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amlodipine besilate + irbesartan (DSP8153)

✓ Approved

Sumitomo Pharma Co., Ltd. · AGTR1 · Small Molecule

What is amlodipine besilate + irbesartan?

amlodipine besilate + irbesartan is a small molecule developed by Sumitomo Pharma Co., Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesDSP8153
CompanySumitomo Pharma Co., Ltd.
Drug ClassSmall Molecule
Molecular TargetAGTR1, CACNA1C
RouteOral (PO)
StatusApproved

Mechanism of Action

Molecular Targets

amlodipine besilate + irbesartan acts on 2 molecular targets:

AGTR1angiotensin II receptor type 1 (HAT1R, AT1)
CACNA1Ccalcium voltage-gated channel subunit alpha1 C (CACNL1A1, CACNA1C-IT2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

amlodipine besilate + irbesartan is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedEuropean journal of case reports in internal medicine2026-11-11

Combined Calcium Channel Blocker And Angiotensin-Converting Enzyme Inhibitor Overdose.

Kahal Fares F, Guérard-Poirier Natasha N, Ji Cheng C, Gursahaney Ashvini A et al.

Combined overdoses of angiotensin-converting enzyme inhibitors and calcium channel blockers are rare but associated with more severe toxicity than either agent alone. A 48-year-old woman presented to the emergency department nine hours after intentionally ingesting 40 tablets of amlodipine (10 mg) and 40 tablets of ramipril (10 mg). On arrival, she was hypotensive and tachycardic. Initial management included fluids, intravenous calcium and insulin bolus followed by high-dose insulin euglycaemic therapy (HIET). Despite escalating vasopressor support, she developed mixed vasoplegic and cardiogenic shock complicated by acute kidney injury, fluid overload, respiratory failure and metabolic acidosis, necessitating intubation and continuous renal replacement therapy. Improvement in haemodynamics was only achieved by day 9. She was transferred from the intensive care unit (ICU) on day 20 with residual weakness from ICU-acquired myopathy and was ultimately discharged after 66 days, with a prolonged hospitalisation attributed to delirium and deconditioning. Severe combined angiotensin-converting enzyme inhibitors (ACEI) and calcium channel blockers (CCB) overdose may cause prolonged, refractory haemodynamic instability requiring extended high-dose insulin euglycaemic therapy (HIET), vasoactive support and fluid administration. Concentrated insulin, dextrose and vasopressor preparations may help mitigate fluid overload. Angiotensin II may be a potential treatment for refractory vasoplegia, although evidence and availability remain limited. Secondary complications can prolong recovery beyond the duration of drug toxicity. This case highlights the need for individualised, multidisciplinary management, early HIET, vasoactive support and fluid-sparing strategies in severe combined ACEI and CCB overdose. Management of severe combined calcium channel blocker and angiotensin-converting enzyme inhibitor overdose may require prolonged resuscitation with high-dose insulin euglycaemic therapy, vasoactive support and fluid administration. The cumulative fluid requirements of these therapies, combined with complications such as acute kidney injury, can contribute to severe fluid overload. The use of concentrated insulin, dextrose and vasopressor preparations may help limit the iatrogenic fluid accumulation.Clinicians should anticipate and proactively manage secondary complications, including acute kidney injury, volume overload, respiratory failure and infection, as these complications may independently prolong recovery beyond the expected duration of drug toxicity.Combined angiotensin-converting enzyme inhibitor and calcium channel blocker overdose lacks established management guidelines and requires individualised, multidisciplinary care based on clinical severity and response to therapy.

PubMedJournal of biomolecular structure & dynamics2026-11-10

Integrated molecular modeling and in vitro validation identify new acetylcholinesterase-inhibitory scaffolds among FDA-approved drugs.

Kumar Ram R, Das Modak Sanjib S, Babu M Arockia MA, Sinha Suman S

Acetylcholinesterase (AChE) inhibition remains a clinically validated strategy for the symptomatic management of Alzheimer's disease (AD). However, the limited long-term efficacy of currently available inhibitors continues to drive the search for new scaffolds, making drug repurposing an attractive strategy for accelerating drug discovery. Here, an integrated structure-guided workflow combining molecular docking, molecular dynamics (MD) simulations, MMGBSA binding free-energy analysis, dynamic interaction profiling, and in vitro enzyme inhibition assays was employed to investigate the AChE inhibitory potential of FDA-approved drugs. The docking study identified lumacaftor, olaparib, fexofenadine, and vibegron as the highest-ranked compounds, while MMGBSA predicted favourable binding energetics for lumacaftor, pemetrexed, olaparib, and cilostazol. MD simulations showed that most of the compounds remained favourably accommodated within the AChE active-site gorge while maintaining overall structural integrity of the enzyme. In vitro enzyme inhibition assays identified olaparib, cilostazol, and miconazole with the lowest measured IC50 values (2.86, 2.88, and 2.89 μM, respectively), while vibegron, irbesartan, pemetrexed, lumacaftor, and indomethacin also showed measurable inhibition. Fexofenadine showed 51.26 ± 4.81% inhibition at 20 μM, but its IC50 was not determined. Differences between computational predictions and experimental activity highlight the utility of computational approaches for compound prioritization rather than quantitative prediction of biological activity. Taken together, this study identified FDA-approved drugs with, to the best of our knowledge, previously unreported AChE inhibitory activity and provided mechanistic insights into AChE-ligand recognition. These compounds represent preliminary, experimentally supported AChE-interacting scaffolds for further biochemical, pharmacological, and in vivo investigation.

PubMedNeuroscience2026-11-10

Association of metoprolol with temporal changes in SIRT1, oxidative stress, and inflammatory biomarkers.

Gupta Sandeep Kumar SK, Kalita Jayantee J, Pandey Prakash C PC, Mahajan Roopali R et al.

There is a paucity of studies on the effect of beta-blocker on sirtuins (SIRT1)-mediated inflammation and oxidative stress in ischemic stroke. We report the effect of metoprolol on the temporal kinetics of SIRT1-mediated oxidative stress markers [catalase (CAT), glutathione peroxidase (GPx), malondialdehyde (MDA), and reactive oxygen species (ROS)], proinflammatory cytokines (TNFα and IL1β), and their association with outcomes. This was a sub-analysis of our earlier study on effect of beta-blocker in acute stroke. Forty-eight patients within 3-days of ischemic stroke were included. Their demographic characteristics, risk factors for stroke, GCS/NIHSS score, hematological and biochemical parameters, electrocardiogram, echocardiography, and cranial-MRI findings were noted. SIRT1, TNFα, and IL1β mRNA fold-changes were measured by using real-time PCR, and GPx, CAT, MDA, and ROS were measured by using a spectrophotometer. These biomarkers were also measured in 59 healthy-controls. The outcome was defined at 1 and 3-months using the modified Rankin Scale. Twenty-eight patients received metoprolol, and 20 received amlodipine. There is a gradual reduction in TNFα, IL1β, ROS, and MDA and an increase in CAT level in both groups; however, more marked in the metoprolol group. On day 15, the metoprolol group had a comparable level of SIRT1, TNFα, IL1β, and CAT to those with the healthy controls. Metoprolol in acute ischemic stroke helps in upregulating SIRT1 and CAT and downregulating TNFα and IL1β; however, the overall p-value for treatment-by-time interaction was insignificant. The patients in the metoprolol group had a better outcome at 3-months. A large study is needed to confirm these findings.

PubMedPediatric nephrology (Berlin, Germany)2026-11-09

Persistent systemic hypertension in a child with carbonic anhydrase II deficiency.

Arslan Bengü B, Polat Recep R, Çelakıl Mehtap M

Carbonic anhydrase II (CA II) deficiency is a rare autosomal recessive disorder classically characterized by osteopetrosis, renal tubular acidosis (RTA), and intracranial calcifications. We report a 10-year-old girl with genetically confirmed CA II deficiency who developed acute severe hypertension after previously documented normotension. Blood pressure reached 160/100 mmHg and was accompanied by headache, vomiting, and transient neurological symptoms requiring intravenous antihypertensive therapy. Hypertension persisted beyond the acute episode and was confirmed by ambulatory blood pressure monitoring (ABPM) despite treatment, requiring long-term antihypertensive therapy. Serial ABPM during follow-up subsequently demonstrated sustained blood pressure control, permitting stepwise dose reduction and eventual discontinuation of amlodipine approximately two years after presentation. Systemic hypertension has not previously been reported in CA II deficiency. This single-patient observation is hypothesis-generating and does not establish a causal relationship.

PubMedAmerican journal of therapeutics2026-11-06

Amlodipine-associated Angioedema.

Lee Mikyung L ML, Delijani David D, Vittorio Timothy T, Lee David N DN et al.

PubMedRenal failure2026-11-04

Effect of Kunxian capsule, a novel Tripterygium wilfordii preparation, on reducing proteinuria and slowing renal function decline in diabetic kidney disease: a 48-week randomized controlled trial.

Chen Shengnan S, Gao Yajuan Y, Liang Zishen Z, Zhang Yixue Y et al.

Diabetic kidney disease (DKD), a leading cause of chronic kidney disease, remains a clinical challenge despite renin-angiotensin system blockade. This study evaluated the efficacy and safety of adding Kunxian capsule to standard therapy with irbesartan in patients with DKD. Eighty patients with DKD were randomly assigned to either the experimental group (standard therapy with irbesartan plus Kunxian capsule) or the control group (standard therapy with irbesartan) for 48 weeks. Primary outcomes included the proteinuria remission rate, degree of proteinuria reduction, and median time to remission. Secondary outcomes included the slope of eGFR decline and the incidence of renal composite hard endpoint. Safety was assessed by monitoring adverse events. This trial was registered in ClinicalTrials.gov on March 2, 2021 (No. NCT04981613). In the intention-to-treat analysis, the experimental group had a higher proteinuria remission rate (57.50% vs. 25.00%), a shorter median time to remission (5 months vs. not reached), and a greater reduction in 24-hour urinary protein than the control group. A lower incidence of renal composite hard endpoint was observed in the experimental group (10.00% vs. 32.50%), accompanied by a slower eGFR decline. No significant differences in the incidence of adverse events were observed between the two groups. Inflammatory markers, including C-reactive protein and erythrocyte sedimentation rate, were significantly reduced in the experimental group. Adding Kunxian capsule to standard therapy with irbesartan improved the proteinuria remission rate and attenuated renal function decline in patients with DKD, supporting its potential as a promising adjunctive therapy.

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