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更新于：2026-07-18

SRC inhibitors(Wyeth-Ayerst Research)

更新于：2026-07-18

概要

概要

基本信息

药物类型

小分子化药

别名

4-[(2,4-dichlorophenyl)amino]-6,7-dimethoxy-3-quinolinecarbonitrile (2a)

靶点

SRC

作用方式

抑制剂

作用机制

SRC抑制剂(酪氨酸蛋白激酶SRC抑制剂)

治疗领域

肿瘤

在研适应症-

非在研适应症

肿瘤

原研机构

Wyeth-Ayerst Research

在研机构-

非在研机构

Wyeth-Ayerst Research

权益机构-

最高研发阶段无进展临床前

首次获批日期-

最高研发阶段(中国)-

特殊审评-

结构/序列

分子式C18H13Cl2N3O2

InChIKeyIUZCVUGIDCZCEQ-UHFFFAOYSA-N

CAS号331662-50-1

关联

100 项与 SRC inhibitors(Wyeth-Ayerst Research) 相关的临床结果

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100 项与 SRC inhibitors(Wyeth-Ayerst Research) 相关的转化医学

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100 项与 SRC inhibitors(Wyeth-Ayerst Research) 相关的专利（医药）

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153

项与 SRC inhibitors(Wyeth-Ayerst Research) 相关的文献（医药）

2026-06-01·CYTOKINE

CSF3R signalling beyond granulopoiesis: new paradigms in female reproductive biology

Review

作者: Goyal, Sameer N ; Ansari, Rashid ; Awathale, Sanjay N

The Colony-Stimulating Factor 3 Receptor (CSF3R), the receptor for granulocyte colony-stimulating factor (G-CSF), has expanded from a hematopoietic regulator to a multifunctional signalling molecule with significant relevance in gynaecological biology. High-resolution transcriptomic and proteomic studies now identify CSF3R expression in ovarian granulosa cells, endometrial epithelium, cervical tissue, placental trophoblasts, and gynaecologic tumour microenvironments, highlighting its integration into immune, endocrine, and tissue-remodeling networks. Structurally anchored by Box1/Box2 motifs, CSF3R initiates key intracellular pathways JAK-STAT, MAPK/ERK, PI3K-AKT-mTOR, SRC-family kinases, and Nf-κB governing cellular survival, proliferation, angiogenesis, metabolic activity, inflammation, and epithelial-mesenchymal transition. Dysregulated CSF3R signalling contributes to major gynaecological disorders. In polycystic ovary syndrome (PCOS), chronic inflammation and altered CSF3R-STAT3/Nf-κB activity disturb follicular maturation and endocrine-metabolic balance. In endometriosis, CSF3R-associated neutrophil activation, MMP induction, and ERK-driven angiogenesis sustain lesion growth and chronic pelvic inflammation. During implantation, defective CSF3R-mediated STAT3 signalling impairs decidualization, immune tolerance, and trophoblast invasion, contributing to implantation failure and recurrent pregnancy loss. In ovarian and endometrial cancers, CSF3R drives tumour proliferation, EMT, angiogenesis, and recruitment of immunosuppressive myeloid-derived suppressor cells. Therapeutically, targeting G-CSF3R-linked pathways offers emerging opportunities. Approaches include JAK inhibitors, PI3K/mTOR inhibitors, SRC inhibitors, STAT3 antagonists, and investigational anti-G-CSF/anti-CSF3R monoclonal antibodies. G-CSF therapy has also shown benefits in improving endometrial receptivity in select cases of reproductive failure. This review explored CSF3R biology, signalling, disease involvement, and therapeutic potential, positioning G-CSF3R as an emerging, actionable node in reproductive medicine and gynaecologic oncology.

2026-05-18·Theranostics

Inhibition of SRC prevents bone metastasis of breast cancer by blocking metastatic cell motility and bone directionality

Article

作者: Lim, Sung-Chul ; Kang, Minjae ; Shim, Wan Seob ; Kwon, Minju ; Choi, Yong June ; Kang, Keon Wook ; Choi, Munkyung ; Oh, Seungseok ; Kim, Myung Jun ; Tran, Phuong Thao ; Kim, Yong-Chul ; Lee, Yujeong

Rationale:

Breast cancer bone metastasis remains a major cause of mortality with limited effective therapies. Although SRC is one of the earliest identified oncogenic kinases and has been extensively studied as a regulator of cancer progression and migration, it has not yet been successfully translated into an effective therapeutic target in solid tumors, highlighting the need to redefine SRC-targeted strategies in this context.

Methods:

Genetic deletion and pharmacological approaches were employed to interrogate SRC function, including comparative evaluation of conventional kinase inhibitors and next-generation inhibitors targeting both kinase and scaffolding functions. Cytoskeletal remodeling and cell motility were assessed via F-actin organization and focal adhesion signaling. Preclinical bone metastasis models were used to assess the extent of bone metastasis. Therapeutic efficacy was evaluated under both monotherapy and combination regimens with gemcitabine/bisphosphonate or anti-PD-1.

Results:

SRC phosphorylation regulated the activation of cytoskeletal regulators FAK and paxillin, thereby controlling cancer cell motility. Genetic deletion or pharmacological inhibition of SRC significantly suppressed cell motility, reduced F-actin remodeling, increased bone density, and inhibited bone metastasis in vivo. SRC inhibition also attenuated immune evasion, enhanced anti-tumor immunity, and synergized with anti-PD-1 or gemcitabine/bisphosphonate therapies. Notably, a next-generation SRC inhibitor that targets both catalytic activity and scaffolding function achieved more potent suppression of metastatic signaling and bone metastasis than conventional SRC inhibitors.

Conclusions:

This study demonstrates that SRC plays distinct and essential roles in cancer cell motility, osteoclast activation, and immune evasion, which collectively drive breast cancer bone metastasis. These findings establish SRC as a critical therapeutic target and suggest that dual inhibition of its kinase and scaffolding functions represents a more effective strategy than conventional approaches.

2026-02-01·CANCER LETTERS

SRC at the crossroads of KRAS inhibitor resistance: Mechanisms and therapeutic opportunities

Review

作者: Kang, Rui ; Huang, Huocong ; Westover, Kenneth D ; Zeh, Herbert J ; Lee, Yong J ; Kim, Alex ; Zhao, Dan ; Song, Xinxin ; Zhou, Zhuan ; Qu, Zhaoxia ; Tian, Hui

Kirsten rat sarcoma (KRAS) mutations are among the most common oncogenic drivers in human cancers, particularly in non-small cell lung cancer (NSCLC), colorectal cancer (CRC), and pancreatic ductal adenocarcinoma (PDAC). The development of allele-specific KRAS inhibitors, especially those targeting the KRAS^G12C variant, represents a landmark achievement in precision oncology. Yet their therapeutic benefit is often transient, as tumors rapidly develop seemingly heterogeneous resistance mechanisms. Increasing evidence implicates SRC, a non-receptor tyrosine kinase frequently hyperactivated in KRAS-mutant cancers, as a central regulator of resistance. This review integrates current evidence supporting SRC's role in mediating diverse resistance pathways, including mitogen-activated protein kinase (MAPK) reactivation, transcriptional/epigenetic reprogramming, metabolic adaptation, multidrug resistance, cell death evasion, and remodeling of the tumor microenvironment. We also critically examine the shortcomings of early-generation SRC inhibitors in solid tumors and highlight emerging therapeutic avenues such as next-generation inhibitors, proteolysis-targeting chimera (PROTAC) degraders, and biomarker-guided combination strategies. By connecting molecular insights with preclinical and clinical findings, this review positions SRC as a therapeutically actionable vulnerability in KRAS-driven cancers and outlines a translational framework for overcoming drug resistance.

100 项与 SRC inhibitors(Wyeth-Ayerst Research) 相关的药物交易

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