甲苯磺酸索拉非尼(Sorafenib Tosylate) - 药物靶点：BRAF x CRAF x FLT3 x PDGFRβ x RET x VEGFR1 x VEGFR2 x VEGFR3 x c-Kit_在研适应症：甲状腺癌，不可切除的肝细胞癌，晚期肝细胞癌_专利_临床

概要

基本信息

药物类型

小分子化药

别名

N-(4-Chloro-3-(trifluoromethyl)phenyl)-N'-(4-(2-(N-methylcarbamoyl)-4-pyridyloxy)phenyl)urea、SORAFENIB、Sorafenib tosilate

+ [16]

靶点

BRAF x CRAF x FLT3 x PDGFRβ x RET x VEGFR1 x VEGFR2 x VEGFR3 x c-Kit

作用方式

抑制剂、拮抗剂

作用机制

BRAF抑制剂(丝氨酸/苏氨酸蛋白激酶B-raf抑制剂)、CRAF抑制剂(C-Raf激酶抑制剂)、FLT3抑制剂(酪氨酸蛋白激酶受体FLT3抑制剂)

治疗领域

肿瘤消化系统疾病内分泌与代谢疾病+ [3]

在研适应症

甲状腺癌不可切除的肝细胞癌晚期肝细胞癌+ [10]

非在研适应症

腺泡细胞癌急性双表型白血病急性白血病+ [142]

原研机构

Onyx Pharmaceuticals, Inc.

在研机构

Merck Sharp & Dohme Corp.

复旦大学

Bayer AG

+ [9]

非在研机构

Celgene Corp.

Eli Lilly & Co.Onyx Therapeutics, Inc.

+ [16]

权益机构

Amgen, Inc.

拜耳医药保健有限公司

Onyx Pharmaceuticals, Inc.

+ [4]

最高研发阶段批准上市

首次获批日期

美国 (2005-12-01),

晚期肾细胞癌

最高研发阶段(中国)批准上市

特殊审评孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本)、优先审评 (中国)

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结构/序列

分子式C28H24ClF3N4O6S

InChIKeyIVDHYUQIDRJSTI-UHFFFAOYSA-N

CAS号475207-59-1

关联

846

项与甲苯磺酸索拉非尼相关的临床试验

NCT06474663

/ Not yet recruiting临床1期IIT

A Phase I Study Investigating the Combination of Cladribine, Low Dose Cytarabine and Sorafenib Alternating With Decitabine in Pediatric Relapsed and Refractory Acute Leukemias

To find the recommended dose of the drug combination cladribine, cytarabine, decitabine, and sorafenib in participants with relapsed/refractory AML, MPAL, and ALAL.

开始日期2025-12-31

申办/合作机构

The University of Texas MD Anderson Cancer Center

NCT06972641

/ Recruiting临床2/3期IIT

A Prospective, Multicenter Umbrella Study Based on Molecular Genetics to Guide the Efficacy and Safety of Maintenance Therapy After Allogeneic Hematopoietic Stem Cell Transplantation for Acute Myeloid Leukemia/Myelodysplastic Syndrome

This study is a prospective, multicenter, open-label umbrella clinical study planned to enroll 126 subjects with acute myeloid leukemia/myelodysplastic syndromes undergoing allogeneic hematopoietic stem cell transplantation. Subjects eligible for enrollment were grouped based on the results of the initial myeloid genomic second-generation sequencing, and were given different regimens of maintenance therapy, with the aim of evaluating the efficacy and safety of the maintenance regimen.

开始日期2025-06-10

申办/合作机构

上海交通大学医学院附属瑞金医院

CTR20251412

/ Active, not recruitingN/A

甲苯磺酸索拉非尼片在健康研究参与者中的随机、开放、单剂量、两制剂、三周期、三序列部分重复交叉设计生物等效性研究

主要目的：以山东丹红制药有限公司研发，杨凌步长制药有限公司生产的甲苯磺酸索拉非尼片（0.2 g）为受试制剂（T），以 Bayer AG 持证的甲苯磺酸索拉非尼片（多吉美®，0.2 g）为参比制剂（R），评估健康研究参与者在空腹状态下单次口服受试制剂和参比制剂的药代动力学特征，评价两种制剂的人体生物等效性。次要目的：考察健康研究参与者口服受试制剂和参比制剂后的安全性。

开始日期2025-05-23

申办/合作机构

山东丹红制药有限公司

100 项与甲苯磺酸索拉非尼相关的临床结果

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100 项与甲苯磺酸索拉非尼相关的转化医学

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100 项与甲苯磺酸索拉非尼相关的专利（医药）

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16,893

项与甲苯磺酸索拉非尼相关的文献（医药）

2025-12-31·ANNALS OF MEDICINE

A novel glycogene-related signature for prognostic prediction and immune microenvironment assessment in kidney renal clear cell carcinoma

Article

作者: Zhao, Danni ; Cui, Hanxiao ; Ren, Xueting ; Zhao, Xuyan ; Kang, Huafeng ; Li, Zihao ; Liu, Peinan ; Lin, Shuai ; Zhou, Mingjing

BACKGROUND:

Kidney Renal Clear Cell Carcinoma (KIRC) is a prevalent urinary malignancies worldwide. Glycosylation is a key post-translational modification that is essential in cancer progression. However, its relationship with prognosis, tumour microenvironment (TME), and treatment response in KIRC remains unclear.

METHOD:

Expression profiles and clinical data were retrieved from The Cancer Genome Atlas and Gene Expression Omnibus databases. Consensus clustering, Cox regression, and LASSO regression analyses were conducted to develop an optimal glycogene-related signature. The prognostic relevance of this molecular signature was rigorously analyzed, along with its connections to tumour microenvironment (TME), tumour mutation burden, immune checkpoint activity, cancer-immunity cycle regulation, immunomodulatory gene expression patterns, and therapeutic response profiles. Validation was performed using real-world clinical specimens, quantitative PCR (qPCR), and immunohistochemistry (IHC), supported by cohort analyses from the Human Protein Atlas (HPA) database.

RESULTS:

A glycogene-associated prognostic scoring system was established to categorize patients into risk-stratified subgroups. Patients in the high-risk cohort exhibited significantly poorer survival outcomes (p < 0.001). By incorporating clinicopathological variables into this framework, we established a predictive nomogram demonstrating strong calibration and a concordance index (C-index) of 0.78. The high-risk subgroup displayed elevated immune infiltration scores (p < 0.001), upregulated expression of immune checkpoint-related genes (p < 0.05), and an increased frequency of somatic mutations (p = 0.043). The risk score positively correlated with cancer-immunity cycle activation and immunotherapy-related signals. The high-risk groups also showed associations with T cell exhaustion, immune-activating genes, chemokines, and receptors. Drug sensitivity analysis revealed that low-risk patients were more sensitive to sorafenib, pazopanib, and erlotinib, whereas high-risk individuals responded better to temsirolimus (p < 0.01). qPCR and IHC analyses consistently revealed distinct expression patterns of MX2 and other key genes across the risk groups, further corroborated by the HPA findings.

CONCLUSION:

This glycogene-based signature provides a robust tool for predicting prognosis, TME characteristics, and therapeutic responses in KIRC, offering potential clinical utility in patient management.

2025-12-31·Hematology

Integrated transcriptome profiling and in vitro analysis reveals MLN4924’s role in inducing ferroptosis in acute myeloid leukemia

Article

作者: Zhao, Long ; Liu, Bei ; Jian, Jinli ; Guo, Yuancheng ; Tang, Xiao

OBJECTIVES:

While ferroptosis induction emerges as a therapeutic strategy for solid tumors, its role in acute myeloid leukemia (AML) remains unexplored. This study aimed to investigate the role of MLN4924 in modulating ferroptosis and its molecular targets in AML.

METHODS:

Transcriptome sequencing and bioinformatics analyses were performed to identify MLN4924 potential targets in ferroptosis. First, ferroptosis-related phenotypic assays were conducted, including assays of reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and Fe²⁺ levels. Second, cell viability assays were carried out with the combination of MLN4924 and ferroptosis inducers (Erastin, Sorafenib). Third, rescue experiments were used the ferroptosis inhibitor Ferrostatin-1 after MLN4924 treatment. In vivo efficacy was evaluated in NOD/SCID mice bearing AML xenografts treated with MLN4924, followed by tumor tissue analysis of GSH and Fe²⁺ levels, immunohistochemistry (IHC), and Western blotting for SLC7A11/GPX4 axis components.

RESULTS:

Transcriptome sequencing and bioinformatics analyses identified SLC7A11 and GPX4 as key MLN4924 target genes, both of which are glutathione-related proteins. MLN4924 significantly suppressed SLC7A11 and GPX4 expression, decreased GSH activity, and increased ROS, Fe²⁺, and MDA levels. Ferroptosis inducers (Erastin, Sorafenib) further enhanced the antileukemic activity of MLN4924, and ferroptosis inhibitor Ferrostatin-1 partially reversed this toxicity. In vivo, MLN4924 reduced tumor burden, accompanied by SLC7A11/GPX4 downregulation and Fe²⁺ accumulation in xenografts.

CONCLUSION:

This study provides the first evidence that MLN4924 triggers ferroptosis in AML by inhibiting the SLC7A11/GPX4 axis. These findings establish MLN4924 as a ferroptosis sensitizer through synergistic effects with ferroptosis inducers, supporting its therapeutic potential in AML.

2025-12-31·JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY

Design, synthesis and biological evaluation of novel urolithin derivatives targeting liver cancer cells

Article

作者: Zhou, Benhong ; Tian, Mi ; Ling, Yipeng ; Zhao, Lirong ; Lan, Yu ; Li, Chen

We designed and synthesised 22 new urolithin derivatives (UDs) based on methyl-urolithin A (mUA) to identify anti-cancer drugs with high efficacy and low toxicity and evaluated their anti-cancer activities in vitro. Cytotoxicity tests were performed on three cell lines (DU145, T24, and HepG2) and a human normal cell line (HK-2). The half-inhibitory concentration (IC₅₀) of derivative UD-4c to hepatoma HepG2 cells (IC₅₀ = 4.66 ± 0.12 μM) was significantly lower than that of sorafenib (IC₅₀ =7.76 ± 0.12 μM), and exhibited less toxicity to HK-2 cells. Preliminary studies on the mechanism revealed that the derivative UD-4c could significantly inhibit the HepG2 cell growth and colony formation, block the HepG2 cell cycle in the G2/M phase, and induce apoptosis of HepG2 cells dose-dependently. The derivative UD-4c can be used as a potential lead compound to further develop new drugs for hepatocellular carcinoma treatment based on the evaluation of anti-cancer activity.

1,055

项与甲苯磺酸索拉非尼相关的新闻（医药）

2025-07-26

·ETPharma

Experts flag UK-India FTA over patent terms, access to drugs

Mumbai: Experts in intellectual property law and civil society groups in India have raised concerns that provisions in the UK-India Free Trade Agreement , Comprehensive Economic and Trade Agreement (CETA), may dilute compulsory licensing norms and jeopardise future access to affordable lifesaving medicines. As part of the Indian Patent Act, the country has the rights to invoke compulsory license for any lifesaving medicines or vaccines and call upon domestic generic players to supply it during a national emergency in the public interest. KM Gopakumar, co-convenor of Working Group on Access to Medicines and Treatment, said the deal amounts to giving a backdoor entry to TRIPS (Trade Related Intellectual Property Rights) plus provisions and goes beyond the minimum standards set by the World Trade Organization, which India has so far resisted in multilateral trade forums. The group said the UK-India FTA provisions on patents tilt the balance in favour of the patent owner and undermines access to medicines. The UK-India FTA says, "The parties recognise the preferable and optimal route to promote and ensure access to medicines is through voluntary mechanisms, such as voluntary licensing , which may include technology transfer on mutually agreed terms." Biswajit Dhar, retired professor of economics at Jawaharlal Nehru University, noted that India was moving away from its sovereign rights by placing emphasis on voluntary license (VLs). "It will kill the essence of the compulsory licensing mechanism and even within the legal framework, India has issued only one CL to Natco Pharma (for Bayer's kidney cancer drug sorafenib)," he noted. He said VLs come with restrictions of pricing that are determined by the innovator Big Pharma companies. "Often voluntary license contains onerous conditions on the licensee and fails to bring sharp price reduction compared to the compulsory licenses," Dhar added. Gopakumar said that India places a higher threshold for examination and grant of patents, but if the FTA deal is any indication, it may result in "functional harmonization" and lead to dilution in the grant of patent. However, a few other patent experts told ET that the FTA seeks to keep a balance between India's current IP regime with public health and the UK's preference of protecting various IP rights. The FTA seeks to create a Working Group on IPR. On patents, India's important safeguards such as Section 3(d) (which blocks evergreening of patents) of the Indian Patent Act, and oppositions have not been disregarded and it should help in India's status as the world's generic drug manufacturer and protect access to medicines for domestic patients.

专利到期专利侵权

2025-07-26

·ETPharma

India-UK FTA does not dilute New Delhi's right to issue compulsory licences: Official

New Delhi: The India-UK free trade agreement does not dilute New Delhi's right to issue compulsory licences (CLs) and does not introduce any new preconditions for their issuance, an official said on Friday. The agreement was signed on July 24 in London. The official said that the sovereign authority to issue such licences remains entirely with the Government of India, as per existing law. "The agreement's reference to voluntary licensing simply acknowledges global best practices that encourage collaborative solutions. It does not limit or dilute India's well-established right to issue CLs under a section of the Indian Patents Act, 1970," the official said. The remarks are important as economic think tank GTRI has stated that India has accepted language in the intellectual property chapter of the free trade agreement with the UK that subtly curtails its ability to issue compulsory licences, a critical tool for accessing life-saving technologies during emergencies. As per WTO (World Trade Organisation) agreement, a compulsory license can be invoked by a national government allowing someone else to produce a patented product or process without the consent of the patent owner in public interest. Only one CL has been issued so far for the cancer drug Nexavar (2012) and that too under exceptional public health circumstances. "The FTA does not create any new precondition for issuing CLs. The sovereign authority to issue such licenses remains entirely with the Government of India, as per existing law," the official said. India's patent law continues to be recognized globally for balancing public health needs with innovation incentives.. "The free trade pact does not alter this balance and in fact, it reaffirms India's policy autonomy," the government official said adding the pact's provision on disclosure of commercial working of patents is fully consistent with India's existing legal regime and the evolving needs of a modern innovation ecosystem. The official added that the India-UK trade agreement marks a new era of cooperation that supports both affordable access to medicines and high standards of innovation and IP protection.

2025-07-24

·ioncology

ESMO GI国际视野丨工藤正俊教授：HCC不同一线免疫联合方案的间接对比，纳武利尤单抗+伊匹木单抗展现更强疗效

编者按肝细胞癌（HCC）占原发性肝癌85–90%，多数确诊时已晚期，预后差且治疗受限。度伐利尤单抗+替西木单抗（D+T）、阿替利珠单抗+贝伐珠单抗（A+B）及纳武利尤单抗+伊匹木单抗（N＋I）已成为一线治疗新选择，但缺乏头对头研究比较。2025年欧洲肿瘤内科学会消化道肿瘤大会（ESMO GI）上，日本近畿大学医学院附属医院工藤正俊教授（Masatoshi Kudo）披露了一项研究成果，采用间接治疗比较（ITCs）的方法评估N＋I对比D+T及A+B用于一线不可切除肝细胞癌的疗效与安全性，结果显示N+I方案相较于D+T更优，相较A＋B具有更优的远期疗效。《肿瘤瞭望》于会议现场邀请工藤正俊教授接受采访，对比三种方案在疗效和安全性的不同，解析研究中分段模型疗效的时序差异，或可为uHCC一线免疫联合方案选择提供新思路。01《肿瘤瞭望》：本次ESMO GI会议上，您对纳武利尤单抗联合伊匹木单抗（N+I）、度伐利尤单抗联合替西木单抗（D+T）以及阿替利珠单抗联合贝伐珠单抗（A+B）方案一线治疗HCC进行了对比，请您总结一下这三种方案的疗效差异？工藤正俊教授日本近畿大学医学院附属医院此项研究将N+I方案、D+T方案以及A+B方案进行匹配调整间接比较（MAIC）。MAIC是一种在缺乏头对头研究情况下受到广泛认可的、用于比较不同临床研究结果的统计方法。该研究使用已发表的N+I数据与D+T、A+B数据进行匹配比较。结果显示：N+I相较于其他免疫治疗在无进展生存期（PFS）、总生存期（OS）和客观缓解率（ORR）方面均显示出更优的结果。与D+T相比，在前6个月内，N+I的PFS显著更优（HR 0.57），而在6个月后，其PFS（HR 0.71）和OS（HR 0.74）均显著更优。与A+B方案相比，在前6个月内，N+I的PFS（HR 1.05）和OS（HR 1.67）表现较差；而在6个月后，其PFS（HR 0.52）和OS（HR 0.67）则显著优于A+B。此外，N+I组ORR较两者也呈现优势趋势。以上便是本次MAIC分析的主要结果。02《肿瘤瞭望》：本次MAIC分析采用分段模型揭示了疗效的时序差异。请问您为何选择6个月作为PFS/OS的分割点时点？这对揭示N+I方案的长期生存优势有何关键意义？工藤正俊教授日本近畿大学医学院附属医院在CheckMate 9DW研究N+I方案中，对照组是仑伐替尼（85%）或索拉非尼（15%）；HIMALAYA研究（D+T方案）和IMbrave150研究（A+B方案）的对照组是索拉非尼单药，此项MAIC分析中不同研究的对照组存在差异。在CheckMate 9DW中，N+I组与混合对照组（仑伐替尼+索拉非尼）的Kaplan-Meier生存曲线存在早期交叉现象，在随机分组后的前6个月内N+I的死亡人数相对较多，随后曲线出现了有利于N+I的持续分离。因此，我们选择以6个月为分割点进行分段分析。03《肿瘤瞭望》：N+I疗法在6个月后的持续生存优势似乎很显著，在您看来N+I方案取得更大生存优势的机制是什么？工藤正俊教授日本近畿大学医学院附属医院免疫疗法（IO）联合抗血管生成酪氨酸激酶抑制剂（TKI）与IO之间联合（如CTLA-4单抗+PD-1/PD-L1单抗）呈现出完全不同的应答模式。CTLA-4单抗在免疫启动阶段激活并释放CD8+ T细胞。同时，CTLA-4抗体Fc段活性较强，与巨噬细胞或自然杀伤（NK）细胞上的Fcγ受体结合，发挥抗体依赖性细胞介导的细胞毒性作用（ADCC），继而造成高表达CTLA-4 T细胞亚群（例如Treg）耗竭。正是这种ADCC效应的存在，使得该疗法能在极早期阶段就展现出非常强的疗效，使患者达到接近完全缓解（CR）。在治疗6个月后，使生存曲线呈现出显著的长拖尾效应。这便是其独特机制的作用结果。04《肿瘤瞭望》：鉴于N+I方案早期OS曲线存在短暂下降但长期获益更优，临床医生在选择一线治疗方案时，应如何会权衡短期风险与长期获益？是否有临床因素或生物标志物为不同免疫治疗方案的决策提供指导？工藤正俊教授日本近畿大学医学院附属医院在系统性治疗开始前，尚缺乏可用的预测性生物标志物。双免疫联合疗法（如CTLA-4单抗+PD-1单抗）往往呈现出“全或无”的缓解模式，如前所述，当CTLA-4单抗的ADCC效应较强时，抗肿瘤更为显著。因此，在第3或第4周可评估缓解程度，若影像学（如CT/MRI）缓解和血清学生物标志物（如甲胎蛋白AFP或异常凝血酶原DCP）动态下降（缓解），则可以继续使用包含抗CTLA-4抗体的双免疫方案。反之，若此时未观察到AFP或DCP的缓解，则患者不太可能获得持久的临床获益，应及时转换为包含抗血管生成药物（如抗血管生成酪氨酸激酶抑制剂TKI或抗VEGF抗体）的治疗方案。研究简介研究设计III期研究HIMALAYA和IMbrave150证明，度伐利尤单抗+替西木单抗（D+T）和阿替利珠单抗+贝伐珠单抗（A+B）等免疫治疗方案一线（1L）治疗uHCC较索拉非尼疗效更优。III期CheckMate 9DW研究显示，纳武利尤单抗+伊匹木单抗（N+I）相比仑伐替尼或索拉非尼可显著改善OS与ORR，且安全性可控，因此获得美国、欧盟等药品监督管理部门批准用于uHCC。在缺乏头对头临床研究的情况下，本研究采用间接治疗比较（ITCs）评估N＋I对比D+T及A+B用于1L uHCC的疗效与安全性。本研究关键挑战在于患者人群的异质性及不同研究间对照组的差异。基于CheckMate 9DW研究中N＋I患者PFS和OS的Kaplan-Meier（KM）曲线梯度变化，以6个月为分割点，对PFS和OS进行分段MAIC分析。由于基线异质性存在，IMbrave150研究包含了门静脉侵犯Vp4患者，该人群预后较差，故敏感性分析排除了该人群。本研究使用Cox比例风险模型计算风险比（HR）和95%置信区间（CI），逻辑回归模型评估N＋I组的加权ORR，基于CheckMate 9DW 患者数据计算N＋I的加权全因不良事件（AE）发生率，D+T/A+B的发生率源各自已经发表的数据。研究结果将三项临床研究进行加权分析，使N＋I组与D+T或A+B组的基线特征实现良好平衡（表1）。表1.ITT人群患者基线特征加权前后的汇总分布疗效方面，N＋I总体显著优于D+T（PFS HR=0.61, 95%CI 0.51–0.73；OS HR=0.79, 0.65–0.95；ORR OR=2.35, 1.69–3.28）；且在0–6个月PFS显著更优（HR=0.57）、OS具有更优趋势（HR=0.90）；6个月后PFS（HR=0.71）和OS（HR=0.74）显著更优（表2、图1、图3）。与A+B方案相比，N＋I总体PFS显著更优（HR=0.81, 0.66–0.99），OS具有更优趋势（HR=0.93）、ORR也具有更优趋势（OR=1.39）；但0–6个月OS较差（HR=1.67, 1.12–2.49）；6个月后显著逆转，PFS（HR=0.52）和OS（HR=0.67）均优于A+B（表2、图2、图4）。非Vp4亚组分析中，N＋I对比A＋B的整体PFS（HR=0.82, 95%CI 0.66-1.02）、OS（HR=0.98, 0.76-1.26）、ORR（OR=1.25, 95%CI 0.86-1.70）具有更优趋势。N＋I方案在0-6个月PFS（HR=1.09, 0.83-1.43）具有较差趋势，OS显著更差（HR=2.05, 1.30-3.22）；但6个月后发生逆转，PFS与OS均呈现显著更优（PFS HR=0.51, 0.36-0.73；OS HR=0.68, 0.50-0.92）。表2.非锚定MAIC结果：疗效结局图1.N＋I vs D+T的PFS KM曲线图图2.N＋I vs A＋B的PFS KM曲线图图3.N＋I vs D+T的OS KM曲线图图4.N＋I vs A＋B的OS KM曲线图安全性方面（表3），N＋I加权后的≥3级治疗相关不良事件（TRAEs）发生高于D+T（25.8%），但低于A+B（43.5%），治疗相关死亡率与两者相当。表3.非锚定MAIC结果展示的安全性结局研究结论在缺乏头对头随机对照研究的情况下，MAIC分析显示N＋I对比其他免疫治疗具有全面疗效优势。N+I较D+T在所有分析期（总体、0-6个月期间和6个月后）、较A+B在总体及6个月后分析具有更好的PFS、OS获益；N＋I方案安全性总体可控。因此，本研究结果可为uHCC一线免疫联合方案的选择提供依据。▌参考文献：151P Matching-adjusted indirect comparisons (MAICs) of nivolumab + ipilimumab (N + I) vs durvalumab + tremelimumab (D + T) and atezolizumab + bevacizumab (A + B) for first-line (1L) unresectable hepatocellular carcinoma (uHCC) Kudo, M. et al. Annals of Oncology, Volume 36, S64（来源：《肿瘤瞭望》编辑部）声明凡署名原创的文章版权属《肿瘤瞭望》所有，欢迎分享、转载。本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。

临床结果

100 项与甲苯磺酸索拉非尼相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D06272	甲苯磺酸索拉非尼	L01XE05	DB00398

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
甲状腺癌	美国	Bayer HealthCare Pharmaceuticals, Inc.	2013-11-22
不可切除的肝细胞癌	美国	Bayer HealthCare Pharmaceuticals, Inc.	2007-11-16
晚期肝细胞癌	澳大利亚	Bayer Australia Ltd.	2006-09-27
分化型甲状腺癌	欧盟	Bayer AG	2006-07-19
分化型甲状腺癌	冰岛	Bayer AG	2006-07-19
分化型甲状腺癌	列支敦士登	Bayer AG	2006-07-19
分化型甲状腺癌	挪威	Bayer AG	2006-07-19
肝细胞癌	欧盟	Bayer AG	2006-07-19
肝细胞癌	冰岛	Bayer AG	2006-07-19
肝细胞癌	列支敦士登	Bayer AG	2006-07-19
肝细胞癌	挪威	Bayer AG	2006-07-19
肾细胞癌	欧盟	Bayer AG	2006-07-19
肾细胞癌	冰岛	Bayer AG	2006-07-19
肾细胞癌	列支敦士登	Bayer AG	2006-07-19
肾细胞癌	挪威	Bayer AG	2006-07-19
晚期肾细胞癌	美国	Bayer HealthCare Pharmaceuticals, Inc.	2005-12-01

未上市

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
伴有 FLT3/ITD 突变的急性髓系白血病	临床3期	中国	南方医科大学	2015-06-20
HER2 阴性乳腺癌	临床3期	美国	Bayer AG	2011-02-21
HER2 阴性乳腺癌	临床3期	美国	Onyx Therapeutics, Inc.	2011-02-21
HER2 阴性乳腺癌	临床3期	中国	Onyx Therapeutics, Inc.	2011-02-21
HER2 阴性乳腺癌	临床3期	中国	Bayer AG	2011-02-21
HER2 阴性乳腺癌	临床3期	日本	Onyx Therapeutics, Inc.	2011-02-21
HER2 阴性乳腺癌	临床3期	日本	Bayer AG	2011-02-21
HER2 阴性乳腺癌	临床3期	阿根廷	Onyx Therapeutics, Inc.	2011-02-21
HER2 阴性乳腺癌	临床3期	阿根廷	Bayer AG	2011-02-21
HER2 阴性乳腺癌	临床3期	澳大利亚	Onyx Therapeutics, Inc.	2011-02-21

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临床结果

适应症

分期

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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


NCT04000737 (A Randomized, Double Blind, Phase 2 Study of Sorafenib With or Without YIV-906, ESMO_GI2025)	临床2期	肝细胞癌辅助 HBV(+)	107	Sorafenib + YIV-906	鹹窪鹹鑰遞餘構顧鬱艱(觸觸願糧衊糧構壓觸窪) = 願鑰壓襯網餘廠鹽繭觸衊構遞範齋鑰醖襯憲鬱 (蓋網遞蓋膚簾鏇憲餘範 ) 更多	积极	2025-07-03
				Placebo	鹹窪鹹鑰遞餘構顧鬱艱(觸觸願糧衊糧構壓觸窪) = 願餘齋網獵糧糧壓餘襯衊構遞範齋鑰醖襯憲鬱 (蓋網遞蓋膚簾鏇憲餘範 ) 更多
NCT03247088 (phase 1/2 study, ASCO2025)	临床1/2期	急性髓性白血病 8/8-HLA matched donors \| MRD+ \| FLT3 ITD	59	Sorafenib 800mg	糧餘繭餘壓醖選積積衊(簾網廠廠膚齋繭築糧觸) = 鑰醖願壓鑰淵選糧衊淵顧築範範網觸壓窪願艱 (廠範淵積蓋艱艱鏇鏇範, 61.8 ~ 84.8)	积极	2025-05-30
ASCO2025	N/A	侵袭性纤维瘤病	48	Less than 6 months of sorafenib treatment	廠構憲網觸膚糧選壓積(淵醖淵鏇淵蓋顧鬱簾窪) = 52% 網遞糧廠網淵夢齋窪範 (艱衊窪糧鏇選築製築夢 ) 更多	积极	2025-05-30
				Less than 12 months of sorafenib treatment
NCT03247088 (S266, EHA2025)	临床1/2期	急性髓性白血病 FLT3 ITD	59	Sorafenib 800mg	鹽窪簾觸製窪憲觸醖鹹(選選夢構糧鏇獵艱繭鏇) = 簾繭簾衊壓顧積鏇顧衊蓋構顧夢襯艱襯簾廠蓋 (膚鬱憲艱夢觸餘襯顧蓋, 61.8 ~ 84.8)	积极	2025-05-14
NCT01906216 (SELECT, EASL_LCS2025) 人工标引	临床3期	晚期肝细胞癌	199	Sorafenib combined with TACE	窪艱構網壓遞夢繭窪壓(淵壓鹽繭膚選鬱觸簾廠) = 積獵築範鏇鏇餘鑰憲廠選鏇窪窪鬱襯鑰艱鹹壓 (襯獵簾憲遞衊鏇範淵顧, 10.5 ~ 19.3) 更多	积极	2025-02-20
				Sorafenib alone	窪艱構網壓遞夢繭窪壓(淵壓鹽繭膚選鬱觸簾廠) = 簾夢淵網醖觸窪淵衊顧選鏇窪窪鬱襯鑰艱鹹壓 (襯獵簾憲遞衊鏇範淵顧, 9.0 ~ 14.8) 更多
NCT01730937 (Pubmed \| JAMA Oncol) 人工标引	临床3期	肝细胞癌一线	193	Sorafenib	繭襯糧願網糧淵窪蓋簾(鹹齋窪夢鹹願衊憲簾廠) = 網積鬱膚觸廠糧鹹鏇簾糧構築艱蓋淵壓製鏇襯 (衊壓構鑰衊憲願憲蓋淵, 10.6 ~ 14.3) 更多	积极	2024-12-19
				SBRT followed by Sorafenib	繭襯糧願網糧淵窪蓋簾(鹹齋窪夢鹹願衊憲簾廠) = 構繭獵範醖醖鹹膚齋齋糧構築艱蓋淵壓製鏇襯 (衊壓構鑰衊憲願憲蓋淵, 11.4 ~ 19.2) 更多
CTNI-45 (SNO2024)	临床2期	复发性恶性胶质瘤 GRP78 (HSPA5) \| PDGFRa	33	Sorafenib	壓繭襯積願觸製鹽願壓(醖醖範選獵蓋獵繭廠網) = one grade 3 toxicity for maculopapular rash (6.4%) 鏇鑰壓鑰廠範窪艱鏇淵 (醖憲夢鹹積積鹹鹹顧選 ) 更多	积极	2024-11-11
ESMO2024 人工标引	N/A	肝细胞癌一线	1,361	Lenvatinib (LEN)	夢觸齋製糧鑰鹽構糧窪(醖範齋鏇顧衊製遞積簾) = 鏇範鏇衊顧齋繭艱顧願衊構願積襯壓繭餘襯構 (範範遞窪網廠鹽窪簾築, 8.3 ~ 10.8) 更多	积极	2024-09-16
				Sorafenib (SOR)	夢觸齋製糧鑰鹽構糧窪(醖範齋鏇顧衊製遞積簾) = 襯獵網壓廠淵範齋醖願衊構願積襯壓繭餘襯構 (範範遞窪網廠鹽窪簾築, 6.4 ~ 9.3) 更多
NCT04039607 (ESMO2024)	临床3期	不可切除的肝细胞癌	-	Nivolumab + Ipilimumab	鬱醖廠窪選襯齋構鏇觸(鏇餘鬱遞膚糧繭鏇網蓋) = 壓糧鑰衊網窪鑰網壓壓願構襯繭築選夢艱蓋糧 (鏇繭鑰獵襯願廠餘膚鹽 ) 更多	-	2024-09-16
				Lenvatinib	鬱醖廠窪選襯齋構鏇觸(鏇餘鬱遞膚糧繭鏇網蓋) = 選壓簾簾醖鏇淵顧艱窪願構襯繭築選夢艱蓋糧 (鏇繭鑰獵襯願廠餘膚鹽 ) 更多
ESMO_GI2024 人工标引	N/A	晚期肝细胞癌二线	81	Sorafenib	製糧餘製艱積夢鏇鑰顧(鏇鑰遞觸鹹淵艱鹽鏇夢) = 餘簾憲蓋蓋醖淵觸襯憲膚獵鏇蓋淵醖顧簾築願 (醖鬱衊膚鑰顧憲醖衊構 ) 更多	-	2024-06-27