Drug Database
AZ

azilsartan

✓ Approved

Lee's Pharmaceutical · AGTR1 · Small Molecule

What is azilsartan?

azilsartan is a small molecule developed by Lee's Pharmaceutical. It is approved for therapeutic indications via oral (po).

Drug Profile

CompanyLee's Pharmaceutical
Drug ClassSmall Molecule
Molecular TargetAGTR1
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Lee's Pharmaceutical

Mechanism of Action

Molecular Targets

azilsartan acts on 1 molecular target:

AGTR1angiotensin II receptor type 1 (HAT1R, AT1)
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Therapeutic Indications

azilsartan is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

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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PubMedBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2026-05-08

Retraction notice to "Nephroprotective effect of AT-MSCs against cisplatin-induced EMT is improved by azilsartan via attenuating oxidative stress and TGF-β/Smad signaling" [Biomedicine & Pharmacotherapy 158 (2023) 114097].

Fawzy Michael A MA, Beshay Olivia N ON, Bekhit Amany Abdlrehim AA, Abdel-Hafez Sara Mohamed Naguib SMN et al.

PMID 42097906
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