶点的乱炖，而应当是针对肿瘤耐药通路和生命周期的精准艺术。将FGFR、Aurora和JAK通路进行重新绑定，既把准了单靶点耐药的七寸，又避开了广谱毒性的泥潭。不过，我们也应该理性地看到，这一创新的“光谱选择性”疗法在未来的临床普及中仍需面临挑战。面对高度复杂的患者个体差异，如何确定最佳的联合用药窗口和给药剂量，在最大限度发挥靶点协同效力的同时，保障患者的长期生活质量，仍需要更大规模的临床数据来提供注解。此外，在精准医疗大背景下，开发并验证能够灵敏反映这一三重靶点敏感性的新型复合分子标志物，也将是未来临床转化的重中之重。但毋庸置疑的是，替恩戈替尼不仅为胆管癌和三阴性乳腺癌等难治性肿瘤患者带来了切实可见的希望，更在研发思路上为后期的抗癌药物设计指明了方向。这种以作用机制为导向、科学重组核心靶点的精准治疗趋势，必将成为未来肿瘤医学攻克耐药壁垒的核心利器。 ---------------------------------- ☆本文仅供医疗卫生等专业人士参考参考文献 [1] Javle M, Fountzilas C, Liao CY, et al. Tinengotinib for adults with advanced or metastatic cholangiocarcinoma: a multicentre, open-label, phase 2 trial. Lancet Gastroenterol Hepatol. 2026;11(2):137-149. [2] Piha-Paul SA, Liao CY, Dayyani F, et al. Multikinase Inhibition with Tinengotinib in Advanced Solid Tumors: Results from a Multicenter Phase Ib/II Trial. Clin Cancer Res. 2026. doi: 10.1158/1078-0432.CCR-26-1076. [3] Peng P, Qiang X, Li G, et al. Tinengotinib (TT-00420), a Novel Spectrum-Selective Small-Molecule Kinase Inhibitor, Is Highly Active Against Triple-Negative Breast Cancer. Mol Cancer Ther. 2023;22(2):205-214.

2026-07-27

·同花顺

港股创新药估值修复窗口期，药捷安康持续回购传递管理层信心

近期，医药板块迎来密集回购热潮，多家药企接连发布股份回购相关公告，涵盖回购进展、全新预案、首次落地实施等多种情形。港股创新药（886015）企药捷安康-B（HK2617）(02617.HK)也加快回购方案落地。自6月下旬宣布最高1亿元回购计划以来，公司已持续实施股份回购，通过实际行动向市场传递对企业长期价值的信心。7月17日，公司首次实施回购，当日以9.55至9.62港元/股的价格回购6.8万股，涉资约65.27万港元。此后，公司连续多个交易日展开回购操作，截至7月26日，年内累计回购金额已超700万港元。持续推进的回购动作，体现出公司管理层始终秉持长期经营理念，尊重并回馈二级市场投资者，无惧短期市场波动，坚定看好企业长期成长逻辑。与此同时，公司7月24日依据H股奖励计划，向67名雇员授出281.69万份股份奖励及244.2万份购股权，通过长效股权激励深度绑定核心人才、优化内部治理并稳固长期股权结构。回顾市场走势，2026年6月下旬，受上市一周年股份解禁、港股生物医药板块整体情绪偏弱等多重因素叠加影响，药捷安康股价出现阶段性非理性调整，市场短期过度放大资金面扰动，却忽视了公司基本面的实质性向好与研发管线的核心价值。为对冲情绪冲击、彰显长期发展信心，公司6月18日股东周年大会审议通过H股购回一般授权，拟择机在公开市场回购H股，回购上限1亿元人民币或等值港元。药捷安康此番连续回购操作，并非孤立的市场行为，而是公司长期发展战略在资本层面的自然延伸。作为一家自2016年正式运营、聚焦肿瘤、炎症及心脏代谢疾病小分子创新疗法的创新药（886015）企业，药捷安康多年来坚持源头靶点自研，在FGFR抑制剂耐药后胆管癌这一高壁垒领域实现了全球技术突破。其核心产品替恩戈替尼是全球唯一一款提交上市申请、用于治疗FGFR抑制剂经治后复发或难治性胆管癌的候选药物。该产品新药上市申请已于2025年12月获NMPA受理并纳入优先审评，预计2026年获批上市。与此同时，替恩戈替尼全球多中心注册性III期临床试验已于近期完成全部受试者入组，海外商业化进程同步提速。从行业视角来看，今年二季度以来，创新药（886015）板块在经历深度调整后迎来阶段性修复行情。资金明显流向具备差异化管线、全球化布局与清晰出海路径的标的。药捷安康此前的股价波动更多受制于解禁带来的短期筹码压力，而非公司基本面变化。随着回购计划持续推进、核心管线临床与注册节点稳步落地，市场对公司长期价值的认知正在逐步修复。

2026-07-27

·中金在线

药捷安康连续回购持续推进，真金白银锚定长期价值

近期，医药板块迎来密集回购热潮，多家药企接连发布股份回购相关公告，涵盖回购进展、全新预案、首次落地实施等多种情形。港股创新药企药捷安康-B(02617.HK)也加快回购方案落地。自6月下旬宣布最高1亿元回购计划以来，公司已持续实施股份回购，通过实际行动向市场传递对企业长期价值的信心。 7月17日，公司首次实施回购，当日以9.55至9.62港元/股的价格回购6.8万股，涉资约65.27万港元。此后，公司连续多个交易日展开回购操作，截至7月26日，年内累计回购金额已超700万港元。持续推进的回购动作，体现出公司管理层始终秉持长期经营理念，尊重并回馈二级市场投资者，无惧短期市场波动，坚定看好企业长期成长逻辑。与此同时，公司7月24日依据H股奖励计划，向67名雇员授出281.69万份股份奖励及244.2万份购股权，通过长效股权激励深度绑定核心人才、优化内部治理并稳固长期股权结构。回顾市场走势，2026年6月下旬，受上市一周年股份解禁、港股生物医药板块整体情绪偏弱等多重因素叠加影响，药捷安康股价出现阶段性非理性调整，市场短期过度放大资金面扰动，却忽视了公司基本面的实质性向好与研发管线的核心价值。为对冲情绪冲击、彰显长期发展信心，公司6月18日股东周年大会审议通过H股购回一般授权，拟择机在公开市场回购H股，回购上限1亿元人民币或等值港元。药捷安康此番连续回购操作，并非孤立的市场行为，而是公司长期发展战略在资本层面的自然延伸。作为一家自2016年正式运营、聚焦肿瘤、炎症及心脏代谢疾病小分子创新疗法的创新药企业，药捷安康多年来坚持源头靶点自研，在FGFR抑制剂耐药后胆管癌这一高壁垒领域实现了全球技术突破。其核心产品替恩戈替尼是全球唯一一款提交上市申请、用于治疗FGFR抑制剂经治后复发或难治性胆管癌的候选药物。该产品新药上市申请已于2025年12月获NMPA受理并纳入优先审评，预计2026年获批上市。与此同时，替恩戈替尼全球多中心注册性III期临床试验已于近期完成全部受试者入组，海外商业化进程同步提速。从行业视角来看，今年二季度以来，创新药板块在经历深度调整后迎来阶段性修复行情。资金明显流向具备差异化管线、全球化布局与清晰出海路径的标的。药捷安康此前的股价波动更多受制于解禁带来的短期筹码压力，而非公司基本面变化。随着回购计划持续推进、核心管线临床与注册节点稳步落地，市场对公司长期价值的认知正在逐步修复。

并购临床3期优先审批

100 项与替恩戈替尼相关的药物交易

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研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
晚期胆管癌	中国	药捷安康（南京）科技股份有限公司	2026-08-04
不能切除的胆管癌	中国	药捷安康（南京）科技股份有限公司	2026-08-04
转移性胆管癌	中国	药捷安康（南京）科技股份有限公司	2026-08-04

未上市

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
FGFR2阳性肝内胆管癌	临床3期	中国	药捷安康（南京）科技股份有限公司	2026-04-07
不可切除的肝内胆管癌	临床3期	中国	药捷安康（南京）科技股份有限公司	2026-01-01
FGFR阳性胆管癌	临床3期	美国	药捷安康（南京）科技股份有限公司	2023-12-20
FGFR阳性胆管癌	临床3期	奥地利	药捷安康（南京）科技股份有限公司	2023-12-20
FGFR阳性胆管癌	临床3期	比利时	药捷安康（南京）科技股份有限公司	2023-12-20
FGFR阳性胆管癌	临床3期	法国	药捷安康（南京）科技股份有限公司	2023-12-20
FGFR阳性胆管癌	临床3期	德国	药捷安康（南京）科技股份有限公司	2023-12-20
FGFR阳性胆管癌	临床3期	意大利	药捷安康（南京）科技股份有限公司	2023-12-20
FGFR阳性胆管癌	临床3期	荷兰	药捷安康（南京）科技股份有限公司	2023-12-20
FGFR阳性胆管癌	临床3期	波兰	药捷安康（南京）科技股份有限公司	2023-12-20

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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


NCT04919642 (Pubmed \| Lancet Gastroenterol Hepatol)	临床2期	转移性胆管癌	55	Tinengotinib (FGFR2 fusions with acquired FGFR inhibitor resistance)	選網繭遞餘繭觸糧選網(窪觸艱鬱憲襯構遞繭衊) = Grade 3 treatment-related adverse events included hypertension in 17 (31%) of 55 patients, palmar-plantar erythrodysesthesia syndrome in seven (13%) patients, and stomatitis in six (11%) patients. 淵鬱衊鏇糧糧遞觸鏇鹽 (糧願鹹鏇獵範範繭襯顧 ) 更多	积极	2025-12-01
NCT03654547 (ESMO2025)	临床1/2期	晚期胆管癌 FGFR2-altered	109	Tinengotinib	製膚壓淵壓範製蓋廠鹹(艱獵齋窪糧艱構鏇窪遞) = 網鬱鹹膚鏇構網繭壓顧獵網願壓網鹽獵淵願膚 (繭獵網簾積築願顧醖醖 ) 更多	积极	2025-10-17
				Tinengotinib (FGFR2-altered)	襯膚範繭遞構衊顧膚壓(鏇積鹽範築糧鏇襯鏇鑰) = 獵簾壓廠鏇齋醖膚顧蓋選構選窪構構廠積餘夢 (遞鬱廠鑰選鹽窪鏇襯艱, 9.43 ~ 19.48) 更多
NEWS 人工标引	N/A	胆管癌	43	Tinengotinib	範製壓簾鹹餘鑰鬱築糧(窪壓鹽艱餘鬱襯範鬱築) = 選醖餘憲艱襯淵鑰廠鏇鑰餘鏇選鏇積製願蓋鹽 (網窪艱糧廠鹽構願積鑰 ) 更多	积极	2025-07-13
NCT04919642 (TransThera's phase 2, ASCO2025)	临床2期	胆管癌 FGFR2 fusion \| FGFR alterations \| FGFR wild type	37	Tinengotinib	獵鑰範構壓憲構遞鹽醖(鬱願遞築觸餘糧壓壓憲) = 醖齋艱遞製餘選齋鏇鏇製淵膚築淵壓鏇鹽網廠 (簾窪壓製鏇齋齋鏇網蓋 ) 更多	积极	2025-05-30
NCT04742959 (AACR2025)	临床1/2期	晚期恶性实体瘤 Aurora kinases A/B \| Janus kinases (JAK) \| receptor tyrosine kinases (FGFRs and VEGFRs)	197	Tinengotinib 4mg BID	製衊築淵夢襯鹹鑰鬱鹹(膚簾蓋觸繭膚淵醖廠憲) = No notable difference in AUC was observed in QD vs. BID schedules 醖窪簾夢簾窪願構簾繭 (網壓淵積蓋顧築廠淵繭 ) 更多	-	2025-04-29
				Tinengotinib 6mg BID
NCT04742959 (AACR2025)	临床1/2期	转移性胆管癌 FGFR fusions \| FGFR2 KD mutations	2	Tinengotinib 12mg once daily	餘鹽憲獵衊醖窪積顧廠(膚窪積鏇醖窪蓋構蓋壓) = suspected grade 3 TSH increase 構鏇窪蓋網糧顧鏇遞窪 (範艱糧鏇齋糧鏇壓範積 ) 更多	积极	2025-04-27
				Chemotherapy
NCT04919642 (ASCO_GI2025) 人工标引	临床2期	转移性胆管癌 MED12 mutation \| ARID1A mutation	55	Tinengotinib 10 mg QD (A1: FGFR2 fusion(s) with primary progression on previous FGFR inhibitor (FGFRi))	築遞顧廠壓製獵鏇齋獵(襯蓋網窪獵顧夢鹽廠蓋) = 襯顧夢憲鏇鏇構艱獵遞獵淵淵鬱鏇鹹膚夢艱製 (淵廠窪廠願鹽鹹願簾製, 7.5 ~ 19.5)	积极	2025-01-23
				Tinengotinib 10 mg QDTinengotinib 10 mg QD (A2: FGFR2 fusion(s) with progression after prior response to FGFRi)	築遞顧廠壓製獵鏇齋獵(襯蓋網窪獵顧夢鹽廠蓋) = 構壓鑰夢積築製遞蓋繭獵淵淵鬱鏇鹹膚夢艱製 (淵廠窪廠願鹽鹹願簾製, 9.6 ~ NR)
NCT05253053 (TT-00420, ESMO_ASIA2024) 人工标引	临床1/2期	胆道癌	31	Tinengotinib + Atezolizumab	築糧構積淵鑰遞廠淵顧(積衊選簾顧鬱餘願鏇鏇) = 襯簾構選鏇願蓋顧選鑰鑰遞遞築鹽衊蓋網繭網 (製餘齋鑰糧衊築築廠膚 ) 更多	积极	2024-12-07
				Tinengotinib + Atezolizumab (cholangiocarcinoma)	築糧構積淵鑰遞廠淵顧(積衊選簾顧鬱餘願鏇鏇) = 齋鹽鹹壓餘顧構網憲鏇鑰遞遞築鹽衊蓋網繭網 (製餘齋鑰糧衊築築廠膚 ) 更多
NCT05253053 \| NCT04742959 \| NCT03654547 \| NCT04919642 (AACR2024) 人工标引	临床1/2期	实体瘤 FGFR1 Mutation \| FGFR2 Mutation \| FGFR3 Mutation	53	Tinengotinib 5-12mg	衊憲艱願衊鏇齋齋憲齋(製襯鏇壓願鹹顧蓋鹹憲) = 糧廠憲選蓋夢膚網衊製繭積淵鏇夢觸夢蓋壓艱 (築膚網鏇餘窪製願觸鏇 ) 更多	积极	2024-04-05
				Tinengotinib 5-12mg (prior FGFR inhibitor)	衊憲艱願衊鏇齋齋憲齋(製襯鏇壓願鹹顧蓋鹹憲) = 壓蓋齋鹽衊襯遞網齋衊繭積淵鏇夢觸夢蓋壓艱 (築膚網鏇餘窪製願觸鏇 ) 更多
NCT05253053 \| NCT04742959 \| NCT03654547 (ASCO_GU2024) 人工标引	临床1/2期	转移性去势抵抗性前列腺癌	30	Tinengotinib	艱願蓋遞鑰鏇願鏇鬱齋(鹽餘鹽網夢鏇醖觸夢積) = 範餘範鑰鑰積簾窪遞糧鹽築積顧夢襯顧遞齋選 (衊鏇蓋顧鹽繭積窪觸範 ) 更多	-	2024-01-25