预约演示
更新于：2026-06-22
Atrasentan Hydrochloride
盐酸阿曲生坦
更新于：2026-06-22
概要
基本信息
最高研发阶段批准上市 |
首次获批日期 美国 (2025-04-02), |
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 (欧盟)、附条件批准 (中国)、孤儿药 (日本)、特殊审批 (美国)、优先审评 (中国) |
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结构/序列
分子式C29H38N2O6 |
InChIKeyMOTJMGVDPWRKOC-QPVYNBJUSA-N |
CAS号173937-91-2 |
关联
27
项与 盐酸阿曲生坦 相关的临床试验NCT07498335
A Single-arm, Multicenter, Phase III Study to Assess Efficacy, Pharmacokinetics, Safety and Tolerability of Atrasentan in Pediatric Patients of 2 to <18 Years of Age With Primary Immunoglobulin A Nephropathy (IgAN)
NCT06952426
A Mobile App-Based, Prospective, Observational Study to Evaluate Disease Burden and Treatment Patterns in Immunoglobulin A Nephropathy (IgAN) in the US
NCT05834738
A Randomized, Double-blind, Placebo-controlled, Crossover Study of Atrasentan in Subjects With IgA Nephropathy on Sodium-glucose Cotransporter-2 Inhibitors (SGLT2i)
100 项与 盐酸阿曲生坦 相关的临床结果
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100 项与 盐酸阿曲生坦 相关的转化医学
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100 项与 盐酸阿曲生坦 相关的专利（医药）
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446
项与 盐酸阿曲生坦 相关的文献（医药）2026-06-01LANCET
Atrasentan in patients with IgA nephropathy (ALIGN): final 2·5-year results from a randomised, double-blind, placebo-controlled, phase 3 trial
Article
BACKGROUND:
Atrasentan, a selective endothelin A receptor antagonist, reduced proteinuria in the prespecified interim analysis (week 36) of the ALIGN trial in adults with IgA nephropathy. We assessed whether atrasentan slowed estimated glomerular filtration rate (eGFR) decline after 2·5 years' treatment.
METHODS:
We performed a randomised, double-blind, placebo-controlled, phase 3 trial (133 sites, 20 countries). Adults with biopsy-proven IgA nephropathy, eGFR of at least 30 mL/min per 1·73 m2, and urinary protein excretion of at least 1·0 g/day while receiving renin-angiotensin system inhibition were enrolled (main stratum). An exploratory stratum enrolled participants also receiving an SGLT2 inhibitor. Participants were randomly assigned (1:1) to oral atrasentan 0·75 mg once daily or placebo for 132 weeks, followed by a 4-week off-treatment follow-up. The key secondary endpoint was change from baseline to week 136 in eGFR in the main stratum, assessed in all randomised patients (excluding data after intercurrent events, defined as initiation of restricted or alternative IgA nephropathy medications or kidney replacement therapy). Safety was assessed in all randomised patients who received at least one dose of study treatment. ALIGN is registered with ClinicalTrials.gov, NCT04573478; the double-blind section is complete, and the open-label extension is ongoing.
FINDINGS:
Between March 15, 2021, and April 28, 2023, 404 participants were randomly assigned (main stratum: 340; SGLT2 inhibitor stratum: 64). In the main stratum, change from baseline in eGFR at week 136 was -7·5 mL/min per 1·73 m2 (95% CI -9·2 to -5·8) with atrasentan and -9·9 mL/min per 1·73 m2 (-11·7 to -8·1) with placebo (between-group difference 2·4 mL/min per 1·73 m2; 95% CI -0·1 to 4·8; p=0·057). The between-group difference in eGFR change from baseline at end of treatment (week 132) was 2·6 mL/min per 1·73 m2 (95% CI 0·1-5·0), and the difference in total eGFR slope (baseline to week 136) was 1·4 mL/min per 1·73 m2 per year (95% CI 0·5-2·3). In the SGLT2 inhibitor stratum, the difference in eGFR change from baseline at week 136 between atrasentan and placebo was 9·1 mL/min per 1·73 m2 (95% CI 3·0-15·2). Treatment-emergent adverse events were well balanced between atrasentan and placebo, with no new safety signals. In the main stratum, fluid retention adverse events occurred in 24 (14%) of 169 patients receiving atrasentan and 20 (12%) of 170 receiving placebo.
INTERPRETATION:
Atrasentan reduced proteinuria and preserved kidney function after 2·5 years. This effect was present with or without concomitant SGLT2 inhibitor use. Atrasentan was well tolerated.
FUNDING:
Novartis.
2026-06-01ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Endothelial DNA Damage Orchestrates Cardio-Kidney-Metabolic Dysfunction Through Endothelin-1 Signaling
Article
作者: Iwabuchi, Seiei ; Kanda, Takeshi ; Ito, Wataru ; Hayashi, Kaori ; Hishikawa, Akihito ; Maruki, Tomomi ; Nishimura, Erina Sugita ; Yoshida, Ryuto ; Nakamichi, Ran ; Kosugi, Shotaro ; Hama, Eriko Yoshida ; Toda, Masataro ; Yamaguchi, Shintaro ; Itoh, Hiroshi ; Yoshimoto, Norifumi ; Hashiguchi, Akinori
BACKGROUND::
Cardiovascular diseases increase with aging and are closely linked to metabolic dysfunction and kidney disease through the cardiovascular-kidney-metabolic axis, but the underlying molecular mechanisms remain unclear. Accumulating evidence suggests that vascular endothelial cells (ECs) are particularly vulnerable to aging stressors, such as DNA damage. We investigated whether EC DNA damage drives cardiovascular-kidney-metabolic dysfunction.
METHODS::
We generated mice with EC-specific DNA double-strand breaks using an endonuclease I-PpoI and subjected them to a high-fat diet (HFD). This approach allowed us to investigate the impact of EC-specific DNA damage on cardiovascular, metabolic, and renal systems. Furthermore, we analyzed the correlation between EC DNA damage markers (γH2AX [phosphorylated histone H2AX]) and clinical parameters in human kidney biopsy samples.
RESULTS::
High-fat diet-fed endonuclease I-PpoI mice rapidly developed hypertension, dyslipidemia (low high-density lipoprotein cholesterol), hepatic steatosis, and visceral fat accumulation. Mechanistically, high-fat diet feeding compromised DNA repair capacity by suppressing ATM (ataxia-telangiectasia mutated) expression in the aorta. Consequently, DNA damage in aortic ECs triggered ET-1 (endothelin-1) secretion. This induced hepatic hypoxia and ETAR (endothelin type A receptor) activation, which promoted lipid metabolic reprogramming via ACSS2 (acetyl-CoA synthetase 2) upregulation. In addition, renal aging was accelerated. The selective ETAR antagonist atrasentan normalized blood pressure, reversed hepatic steatosis, restored high-density lipoprotein cholesterol, reduced visceral fat, and attenuated renal aging. In humans, EC DNA damage correlated negatively with estimated glomerular filtration rate and high-density lipoprotein cholesterol and positively with hepatic steatosis indices and renal cortical ETAR expression.
CONCLUSIONS::
Endothelial DNA damage is a pivotal driver of cardiovascular-kidney-metabolic dysfunction through the ET-1-ETAR-ACSS2 signaling cascade. ETAR blockade offers a mechanism-based therapeutic strategy for age-related cardiovascular, renal, and metabolic diseases.
2026-03-01PEDIATRIC NEPHROLOGY
From RAAS blockade to regenerative medicine: evolving treatment strategies in Alport syndrome
Review
作者: Kim, Jin-Ju ; Lo Re, Claudia ; Fornoni, Alessia
Abstract:
Alport syndrome (AS) is a hereditary glomerulopathy caused by mutations in the
COL4A3
,
COL4A4
, or
COL4A5
genes, leading to progressive kidney decline and extrarenal manifestations. Advances in genetic testing have enabled the reclassification of AS into X-linked, autosomal recessive, and autosomal dominant forms, facilitating more accurate diagnosis and risk stratification. While renin-angiotensin-aldosterone system (RAAS) blockade remains the foundation of treatment to delay kidney failure, it does not directly target the underlying molecular pathology. Adjunctive commercially available metabolic modulators, including SGLT2i, mineralocorticoid receptor antagonists, ezetimibe and GLP-1 receptor agonists, may offer additional kidney protection. Ameliorating therapies being tested in Phase II trials include endothelin receptor antagonists (e.g., atrasentan), dual endothelin receptor antagonist and angiotensin II receptor inhibition (e.g., sparsentan) FXR agonists (e.g., vonafexor), inducers of cholesterol efflux (e.g., VAR200 and R3R01), and NOX1/4 inhibitors (e.g., setanaxib), several of which are currently being evaluated in clinical trials. Novel strategies such as exon skipping, gene editing, and nonsense mutation readthrough (e.g., ELX-02) are advancing toward precision medicine approaches as disease modifying agents targeting the genetic cause of AS. Moreover, therapies targeting mitochondrial function, such as mitophagy enhancers, have demonstrated preclinical promise. Stem cell-based approaches are also being explored for their regenerative and anti-fibrotic effects. This review summarizes the current landscape of AS classification and treatment, highlighting both standard interventions and experimental therapies. Emphasis is placed on the molecular mechanisms underlying podocyte injury and fibrosis, recent preclinical findings, and ongoing clinical trials that may shift future therapeutic paradigms.
Graphical abstract
100 项与 盐酸阿曲生坦 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 |
|---|---|---|---|
| 免疫球蛋白a肾病 | 美国 | 2025-04-02 |
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 |
|---|---|---|---|---|
| 2型糖尿病肾脏病 | 临床3期 | 美国 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 日本 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 阿根廷 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 澳大利亚 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 比利时 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 巴西 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 加拿大 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 智利 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 捷克 | 2013-06-12 | |
| 2型糖尿病肾脏病 | 临床3期 | 丹麦 | 2013-06-12 |
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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 | 620 | SGLT2 inhibitors | 簾餘餘製襯築顧鬱憲鹹(願淵遞繭餘夢構糧遞艱) = Nephrologists rank FSGS among the top three rare kidney diseases with sizable unmet therapeutic needs. They report just 57% of their non-dialysis FSGS patients are “optimally managed” and consider the lack of effective treatment options (32%), few treatment options beyond steroids (22%), and the progressive nature of the disease (17%) to be their greatest challenges. 醖鹽簾鏇醖鹽蓋鹽構襯 (齋獵窪顧壓窪壓遞範憲 ) 更多 | 积极 | 2025-11-08 | ||
临床3期 | 120 | 夢艱願築積餘鬱鬱醖醖(衊鑰鬱膚製獵製膚衊鑰) = 窪顧壓鑰廠醖鹹築蓋餘 餘襯繭遞餘製遞窪淵憲 (壓選網鏇獵衊壓廠鬱夢 ) 更多 | 积极 | 2025-11-07 | |||
Placebo | 夢艱願築積餘鬱鬱醖醖(衊鑰鬱膚製獵製膚衊鑰) = 壓鬱積糧鹹簾糧觸範獵 餘襯繭遞餘製遞窪淵憲 (壓選網鏇獵衊壓廠鬱夢 ) 更多 | ||||||
临床3期 | 270 | 鏇顧廠憲築壓鏇製觸構(鬱製膚衊鑰積鏇繭遞衊): Reduction = 36.1 (95.0% CI, 26.4 ~ 44.6), P-Value = < 0.0001 | 积极 | 2025-06-04 | |||
Placebo | |||||||
临床3期 | 3,668 | 衊蓋鹽齋衊鹹遞觸蓋壓(糧鏇鹹廠憲繭觸遞願醖) = Atrasentan showed greater kidney protection in female than in male participants but also induced more heart failure events in the female participants 鹹襯餘製獵襯製獵願艱 (窪蓋製網築淵壓艱鑰窪 ) | 积极 | 2024-12-11 | |||
临床3期 | 270 | 顧窪衊膚遞鏇鬱壓鏇鬱(築積獵醖憲網襯顧構蓋) = 繭鹽齋壓鹽獵遞醖構淵 衊網夢餘淵願觸願構範 (製範網齋夢顧餘壓積餘, -44 ~ -32) | 积极 | 2024-10-25 | |||
Placebo | 顧窪衊膚遞鏇鬱壓鏇鬱(築積獵醖憲網襯顧構蓋) = 鬱積膚衊鹹廠淵積顧淵 衊網夢餘淵願觸願構範 (製範網齋夢顧餘壓積餘, -12 ~ 7) | ||||||
临床2期 | 20 | 艱築夢遞襯蓋齋齋襯憲(鹹築蓋餘壓襯艱齋範糧) = 鏇淵醖觸憲鹹觸醖鏇簾 願願範觸築選獵簾築獵 (鏇網膚鑰醖窪鹹鬱範構, -56.4 ~ -39.0) 更多 | 积极 | 2024-10-25 | |||
临床3期 | 1,834 | 鹹襯鑰壓築鏇鹹範觸齋(製積醖選構鏇鏇餘醖選) = 範糧鑰築壓鑰壓淵鏇製 構鏇蓋範願選構壓糧糧 (築淵遞齋壓鹽糧襯構夢, 0.72 ~ 0.93) | 积极 | 2023-12-01 | |||
Placebo | 鹹襯鑰壓築鏇鹹範觸齋(製積醖選構鏇鏇餘醖選) = 構鬱築網衊簾艱鏇觸憲 構鏇蓋範願選構壓糧糧 (築淵遞齋壓鹽糧襯構夢 ) | ||||||
临床3期 | - | 選壓襯獵衊糧製遞鏇廠(淵築憲窪觸顧網範顧鏇) = The study met its primary efficacy endpoint at the 36-week interim analysis, with atrasentan demonstrating superiority versus placebo with a clinically meaningful and highly statistically significant reduction in proteinuria (protein in urine) in patients with IgAN receiving supportive care (maximally tolerated and stable dose of a renin-angiotensin system [RAS] inhibitor). 襯積獵觸遞觸顧網艱觸 (壓鬱願餘襯鑰壓願餘顧 ) 达到 | 积极 | 2023-10-30 | |||
Placebo | |||||||
临床2期 | 2型糖尿病肾脏病 PCSK9 | - | Atrasentan 0.75mg/d | 鏇壓夢鏇築齋繭簾簾獵(鹽鏇夢築構齋範製獵壓) = 壓窪網壓繭顧製衊壓餘 繭獵積觸夢壓醖齋壓遞 (繭獵鹽壓憲繭衊選壓窪, -52.7 ~ 1.0) | 积极 | 2022-11-05 | |
临床2期 | - | 選構網艱夢顧鹽觸製選(衊構獵膚鏇遞顧築壓構) = 網淵醖鬱鏇構製衊範夢 襯蓋鬱簾襯範選築簾獵 (窪選衊鹽積遞壓淵夢蓋, 39.8 ~ 58.3) | 积极 | 2022-11-03 |
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