预约演示
更新于：2026-01-31
Navarixin
更新于：2026-01-31
概要
基本信息
在研机构- |
权益机构- |
最高研发阶段终止临床2期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
登录后查看时间轴
结构/序列
分子式C21H23N3O5 |
InChIKeyRXIUEIPPLAFSDF-CYBMUJFWSA-N |
CAS号473727-83-2 |
关联
10
项与 Navarixin 相关的临床试验NCT03473925
A Phase II Study of Navarixin (MK-7123) in Combination With Pembrolizumab (MK-3475) in Participants With Selected Advanced/Metastatic Solid Tumors
NCT01068145
Randomized, Double-Blind, Multiple-Dose, Placebo-Controlled, Incomplete Crossover, Two-Part Study to Evaluate the Dose Response of SCH 527123 on Sputum Neutrophilia Following Ozone Challenge in Healthy Subjects and COPD Patients
NCT01006161
Proof-of-Concept and Dose Range-Finding Study of SCH 527123 in Subjects With Severe Asthma
100 项与 Navarixin 相关的临床结果
登录后查看更多信息
100 项与 Navarixin 相关的转化医学
登录后查看更多信息
100 项与 Navarixin 相关的专利（医药）
登录后查看更多信息
81
项与 Navarixin 相关的文献（医药）2026-03-01CANCER LETTERS
NR4A2 induces perineural invasion in head and neck squamous cell carcinoma and pancreatic ductal adenocarcinoma via CXCL5/CXCR2 signaling axis
Article
作者: Macha, Muzafar A ; Ganguly, Koelina ; Chaudhary, Sanjib ; Lele, Subodh M ; Lakshmanan, Imayavaramban ; Pothuraju, Ramesh ; Appadurai, Muthamil Iniyan ; Batra, Surinder Kumar ; Nasser, Mohd Wasim ; Ganti, Apar Kishor ; Cox, Jesse L ; Wang, Han-Jun
Perineural invasion (PNI) is associated with worse prognosis in various malignancies. Targeting PNI may hinder the tumor metastasis in head and neck squamous cell carcinoma (HNSCC) and pancreatic ductal adenocarcinoma (PDAC). We investigated the role of nuclear receptor subfamily 4 group A2 (NR4A2/Nurr1) mediated neuronal invasion in HNSCC and PDAC tumor progression. Aberrant expression of NR4A2 was observed in these tumors, and high levels of NR4A2 were associated with worse survival. The whole genome chromatin immunoprecipitation (ChIP) sequencing with NR4A2 antibody illustrated several genes associated with axonal guidance, suggesting its potential role in PNI. Treatment with conditioned-media (CM) collected from NR4A2-depleted cancer cells showed significantly decreased neurite outgrowths in dorsal root ganglion. Cytokine array analysis revealed several soluble factors, such as CXCL5, CCL2, IGBP2, and TIMP-2, that may be involved in neuritogenesis; these factors are decreased in CM of NR4A2-depleted cells. Further treatment with CXCL5 ligand significantly induced neuritogenesis, while the neurite outgrowth was abrogated when cotreated with CXCR2 (receptor for CXCL5) inhibitor SCH527123. Upregulation of Rac1 and phospho-AKT (S473) downstream signaling of CXCL5 was observed, and the CXCR2 inhibitor abrogated this effect in neuronal cells. Moreover, CM from CXCL5-depleted cells showed reduced neurite length. NR4A2 knockdown in UMSCC1 cells impaired tumor formation in vivo, and the xenograft tissues exhibited significant downregulation of CXCL5, providing direct in vivo evidence for the NR4A2-CXCL5 axis in tumor progression. NR4A2 is a key driver of CXCL5-mediated PNI and the NR4A2/CXCL5/CXCR2 signaling axis is a potential therapeutic target in HNSCC and PDAC.
2026-02-01BIOMEDICINE & PHARMACOTHERAPY
CXCR2 antagonism as a promising therapeutic approach for pulmonary fibrosis therapy
Article
作者: Melo, Eliza Mathias ; Resende, Filipe ; Soriani, Frederico Marianetti ; Teixeira, Mauro Martins ; Brandolini, Laura ; Dutra, Rafael Cypriano ; Queiroz-Junior, Celso Martins ; Bianchini, Gianluca ; Ascenção, Fernando Roque ; Aramini, Andrea ; Tomassetti, Mara ; Amatruda, Mario
Pulmonary inflammation is a central feature of several chronic lung diseases. The chemokine receptor CXCR2 plays a key role in regulating recruitment and activation of leukocytes and other cell types involved in acute and chronic inflammation of the lungs. In this study, we evaluated and compared the anti-inflammatory effects of four CXCR2 antagonists - DF2755A, AZD-5069, SX-682, and SCH527123 - in a murine model of bleomycin-induced lung injury. C57BL/6 mice received intranasal bleomycin and were treated once a day with known active doses of the antagonists by oral gavage. Following disease induction through bleomycin inoculation on day 0, animals were either treated at days 0-2 and then evaluated at day 2 (focus on the early inflammatory response) or treated from days 0-16 (preventive schedule) or from days 8-16 (therapeutic schedule) and then evaluated at day 16 (focus on fibrosis). We assessed inflammatory responses in bronchoalveolar lavage fluid (BALF) and lung tissue by analyzing total and differential leukocyte counts, cytokine levels, myeloperoxidase (MPO) activity, BALF protein content, and lung histopathology. All compounds displayed anti-inflammatory effects (day 2), with DF2755A and AZD-5069 standing out for their greater efficacy in reducing early neutrophils influx. Importantly, DF2755A and SX-682 were particularly effective in mitigating fibrosis and chronic inflammatory changes when administered in both preventive and therapeutic schedules, even at later stages of disease progression. These findings underscore the potential of CXCR2 antagonism, especially with DF2755A, as a promising strategy to limit inflammation and fibrosis in experimental lung injury.
2026-01-01FASEB BioAdvances
Unlocking the Power of
CXCR2
Inhibition to Overcome Gemcitabine Resistance in Pancreatic Cancer
Article
作者: Bhatia, Rakesh ; Kumar, Sushil ; Batra, Surinder K. ; Singh, Rakesh K. ; Molczyk, Caitlin ; Johnson, Esther ; Saxena, Sugandha ; Sturgeon, Reegan ; Bhyravbhatla, Namita
ABSTRACT:
Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer‐related mortality, characterized by intrinsic resistance to conventional therapies and limited effective treatment options. In this study, we investigated the role of the CXCR2 axis in PDAC therapy resistance. CXCR2, a chemokine receptor, is actively involved in inflammation, tumor angiogenesis, and metastasis. Our working hypothesis is that CXCR2 contributes to PDAC chemotherapy resistance. To test this, we generated gemcitabine‐resistant (GemR) lines using T3M4 and CD18/HPAF (CD18) cell lines. Baseline expression of CXCL1, CXCL5, and CXCL8 ligands was higher in GemR cells compared to parental cells. Upon gemcitabine treatment, parental cells exhibited a greater increase in CXCL1 and CXCL8 expression than GemR cells. Further analysis in T3M4 cells revealed a dose‐ and time‐dependent increase in CXCL1 and CXCL8 expression following gemcitabine exposure. Next, we assessed whether targeting CXCR2 could enhance the therapeutic response. We treated parental and GemR cell lines with gemcitabine in combination with a CXCR2 antagonist, Navarixin. Notably, lower concentrations of gemcitabine combined with Navarixin were more effective than higher concentrations of gemcitabine alone in GemR cell lines. In both parental and GemR xenograft models, combination therapy with Navarixin and gemcitabine demonstrated superior antitumor and antimetastatic activity compared to either treatment alone. In conclusion, these findings highlight the critical role of the CXCR2 axis in PDAC therapy resistance. Targeting CXCR2 enhances gemcitabine efficacy, offering a potential therapeutic strategy to overcome resistance in PDAC.
100 项与 Navarixin 相关的药物交易
登录后查看更多信息
研发状态
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 去势抵抗性前列腺癌 | 临床2期 | 美国 | 2018-04-10 | |
| 去势抵抗性前列腺癌 | 临床2期 | 澳大利亚 | 2018-04-10 | |
| 去势抵抗性前列腺癌 | 临床2期 | 加拿大 | 2018-04-10 | |
| 去势抵抗性前列腺癌 | 临床2期 | 以色列 | 2018-04-10 | |
| 去势抵抗性前列腺癌 | 临床2期 | 韩国 | 2018-04-10 | |
| 转移性非小细胞肺癌 | 临床2期 | 美国 | 2018-04-10 | |
| 转移性非小细胞肺癌 | 临床2期 | 澳大利亚 | 2018-04-10 | |
| 转移性非小细胞肺癌 | 临床2期 | 加拿大 | 2018-04-10 | |
| 转移性非小细胞肺癌 | 临床2期 | 以色列 | 2018-04-10 | |
| 转移性非小细胞肺癌 | 临床2期 | 韩国 | 2018-04-10 |
登录后查看更多信息
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 | 105 | 獵範壓窪顧艱鑰齋憲餘(襯願齋製餘鬱鏇繭鑰簾) = grade 3 transaminase elevation occurred in 3/48 (6%) receiving navarixin 100 mg 觸構衊顧積鑰衊憲淵齋 (襯膚鹽簾製廠選獵範憲 ) 更多 | 不佳 | 2024-02-01 | |||
临床2期 | 107 | (Navarixin 30 mg + Pembrolizumab 200 mg) | 鏇繭鹹淵憲壓築網積廠 = 顧願構艱壓膚憲顧構鏇 膚鹽蓋夢網鹹鹽願簾製 (觸範餘網壓齋構製簾蓋, 鹽襯積鹽範鹽鹹鑰壓憲 ~ 艱願衊夢醖襯鏇簾壓願) 更多 | - | 2022-06-29 | ||
(Navarixin 100 mg + Pembrolizumab 200 mg) | 鏇繭鹹淵憲壓築網積廠 = 觸簾選窪網壓蓋衊鏇憲 膚鹽蓋夢網鹹鹽願簾製 (觸範餘網壓齋構製簾蓋, 簾繭衊蓋鏇衊齋鹽鹹鹹 ~ 齋範製遞鏇鹹鏇繭艱齋) 更多 | ||||||
临床2期 | 616 | MK-7123 50 mg | 窪憲鏇膚衊構齋簾糧餘(醖夢鏇鹹繭簾繭網築窪) = 鹽衊獵餘鬱選蓋艱觸窪 膚鬱顧壓願蓋獵醖醖衊 (觸憲繭獵醖壓餘窪夢醖 ) 更多 | - | 2015-05-01 | ||
临床2期 | 37 | Rescue medication+Navarixin (Navarixin) | 選鬱憲選繭構觸蓋鑰範 = 鬱蓋壓網遞糧鹹廠積築 蓋糧艱蓋願憲衊繭憲選 (襯醖簾築簾選艱願觸鏇, 夢夢繭艱醖鑰蓋蓋獵範 ~ 膚艱顧艱壓夢蓋窪蓋鏇) 更多 | - | 2014-11-18 | ||
Placebo (Placebo) | 選鬱憲選繭構觸蓋鑰範 = 衊鏇糧膚顧艱艱獵鹽窪 蓋糧艱蓋願憲衊繭憲選 (襯醖簾築簾選艱願觸鏇, 網襯鑰壓醖構範鑰廠範 ~ 鏇範鹽餘積憲築觸鏇淵) 更多 | ||||||
临床2期 | 616 | Placebo+Navarixin (Navarixin 10 mg) | 鏇積廠網簾製網廠鑰製(積觸網鹽蓋夢夢廠鹹遞) = 積衊構膚鏇憲願糧糧鏇 憲構憲憲築範願艱襯築 (網窪壓簾鹽鑰製廠廠製, 0.022) 更多 | - | 2014-11-17 | ||
Placebo+Navarixin (Navarixin 30 mg) | 鏇積廠網簾製網廠鑰製(積觸網鹽蓋夢夢廠鹹遞) = 網蓋觸艱簾艱襯齋構醖 憲構憲憲築範願艱襯築 (網窪壓簾鹽鑰製廠廠製, 0.023) 更多 | ||||||
临床2期 | 19 | (Navarixin) | 獵積齋蓋壓壓遞夢網憲(簾夢顧廠觸淵廠衊鏇鏇) = 醖繭糧廠繭餘醖齋簾醖 繭壓膚淵窪淵願簾襯鑰 (構醖遞顧餘艱觸齋憲築, 27.377) 更多 | - | 2014-10-06 | ||
Placebo (Placebo) | 獵積齋蓋壓壓遞夢網憲(簾夢顧廠觸淵廠衊鏇鏇) = 餘範衊廠繭鬱廠鏇廠鏇 繭壓膚淵窪淵願簾襯鑰 (構醖遞顧餘艱觸齋憲築, 27.377) 更多 | ||||||
临床2期 | 31 | (Navarixin) | 選遞網蓋艱襯鏇窪艱衊(膚簾願選窪製餘夢廠衊) = 獵衊製壓夢網鬱蓋顧鹽 壓齋夢憲鑰範選鹽襯壓 (範蓋鹹築鹹繭鏇醖鬱獵, 15.05) 更多 | - | 2014-10-06 | ||
Placebo (Placebo) | 選遞網蓋艱襯鏇窪艱衊(膚簾願選窪製餘夢廠衊) = 顧淵簾窪鏇醖艱簾襯構 壓齋夢憲鑰範選鹽襯壓 (範蓋鹹築鹹繭鏇醖鬱獵, 13.26) 更多 | ||||||
临床1期 | - | 18 | 觸選鑰壓選遞蓋鑰鏇齋(遞構憲壓淵範製糧積遞) = 糧遞顧鏇襯願餘構艱醖 願餘廠願壓製糧鑰網製 (製醖醖鑰艱網繭廠壓壓 ) | - | 2010-03-01 | ||
Prednisolone 50 mg | 觸選鑰壓選遞蓋鑰鏇齋(遞構憲壓淵範製糧積遞) = 鹽鹽壓壓顧衊糧積簾夢 願餘廠願壓製糧鑰網製 (製醖醖鑰艱網繭廠壓壓 ) |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
生物医药百科问答
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用