预约演示
更新于：2026-10-21
Gandotinib
更新于：2026-10-21
概要
基本信息
药物类型 小分子化药 |
别名 Gandotinib (USAN)、LY-2784544、LY2784544 |
作用方式 激动剂、抑制剂 |
作用机制 GPR39 激动剂(G protein-coupled receptor 39 agonists)、JAK2抑制剂(酪氨酸蛋白激酶JAK2抑制剂) |
原研机构 |
在研机构 |
非在研机构- |
权益机构- |
最高研发阶段临床2期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
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结构/序列
分子式C23H25ClFN7O |
InChIKeySQSZANZGUXWJEA-UHFFFAOYSA-N |
CAS号1229236-86-5 |
关联
3
项与 Gandotinib 相关的临床试验NCT01520220
A Phase 1 Study of LY2784544 Testing Alternative Dosing Regimens in Patients With Myeloproliferative Neoplasms
NCT01594723
A Phase 2 Study of LY2784544 in Patients With Myeloproliferative Neoplasms
NCT01134120
A Phase 1 Study of LY2784544 in Patients With JAK2 V617F-Positive Myeloproliferative Disorders
100 项与 Gandotinib 相关的临床结果
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100 项与 Gandotinib 相关的转化医学
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100 项与 Gandotinib 相关的专利（医药）
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55
项与 Gandotinib 相关的文献（医药）2026-01-06CLINICAL AND EXPERIMENTAL IMMUNOLOGY
Dermatomyositis is characterized by TYK2-dependent STAT3 activation
Article
作者: Fornaro, M ; Cacciapaglia, F ; Del Vescovo, S ; Iannone, F ; Girolamo, F ; Natuzzi, D ; Bizzoca, R
Abstract:
Dermatomyositis (DM) is characterized by activation of cytokine pathways that signal through the Janus kinase/signal transducer and activator of transcription (JAK/STAT) axis, although the relative contribution of individual JAK family members remains unclear. Peripheral blood mononuclear cells were isolated from patients with active DM (n = 5), rheumatoid arthritis (RA, n = 7), systemic sclerosis (SSc, n = 7), and healthy donors (HD, n = 5). Phosphorylated STAT3 (pSTAT3) levels were assessed by flow cytometry in CD4+ and CD14+ cells under basal conditions and following selective inhibition of JAK1 (abrocitinib), JAK2 (gandotinib), JAK3 (decernotinib), or TYK2 (deucravacitinib). Under basal conditions, DM displayed the highest pSTAT3 levels in CD4+ cells (median 38.3%), significantly exceeding those observed in HDs (0.9%, P < 0.05) and SSc (8.6%, P < 0.05), while RA showed intermediate levels (17.7%). CD14+ cells from DM patients also demonstrated increased pSTAT3 compared with HDs (9.7% vs 1.4%, P < 0.05), without significant differences versus RA or SSc. Selective JAK inhibition revealed distinct disease-specific patterns. In DM, only TYK2 inhibition significantly reduced pSTAT3 levels in both CD4+ and CD14+ cells (P < 0.05), whereas in RA, pSTAT3 was modulated by inhibition of multiple JAK family members. No significant effects were observed in HDs or SSc patients. These findings identify a selective TYK2-dependent STAT3 activation signature in circulating immune cells from patients with DM, distinguishing this disease from other autoimmune conditions and supporting TYK2 as a potential therapeutic target in DM.
2025-03-01JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Article
作者: Xu, Guangen ; Zhu, Renjun ; Dai, Qingfeng ; Zhang, Guolin ; Xu, Yuhong ; Li, Yaoqing ; Hu, Gengyuan ; Tao, Kelong ; Xu, Chuchu
ABSTRACT:
The main reason for the failure of chemotherapy therapies based on 5‐Fluorouracil (5‐Fu) is the development of resistance to 5‐Fu in cancer patients, particularly those with colorectal cancer. Tissue inhibitor of metalloproteinases 2 (TIMP‐2) has been shown to be associated with colorectal cancer (CRC), but its correlation with 5‐Fu resistance in colorectal cancer has not been thoroughly studied. We screen the expression of different cytokines through Cytokine array. CCK‐8 assay was conducted to evaluate the IC50 of 5‐Fu and cell proliferation. ELISA and RT‐qPCR were performed to detect TIMP‐2 expression levels in cells and patient serum. Western blotting was utilised to analyse the differences in the expression of proteins related to signalling pathways in cells. Through cytokine array screening, we found that the expression of TIMP‐2 was significantly increased in CRC drug‐resistant cell lines. In addition, the expression of TIMP‐2 in the serum of patients with CRC resistance to 5‐Fu was significantly increased. Subsequent mechanistic experiments showed that TIMP‐2 regulated the resistance of CRC cells to 5‐Futhrough the JAK–STAT signalling pathway. Moreover, anti‐TIMP‐2 antibody or small molecule drug LY2784544 targeting the JAK–STAT signalling pathway can effectively reverse the resistance of CRC cells to 5‐Fu. It is exactly TIMP‐2 that mediates the resistance of CRC to 5‐Fu through the JAK–STAT signalling pathway. Targeting drugs for TIMP‐2 or the JAK–STAT signalling pathway are expected to be opportunities to reverse 5‐Fu resistance in CRC.
2024-12-01Molecular diversity
First report on chemometrics-driven multilayered lead prioritization in addressing oxysterol-mediated overexpression of G protein-coupled receptor 183
Article
作者: Probir Kumar Ojha ; Arnab Bhattacharjee ; Supratik Kar
Contemporary research has convincingly demonstrated that upregulation of G protein-coupled receptor 183 (GPR183), orchestrated by its endogenous agonist, 7α,25-dihydroxyxcholesterol (7α,25-OHC), leads to the development of cancer, diabetes, multiple sclerosis, infectious, and inflammatory diseases. A recent study unveiled the cryo-EM structure of 7α,25-OHC bound GPR183 complex, presenting an untapped opportunity for computational exploration of potential GPR183 inhibitors, which served as our inspiration for the current work. A predictive and validated two-dimensional QSAR model using genetic algorithm (GA) and multiple linear regression (MLR) on experimental GPR183 inhibition data was developed. QSAR study highlighted that structural features like dissimilar electronegative atoms, quaternary carbon atoms, and CH2RX fragment (X: heteroatoms) influence positively, while the existence of oxygen atoms with a topological separation of 3, negatively affects GPR183 inhibitory activity. Post assessment of true external set prediction capability, the MLR model was deployed to screen 12,449 DrugBank compounds, followed by a screening pipeline involving molecular docking, druglikeness, ADMET, protein-ligand stability assessment using deep learning algorithm, molecular dynamics, and molecular mechanics. The current findings strongly evidenced DB05790 as a potential lead for prospective interference of oxysterol-mediated GPR183 overexpression, warranting further in vitro and in vivo validation.
3
项与 Gandotinib 相关的新闻（医药）2026-10-19
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2026-07-12
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2022-09-11
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蛋白降解靶向嵌合体小分子药物紧急使用授权抗体药物偶联物基因疗法
100 项与 Gandotinib 相关的药物交易
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外链
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| D10365 | Gandotinib | - |
研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 蕈样真菌病 | 临床2期 | 美国 | 2012-05-22 | |
| 蕈样真菌病 | 临床2期 | 澳大利亚 | 2012-05-22 | |
| 蕈样真菌病 | 临床2期 | 奥地利 | 2012-05-22 | |
| 蕈样真菌病 | 临床2期 | 加拿大 | 2012-05-22 | |
| 蕈样真菌病 | 临床2期 | 法国 | 2012-05-22 | |
| 蕈样真菌病 | 临床2期 | 德国 | 2012-05-22 | |
| 蕈样真菌病 | 临床2期 | 意大利 | 2012-05-22 | |
| 蕈样真菌病 | 临床2期 | 西班牙 | 2012-05-22 | |
| 蕈样真菌病 | 临床2期 | 瑞典 | 2012-05-22 | |
| 真性红细胞增多症 | 临床2期 | 美国 | 2012-05-22 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 骨髓增生性疾病 JAK2 V617F Mutation | 138 | 蓋鑰願齋壓鹹觸觸憲選(簾醖廠繭遞窪製範範艱) = 憲網壓簾窪範窪鏇繭壓 簾糧鬱餘構膚選範夢範 (遞觸齋觸鹽艱繭範餘構 ) 更多 | 积极 | 2018-08-01 | ||
临床1期 | - | 餘鏇艱網淵壓齋廠壓餘(獵襯鏇膚鏇構糧壓遞艱) = approximately 6h 窪獵艱鏇壓簾鏇餘窪鬱 (鹹遞衊鬱遞糧糧鏇觸鹽 ) | - | 2017-10-01 |
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