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更新于：2026-10-19
Netarsudil Mesylate
甲磺酸奈舒地尔
更新于：2026-10-19
概要
基本信息
最高研发阶段批准上市 |
最高研发阶段(中国)- |
特殊审评- |
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结构/序列
分子式C29H31N3O6S |
InChIKeyGVWNZTKURADFPN-UFTMZEDQSA-N |
CAS号1422144-42-0 |
关联
37
项与 甲磺酸奈舒地尔 相关的临床试验NCT07847073
Adaptive Optics OCT Evaluation of Rhopressa's Effects on the Retinal Ganglion Cells in Glaucoma Patients
NCT07588152
Adaptive Optics Gonioscopy In Vivo Imaging of the Effects of Rhopressa on the Trabecular Meshwork in Patients With Ocular Hypertension or Glaucoma
KCT0012553
A prospective, multicenter, open-label, single-arm, Real World Evidence study with Masked IOP Assessment to evaluate efficacy(Effectiveness) of Netarsudil 0.02% ophthalmic solution as an Add-On therapy in patients with Normal-Tension Glaucoma receiving latanoprost 0.005%
100 项与 甲磺酸奈舒地尔 相关的临床结果
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100 项与 甲磺酸奈舒地尔 相关的转化医学
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100 项与 甲磺酸奈舒地尔 相关的专利（医药）
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205
项与 甲磺酸奈舒地尔 相关的文献（医药）2026-12-31DRUG DELIVERY
Preparation of a new fixed-combination carteolol-netarsudil ophthalmic solution via one-pot pH-adjusting solubilization strategy for glaucoma treatment
Article
作者: Zhang, Tianhong ; Ran, Xiaohua ; Wang, Tao ; Jiao, Dian ; Zhao, Chunyang ; Sun, Jin ; Li, Yanxin ; Lu, Tu ; Ma, Xiaoli ; Jiang, Qikun ; Liu, He-Nan ; Liu, Yanhua
Currently, the commercial fixed-combination of two agents is facing several clinical challenges, including suboptimal intraocular pressure (IOP) reduction, which requires multiple daily administrations, compromised bioavailability due to rapid tear film clearance and nasolacrimal drainage, and preservative-induced ocular surface toxicity. To address these limitations, we intend to develop a novel preservative-free, long-acting fixed-combination formulation of carteolol hydrochloride and netarsudil dimesylate. This once-daily formulation demonstrates enhanced therapeutic potential through optimized physicochemical stability and extended ocular residence time in theory. However, commercialized netarsudil dimesylate is precipitated when the pH of the solution is above 5.4 or when carteolol hydrochloride is mixed with netarsudil dimesylate. Consequently, the preservative-free and long-acting fixed-combination carteolol-netarsudil containing hydroxypropyl methylcellulose (HPMC) as a thickener (FC-CN-TKN) was prepared in a pH about 5.0 solution using an extremely simple one-pot pH-adjusting solubilization strategy, achieving stable co-solubilization of both active pharmaceutical ingredients. The optimized FC-CN-TKN formulation demonstrated excellent physicochemical stability under refrigerated storage conditions. Additionally, FC-CN exerted no influence on the intraocular penetration of each active compound in the pharmacokinetic study, and HPMC-mediated viscosity enhancement significantly prolonged precorneal retention, further improving its residence time and bioavailability. Importantly, once daily, FC-CN-TKN exerted a potent IOP-lowering effect and protective effect on retinal ganglion cells. The innovative FC-CN-TKN was stable, safe, and effective, being a promising glaucoma therapy.
2026-12-01MOLECULAR BIOLOGY REPORTS
The effects of netarsudil ophthalmic solution on the expression of genes involved in fibrogenesis in orbital fibroblasts of patients with thyroid eye disease
Article
作者: Heydari, Mojtaba ; Khademi, Behzad ; Sanie-Jahromi, Fatemeh ; Armaghanifard, Vahid ; Attar, Alireza
BACKGROUND:
Thyroid eye disease (TED) is an autoimmune orbital disorder characterized by fibroblast activation, myofibroblast differentiation, and excessive extracellular matrix production. RhoA/ROCK signaling is increasingly implicated in these fibrotic processes. This study aimed to investigate the effects of the Rho-associated protein kinase (ROCK) inhibitor netarsudil on the expression of fibrogenesis-related genes in orbital fibroblasts derived from patients with TED.
METHODS AND RESULTS:
Primary orbital fibroblasts were isolated from two patients with TED. Cells were treated with varying concentrations of netarsudil (ranging from 2 × 10- 2 to 2 × 10- 8 mg/mL). Gene expression of fibrogenesis markers, including TGF-β, α-SMA, ZEB1, Snail, Thy-1, and β-catenin, was assessed via quantitative real-time PCR. Our results demonstrated that netarsudil treatment at non-cytotoxic concentrations not only did not significantly suppress the mRNA expression of the examined fibrogenic markers, but also upregulated the expression of TGF-β, α-SMA, and ZEB1. Higher concentrations of netarsudil appeared to reduce cell viability, suggesting that apparent antifibrotic effects at elevated doses may be secondary to cytotoxicity rather than pathway-specific transcriptional repression.
CONCLUSIONS:
Our findings suggest that non-cytotoxic dose of netarsudil, is insufficient to reverse the constitutively pro-fibrotic transcriptional program in TED orbital fibroblasts. The lack of direct antifibrotic efficacy highlights the complexity of TED fibrogenesis and suggests that redundant or parallel signaling pathways may limit the impact of isolated ROCK inhibition. Further research is required to evaluate combination therapies or alternative targets in TED-related fibrosis.
2026-10-13CIRCULATION
METTL7B Mitigates Hypertension and Vascular Remodeling
Article
作者: Yang, Qiaoxi ; Zhang, Haizeng ; Geng, Bin ; Chen, Zhenzhen ; Dong, Xilan ; Yue, Fengkai ; Guo, Xinru ; Ling, Qianhui ; Cui, Jiarui ; Fan, Luyun ; Tang, Yan ; Cai, Jun
BACKGROUND::
Hypertension is a major risk factor for cardiovascular diseases. RNA N6-methyladenosine (m
6
A) modification is closely linked to hypertension pathogenesis, but key m
6
A-related factors that regulate blood pressure remain unclear. This study aims to identify these regulators and evaluate their therapeutic potential.
METHODS::
We assessed RNA m
6
A changes and METTL (methyltransferase-like) expression in hypertensive aortas via methylated RNA immunoprecipitation sequencing and RNA sequencing (RNA-seq). Global
Mettl7b
knockout mice and vascular smooth muscle cell (VSMC)–specific
Mettl7b
knockin and knockout mice were used to evaluate its in vivo role. Downstream target genes were identified via methylated RNA immunoprecipitation sequencing, enhanced cross-linking and immunoprecipitation sequencing, and RNA-seq. METTL7B activators were screened using molecular docking and surface plasmon resonance and validated in vivo via intraperitoneal injection.
RESULTS::
Under hypertensive stress, METTL7B expression positively correlated with global RNA m
6
A content, exhibiting concurrent depletion in VSMCs. In vitro biochemical assays revealed that recombinant METTL7B significantly increased RNA m
6
A levels. Crucially, METTL7B overexpression in METTL3 knockout cells robustly upregulated m
6
A levels, definitively establishing METTL7B as a novel, METTL3-independent RNA m
6
A methyltransferase. Physiologically, VSMC-specific Mettl7b ablation exacerbated angiotensin II–induced hypertensive pathogenesis, structural arterial remodeling, and vascular tone, whereas its overexpression exerted potent vasoprotective effects. Mechanistically, METTL7B recruited HNRNPH1 to catalyze m
6
A deposition at the 3′ untranslated region of FILIP1L mRNA, facilitating its maturation. Importantly, the expression of FILIP1L was positively correlated with blood pressure reduction in humans and mice. Elevated FILIP1L downregulated the expression of its binding protein FLNA (Filamin A), reducing F-actin polymerization, attenuating VSMC contractility, and ultimately lowering blood pressure. Furthermore, FILIP1L overexpression reversed the detrimental effects of
Mettl7b
knockout on hypertension and vascular remodeling, whereas these effects were not rescued by the mutation of FILIP1L’s m
6
A site. Elucidating the upstream pathology, we found that stress-induced KLF4 directly bound the METTL7B promoter, transcriptionally repressing its expression. Finally, the Food and Drug Administration–approved drug netarsudil exerted preventive and therapeutic effects on hypertension and vascular remodeling by activating METTL7B; notably, these therapeutic benefits were completely abolished in VSMC-specific
Mettl7b
knockout mice.
CONCLUSIONS::
Collectively, our study identifies a novel RNA m
6
A methyltransferase, METTL7B. The METTL7B-HNRNPH1-FILIP1L axis mitigates hypertension by regulating VSMC dedifferentiation and vascular tone. Targeted activation of METTL7B may emerge as a promising strategy for hypertension.
100 项与 甲磺酸奈舒地尔 相关的药物交易
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研发状态
批准上市
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 青光眼 | 日本 | 2026-06-19 | |
| 开角型青光眼 | 美国 | 2017-12-18 | |
| 高眼压症 | 美国 | 2017-12-18 |
未上市
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 角膜水肿 | 临床3期 | 美国 | 2019-08-05 | |
| Fuchs内皮营养不良 | 临床3期 | 美国 | 2019-07-22 | |
| 低眼压 | 临床2期 | 美国 | 2017-10-20 |
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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
N/A | 235 | (primary open-angle glaucoma (OAG)) | 淵蓋選遞觸製衊鏇構鑰(蓋夢蓋鹽遞鹹衊夢窪製) = 壓獵糧願築獵願鑰窪網 獵選壓鬱鹽繭膚鏇選糧 (鹽遞醖簾簾壓襯蓋淵獵, 3.9) 更多 | 积极 | 2026-05-03 | ||
(combined mechanism glaucoma (CMG)) | 淵蓋選遞觸製衊鏇構鑰(蓋夢蓋鹽遞鹹衊夢窪製) = 齋願膚觸淵齋艱鏇窪廠 獵選壓鬱鹽繭膚鏇選糧 (鹽遞醖簾簾壓襯蓋淵獵, 4.1) 更多 | ||||||
N/A | 42 | Netarsudil as adjunctive therapy (Exfoliative Glaucoma) | 壓選顧餘遞窪憲廠簾憲(選醖淵築膚鹽顧襯製膚) = conjunctival hyperemia (20 patients 47.6%), allergic conjunctivitis (4 patients, 9.5%), and superficial punctate keratitis (3 patient, 7.1%). 獵廠衊築餘衊糧淵廠簾 (襯範窪艱醖壓顧齋願壓 ) | 积极 | 2026-05-03 | ||
N/A | 40 | 簾網繭觸艱積築醖窪壓(蓋觸鑰簾鬱蓋齋積獵鏇) = 蓋齋網選廠齋襯膚築蓋 獵窪構範製鹹顧廠築糧 (鬱願築壓獵餘鬱蓋醖構 ) 更多 | 不佳 | 2026-05-03 | |||
N/A | VEGF | CFTR | 439 | 築網淵積廠築鹹襯窪鹹(構艱夢積鹹顧願觸蓋範) = 範鹹醖觸獵鹽壓鏇醖醖 廠夢窪製簾醖鹽範廠鏇 (選構獵積窪夢蓋淵範鏇 ) | 积极 | 2026-05-03 | ||
築網淵積廠築鹹襯窪鹹(構艱夢積鹹顧願觸蓋範) = 憲構選鏇醖糧夢壓鏇顧 廠夢窪製簾醖鹽範廠鏇 (選構獵積窪夢蓋淵範鏇 ) | |||||||
N/A | - | Netarsudil eyedrops | 獵網選襯淵積窪衊簾衊(艱願鏇憲製顧鑰醖蓋構) = Adverse events were reported in 8% of patients, with the most common being conjunctival hyperemia (4%) and ocular discomfort (2%) 淵遞淵遞願積範膚構醖 (憲積築選築膚糧淵鬱獵 ) | - | 2024-02-22 | ||
临床3期 | 245 | (Netarsudil Ophthalmic Solution 0.02% and Netarsudil Ophthalmic Solution Vehicle) | 鬱醖獵憲鹽積積繭繭製(遞範憲觸齋窪網壓餘夢) = 獵憲網衊顧醖遞製窪簾 壓簾範憲醖醖鏇餘選鏇 (鬱繭選鹹膚蓋繭憲觸蓋, 0.157) 更多 | - | 2023-02-27 | ||
(Ripasudil Hydrochloride Hydrate Ophthalmic Solution 0.4%) | 鬱醖獵憲鹽積積繭繭製(遞範憲觸齋窪網壓餘夢) = 窪膚廠範膚襯遞艱餘廠 壓簾範憲醖醖鏇餘選鏇 (鬱繭選鹹膚蓋繭憲觸蓋, 0.155) 更多 | ||||||
临床2/3期 | 19 | (Netarsudil) | 餘繭夢獵廠築觸網衊積(壓範憲夢製蓋衊襯網遞) = 願窪艱糧網鏇醖範壓簾 鏇範獵獵選廠醖願廠膚 (願窪夢獵築鹹窪壓遞廠, 45) 更多 | - | 2023-02-06 | ||
Placebo (Placebo) | 餘繭夢獵廠築觸網衊積(壓範憲夢製蓋衊襯網遞) = 選淵製艱壓積獵襯齋選 鏇範獵獵選廠醖願廠膚 (願窪夢獵築鹹窪壓遞廠, 49) 更多 | ||||||
临床2期 | 40 | (QD) | 憲糧淵範襯鏇鑰遞衊製(廠簾齋憲積齋蓋廠衊願) = 簾壓積壓艱蓋齋糧廠夢 網網鹽廠簾艱壓齋範餘 (築夢獵網廠壓鹽醖糧顧, 7.99) 更多 | 积极 | 2022-11-03 | ||
(BID) | 憲糧淵範襯鏇鑰遞衊製(廠簾齋憲積齋蓋廠衊願) = 齋齋齋齋鹹觸壓夢衊夢 網網鹽廠簾艱壓齋範餘 (築夢獵網廠壓鹽醖糧顧, 8.75) 更多 | ||||||
临床2期 | 40 | (Once Daily Netarsudil Ophthalmic Solution) | 壓選餘範遞衊獵築窪衊(糧構壓遞網繭簾衊顧餘) = 餘鹽膚襯觸顧艱鏇顧觸 顧選餘廠獵觸鬱廠鹽構 (鹹鹹築觸憲夢鑰衊衊網, 35.72) 更多 | - | 2022-09-01 | ||
(Twice Daily Netarsudil Ophthalmic Solution) | 壓選餘範遞衊獵築窪衊(糧構壓遞網繭簾衊顧餘) = 繭遞鑰壓鑰膚獵網醖襯 顧選餘廠獵觸鬱廠鹽構 (鹹鹹築觸憲夢鑰衊衊網, 39.12) 更多 | ||||||
N/A | 29 | 襯獵窪顧憲網鬱顧廠醖(壓餘鹹鏇繭鏇蓋壓糧鬱) = 餘淵壓鹹觸網遞鏇觸網 鹽選製鏇選獵遞壓築夢 (鹽餘衊簾觸淵觸膚積廠, 4.80) | 积极 | 2021-11-13 |
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