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azilsartan

✓ Approved

Lee's Pharmaceutical · AGTR1 · 小分子

什么是 azilsartan？

azilsartan 是一种小分子，由Lee's Pharmaceutical研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

公司Lee's Pharmaceutical
药物类别小分子
分子靶点AGTR1
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Lee's Pharmaceutical

作用机制

分子靶点

azilsartan 作用于 1 个分子靶点：

AGTR1angiotensin II receptor type 1 (HAT1R, AT1)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

azilsartan 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersHypertension✓ Approved

相关研究文献

PubMedJournal of diabetes research2026-09-09

Azilsartan Ameliorates Diabetic Kidney Disease Through Modulation of Inflammation, Pyroptosis, and Mitochondrial Dysfunction.

Li Wang W, Hao Fang F, Lijia Xu X

To investigate the protective effects of Azilsartan (AZL) on kidney injury in diabetic nephropathy (DKD) mice and high glucose (HG)-induced mesangial cell damage, and to clarify whether these effects are mediated through the regulation of mitochondrial reactive oxygen species (mtROS) and NLRP3 inflammasome-mediated pyroptosis. SPF male C57BL/6 mice, aged 6-8 weeks, were adapted for 1 week and randomly divided into a control group and a DKD group. The DKD model was established through right nephrectomy combined with a high-fat diet and intraperitoneal injection of streptozotocin (STZ, 50 mg/kg). After successful modeling, the two groups were further divided into a saline subgroup and an AZL intervention subgroup, with continuous intervention for 8 weeks. In vitro, mesangial cells from mice during the logarithmic growth phase were divided into normal glucose (NG) and HG groups, further setting up saline control and AZL intervention subgroups. MitoQ, a mitochondrial-targeted antioxidant, was used to verify the role of mtROS. Parameters including systolic blood pressure, blood glucose, serum creatinine, and urinary albumin-to-creatinine ratio (UACR) were measured in mice. Kidney pathology was observed by PAS staining. Western blotting was used to detect the expression of NLRP3, cleaved-Caspase1, GSDMD-N, and other pyroptosis-related proteins in kidney tissues and mesangial cells. ELISA was used to measure the concentration of IL-1β in serum and cell supernatants. Mitochondrial morphology, membrane potential, and mtROS levels in mesangial cells were observed using laser confocal microscopy. ATP content in cells was measured by chemiluminescence, and cell injury was assessed by LDH assay. In vivo, compared to the control group, the DKD+Saline group showed significantly increased systolic blood pressure, blood glucose, serum creatinine, and UACR, with evident mesangial matrix expansion and enhanced activation of the NLRP3 inflammasome and pyroptosis. AZL intervention significantly improved these abnormalities. In vitro, HG induced mitochondrial structural damage, decreased membrane potential, reduced ATP generation, and increased mtROS levels in mesangial cells while also activating NLRP3 inflammasome-mediated pyroptosis. AZL intervention significantly reversed these changes, and MitoQ, by inhibiting mtROS, mimicked the protective effects of AZL. AZL improves renal function and pathology in DKD mice, potentially through both hemodynamic (blood pressure lowering) and nonhemodynamic mechanisms. In vitro evidence indicates that AZL suppresses HG-induced mesangial cell pyroptosis by inhibiting mtROS generation and NLRP3 inflammasome activation.

PMID 42713967
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PubMedCurrent hypertension reviews2026-08-24

Emerging Pharmacological Therapies for Hypertension.

Mahajan Pritesh P, Pagar Ashish A, Baviskar Kajal K, Kachave Ramanlal R

This review provides a general overview of the physiological effects and pharmacokinetic properties that affect the absorption, distribution, metabolism, and elimination of recently developed antihypertensive drugs, such as fimasartan, azilsartan, zilebesiran, aprocitentan, and esaxerenone. It provides an opportunity to understand the pharmacologic properties of drugs like esaxerenone, a non-steroidal selective mineralocorticoid receptor antagonist; aprocitentan, a dual endothelin receptor antagonist; and zilebesiran, a small interfering RNA (siRNA) therapeutic that inhibits hepatic angiotensinogen synthesis. Mechanistic differences among these agents are also highlighted; for instance, fimasartan and azilsartan inhibit the angiotensin II receptor, whereas other medications alter mineralocorticoid activity or endothelial pathways. The review further discusses the clinical implications of these mechanisms in hypertension management and supports informed therapeutic decisionmaking by providing a detailed understanding of the pharmacological and mechanistic profiles of these emerging antihypertensive therapies.

PMID 42634574
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PubMedInternational microbiology : the official journal of the Spanish Society for Microbiology2026-08-08

Identification of hypertension-associated bacterial key genes as potential targets and therapeutic agents through integrated bioinformatics approach.

Sumi Most Shermin Akter MSA, Islam Rahat Md Tahalil MT, Resma Most Nusrat Jahan MNJ, Ahmed Md Feroj MF et al.

Hypertension (HTN) is a major global health burden and a leading risk factor for cardiovascular morbidity and mortality. Although numerous studies have explored host genetic factors and molecular mechanisms underlying HTN, increasing evidence indicates that gut microbiota dysbiosis also contributes to disease development. However, the specific microbial genes involved in HTN pathogenesis and their potential therapeutic targeting remain largely unexplored. This study aimed to identify HTN-associated differentially abundant bacterial genes (DAGs), prioritize bacterial key genes (bKGs) from among them, and repurpose potential therapeutic agents targeting these bKGs using an integrated bioinformatics framework. A total of 167 stool (fecal) microbiome samples, comprising 72 samples from HTN patients and 95 samples from HCs, were analyzed using publicly available 16 S rRNA sequencing data. After quality processing and clustering at 97% similarity, 95,361 representative operational taxonomic units were obtained. Microbial diversity analysis revealed significant alterations in community composition between HTN and HC groups. Differential abundance analysis identified 24 significantly altered bacterial genera associated with HTN. Functional prediction analysis further revealed 28 differentially abundant metabolic pathways and 631 differentially abundant bacterial genes (DAGs) potentially involved in HTN pathogenesis. From these DAGs, protein-protein interaction network analysis prioritized ten hub genes as bKGs (alsB, ampC, gsiB, araC, coaA, dnaB, fruA, ssuA, minE and tsx) representing potential microbial therapeutic targets. Structure-based molecular docking identified five approved drugs, namely Azilsartan, Eplerenone, Candesartan, Conivaptan, and Telmisartan, as top-ranked compounds exhibiting strong binding affinities toward the proposed targets. ADMET evaluation suggested favorable pharmacokinetic and safety profiles for Azilsartan, Eplerenone, and Candesartan. Furthermore, molecular dynamics simulation analyses confirmed that Eplerenone and Candesartan exhibited greater structural stability and sustained binding interactions, suggesting their potential as promising therapeutic candidates for HTN management. Therefore, this study identifies microbial gene signatures potentially involved in HTN and proposes a microbiome-guided drug repurposing strategy targeting bacterial functional pathways. These findings provide novel insights into microbiota-host interactions in HTN and highlight promising therapeutic candidates that warrant further experimental and clinical validation.

PMID 42570071
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PubMedAmerican journal of cardiovascular drugs : drugs, devices, and other interventions2026-08-08

Antihypertensive Efficacy and Safety of Angiotensin Receptor Blockers (ARBs) with and without Inverse Agonism: A Systematic Review and Network Meta-analysis.

Liu Jing J, Geng Jialu J, Liu Jiakun J, Hu Lei L et al.

While not all angiotensin receptor blockers (ARBs) exhibit inverse agonistic activity, certain ARBs with this property may offer greater potential for blood pressure (BP) reduction compared with ARBs without inverse agonism. This study aimed to evaluate the antihypertensive efficacy and safety of ARBs with or without inverse agonism. A systematic literature review and network meta-analysis identified randomized clinical trials (RCTs) of first-line monotherapy for mild-to-moderate hypertension: azilsartan medoxomil (AZL-M), candesartan, olmesartan, losartan, valsartan, telmisartan, irbesartan, allisartan isoproxil, sacubitril/valsartan, sacubitril/allisartan, or placebo. Treatments were grouped as ARBs with or without inverse agonism, angiotensin receptor neprilysin inhibitors (ARNIs), and placebo. AZL-M was separately analyzed as part of ARBs with inverse agonism. BP changes and adverse events (AEs) were assessed. Of 2659 RCTs screened, 23 studies were analyzed. ARBs with inverse agonism demonstrated superior systolic BP and diastolic BP reductions compared with ARBs without inverse agonism, ARNIs, and placebo. When analyzed separately, AZL-M significantly outperformed ARBs without inverse agonism in systolic BP and diastolic BP reduction and was superior to other ARBs with inverse agonism in systolic BP reduction. Surface under the cumulative ranking curves (SUCRA) indicated AZL-M had the highest probability of being the best treatment for systolic BP (98%) and diastolic BP (95%) reduction. This study supports that ARBs with inverse agonism, especially AZL-M, have a better BP-lowering efficacy compared with ARBs without inverse agonism and ARNIs, while maintaining favorable safety profiles. Future research is encouraged to explore the effects on long-term outcomes, combination therapies, and safety in diverse populations.

PMID 42570044
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PubMedCEN case reports2026-06-22

Development of IgA nephropathy following risankizumab therapy for psoriatic arthritis: a case report.

Yagasaki Motohiro M, Yamada Koshi K, Koshida Takeo T, Takagi Miyuki M et al.

IgA nephropathy (IgAN) has been reported in association with several biologic agents; however, renal events related to selective interleukin (IL)-23p19 inhibition remain poorly characterized. We report a case of biopsy-proven IgAN that became clinically apparent after initiation of risankizumab for psoriatic arthritis. A 37-year-old man with psoriatic arthritis achieved marked improvement in joint and skin manifestations after starting risankizumab in October 2022. Thereafter, kidney function gradually declined, with the estimated glomerular filtration rate decreasing from approximately 90-100 to 69.9 mL/min/1.73 m2 by August 2023, accompanied by proteinuria and microscopic hematuria. Despite supportive therapy with azilsartan and dapagliflozin, kidney function continued to worsen and proteinuria persisted, prompting a percutaneous kidney biopsy in February 2025. Light microscopy showed mesangial and focal endocapillary hypercellularity without crescents. Immunofluorescence demonstrated granular mesangial deposits of IgA and C3, and KM-55 staining was positive, indicating glomerular deposition of galactose-deficient IgA1; electron microscopy revealed para-mesangial electron-dense deposits. The biopsy was consistent with primary IgAN (Oxford classification M0E1S0T0C0). We administered steroid pulse therapy according to the Pozzi protocol (methylprednisolone 500 mg/day for 3 consecutive days), achieving remission of urinary abnormalities with modest improvement in kidney function, while risankizumab was continued. This case highlights the need for periodic urinalysis and kidney function monitoring during IL-23-targeted therapy and suggests that IgAN-directed treatment may be effective even when continuation of the biologic agent is clinically necessary.

PMID 42329487
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PubMedJournal of translational medicine2026-05-12

Paraxanthine and azilsartan attenuate gentamicin-induced renal fibrosis via modulation of TGF-β1/Smad3/7 signaling and miRNA-21/miRNA-200b expression.

Rizk El-Adwy Nany Saad NS, El-Ashmawy Nahla E NE, Al-Ashmawy Ghada M GM, Khedr Naglaa F NF

Renal fibrosis is a key contributor to chronic kidney disease progression. The TGF-β1/Smad signaling pathway, particularly Smad2 and Smad3 mediate pro-fibrotic responses, while Smad7 exerts inhibitory effects. The study aimed to evaluate the therapeutic potential of paraxanthine (Para), an active caffeine metabolite, and azilsartan (Azil), an angiotensin II receptor blocker, in attenuating gentamicin (GM)-induced renal fibrosis through targeting Smad pathway and miRNA-21/200b. Seventy male albino mice were randomized into seven groups (n = 10): Control, GM, SIS3 + GM, Para + GM, Azil + GM, Para + SIS3 + GM, and Azil + SIS3 + GM. GM (40 mg/kg, I.P.) was administered daily for 7 days. Subsequently, Para (20.5 mg/kg) and Azil (5 mg/kg) were given orally, while SIS3 (2 mg/kg, I.P.) was administered for 7 days. Serum and urine renal function markers were measured. Renal histopathology, protein expression of TGF-β1, CTGF, Smad3, Smad2 and Smad7, and gene expression of miRNA-21 and miRNA-200b were evaluated. GM caused significant (p < 0.001) nephrotoxicity with elevated BUN, serum creatinine, urinary albumin/creatinine ratio, and KIM-1 and increased fibrosis and marked type I collagen deposition compared to normal control. However, treatments with Para & Azil resulted in significant (p < 0.05) improvement in renal functions. Pro-fibrotic markers TGF-β1, connective tissue growth factor (CTGF), Type I Collagen, Smad 2 and Smad3 were reduced, while Smad7 was increased in treated groups versus GM group. Additionally, miRNA-21 was downregulated and miRNA-200b was upregulated following treatments. Paraxanthine and azilsartan demonstrated significantl restoring of kidney function and suppressing fibrotic progression. Their actions were mediated through regulation of Smad3/7 signaling and modulation of miRNA-21 and miRNA-200b expression, highlighting these pathways as promising therapeutic targets for the treatment of renal fibrosis.

PMID 42116184
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