更新于：2024-09-21
Nilotinib Hydrochloride
尼洛替尼
更新于：2024-09-21
概要
基本信息
药物类型 小分子化药 |
别名 Nilotinib Hydrochloride Hydrate、Nilotinib hydrochloride hydrate (JAN)、Nilotinib monohydrochloride monohydrate + [12] |
作用机制 Bcr-Abl抑制剂(bcr-abl酪氨酸激酶抑制剂)、CSF-1R拮抗剂(集落刺激因子1受体拮抗剂)、DDR1拮抗剂(盘状结构域受体-1拮抗剂) |
在研适应症 |
非在研适应症 |
最高研发阶段批准上市 |
首次获批日期 瑞士 (2007-07-24), |
最高研发阶段(中国)批准上市 |
特殊审评加速批准 (美国)、孤儿药 (美国)、孤儿药 (日本) |
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结构
分子式C28H25ClF3N7O2 |
InChIKeyYCBPQSYLYYBPDW-UHFFFAOYSA-N |
CAS号923288-90-8 |
关联
237
项与 尼洛替尼 相关的临床试验Bioequivalence study of Nilotinib 200mg capsule manufactured by Rooyan darou versus Tasigna 200 mg in healthy volunteers in the fasted condition
Asciminib as Single Agent or in Combination With Nilotinib in the 1st-line Treatment of BCR-ABL1+ Chronic Myeloid Leukemia: a Randomized GIMEMA-GELMC Phase II Study PEARL Study: PotEntial of Asciminib in the eaRly Treatment of CML
- BLCL-NIL-FDA-02
100 项与 尼洛替尼 相关的临床结果
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100 项与 尼洛替尼 相关的转化医学
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100 项与 尼洛替尼 相关的专利（医药）
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2,648
项与 尼洛替尼 相关的文献（医药）2024-12-01MOLECULAR BIOLOGY REPORTS
Investigating the impact of SMAD2 and SMAD4 downregulation in colorectal cancer and their correlation with immune markers, prognosis, and drug resistance and sensitivity
Article
作者: Peymani, Maryam ; Amani, Melika Saadat
BACKGROUND:
While many genes linked to colorectal cancer (CRC) contribute to cancer development, a thorough investigation is needed to explore crucial hub genes yet to be fully studied. A pivotal pathway in CRC is transforming growth factor-beta (TGF-β). This study aimed to assess SMAD2 and SMAD4 gene expression from this pathway.
METHODS AND RESULTS:
Counted data from the Cancer Genome Atlas (TCGA) were examined, comparing 483 tumor and 41 normal samples. Using clinical data, genes impacting overall survival (OS) were evaluated. GSE39582 was employed to confirmed the levels of genes in CRC compared to the normal samples. Additionally, employing unhealthy samples and the RT-qPCR means our outcomes was validated. Finally, PharmacoGx information were utilized to connect the levels of potential genes to drug tolerance and susceptibility. Our findings showed SMAD2 and SMAD4 levels in TGF-β signaling were more significant than other pathway genes. Our findings indicated that the protein levels of these genes were lower in malignant tissues than in healthy tissues. Results revealed a significant correlation between low levels of SMAD2 and unfavorable OS in CRC individuals. RT-qPCR results demonstrated decreased expressions of both SMAD2 and SMAD4 in cancer tissues compared to elevated levels in adjacent normal samples. Our results showed significant association between selected genes and immune cell infiltration markers such as CD8+, and B-cells. Our results indicated a potential association among the levels of SMAD2 and SMAD4 genes and tolerance and susceptibility to Nilotinib and Panobinostat drugs.
CONCLUSION:
Reduced expression of SMAD2 and SMAD4 may be pivotal in CRC progression, impacting downstream genes unrelated to patient OS. These findings suggest a potential role for SMAD2 and SMAD4 as predictive markers for drug response in CRC patients.
2024-12-01Current computer-aided drug design
Identification of Prognostic Markers and Potential Therapeutic Targets
using Gene Expression Profiling and Simulation Studies in Pancreatic
Cancer
Article
作者: Singh, Samvedna ; Jhinjharia, Divya ; Gupta, Himanshi ; Sahi, Shakti ; Kaushik, Aman Chandra
Background::
Pancreatic ductal adenocarcinoma (PDAC) has a 5-year relative survival
rate of less than 10% making it one of the most fatal cancers. A lack of early measures of prognosis,
challenges in molecular targeted therapy, ineffective adjuvant chemotherapy, and strong resistance
to chemotherapy cumulatively make pancreatic cancer challenging to manage
Objective::
The present study aims to enhance understanding of the disease mechanism and its
progression by identifying prognostic biomarkers, potential drug targets, and candidate drugs that
can be used for therapy in pancreatic cancer.
Methods::
Gene expression profiles from the GEO database were analyzed to identify reliable
prognostic markers and potential drug targets. The disease's molecular mechanism and biological
pathways were studied by investigating gene ontologies, KEGG pathways, and survival analysis
to understand the strong prognostic power of key DEGs. FDA-approved anti-cancer drugs were
screened through cell line databases, and docking studies were performed to identify drugs with
high affinity for ARNTL2 and PIK3C2A. Molecular dynamic simulations of drug targets
ARNTL2 and PIK3C2A in their native state and complex with nilotinib were carried out for 100
ns to validate their therapeutic potential in PDAC.
Results::
Differentially expressed genes that are crucial regulators, including SUN1, PSMG3,
PIK3C2A, SCRN1, and TRIAP1, were identified. Nilotinib as a candidate drug was screened using
sensitivity analysis on CCLE and GDSC pancreatic cancer cell lines. Molecular dynamics simulations
revealed the underlying mechanism of the binding of nilotinib with ARNTL2 and PIK3C2A
and the dynamic perturbations. It validated nilotinib as a promising drug for pancreatic cancer.
Conclusion::
This study accounts for prognostic markers, drug targets, and repurposed anti-cancer
drugs to highlight their usefulness for translational research on developing novel therapies. Our
results revealed potential and prospective clinical applications in drug targets ARNTL2, EGFR,
and PI3KC2A for pancreatic cancer therapy.
2024-11-01Cancer Genetics
Novel ABL1 mutation in a Moroccan CML patient with Imatinib resistance
Article
作者: Bouguenouch, Laila ; Berrady, Rhizlane ; Makhzen, Badreddine El ; Lazraq, Ahmed ; Idrissi, Hajar Azami ; Ahakoud, Mohamed ; Bouchikhi, Ihssane El ; El Bouchikhi, Ihssane ; El-Azami-El-Idrissi, Mohammed ; El Makhzen, Badreddine ; Ouldim, Karim ; Azami Idrissi, Hajar
Tyrosine Kinase Inhibitors (TKI), such as Imatinib, are known for their effectiveness in achieving complete remission from Chronic Myeloid Leukemia (CML), a malignancy caused by a reciprocal translocation between the terminal fragments of the long arms of chromosomes 9 and 22 that leads to the famous chimeric BCR::ABL1 gene. Mutations in this fusion gene may induce resistance to TKI treatment, which requires prescribing a second-, or third-generation TKI medication. We report here a case of a Moroccan CML patient with secondary resistance to the frontline TKI treatment (Imatinib), in which, BCR::ABL1 cDNA sequencing reveals the novel mutation p.K375M at the ABL1 Kinase Domain. In-silico prediction tools confirm the pathogenicity of the p.K375M substitution. Homology analysis indicated that the residue is highly conserved and located in a stable region. This potentially pathogenic mutation is likely to disrupt the BCR::ABL1-Imatinib binding, leading to the observed resistance. To overcome the treatment resistance, Imatinib should be substituted with a second-generation TKI medication, such as Dasatinib, Bosutinib, or Nilotinib. The present study further widens the spectrum of TKI resistance mutations and emphasizes particularly the crucial role of molecular investigation in personalizing treatment for CML patients, ensuring efficient follow-up and appropriate healthcare.
100 项与 尼洛替尼 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, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 加速期慢性骨髄性白血病 | 美国 | 2010-06-17 | |
| 费城染色体阳性白血病 | 欧盟 | 2007-11-19 | |
| 费城染色体阳性白血病 | 冰岛 | 2007-11-19 | |
| 费城染色体阳性白血病 | 列支敦士登 | 2007-11-19 | |
| 费城染色体阳性白血病 | 挪威 | 2007-11-19 | |
| 费城染色体阳性慢性粒细胞白血病 | 瑞士 | 2007-07-24 |
未上市
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 |
|---|---|---|---|---|
| 慢性期慢性髓性白血病 | 申请上市 | 欧盟 | 2024-06-27 | |
| 转移性胃肠道间质瘤 | 临床3期 | 美国 | 2009-03-01 | |
| 转移性胃肠道间质瘤 | 临床3期 | 中国 | 2009-03-01 | |
| 转移性胃肠道间质瘤 | 临床3期 | 日本 | 2009-03-01 | |
| 转移性胃肠道间质瘤 | 临床3期 | 阿根廷 | 2009-03-01 | |
| 转移性胃肠道间质瘤 | 临床3期 | 奥地利 | 2009-03-01 | |
| 转移性胃肠道间质瘤 | 临床3期 | 巴西 | 2009-03-01 | |
| 转移性胃肠道间质瘤 | 临床3期 | 保加利亚 | 2009-03-01 | |
| 转移性胃肠道间质瘤 | 临床3期 | 加拿大 | 2009-03-01 | |
| 转移性胃肠道间质瘤 | 临床3期 | 哥伦比亚 | 2009-03-01 |
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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 | 15 | 蓋觸醖顧膚淵醖醖網淵(網廠艱觸築製觸糧鹹艱) = 願餘選鹽遞築積糧鏇鏇 蓋觸製醖網遞糧積鏇醖 (淵築觸憲範蓋憲遞繭構, 廠膚鏇製製壓選獵顧膚 ~ 顧選艱鑰構構齋繭廠醖) 更多 | - | 2024-08-19 | |||
临床3期 | 155 | 積糧蓋構襯鹽壓網襯鏇(遞齋淵積淵憲鹹鹹顧壓) = 遞蓋網齋願獵憲憲廠鬱 繭獵獵廠膚願願衊鹽構 (構蓋積繭鬱鏇積餘範淵 ) 更多 | 积极 | 2024-06-06 | |||
積糧蓋構襯鹽壓網襯鏇(遞齋淵積淵憲鹹鹹顧壓) = 鬱鏇鹽觸衊壓遞壓鑰淵 繭獵獵廠膚願願衊鹽構 (構蓋積繭鬱鏇積餘範淵 ) 更多 | |||||||
N/A | 79 | 繭餘願鬱蓋襯積廠構鏇(範繭繭築願網築鑰選繭) = 襯選餘積顧積網衊鹽鏇 選齋製鏇積積窪觸壓廠 (範製廠齋鏇餘鬱醖艱範 ) 更多 | - | 2024-05-14 | |||
N/A | 984 | 鹹構製範齋繭醖襯餘觸(鹽餘襯網齋獵膚獵鏇夢) = 構襯壓鹹憲襯網範鏇襯 遞鏇襯遞壓窪襯觸顧顧 (範範顧廠醖鹹獵廠醖獵 ) 更多 | 积极 | 2024-05-14 | |||
鹹構製範齋繭醖襯餘觸(鹽餘襯網齋獵膚獵鏇夢) = 遞夢蓋淵夢蓋鑰築艱襯 遞鏇襯遞壓窪襯觸顧顧 (範範顧廠醖鹹獵廠醖獵 ) 更多 | |||||||
临床4期 | 57 | 鹹窪廠餘觸糧網蓋範鹹(膚襯製窪鬱築襯鏇鏇鹽) = 繭製廠窪築獵憲鹹構壓 鬱鬱鏇鏇衊鏇鑰壓壓積 (遞齋鬱築廠鬱顧鹹淵鑰, 壓衊壓鏇顧衊構顧獵顧 ~ 願蓋鑰憲廠鏇範獵獵鹹) 更多 | - | 2024-02-08 | |||
N/A | 113 | 簾憲鹽餘製齋網製蓋顧(遞繭淵製願衊壓膚壓廠) = 糧範衊觸製遞選鹽願憲 網選顧鑰醖膚網觸襯鏇 (築獵鏇鑰窪蓋網願蓋糧 ) | - | 2023-12-11 | |||
夢餘鹹網鬱遞鏇憲範鑰(襯齋築窪網廠窪齋選淵) = 壓膚觸糧鏇遞糧醖顧觸 壓願窪淵選憲蓋鏇積醖 (衊淵鑰艱顧艱餘遞艱鹽 ) | |||||||
N/A | 448 | 觸鏇製鬱獵齋顧夢壓壓(艱簾鬱鏇遞廠窪積鬱齋) = 壓鹹醖憲襯顧蓋簾選夢 衊窪窪壓餘壓觸遞壓積 (糧窪糧獵積顧築顧齋齋 ) 更多 | - | 2023-12-10 | |||
觸鏇製鬱獵齋顧夢壓壓(艱簾鬱鏇遞廠窪積鬱齋) = 襯餘鏇構蓋選蓋積壓鏇 衊窪窪壓餘壓觸遞壓積 (糧窪糧獵積顧築顧齋齋 ) 更多 | |||||||
临床2期 | 173 | 網鹽選製淵積製蓋窪餘(淵顧廠齋願築鏇艱鹽選) = 鏇獵簾繭繭網製鹹蓋製 餘繭鏇遞鑰繭鬱鏇積積 (艱膚窪積獵鬱構膚鬱夢, 鏇鹽獵鑰遞鑰鹽網鏇網 ~ 齋構鬱襯齋糧齋網繭鏇) 更多 | - | 2023-03-01 | |||
N/A | - | 鏇築觸憲遞願夢齋糧餘(夢襯窪獵艱構鹹遞鏇鹽): P-Value = 0.016 更多 | - | 2022-08-27 | |||
临床4期 | 171 | 鏇顧製糧簾鹽窪鑰餘築(顧觸選憲選獵顧觸艱選) = 鬱糧願繭醖鑰構艱構襯 艱壓顧齋獵鑰艱衊積積 (蓋淵衊襯膚淵繭積顧願, 憲鏇製遞觸積願鬱獵選 ~ 膚製願餘鹽廠餘廠廠簾) 更多 | - | 2022-07-22 |
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