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felodipine + ramipril (ramipril/felodipine / Tazko / Triapin Mite)

✓ Approved

Sanofi S.A · CACNA1C · Small Molecule

What is felodipine + ramipril?

felodipine + ramipril is a small molecule developed by Sanofi S.A. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namesramipril/felodipine, Tazko, Triapin Mite
CompanySanofi S.A
Drug ClassSmall Molecule
Molecular TargetCACNA1C, ACE
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Sanofi S.A

Mechanism of Action

Molecular Targets

felodipine + ramipril acts on 2 molecular targets:

CACNA1Ccalcium voltage-gated channel subunit alpha1 C (CACNL1A1, CACNA1C-IT2)
ACEangiotensin I converting enzyme (DCP1, ACE1)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

felodipine + ramipril is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedNeuro-oncology practice2026-09-17

WF-1801: Single-arm pilot study of ramipril for prevention of radiation-induced cognitive decline in glioblastoma patients receiving chemoradiotherapy.

Cramer Christina K CK, Smith Sydney S, Dressler Emily V EV, Page Brandi B et al.

To examine the feasibility of adding ramipril for prevention of cognitive decline to chemoradiation treatment of glioblastoma (GBM). This prospective single-arm study (WF-1801) coordinated by the Wake Forest NCI Community Oncology Research Program Research Base (UG1CA189824) assessed feasibility, tolerability, and potential efficacy of ramipril to prevent treatment-induced cognitive decline in patients with GBM. Inclusion criteria and chemoradiotherapeutic paradigms were mirrored to the standard arm of NRG/RTOG 0825, such that cognitive outcomes could be compared. All patients were treated with ramipril during chemoradiation and for 4 weeks after completion of radiotherapy (RT). Major outcomes were retention and the Clinical Trial Battery Composite (CTB COMP) score of the cognitive tests. Results were compared to the corresponding outcomes from NRG/RTOG 0825. A total of 75 participants were accrued between March 25, 2019 and November 14, 2023: median age was 63 years. The NRG/RTOG 0825 cohort was younger (median 57 years, P < .0001). Overall retention rate at 1-month post-RT (defined as compliant with 75% of doses and completion of cognitive testing) was 48% (1-sided 95% CI: 38%-100%); 61% of patients completed more than 75% of doses and 57% had a CTB COMP score through week 10. The median (range) change in the CTB COMP score at 1 month after RT completion was 0.01 (-82.6, 13.0) versus NRG/RTOG 0825 median of 0.10 (-48.2, 8.6); P = .49. The ramipril intervention did not meet the prespecified feasibility endpoint, neither did the cognitive scores differ significantly from the NRG/RTOG 0925 control group. We expect other agents will be the focus of future cytoprotective trials.

PMID 42750920
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PubMedIndian journal of pharmacology2026-09-02

Ramipril and Olmesartan: Unveiling their pleiotropic potential as immunomodulators.

Dasan Jyothishna J, Yesunesan Anie A, Chandran Vinaya V, Mathew Jyothis J et al.

Studying the pleiotropic effects of medicines can reveal their unexplored therapeutic advantages. It promotes repurposing established drugs or identifying compounds that affect multiple targets. The widely prescribed antihypertensive agents, ramipril and olmesartan, because of their ability to reduce C-reactive protein activity, may also modulate the immune system. The study aims to demonstrate the potential immunomodulatory effects of ramipril and olmesartan, which would be beneficial for the management of inflammation in patients with coexisting hypertension. The anti-inflammatory properties of the drugs were studied in acute and chronic models of inflammation. The immunomodulatory action was evaluated using a neutrophil adhesion test, proinflammatory and anti-inflammatory cytokine assay, and hemagglutination antibody titer assay. Histopathological analyses of rat paw edema were also performed. Both drugs demonstrated enhanced neutrophil adhesion, increased hemagglutination antibody titers, reduced paw edema, and improvement in cellular and structural changes associated with inflammation. Drug treatment also inhibited proinflammatory cytokine production while promoting anti-inflammatory cytokine production. The results indicate the immunomodulatory potential of ramipril and olmesartan at equipotent antihypertensive doses, compared with the standard drugs, in Wistar albino rats. The results reveal that olmesartan exhibits superior immunomodulatory properties compared with Ramipril.

PMID 42683985
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PubMedThe Journal of international medical research2026-08-28

Clinical analyses of angiotensin-converting enzyme inhibitor users presenting with cough to a chest diseases outpatient clinic: A single-center retrospective study.

Bektaş Aksoy Hayriye H, Günaydın Selda S

ObjectiveAngiotensin-converting enzyme inhibitors are widely prescribed for cardiovascular disease and are a well-recognized cause of cough. However, cough in patients treated with angiotensin-converting enzyme inhibitor may also reflect underlying pulmonary disease. This study compared the clinical, laboratory, and medication-related characteristics of angiotensin-converting enzyme inhibitor users presenting with pulmonary and non-pulmonary cough.MethodsThis retrospective single-center study included 199 angiotensin-converting enzyme inhibitor-treated patients who presented with cough to the Chest Diseases Outpatient Clinic of Giresun Training and Research Hospital between October 2021 and January 2025. Patients were classified as having cough with pulmonary or non-pulmonary causes according to available clinical, laboratory, and radiological findings. Non-pulmonary cough was not considered synonymous with confirmed angiotensin-converting enzyme inhibitor-induced cough; however, it indicated the absence of identifiable pulmonary pathology based on retrospective data. Demographic, clinical, laboratory, and angiotensin-converting enzyme inhibitor subtype characteristics were compared.ResultsAmong 199 patients, 153 (76.9%) had pulmonary cough and 46 (23.1%) had non-pulmonary cough. Cough duration was longer (p = 0.044) and dyspnea was more frequent (54.2% vs. 13.0%, p < 0.001) in the pulmonary group. Perindopril use was more common in the non-pulmonary group, whereas ramipril use was more common among patients with pulmonary cough (p = 0.015). In a post hoc analysis limited to patients with documented angiotensin-converting enzyme inhibitor discontinuation and evaluable follow-up notes (n = 78), the overall distribution of cough-response categories differed between the groups (Fisher-Freeman-Halton exact p = 0.039), with complete resolution observed in 33.3% of the patients in the non-pulmonary group and 7.9% patients in the pulmonary group. C-reactive protein levels were higher in the pulmonary group (10.87 vs. 5.67 mg/L, p = 0.010), whereas other hematological parameters did not differ significantly.ConclusionsIn the angiotensin-converting enzyme inhibitor-treated patients presenting with cough, shorter symptom duration, absence of dyspnea, and lower C-reactive protein levels may be more compatible with non-pulmonary or presumed angiotensin-converting enzyme inhibitor-related cough, whereas prolonged cough, dyspnea, and elevated C-reactive protein levels may support the consideration of a pulmonary pathology. These findings are hypothesis-generating and require prospective validation.

PMID 42663438
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PubMedPharmaceuticals (Basel, Switzerland)2026-08-27

Metabolic and Inflammatory Adverse Drug Reactions Associated with Amlodipine: A Descriptive and Disproportionality Analysis of EudraVigilance Reports.

Solomon Crina Cristina CC, Butuca Anca A, Frum Adina A, Dobrea Carmen Maximiliana CM et al.

Background/Objectives: The global rise in obesity-related hypertension, metabolic syndrome, and chronic inflammation calls for a precise characterization of the safety profiles of first-line therapies. While amlodipine is considered metabolically neutral, its real-world impact on dysglycemia and inflammatory biomarkers remains incompletely defined. This study aims to characterize the metabolic and inflammatory adverse drug reaction profile of amlodipine, using the EudraVigilance database. Methods: Descriptive and disproportionality analyses were performed on 41,872 Individual Case Safety Reports recorded prior to 17 May 2026. Amlodipine was compared against major antihypertensive classes (beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, sartans, and diuretics), calculating reporting odds ratios (ROR) and 95% confidence intervals. Results: "Hyperglycaemia" could be considered a safety signal for amlodipine, compared to beta-blockers (e.g., bisoprolol-ROR: 2.56), ACE inhibitors (e.g., ramipril-ROR: 2.82), and sartans (e.g., candesartan-ROR: 3.85). "Metabolic syndrome" was reported for amlodipine with a lower probability than for hydrochlorothiazide (ROR: 0.35). Inflammatory signals (e.g., increased C-reactive protein) appeared less frequently for amlodipine than for certain renin-angiotensin-aldosterone system inhibitors (e.g., perindopril-ROR: 0.53). Conclusions: The disproportionality analysis identified relatively lower reporting frequencies for several metabolic and inflammatory adverse drug reactions, compared with selected antihypertensive agents. These findings represent pharmacovigilance signals that warrant further investigation in analytical epidemiological and clinical studies. Although hyperglycemia was reported disproportionally relative to several comparator drugs, reports of T2DM were less frequently reported for amlodipine. However, these observations should not be interpreted as evidence of differences in clinical risk, because disproportionality analyses cannot establish incidence or causality. Reports of inflammation likely reflect patient comorbidities rather than a direct drug effect. These findings demonstrate that post-marketing surveillance remains essential, even when accounting for the methodological limitations of spontaneous reporting.

PMID 42653674
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PubMedJournal of clinical hypertension (Greenwich, Conn.)2026-08-21

Renin-Angiotensin System Inhibitor Use and Mortality in Older Hypertensive Patients With and Without Dementia: A Nationwide Registry-Based Cohort Study.

Villa Lopez Marta M, Hoang Minh Tuan MT, Xu Hong H, Norgren Jakob J et al.

Cardiovascular risk factors are often undertreated in patients with dementia. Renin-angiotensin system inhibitors (RASI) are first-line treatments for hypertension. We examined the association between RASI and all-cause mortality in hypertensive patients with and without dementia, comparing angiotensin-converting enzyme inhibitors (ACEI) to angiotensin receptor blockers (ARB); and selected individual agents. This nationwide register-based cohort study included data from Swedish national registries 2007-2018. The study included 158 176 hypertensive patients with exposure to RASI medications (21 152 RASI users and 137,024 non-users), after excluding prevalent users. Propensity score matching was used to balance measured confounders. Cox regressions compared mortality risk among RASI users versus non-users, ACEI users versus ARB users, and users of enalapril, ramipril, losartan, and candesartan versus other RASI users. RASI use was associated with lower all-cause mortality (hazard ratio[HR] 0.93, 95% confidence interval[CI] 0.91-0.95, p< 0.001) in the full cohort, and among patients with dementia (HR 0.88, 95% CI 0.85-0.92). Compared to ACEI, ARB were associated with lower mortality in the full cohort (HR 0.90, 95% CI 0.85-0.96), but results were not significant in patients with dementia. The comparison of the individual drugs were consistent with class-level findings. RASI use was associated with lower all-cause mortality among older hypertensive patients, including those with dementia. These observational findings support continued attention to evidence-based hypertension treatment in patients with dementia.

PMID 42625529
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PubMedWorld journal of nephrology2026-08-21

Effect of pentoxifylline on inflammatory markers in non-diabetic chronic kidney disease patients: A prospective, interventional, open label.

Abd El Mobdy Ashraf Hassan AH, Hebah Hayam Ahmed HA, Ezzat Mohammed Ali MA, Eid Mohamed Basant Abdelkarim BA et al.

Pentoxifylline (PTX), a methylxanthine derivative, has been shown to exert notable anti-inflammatory and antiproteinuric actions in diabetic kidney disease, contributing to improved sodium handling, attenuation of renal hypertrophy, and reductions in tumour necrosis factor-alpha (TNF-α), interleukin-6 levels, and albuminuria. To determine the impact of PTX on inflammatory biomarkers and the progression of chronic kidney disease (CKD) in non-diabetic patients. This prospective, interventional, open label, randomized controlled clinical study was conducted on 42 participants aged 18 years or older, of both genders, with CKD stages 3 or 4 and proteinuria < 1 g/24 hours. Participants were placed into two equal groups. Group 1 had standard therapy, including angiotensin-converting enzyme inhibitors (ACEIs; ramipril 1.25 mg), calcium acetate (700 mg), alfacalcidol (0.25 µg), antihypertensives, and diuretics. Group 2 had the same standard therapy plus PTX 400 mg (Trental®) two times per day for six consecutive months. There was no significant relationship between TNF-α and high-sensitivity C-reactive protein (hs-CRP) and participants' gender in both groups. An essential direct correlation was observed between TNF-α and creatinine in both groups. A critical direct correlation was observed between hs-CRP and calcium in group B. There was a significant inverse correlation between the change in TNF-α and estimated glomerular filtration rate, as well as between the change in TNF-α and the urinary protein-to-creatinine ratio. The change in protein creatinine ratio noted in group 2 was mainly due to changes in mean arterial pressure, followed by changes in TNF-α. In non-diabetic CKD patients, adjunctive treatment with PTX was associated with significant decreases in C-reactive protein levels and proteinuria. The reduction in proteinuria was mainly explained by changes in mean arterial pressure, followed by changes in TNF-α, indicating that hemodynamic factors may play a more prominent role than inflammatory modulation in mediating this effect.

PMID 42626272
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