A Randomized, Double-blind, Placebo-controlled Phase 3 Study to Compare the Efficacy and Safety of Sitravatinib Plus Tislelizumab or Placebo Plus Tislelizumab Versus Placebo as Adjuvant Treatment in Patients With Hepatocellular Carcinoma Who Are at High Risk of Recurrence After Surgical Resection

The purpose of this study is to compare the efficacy and safety of sitravatinib plus tislelizumab or placebo plus tislelizumab versus placebo. The study will also compare the recurrence-free survival (RFS) in participants with hepatocellular carcinoma (HCC) who are at high risk of recurrence after surgical resection.

开始日期2023-06-30

申办/合作机构

BeiGene Ltd.

NCT05614453 / Withdrawn临床2期

A Phase II Trial of Tislelizumab in Combination With Sitravatinib for Recurrent/Metastatic Cervical Cancer After Platinum-Based Chemotherapy

The goal of this clinical trial is to learn about the effect of the combination treatment of sitravatinib with tislelizumab in patients with Recurrent/Metastatic Cervical Cancer after Platinum-Based Chemotherapy.
The main question it aims to answer is the percentage of people in the study who have a partial or complete response to the treatment.
Participants will receive treatment under the care of their treating physician and will be reviewed regularly.

开始日期2023-06-01

申办/合作机构

Australia New Zealand Gynaecological Oncology Group

[+1]

NCT05461794 / Terminated临床2期

A Phase 2, Randomized, Open-Label Study to Investigate the Efficacy and Safety of Sitravatinib in Combination With Tislelizumab in Patients With Locally Advanced Unresectable or Metastatic Esophageal Squamous Cell Carcinoma That Progressed on or After Anti-PD-(L)1 Antibody Therapy

The purpose of this study is to investigate the efficacy and safety of sitravatinib in combination with tislelizumab for the treatment of participants with esophageal squamous cell carcinoma

开始日期2022-10-03

申办/合作机构

BeiGene Ltd.

100 项与司曲替尼相关的临床结果

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100 项与司曲替尼相关的转化医学

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100 项与司曲替尼相关的专利（医药）

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项与司曲替尼相关的文献（医药）

2024-04-12·Carcinogenesis

Sitravatinib combined with PD-1 blockade enhances cytotoxic T-cell infiltration by M2 to M1 tumor macrophage repolarization in esophageal adenocarcinoma

Article

作者: Zheng, Ping ; Grayhack, Erin E ; Sweeney, Ryan ; Khan, Alisha F ; Kelly, Ronan J ; Fitzpatrick, John T ; Jobe, Blair A ; Omstead, Ashten N ; Goel, Arul ; Wagner, Patrick L ; Zaidi, Ali H ; Gorbunova, Anastasia ; Kosovec, Juliann E

Abstract:

Esophageal adenocarcinoma (EAC) is a leading cause of cancer-related mortality. Sitravatinib is a novel multi-gene tyrosine kinase inhibitor (TKI) that targets tumor-associated macrophage (TAM) receptors, VEGF, PDGF and c-Kit. Currently, sitravatinib is actively being studied in clinical trials across solid tumors and other TKIs have shown efficacy in combination with immune checkpoint inhibitors (ICI) in cancer models. In this study, we investigated the anti-tumor activity of sitravatinib alone and in combination with PD-1 blockade in an EAC rat model. Treatment response was evaluated by mortality, pre- and post-treatment MRI, gene expression, immunofluorescence and immunohistochemistry. Our results demonstrated adequate safety and significant tumor shrinkage in animals treated with sitravatinib, and more profoundly, sitravatinib and PD-1 inhibitor, AUNP-12 (P < 0.01). Suppression of TAM receptors resulted in increased gene expression of pro-inflammatory cytokines and decreased expression of anti-inflammatory cytokines, enhanced infiltration of CD8+ T cells, and M2 to M1 macrophage phenotype repolarization in the tumor microenvironment of treated animals (P < 0.01). Moreover, endpoint immunohistochemistry staining corroborated the anti-tumor activity by downregulation of Ki67 and upregulation of Caspase-3 in the treated animals. Additionally, pretreatment gene expression of TAM receptors and PD-L1 were significantly higher in major responders compared with the non-responders, in animals that received sitravatinib and AUNP-12 (P < 0.02), confirming that TAM suppression enhances the efficacy of PD-1 blockade. In conclusion, this study proposes a promising immunomodulatory strategy using a multi-gene TKI to overcome developed resistance to an ICI in EAC, establishing rationale for future clinical development.

2024-01-01·Annals of oncology : official journal of the European Society for Medical Oncology

SAPPHIRE: phase III study of sitravatinib plus nivolumab versus docetaxel in advanced nonsquamous non-small-cell lung cancer

Article

BACKGROUND:

Checkpoint inhibitor (CPI) therapy revolutionized treatment for advanced non-small-cell lung cancer (NSCLC); however, most patients progress due to primary or acquired resistance. Sitravatinib is a receptor tyrosine kinase inhibitor that can shift the immunosuppressive tumor microenvironment toward an immunostimulatory state. Combining sitravatinib with nivolumab (sitra + nivo) may potentially overcome initial CPI resistance.

PATIENTS AND METHODS:

In the phase III SAPPHIRE study, patients with advanced non-oncogenic driven, nonsquamous NSCLC who initially benefited from (≥4 months on CPI without progression) and subsequently experienced disease progression on or after CPI combined with or following platinum-based chemotherapy were randomized 1 : 1 to sitra (100 mg once daily administered orally) + nivo (240 mg every 2 weeks or 480 mg every 4 weeks administered intravenously) or docetaxel (75 mg/m² every 3 weeks administered intravenously). The primary endpoint was overall survival (OS). The secondary endpoints included progression-free survival (PFS), objective response rate (ORR), clinical benefit rate (CBR), duration of response (DOR; all assessed by blinded independent central review), and safety.

RESULTS:

A total of 577 patients included randomized: sitra + nivo, n = 284; docetaxel, n = 293 (median follow-up, 17.1 months). Sitra + nivo did not significantly improve OS versus docetaxel [median, 12.2 versus 10.6 months; hazard ratio (HR) 0.86, 95% confidence interval (CI) 0.70-1.05; P = 0.144]. The median PFS was 4.4 versus 5.4 months, respectively (HR 1.08, 95% CI 0.89-1.32; P = 0.452). The ORR was 15.6% for sitra + nivo and 17.2% for docetaxel (P = 0.597); CBR was 75.5% and 64.5%, respectively (P = 0.004); median DOR was 7.4 versus 7.1 months, respectively (P = 0.924). Grade ≥3 treatment-related adverse events were observed in 53.0% versus 66.7% of patients receiving sitra + nivo versus docetaxel, respectively.

CONCLUSIONS:

Although median OS was numerically longer with sitra + nivo, the primary endpoint was not met in patients with previously treated advanced nonsquamous NSCLC. The safety profiles demonstrated were consistent with previous reports.

2023-12-01·European urology oncology

A Phase 2 Study of Sitravatinib in Combination with Nivolumab in Patients with Advanced or Metastatic Urothelial Carcinoma

Article

作者: Kalebasty, Arash Rezazadeh ; Chin, Curtis D ; Bupathi, Manojkumar ; Siefker-Radtke, Arlene ; Goodman, Oscar B ; Heath, Elisabeth ; Mortazavi, Amir ; Yorio, Jeffrey ; Olson, Peter ; Yang, Rui ; Msaouel, Pavlos ; Sweis, Randy F ; Iyer, Gopa ; Shaffer, David ; Adra, Nabil ; Mao, Shifeng ; Latven, Lisa ; Davis, Nancy ; Grivas, Petros ; Milowsky, Matthew I ; Picus, Joel ; Hoimes, Christopher J ; Der-Torossian, Hirak ; Gandhi, Sunil

BACKGROUND AND OBJECTIVE:

Checkpoint inhibitor therapy (CPI) has demonstrated survival benefits in urothelial carcinoma (UC); however, not all patients benefit from CPI due to resistance. Combining sitravatinib, a multitargeted receptor tyrosine kinase inhibitor of TYRO3, AXL, and MERTK (TAM) receptors and VEGFR2, with CPI may improve antitumor responses. Our objective was to assess the efficacy and safety of sitravatinib plus nivolumab in patients with advanced/metastatic UC.

METHODS:

The 516-003 trial (NCT03606174) is an open-label, multicohort phase 2 study evaluating sitravatinib plus nivolumab in patients with advanced/metastatic UC enrolled in eight cohorts depending on prior treatment with CPI, platinum-based chemotherapy (PBC), or antibody-drug conjugate (ADC). Overall, 244 patients were enrolled and treated with sitravatinib plus nivolumab (median follow-up 14.1-38.2 mo). Sitravatinib (free-base capsules 120 mg once daily [QD] or malate capsule 100 mg QD) plus nivolumab (240 mg every 2 wk/480 mg every 4 wk intravenously).

KEY FINDINGS AND LIMITATIONS:

The primary endpoint was objective response rate (ORR; RECIST v1.1). The secondary endpoints included progression-free survival (PFS) and safety. The Predictive probability design and confidence interval methods were used. Among patients previously treated with PBC, ORR, and median PFS were 32.1% and 3.9 mo in CPI-naïve patients (n = 53), 14.9% and 3.9 mo in CPI-refractory patients (n = 67), and 5.4% and 3.7 mo in CPI- and ADC-refractory patients (n = 56), respectively. Across all cohorts, grade 3 treatment-related adverse events (TRAEs) occurred in 51.2% patients and grade 4 in 3.3%, with one treatment-related death (cardiac failure). Immune-related adverse events occurred in 50.4% patients. TRAEs led to sitravatinib/nivolumab discontinuation in 6.1% patients.

CONCLUSIONS AND CLINICAL IMPLICATIONS:

Sitravatinib plus nivolumab demonstrated a manageable safety profile but did not result in clinically meaningful ORRs in patients with advanced/metastatic UC in the eight cohorts studied.

PATIENT SUMMARY:

In this study, the combination of two anticancer drugs, sitravatinib and nivolumab, resulted in manageable side effects but no meaningful responses in patients with bladder cancer.

105

项与司曲替尼相关的新闻（医药）

2024-03-23

·生物探索

Cell Reports Medicine | 复旦大学董琼珠/钦伦秀/陆录发现提高检查点抑制剂疗效的潜在新策略

引言免疫检查点抑制剂，特别是PD-1/PD-L1抑制剂，已被批准用于不可切除的肝细胞癌(HCC)。然而，高耐药率仍然限制了它们的疗效，这突出表明迫切需要了解潜在的机制并制定克服耐药性的策略。2024年3月20日，复旦大学董琼珠、钦伦秀及陆录共同通讯在Cell Reports Medicine 在线发表题为“Disruption of MerTK increases the efficacy of checkpoint inhibitor by enhancing ferroptosis and immune response in hepatocellular carcinoma”的研究论文，该研究证明了高MER原癌基因酪氨酸激酶(MerTK)表达的HCC在两种同基因小鼠模型和接受抗PD-1/PD-L1治疗的患者中表现出抗PD-1/PD-L1耐药。在机制上，MerTK通过ERK/SP1途径通过SLC7A11的上调来限制铁死亡，并通过募集髓源性抑制细胞(MDSCs)促进免疫抑制性肿瘤微环境(TME)的发展，从而使HCC对抗PD-1/PD-L1产生耐药性。Sitravatinib是MerTK的一种抑制剂，通过促进肿瘤铁死亡和减少MDSC向TME的浸润，使耐药HCC对抗PD-L1治疗增敏。肝细胞癌(HCC)仍然是一个全球性的健康挑战，其发病率在全球范围内不断增加临床上，大多数HCC患者被诊断为晚期，治疗选择有限。最近，免疫疗法，如免疫检查点抑制剂(ICIs)抗CTLA4、抗PD-1/PD-L1、它们的联合或与其他药物的联合，在癌症患者中取得了无与伦比的成功。此外，nivolumab、pembrolizumab和atezolizumab等ICIs目前已被美国食品和药物管理局(FDA)批准用于HCC的全身治疗。然而，由于抗PD-1/PD-L1治疗经常出现耐药，反应率仍远不能令人满意，目前仅在约15% - 20%的HCC患者中观察到总体获益率。因此，迫切需要确定最佳患者选择的生物标志物，并确定克服这种耐药性的有效靶点。MER原癌基因酪氨酸激酶(MerTK)是酪氨酸受体激酶TAM家族(TYRO3、AXL和MerTK)的一员，在包括HCC在内的多种恶性肿瘤中高度表达6 (the Human Protein Atlas: proteinatlas.org)。同源蛋白生长抑制特异性蛋白6 (Gas6)和蛋白S (Pros1)都是MerTK活化的天然配体，可诱导MerTK的同二聚化和自磷酸化，激活MEK/ERK、PI3K/AKT、JAK/STAT等下游通路，从而达到肿瘤细胞增殖、抗凋亡、抑制炎症和肿瘤生长的目的。最近的研究表明，MerTK作为一种代谢调节剂，通过整合有氧糖酵解和氧化磷酸化，在调节HCC生长中起着关键作用。此外，MerTK的受体/配体活性已在多种免疫细胞类型中得到证实，并增强抗肿瘤免疫，这对癌症免疫治疗具有重要意义。模式图（Credit: Cell Reports Medicine）铁死亡作为一种代谢调节的细胞死亡形式，在癌症生物学中起着重要的作用。近年来，越来越多的证据表明，对铁死亡的抑制与对常规癌症治疗的耐药性有关，并且靶向铁死亡可能为癌症提供治疗潜力。最近，研究表明，在免疫治疗过程中，对铁死亡的调节可以重塑肿瘤生态位，从而导致T细胞介导的肿瘤根除。在HCC中，铁死亡已被证明在全身治疗(如靶向治疗和化疗)中具有耐药性。该研究发现MerTK是抵抗PD-1/PD-L1阻断的主要机制，通过增加髓源性抑制细胞(MDSC)的浸润，限制肿瘤细胞铁死亡并引起免疫抑制性肿瘤微环境(TME)。MerTK阻断可能有效对抗这种耐药，并使HCC对抗PD-L1治疗敏感。此外，MerTK可作为sitravatinib，联合抗PD-L1联合治疗筛查HCC患者的生物标志物。总之，该研究发现MerTK可以作为患者分层的预测性生物标志物，并且是克服HCC中抗PD-1/PD-L1耐药的有希望的靶点。原文链接https://doi-org.libproxy1.nus.edu.sg/10.1016/j.xcrm.2024.101420责编|探索君排版|探索君文章来源|“iNature”End往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文Nature | 破除传统：为何我们需要重新思考肿瘤的命名方式热文Nature | 2024年值得关注的七项技术热文Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文CRISPR技术进化史 | 24年Cell综述

免疫疗法

2024-02-24

·生物探索

Cell Rep Med | 复旦大学董琼珠/钦伦秀/陆录发现提高肝癌免疫检查点抑制剂疗效的潜在新策略

引言近年来，以免疫检查点抑制剂(ICIs)为代表的肿瘤免疫治疗被认为是癌症治疗领域最成功的方法之一，但病人获益有限，甚至病人获益之后仍可出现耐药问题。2024年2月20日，复旦大学董琼珠、钦伦秀及陆录共同通讯在Cell Reports Medicine 在线发表题为“Disruption of MerTK increases the efficacy of checkpoint inhibitor by enhancing ferroptosis and immune response in hepatocellular carcinoma”的研究论文，该研究表明靶向MerTK可通过增强肝细胞癌的铁死亡和免疫应答来提高免疫检查点抑制剂的疗效。在这项研究中，研究人员证明了MER原癌基因酪氨酸激酶(MerTK)在两种ICI耐药的肝癌小鼠模型和接受抗PD-1/PDL1治疗的肝癌患者中高表达，MerTK是导致肝癌ICIs耐药的“元凶”之一。机制上，MerTK通过ERK/SP1通路上调SLC7A11的表达抑制肝癌细胞铁死亡，并通过募集髓源性抑制细胞(MDSCs)促进肝癌免疫抑制性肿瘤微环境(TME)的形成，从而使肝癌对抗PD-1/PD-L1产生耐药性。Sitravatinib是MerTK的一种抑制剂，通过促进肿瘤细胞铁死亡和减少MDSC向TME的浸润，使耐药HCC对抗PD-L1治疗增敏。肝细胞癌(HCC)仍然是一个全球性的健康挑战，其发病率在全球范围内不断增加。临床上，大多数HCC患者被诊断为晚期，治疗选择有限。最近，免疫疗法，如ICIs抗CTLA4、抗PD-1/PD-L1、它们的联合或与其他药物的联合，在癌症患者中取得了无与伦比的成功。此外，nivolumab、pembrolizumab和atezolizumab等ICIs目前已被FDA批准用于HCC的全身治疗。然而，由于抗PD-1/PD-L1治疗经常出现耐药，反应率仍远不能令人满意，目前仅在约15% - 20%的HCC患者中观察到总体获益率。因此，迫切需要确定最佳患者选择的生物标志物，并确定克服这种耐药性的有效靶点。MerTK是酪氨酸受体激酶TAM家族(TYRO3、AXL和MerTK)的一员，在包括HCC在内的多种恶性肿瘤中高度表达(the Human Protein Atlas: proteinatlas.org)。同源蛋白生长抑制特异性蛋白6 (Gas6)和蛋白S (Pros1)都是MerTK活化的天然配体，可诱导MerTK的同二聚化和自磷酸化，激活MEK/ERK、PI3K/AKT、JAK/STAT等下游通路，从而促进肿瘤细胞增殖、抗凋亡、抑制炎症和肿瘤恶性进程。最近的研究表明，MerTK作为一种代谢调节剂，通过整合有氧糖酵解和氧化磷酸化，在调节HCC生长中起着关键作用。此外，MerTK的受体/配体活性已在多种免疫细胞类型中得到证实，对癌症的免疫治疗具有重要意义。模式图（Credit: Cell Reports Medicine）铁死亡作为一种代谢调节的细胞死亡形式，在癌症生物学中起着重要作用。近年来，越来越多的证据表明，抑制铁死亡与传统癌症治疗的耐药性密切相关，靶向铁死亡可能为癌症治疗提供潜力。最近，研究表明，在免疫治疗过程中，调节铁死亡可以重塑肿瘤免疫微环境，从而导致T细胞介导的肿瘤消除。在HCC中，铁死亡已被证明与肿瘤治疗(如靶向治疗和化疗)耐药相关。该研究表明，MerTK上调SLC7A11表达抑制肿瘤细胞铁死亡，同时通过在HCC微环境中募集MDSCs促进肿瘤TME，从而导致抗PD-L1治疗耐药。靶向MerTK是提高PD-L1抗体治疗效果的有效策略。在PD-L1耐药肝癌中，MerTK抑制剂Sitravatinib和ICIs联合使用可有效增加肿瘤细胞铁死亡，减少肝癌微环境中MDSCs募集，促进CD8+ T细胞活化。该研究表明MerTK可作为ICB疗效预测标志物，并且是克服HCC中抗PD-1/PD-L1耐药的潜在靶点。原文链接https://doi-org.libproxy1.nus.edu.sg/10.1016/j.xcrm.2024.101415责编|探索君排版|探索君文章来源|“iNature”End往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文Nature | 破除传统：为何我们需要重新思考肿瘤的命名方式热文Nature | 2024年值得关注的七项技术热文Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文Nature | 癌症与神经系统的致命舞蹈

免疫疗法

2024-02-23

·今日头条

克服耐药性！复旦大学董琼珠/钦伦秀/陆路发现肝细胞癌潜在治疗靶点和生物标志物

本文为转化医学网原创，转载请注明出处作者：Rainbow 导读：肝细胞癌（HCC）仍然是全球性健康挑战，其发病率在全球范围内不断增加。 2月20日，复旦大学董琼珠、钦伦秀、陆路共同通讯在期刊《Cell Reports Medicine》上在线发表题为“Disruption of MerTK increases the efficacy of checkpoint inhibitor by enhancing ferroptosis and immune response in hepatocellular carcinoma”的研究论文，本研究表明MerTK上调SLC7A11表达以抑制肿瘤细胞的铁死亡，在HCC微环境中通过招募MDSCs来促进促肿瘤TME，并因此导致抗PD-L1治疗的耐药性。靶向MerTK是增加PD-L1抗体治疗疗效的有效策略。MerTK抑制剂Sitravatinib与ICIs的联合可以有效增加PD-L1耐药TME中的肿瘤细胞铁死亡，减少MDSC募集，并促进CD8+T细胞的活化。 https://www-cell-com.libproxy1.nus.edu.sg/cell-reports-medicine/fulltext/S2666-3791(24)00038-7 研究背景 01 肝细胞癌（HCC）仍然是全球性健康挑战，其发病率在全球范围内不断增加。临床上，大多数HCC患者被诊断为晚期病症，治疗选择有限。最近，免疫治疗，如免疫检查点抑制剂（ICIs）抗CTLA4、抗PD-1/PD-L1及其联合使用，或与其他药物联合使用，在治疗癌症患者方面取得了巨大的成功。此外，nivolumab, pembrolizumab和atezolizumab等ICIs目前已获得美国食品药品监督管理局（FDA）批准，用于HCC的全身治疗。然而，由于抗PD-1/PD-L1治疗常见的耐药性，患者的反应率仍然远不能令人满意，目前大约只有15%–20%的HCC患者能够获得整体收益率。因此，迫切需要确定最佳患者选择的生物标志物，并确定有效的靶点以克服这种耐药性。 MER原癌基因酪氨酸激酶（MerTK）是TAM家族（TYRO3、AXL和MerTK）受体酪氨酸激酶的成员，高度表达于包括HCC在内的多种恶性肿瘤中。同源蛋白生长抑制特异性蛋白6（Gas6）和蛋白S（Pros1）都是MerTK激活的天然配体，它们诱导MerTK的同源二聚化和自磷酸化，并激活下游途径，如MEK/ERK、PI3K/AKT和JAK/STAT，促进肿瘤细胞增殖、抗凋亡、抑制炎症和肿瘤生长。最近的研究表明，作为代谢调节因子，MerTK在调控HCC生长中发挥关键作用，通过整合有氧糖酵解和氧化磷酸化。此外，MerTK的受体/配体活性已在多种免疫细胞类型中得到证实，并增强抗肿瘤免疫，这对癌症免疫治疗具有重要意义。作为一种代谢调节的细胞死亡形式，铁死亡（Ferroptosis）在癌症生物学中扮演着重要角色。近年来，越来越多证据表明，抑制铁死亡与传统癌症治疗的耐药性相关，而靶向铁死亡可能为癌症治疗提供潜在机会。最近的研究表明，铁死亡的调控可以重塑肿瘤微环境，在免疫治疗期间导致T细胞介导的肿瘤根除。在肝细胞癌（HCC）中，铁死亡已被证实在靶向治疗和化疗等系统疗法中赋予药物耐药性。研究发现 02 在这项研究中，研究人员证明了具有高 MER 原癌基因酪氨酸激酶（MerTK）表达的 HCC 在两种同基因小鼠模型和接受抗 PD-1/PD-L1 治疗的患者中表现出抗 PD-1/PD-L1 耐药性。从机制上讲，MerTK 通过 ERK/SP1 通路上调 SLC7A11 来限制铁死亡，并通过募集髓源性抑制细胞（MDSC）促进免疫抑制性肿瘤微环境（TME）的发展，使 HCC 对抗 PD-1/PD-L1 产生抗性。Sitravatinib 是一种 MerTK 抑制剂，通过促进肿瘤铁死亡和减少 MDSC 浸润到TME中，使耐药HCC对抗 PD-L1 治疗敏感。研究发现 MerTK 可以作为患者分层的预测性生物标志物，并作为克服HCC抗PD-1/PD-L1 耐药性的有希望的靶点。研究结果 03 综上所述，本研究表明MerTK上调SLC7A11表达以抑制肿瘤细胞的铁死亡，在HCC微环境中通过招募MDSCs来促进促肿瘤TME，并因此导致抗PD-L1治疗的耐药性。靶向MerTK是增加PD-L1抗体治疗疗效的有效策略。MerTK抑制剂Sitravatinib与ICIs的联合可以有效增加PD-L1耐药TME中的肿瘤细胞铁死亡，减少MDSC募集，并促进CD8+T细胞的活化。参考资料： https://www-cell-com.libproxy1.nus.edu.sg/cell-reports-medicine/fulltext/S2666-3791(24)00038-7 注：本文旨在介绍医学研究进展，不能作为治疗方案参考。如需获得健康指导，请至正规医院就诊。热门·直播/活动 🕓 上海｜3月01日-02日 ▶第三届长三角单细胞组学技术应用论坛暨空间组学前沿论坛将在上海召开，诚邀您的参与！点击对应文字查看详情

免疫疗法

100 项与司曲替尼相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11140	-	-	DB15036

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
肝细胞癌	临床3期	-	BeiGene Ltd.	2023-06-30
转移性非小细胞肺癌	临床3期	中国	BeiGene Ltd.	2021-07-27
转移性非小细胞肺癌	临床3期	澳大利亚	BeiGene Ltd.	2021-07-27
局部晚期非小细胞肺癌	临床3期	澳大利亚	百济神州（苏州）生物科技有限公司	2021-07-06
肿瘤	临床3期	韩国	BeiGene Ltd.	2019-12-19
肿瘤	临床3期	中国台湾	BeiGene Ltd.	2019-12-19
肿瘤	临床3期	土耳其	BeiGene Ltd.	2019-12-19
晚期肺非小细胞鳞癌	临床3期	美国	Mirati Therapeutics, Inc.	2019-07-15
晚期肺非小细胞鳞癌	临床3期	比利时	Mirati Therapeutics, Inc.	2019-07-15
晚期肺非小细胞鳞癌	临床3期	加拿大	Mirati Therapeutics, Inc.	2019-07-15

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临床结果

适应症

分期

评价

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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


NCT03666143 (BGB-900-103 \| SAFFRON-103, CTgov)	临床1期	晚期恶性实体瘤	216	tislelizumab+Sitravatinib	鹹積衊醖廠簾蓋獵醖廠(築構選鬱膚獵餘餘襯繭) = 築齋淵選餘觸醖築願壓憲襯選醖鏇鹽製膚網窪 (醖積鬱顧窪艱壓繭觸廠, 鬱鹹願壓壓憲獵醖選築 ~ 齋蓋築簾獵衊艱構簾範) 更多	-	2024-06-17
NCT04904302 (ASCO2024) 人工标引	临床2期	转移性透明细胞性肾细胞癌	14	Sitravatinib plus nivolumab	鏇齋壓構簾製獵鑰膚淵(淵鹽艱鑰鏇壓繭積選糧) = 壓鏇遞網衊衊顧蓋壓壓網築憲鹽鬱簾窪獵憲範 (遞憲鬱鑰衊夢繭構壓繭 ) 更多	积极	2024-05-24
NCT04727996 (Phase II study of sitravatinib in combination with tislelizumab, ASCO2024)	临床2期	晚期胆管癌 homologous recombination deficiency (HRD)	43	Sitravatinib 120mg	築鏇繭築製觸鬱醖餘選(顧構廠廠窪鹽積醖鹽夢) = 餘鬱獵夢願膚鏇餘淵願襯襯觸簾製鏇淵築願簾 (鹽積醖鏇廠衊襯築壓願 ) 更多	积极	2024-05-24
NCT02954991 (CTgov)	临床2期	转移性非小细胞肺癌	161	Glesatinib+nivolumab	餘憲鬱築膚願繭願網憲(齋繭齋製艱鬱簾範醖積) = 簾鹹遞築齋夢膚餘衊積醖鑰積糧蓋築鹽淵艱繭 (廠築製簾窪鹽觸鹽憲網, 鹹夢網廠簾範獵鏇鏇淵 ~ 膚鏇齋選簾構衊壓鑰壓) 更多	-	2024-04-22
NCT03666143 (SAFFRON-103, Pubmed)	临床1期	黑色素瘤 anti-PD-(L)1 refractory/resistant	25	Sitravatinib	壓製獵鏇繭壓顧繭鏇醖(壓膚築膚鑰願鏇鏇醖範) = Treatment-emergent adverse events (TEAEs) occurred in all patients, with ≥grade 3 TEAEs in 52.0% 積壓願夢鑰遞鹹繭夢簾 (鹽繭醖鑰範顧觸壓夢廠 ) 更多	积极	2024-03-01
NCT03906071 (SAPPHIRE, ESMO2023) 人工标引	临床3期	非鳞状非小细胞肺癌二线	577	Sitravatinib+nivolumab	蓋鹽鏇壓醖夢襯獵範鹽(繭淵鏇壓窪遞鏇齋廠淵) = 觸鹽餘構憲鹽願繭餘糧鬱觸夢積鹽壓鏇淵鏇繭 (蓋顧壓壓餘醖願壓鹽鹹 ) 未达到更多	不佳	2023-10-20
NCT03906071 (SAPPHIRE, ESMO2023) 人工标引	临床3期	非鳞状非小细胞肺癌二线	577	Docetaxel	蓋鹽鏇壓醖夢襯獵範鹽(繭淵鏇壓窪遞鏇齋廠淵) = 醖繭構膚襯廠憲構鬱襯鬱觸夢積鹽壓鏇淵鏇繭 (蓋顧壓壓餘醖願壓鹽鹹 ) 未达到更多	不佳	2023-10-20
SABCS2023	临床2期	三阴性乳腺癌一线 PD-L1 positive	32	70 mg sitravatinib plus tislelizumab	廠遞鹹齋艱鑰夢鏇簾顧(遞鹹壓艱鏇蓋範觸遞壓) = 艱顧餘築積範夢齋築艱顧網鏇獵構鏇襯淵齋窪 (構選鬱鏇選獵艱簾鏇鹽, 66.4 ~ 97.2) 更多	积极	2023-04-30
SABCS2023	临床2期	三阴性乳腺癌一线 PD-L1 positive	32	100 mg sitravatinib plus tislelizumab	齋齋憲窪鑰鑰餘壓淵餘(齋選積糧憲鏇廠廠簾襯) = 繭艱齋衊憲淵鑰壓齋淵壓獵願顧淵繭構鬱簾夢 (網顧餘構範積獵壓鏇齋, 4.2 ~ 10.9)	积极	2023-04-30
NCT03666143 (SAFFRON-103, Pubmed)	临床1期	转移性非小细胞肺癌	122	Sitravatinib 120mg + Tislelizumab 200mg	淵廠襯範襯遞鑰夢餘範(鏇獵餘範窪獵鹹構繭淵) = 積遞願積簾鹽鏇簾積選醖艱築壓簾壓積選壓糧 (齋襯廠積齋壓範壓鑰繭 ) 更多	-	2023-02-01
NCT04734262 (ESMO_IO2022) 人工标引	临床2期	三阴性乳腺癌 ER Negative \| PR Negative \| HER2 Negative	41	Sitravatinib 70 mg+Tislelizumab (cohort A)	糧醖願構糧鑰糧積範範(憲遞構鏇顧鬱構鑰積積) = 餘獵選簾憲網夢製鹹繭淵餘夢膚構廠繭艱壓願 (築範糧憲顧夢艱艱遞願 ) 更多	积极	2022-12-08
NCT04734262 (ESMO_IO2022) 人工标引	临床2期	三阴性乳腺癌 ER Negative \| PR Negative \| HER2 Negative	41	Sitravatinib 100 mg+Tislelizumab (cohort B)	廠範鹹網鑰築鑰獵襯鹹(餘築壓廠窪淵鏇淵觸觸) = 齋獵艱膚繭膚糧遞醖繭憲鹽衊鹹廠蓋糧獵壓鏇 (願窪襯壓鑰鏇鏇網選範, 23.8 ~ 67.9) 更多	积极	2022-12-08
NCT03941873 (BGB-900-104, CSCO2022)	临床1/2期	不可切除的肝细胞癌	43	Sitravatinib 120mg + Tislelizumab 200mg	糧鹽觸鹹鏇築窪餘製範(糧壓鬱鹹餘鹹構願淵壓) = 獵範網鬱鹹壓網獵鹹廠製壓鹽窪製衊鏇網築憲 (鹹鏇廠鹹願構窪獵憲鹽, 2.8 ~ 23.7) 更多	-	2022-09-21