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eprosartan mesylate + HCTZ (Teveten Combi / Teveten HCT / Teveten Plus)

✓ Approved

AbbVie, Inc. · AGTR1 · Small Molecule

What is eprosartan mesylate + HCTZ?

eprosartan mesylate + HCTZ is a small molecule developed by AbbVie, Inc.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesTeveten Combi, Teveten HCT, Teveten Plus
CompanyAbbVie, Inc.
Drug ClassSmall Molecule
Molecular TargetAGTR1, SLC12A3
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, AbbVie, Inc.

Mechanism of Action

Molecular Targets

eprosartan mesylate + HCTZ acts on 2 molecular targets:

AGTR1angiotensin II receptor type 1 (HAT1R, AT1)
SLC12A3solute carrier family 12 member 3 (NCCT, NCC)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

eprosartan mesylate + HCTZ is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

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Developing and evaluating per-protocol adherence definitions in a large pragmatic clinical trial: insights from the Diuretic Comparison Project.

Anand Sonia T ST, Hau Cynthia C, Davenport Michael J MJ, Ishani Areef A et al.

Pragmatic clinical trials leveraging real-world data, such as the Diuretic Comparison Project (DCP), present unique challenges in measuring treatment adherence compared to traditional randomized controlled trials. In DCP, medications were managed through routine VA care and monitored via pharmacy claims, requiring tailored methods to assess adherence beyond standard measures like medication possession ratio (MPR). To develop a data-driven approach to define protocol treatment adherence for pragmatic comparative effectiveness trials. Structured EHR pharmacy dispense records guided categorization of treatment changes for two diuretics - chlorthalidone (CTD) and hydrochlorothiazide (HCTZ). We examined fill intervals, total drug supply, filling patterns among others to identify prescribing characteristics informing medication adherence definitions and time censoring for per-protocol analysis. Nonadherence was defined as having a gap (>90-days pause in assigned treatment), switch (receiving the other study medication), or discontinuation (without CTD/HCTZ for >90-days). 5,476 patients met nonadherence criteria - 2,851 (52 %) in CTD and 2,625 (48 %) in HCTZ. Switching occurred earlier in CTD patients, gaps were more common in HCTZ, but discontinuation was similar between groups. Defining adherence requires complex decision-making hybrid framework entailing both clinical and statistical expertise. Pragmatic studies should allow flexibility to generate data-driven, clinically-sensitive measures that appropriately describe trial compliance.

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PubMedEnvironmental toxicology and chemistry2026-10-12

Combined sewer overflows attributable to wet weather season contributing to pharmaceutical pollution: a case study in northern Spain.

Akhrimenko Vladimir V, Cerveny Daniel D, Gonzalez-Gomez Xiana X, Cuenca-Castillo Matías Nicolás MN et al.

The use of combined sewer systems is associated with frequent overflow events and discharges of untreated wastewater containing micropollutants, including active pharmaceutical ingredients (APIs). The aim of this study was to evaluate the impact of weather-related factors on the presence of pharmaceuticals and illicit substances and assess the related environmental risk. To address this goal, three sites in the surroundings of the city of Vitoria-Gasteiz were sampled in April (dry week) and November (wet week): Betoño Pond in the Salburua Wetlands, and Zadorra River before and after receiving the Crispijana wastewater treatment plant's (WWTP) effluent. An environmental risk assessment was performed by measuring the hazard quotients for each compound, in addition to individual chemical enantiomers of amphetamine and 3,4-methylenedioxymethamphetamine. A total of 33 out of 102 substances were detected in at least one of the samples and a minimum of 6 APIs in all sample sites. Post-WWTP samples taken in autumn (wet week) presented the highest cumulative concentration (7739 ng L-1). Risk quotients of 12 APIs in the most contaminated site in the rainy weather sampling period reached values >1: diclofenac (3.12) and eprosartan (1.59).

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Exploiting Neosartorya (Aspergillus) fischeri antifungal protein 2-defined fungal targets for drug repurposing against Candida albicans.

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Invasive fungal infections caused by Candida albicans remain major clinical challenges because of the limited therapeutic options, toxicity, and emerging resistance. Drug repurposing offers a promising strategy to accelerate antifungal discovery by leveraging existing compounds with known safety profiles. In this study, we applied a structure-based drug repurposing approach guided by the antifungal protein Neosartorya (currently Aspergillus) fischeri antifungal protein 2 (NFAP2), which targets fungus-specific intracellular proteins, including glutamate decarboxylase, mitochondrial ATP synthase subunit alpha, and enolase. NFAP2-associated binding pockets were identified and used to virtually screen approved clinically investigated compounds. Selected candidates were further evaluated by molecular docking, followed by in vitro antifungal susceptibility testing and interaction analysis with conventional antifungal agents. In vivo toxicity and therapeutic efficacy were assessed using a Galleria mellonella infection model. Despite predicted binding affinities, most repurposed compounds exhibited limited antifungal activity in vitro, highlighting a disconnect between in silico predictions and biological efficacy. Among the tested compounds, dihydroergocristine mesylate (DHEC) and meclizine dihydrochloride exhibited measurable antifungal effects. Notably, DHEC demonstrated pronounced synergistic interactions with amphotericin B, resulting in near-complete growth inhibition in vitro. In vivo, DHEC + amphotericin B induced no detectable toxicity and significantly improved host survival compared with either drug alone. These findings indicate that NFAP2-guided structure-based drug repurposing can identify compounds targeting fungus-specific vulnerabilities. However, antifungal activity depends on factors beyond binding affinity. Our results highlight integrating computational screening with experimental validation and support repurposed compounds as adjuvants in combination therapies to enhance antifungal efficacy and translational potential.Invasive fungal infections caused by Candida albicans remain a major clinical challenge due to limited therapeutic options, toxicity, and emerging resistance. Drug repurposing offers a promising strategy to accelerate antifungal discovery by leveraging compounds with known safety profiles. A structure-based repurposing framework guided by the antifungal protein NFAP2, which targets fungus-specific intracellular proteins, is presented. Using these biologically informed targets, clinically relevant compounds with antifungal and adjuvant potential were identified. Predicted binding affinity alone did not reliably translate into antifungal activity, highlighting the need for integrated computational and experimental approaches. Notably, dihydroergocristine mesylate (DHEC) showed strong synergistic effects with amphotericin B, resulting in near-complete growth inhibition and improved host survival in vivo. These findings highlight the potential of repurposed compounds as adjuvants and support combination-based strategies targeting fungal-specific vulnerabilities. Furthermore, this work provides a framework for the future development of DHEC-inspired antifungal adjuvant strategies.

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Intestinal epithelial cells (IECs) are highly vulnerable to mitochondrial dysfunction and lethal apoptosis under severe hypoxic stress. However, the upstream genetic determinants governing mucosal redox resilience remain poorly defined. To investigate the mechanisms of intestinal epithelial cell apoptosis under cobalt chloride (CoCl2)-induced hypoxic conditions, we established a CoCl2-induced lethal hypoxia model in IPEC-J2 cells and performed a genome-wide CRISPR-Cas9 screen. This screen identified MINOS1 as an essential gene for tolerance to CoCl2-induced hypoxic cell death. Systematic cell phenotyping and transcriptomic analyses revealed that CoCl2 exposure triggers robust intrinsic apoptosis and oxidative stress, whereas MINOS1 ablation remodels the basal transcriptomic landscape to establish an adaptive pro-survival state. Ultrastructural observation via transmission electron microscopy and subcellular functional assays demonstrated that MINOS1 deficiency eliminates canonical crista junctions (CJs) and induces distinctive concentric, "onion-like" remodeling of the inner mitochondrial membrane. Under severe hypoxia, MINOS1-knockout (KO) enterocytes retained stable mitochondrial membrane potential (ΔΨm), suppressed pathological mitochondrial permeability transition pore (mPTP) opening, sustained antioxidant enzyme (SOD and CAT) activities, and abrogated intracellular ROS accumulation and lipid peroxidation. Pharmacological intervention with the mitochondria-targeted antioxidant Mitoquinone mesylate precisely phenocopied the cytoprotective phenotype of MINOS1 ablation, confirming a mitochondria-dependent redox regulatory mechanism. Crucially, subcellular fractionation assays verified that remodeled concentric mitochondrial membranes form a unique topological barrier that physically sequesters cytochrome c within mitochondria, blocking its cytosolic release and subsequent activation of caspase-9 and caspase-3. Accordingly, MINOS1-deficient enterocytes tolerate extreme hypoxic stress by structurally uncoupling mitochondrial oxidative stress from downstream apoptotic execution. Collectively, these findings establish MINOS1-dependent cristae topology as a fundamental biophysical gatekeeper of intestinal mucosal redox homeostasis, providing a novel structure-targeted therapeutic strategy for hypoxia-associated intestinal disorders.

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Regional citrate anticoagulation combined with nafamostat mesylate for continuous kidney replacement therapy in septic acute kidney injury patients: protocol for a prospective, three-arm, randomised controlled study (RCNM-CKRT).

Xu Qing Q, Zou Hongxia H, Zhou Zhifeng Z, Fu Ping P et al.

Extracorporeal circuit (EC) clotting remains a major challenge in continuous kidney replacement therapy (CKRT). While regional citrate anticoagulation (RCA) is recommended first-line, nafamostat mesylate (NM) offers an alternative with potential anti-inflammatory benefits. This trial aims to compare the effects of RCA, NM and their combination on EC lifespan during CKRT in critically ill acute kidney injury (AKI) patients with sepsis. This is a single-centre, prospective, three-arm, open-label, randomised controlled trial. Critically ill adult patients with AKI with sepsis requiring CKRT will be enrolled. Participants will be randomly assigned (1:1:1) to receive RCA, NM or combined RCA+NM anticoagulation. The primary outcome is EC lifespan. Secondary outcomes include EC survival rates, patient mortality, inflammatory biomarker levels and safety events (eg, bleeding, citrate accumulation). The sample size of 258 patients (86 per group) was calculated to detect a significant difference in the primary outcome with 90% power. Analysis will follow the intention-to-treat principle, using Kaplan-Meier survival analysis and Cox regression for the primary outcome. The RCNM-CKRT trial has been approved by the Biomedical Ethics Review Committee of West China Hospital, Sichuan University. We plan to present the results of our research at an international conference and publish in a peer-reviewed journal. The study data will be available on request, ensuring transparency and accessibility.Trial registration number:ChiCTR2600121436; Pre-results.

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Jiang Wenxin W, Yang Yike Y, Yuan Xiao X, Deng Wei W et al.

Well-regulated trophoblast proliferation, migration, invasion, and cell turnover are essential for normal placental development in humans and rodents. Given the established role of oxidative stress in placentation and the redox activity of iron, we investigated whether ferroptosis-associated redox signaling contributes to trophoblast function and placental development. Placental iron profiling revealed significantly elevated total and ferrous iron levels in first-trimester human villi compared with term placentas, accompanied by the transcript levels of several iron uptake- and reduction-related genes, including TFRC, DMT1, ZIP8, STEAP3, and STEAP4, which were elevated in first-trimester villi. Murine placentas also exhibited gestational changes in iron abundance and iron-homeostasis-related gene expression. HO-1 protein abundance was highest during early gestation and declined thereafter, suggesting a potential association between heme degradation and gestational iron homeostasis. In contrast, placental labile iron pool (LIP) levels showed only modest, statistically nonsignificant changes across gestation, suggesting a relatively stable redox-active iron pool. Immunofluorescence analyses demonstrated spatially distinct expression of ferroptosis-associated regulators, with ACSL4 enriched in invasive trophoblast populations and GPX4 predominantly localized in surrounding decidual tissues, suggesting regional heterogeneity in ferroptosis-associated molecular features during placentation. Functional studies in HTR-8/SVneo trophoblast cells further demonstrated that mild ferroptosis-associated redox perturbation induced by low-dose erastin or ferrous iron enhanced trophoblast migration and invasion without overt cytotoxicity. These effects were attenuated by ferrostatin-1, deferoxamine mesylate (DFOM), or the mitochondria-targeted antioxidant MitoQ and were blunted following FTH1 and TFRC knockdown, indicating that trophoblast responsiveness depends on iron availability and ferroptosis-associated redox signaling. Importantly, these pro-invasive effects were preserved under physiologically relevant hypoxic conditions. Together, our findings support a model in which gestational changes in placental iron homeostasis are associated with ferroptosis-related molecular features, while experimentally induced iron-dependent redox signaling modulates trophoblast behavior. Rather than inducing overt ferroptotic cell death, sublethal iron-dependent redox perturbation may act as a signaling mechanism influencing trophoblast function during placental development.

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