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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

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

Related Research Articles

PubMedBMC nephrology2026-09-18

Nafamostat mesylate versus low-molecular-weight heparin during continuous renal replacement therapy in critically Ill adults: a single-center retrospective cohort study.

Zeng Xianguo X, Xiao Yutong Y, Zhang Chaoqun C, Li Yide Y et al.

Nafamostat mesylate (NM) is frequently used for continuous renal replacement therapy (CRRT) anticoagulation when clinicians wish to avoid sustained systemic anticoagulation, whereas low-molecular-weight heparin (LMWH) is commonly selected when systemic anticoagulation is considered acceptable. However, direct evidence comparing NM with LMWH in adult intensive care unit (ICU) patients undergoing CRRT remains limited. This study compared filter lifespan, circuit-related failure and safety outcomes between NM and LMWH in a real-world ICU CRRT cohort. This single-center retrospective cohort study included adult ICU patients receiving CRRT with NM or LMWH between January 2022 and January 2023. The primary outcome was filter lifespan. In the primary time-to-event analysis, circuit-related filter failure was defined as clotting-related failure or access/device-related failure, while planned and clinical-event-related terminations were censored. Kaplan-Meier analysis, Cox regression with patient-level cluster-robust standard errors, shared-frailty Cox regression, and propensity score-matched analyses were used to compare filter survival, account for repeated circuits within patients, adjust for CRRT prescription factors, and assess robustness. A total of 116 patients contributing 344 filters were included: 31 patients with 132 filters in the NM group and 85 patients with 212 filters in the LMWH group. NM-treated patients had greater illness severity and more pronounced coagulation abnormalities. Unadjusted Kaplan-Meier analysis showed shorter filter survival with NM than with LMWH (log-rank P = 0.007). However, anticoagulant strategy was not significantly associated with circuit-related filter failure in the primary Cox model (HR 1.41; 95% CI 0.88-2.25; P = 0.15), shared-frailty Cox model (HR 1.57; 95% CI 0.85-2.90; P = 0.15), extended Cox model (HR 1.16; 95% CI 0.70-1.90; P = 0.56), or propensity score-matched analyses. Bleeding events were infrequent, precluding a precise comparison of bleeding risk between groups. Anticoagulant strategy was not significantly associated with circuit-related filter failure after adjustment for measured covariates. Because of substantial baseline differences, residual confounding, and limited statistical precision, these findings should not be interpreted as evidence of comparative efficacy, equivalence, noninferiority, or comparable safety. Larger prospective studies with standardized treatment protocols are needed.

PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-09-13

Antitumor potential of pacific plant extracts revealed using tumor spheroids and untargeted metabolomics.

Huchedé Paul P, Abalam Hugo H, Dumontet Vincent V, Leal Jade J et al.

The discovery of novel antitumor compounds remains a pressing need to address the global burden of cancer, particularly to fight treatment resistance and the lack of specificity of conventional therapies. The terrestrial flora from New Caledonia (NC), a biodiversity hotspot in the South Pacific, represents a rich and largely underexplored source of candidate antitumor natural products (NPs). This study aimed to identify the most potent antitumor extracts among a selection of plants from the terrestrial flora of NC and to further characterize their pharmacological potential. Ten extracts prepared from the leaves and bark of Alphitonia neocaledonica (Rhamnaceae), the aerial parts of Coleus forsteri (Lamiaceae), the bark of Scaevola taccada (Goodeniaceae), and the leaves and bark of Xylopia pancheri (Annonaceae) were evaluated across a panel of six tumor cell lines. Cytotoxic activity of identified hits was assessed against HCT116 colorectal carcinoma and Huh-7 hepatocarcinoma tumor spheroids, and selectivity was investigated ex vivo using peripheral blood mononuclear cells (PBMCs). Pharmacological interactions between the active extracts and conventional anticancer agents were subsequently evaluated. Metabolomic profiling of active extracts was performed using ultra-high-performance liquid chromatography coupled with high-resolution mass spectrometry (UHPLCHRMS). Cyclohexane extracts of C. forsteri aerial parts and X. pancheri leaves exhibited cytotoxic activity against several tumor cell lines. Both extracts reduced the area and viability of HCT116 and Huh-7 tumor spheroids, while displaying moderate selectivity toward K562 chronic myeloid leukemia (CML) cells over ex vivo PBMCs. The active extracts displayed dose-dependent synergistic or antagonistic interactions with the conventional anticancer agents 5-fluorouracil (5-FU) and imatinib mesylate (IM). Principal component analysis (PCA) and heatmap visualization of UHPLCHRMS profiles revealed markedly distinct chemical signatures among the ten plant extracts, including between different plant parts of the same species. Partial least squares discriminant analysis (PLS-DA) based on the 30 most discriminating features further showed that the active extracts were enriched in features putatively annotated to abietane-type diterpenoids in C. forsteri and kaurene/trachylobane-type diterpenoids in X. pancheri. This study highlights the antitumor potential of NPs from the terrestrial flora of NC and provides novel evidence of the activity of selected plant extracts, including in physiologically relevant 3D tumor spheroid models. The enrichment of the most active extracts in abietane- and kaurene/trachylobane-type diterpenoids further points to these metabolite families as promising sources of novel anticancer agents.

PubMedTranslational cancer research2026-09-11

A cuproptosis-related lncRNAs-based risk signature for predicting prognosis and immune status in glioma.

Lu Xiangdong X, Zhu Siquan S, Si Junzeng J, Qiu Peng P

Glioma is one of the most prevalent primary malignant brain tumors, characterized by poor prognosis and limited treatment options. Recent studies have identified cuproptosis, a novel copper-dependent form of regulated cell death, as a critical mechanism involved in tumor progression. However, the role of cuproptosis-related long non-coding RNAs (lncRNAs) in glioma remains not fully clarified. This study aimed to develop and validate a prognostic model based on cuproptosis-associated lncRNAs to predict patient outcomes and guide individualizing therapeutic strategies. Transcriptomic profiles and clinical data were obtained from The Cancer Genome Atlas (TCGA), The Genotype-Tissue Expression (GTEx), and the Chinese Glioma Genome Atlas (CGGA) databases. Cuproptosis -related prognostic lncRNAs were filtered via univariate and multivariate Cox and Least absolute shrinkage and selection operator (LASSO) regression analyses, which were selected to establish a prognostic model for glioma. Samples were divided into high- and low-risk groups, and the predictive performance of the prognostic model was evaluated based on receiver operating characteristic (ROC) curves, Kaplan-Meier (K-M) survival curves, and a nomogram. In addition, immune cell infiltration, tumor mutational burden (TMB), immunophenoscore (IPS), Tumor Immune Dysfunction and Exclusion (TIDE) and drug sensitivity were analyzed. Expression levels of selected lncRNAs and proteins were validated using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. An 11-lncRNA signature associated with cuproptosis was established, and the risk score derived from this model was identified as an independent prognostic factor for glioma. The model exhibited excellent predictive ability, with area under the curve (AUC) values of 0.880, 0.913, and 0.866 for 1-, 3-, and 5-year survival, respectively. Higher TMB, immune checkpoint expression, and IPS were observed in the high-risk group and no significant difference was observed in TIDE between risk groups. Drug sensitivity analysis identified TPCA-1, KIN001-135, and ispinesib mesylate as potential therapeutic agents. Expression validation in glioma cells further supported the biological relevance of the selected lncRNAs. This cuproptosis-related lncRNA-based signature demonstrates strong prognostic value and may serve as a promising tool for glioma risk stratification and personalized treatment selection.

PubMedPharmacological reports : PR2026-09-09

Interactions of ACEA and WIN 55,212-2 mesylate with temozolomide and cisplatin in neuroblastoma and glioblastoma cell lines: an isobolographic analysis.

Załuska-Ogryzek Katarzyna K, Wróblewska-Łuczka Paula P, Góralczyk Agnieszka A, Chojnacki Michał M et al.

Glioblastoma is still the most aggressive primary brain tumor in adults. Recently, several advanced experimental treatment options have been proposed for glioblastoma patients, including the application of cannabinoids as an add-on therapy. In the MTT, LDH, and BrdU assays, the anti-proliferative effects of arachidonyl-2'-chloroethylamide (ACEA - a potent selective cannabinoid CB1 receptor agonist) and WIN 55,212-2 mesylate (a non-selective cannabinoid CB1 and CB2 receptor agonist) on neuroblastoma and glioblastoma cell lines (CHP-134, KELLY, U-87MG, T98G, and C6) were determined. The interaction profiles of ACEA and WIN 55,212-2 mesylate in combinations with cisplatin and temozolomide (two chemotherapeutic drugs) in CHP-134, KELLY, U-87MG, T98G, and C6 were assessed isobolographically in the MTT test. Additionally, the impact of ACEA and WIN 55,212-2 mesylate on cannabinoid CB1 receptors expressed on all the tested cell lines was examined with the Western blot technique. Pre-incubation with a selective cannabinoid CB1 receptor antagonist/invert agonist (AM281) and consecutive exposure of the neuroblastoma CHP-134 and glioblastoma T98G cell lines to ACEA or WIN 55,212-2 mesylate at various treatment times (24, 48, and 72 h) in the MTT assay was studied. Expression of Bax and Bcl-2 proteins in response to ACEA or WIN 55,212-2 mesylate treatment was examined with Western blot. ACEA and WIN 55,212-2 mesylate produced anti-proliferative effects on the tested cell lines. The selectivity index for ACEA ranged from 2.61 to 5.95, and that for WIN 55,212-2 mesylate ranged from 4.32 to 12.85. The combinations of ACEA with cisplatin (at the fixed ratio of 1:1) exerted additive interactions in all the tested cell lines. In contrast, WIN 55,212-2 mesylate, when combined with cisplatin, exerted a synergistic interaction in the CHP-134 cell line (p < 0.05) and additive interactions in the remaining (KELLY, U-87MG, T98G, and C6) cell lines in the MTT test. The combinations of ACEA with temozolomide (at the fixed-ratio of 1:1) exerted antagonistic interactions in two (CHP-134 at p < 0.05; and C6 at p < 0.0001) cell lines and additive interactions in three (KELLY, U-87MG, T98G) cell lines in the MTT assay. In contrast, WIN 55,212-2 mesylate, when combined with temozolomide, produced antagonistic interactions in three (KELLY at p < 0.05; T98G at p < 0.01, and C6 at p < 0.01) cell lines and additive interactions in the remaining (CHP-134 and U-87MG) cell lines in the MTT test. Western blot analysis confirmed that all the tested cell lines (CHP-134, KELLY, U-87MG, T98G, and C6) exposed to ACEA or WIN 55,212-2 mesylate changed the expression of cannabinoid CB1 receptors. Pre-incubation with AM281 and subsequent exposition of the CHP-134 and T98G cell lines to ACEA or WIN 55,212-2 mesylate revealed that the prior blockade of cannabinoid CB1 receptors reduced the anti-viability effects of the cannabinoid agonists in the MTT assay, confirming the involvement of cannabinoid CB1 receptors in this cellular response. Additionally, due to Western blot technique it was confirmed that neither Bax, nor Bcl-2 proteins were involved in the anti-proliferative effects of ACEA and WIN 55,212-2 mesylate in the tested CHP-134 and T98G cell lines. WIN 55,212-2 mesylate combined with cisplatin exerted the most desirable synergistic interaction in relation to the anti-proliferative effects in the neuroblastoma (CHP-134) cell line. In contrast, all the antagonistic interactions determined isobolographically for WIN 55,212-2 mesylate in combination with temozolomide in the KELLY, T98G, C6, and those of ACEA with temozolomide in the CHP-134, C6 cell lines in the MTT assay, should not be used clinically, due to the reduction of the anti-viability effects of the tested combinations.

PubMedBiological & pharmaceutical bulletin2026-09-09

Realgar Transforming Solution Triggers Ferroptosis-Associated Death in NB4 Leukemia Cells through Disruption of Iron Homeostasis and Suppression of the SLC7A11/GPX4 Axis.

Yue Zhaorong Z, Liu Qinghong Q, Wang Yanni Y, Wang Ruyue R et al.

Realgar (As4S4) has long been used in traditional medicine, yet its clinical application remains limited due to poor bioavailability and toxicity. Realgar transforming solution (RTS), a bioleached product generated through microbial transformation of realgar, exhibits enhanced anti-tumor activity; however, its underlying mechanism remains unclear. This study investigated whether ferroptosis contributes to the anti-leukemic effects of RTS in NB4 cells, focusing on iron homeostasis and the solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) antioxidant axis. NB4 cells were treated with RTS, arsenic trioxide (ATO), or realgar, and cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Transcriptomic profiling, biochemical assays, fluorescence probes, flow cytometry, and Western blotting were employed to evaluate ferroptosis-related changes. RTS inhibited NB4 cell viability more effectively than ATO or realgar at comparable arsenic concentrations. Transcriptomic analysis indicated significant enrichment of ferroptosis-related pathways. RTS decreased glutathione and superoxide dismutase levels, increased malondialdehyde accumulation and lipid peroxidation, disrupted mitochondrial membrane potential, and elevated intracellular total iron and mitochondrial Fe2+ levels. Additionally, RTS downregulated SLC7A11 and GPX4 and altered the expression of iron metabolism-related proteins, including transferrin receptor protein 1, nuclear receptor coactivator 4, ferritin heavy chain 1, ferroportin 1, iron-responsive element-binding protein 2, and heme oxygenase 1. Moreover, ferrostatin-1 and deferoxamine mesylate partially rescued RTS-induced cytotoxicity and alleviated oxidative damage and iron overload. These results indicate that RTS induces ferroptosis-associated cell death in NB4 cells by disrupting iron homeostasis and inhibiting the SLC7A11/GPX4 axis, supporting further investigation of RTS as a modernized arsenic-based anti-leukemic formulation.

PubMedFrontiers in pharmacology2026-09-08

Pradefovir mesylate and tenofovir amibufenamide for chronic hepatitis B: a systematic review and pragmatic treatment algorithm.

Yang Shuqi S, Zhan Liting L, Wan Zimei Z, Yu Xueping X

Pradefovir mesylate (PDV; approved in China in 2024) and tenofovir amibufenamide (TMF; approved in China in 2021) are novel hepatocyte-targeted nucleotide prodrugs recently approved in China. Their clinical positioning relative to the guideline-endorsed benchmark tenofovir alafenamide (TAF) for chronic hepatitis B management remains undefined, particularly regarding renal/bone safety and drug-drug interaction profiles. To synthesize available evidence and propose a pragmatic treatment selection framework. Narrative review with systematic literature search of Phase 2/3 randomized trials and observational real-world cohort studies (≥48 weeks follow-up, n ≥ 100) comparing PDV or TMF with TDF or TAF, with explicit evidence quality classification. Methods: Systematic review with qualitative synthesis of Phase 2/3 trials and observational cohorts comparing PDV or TMF with TDF or TAF. Risk of bias (RoB 2, NOS) and GRADE certainty were assessed. TMF demonstrated noninferior antiviral efficacy versus TDF through Week 96 with superior renal and bone safety. TMF demonstrated noninferior antiviral efficacy versus TDF through Week 96, with improved renal and bone safety profiles compared with TDF. Retrospective real-world comparisons suggest comparable efficacy to TAF; however, prospective confirmation is needed. PDV demonstrated comparable HBV DNA suppression to TDF at Week 24, with sustained efficacy and favorable safety through Week 96 in Phase 3 trials PDV showed comparable HBV DNA suppression to TDF at Week 24, with Phase 3 data at Weeks 48 and 96 now available in Chinese CHB patients. PDV's CYP3A4-dependent activation creates clinically significant drug-drug interaction potential, whereas TMF and TAF utilize non-CYP pathways with favorable interaction profiles. PDV's CYP3A4-dependent activation raises the theoretical possibility of drug-drug interactions based on in vitro metabolic data, whereas TMF and TAF utilize non-CYP pathways with favorable interaction profiles. Based on currently available evidence, TMF represents a potentially viable TAF alternative for patients with renal/bone risk or anticipated long-term therapy, though definitive therapeutic equivalence requires prospective head-to-head randomized trials. PDV remains an emerging option requiring cautious implementation pending further characterization of its long-term durability, resistance barrier, and drug-drug interaction profile. Conclusion: TMF may represent an alternative to TAF for patients with renal/bone risk or anticipated long-term therapy, though definitive equivalence requires prospective head-to-head randomized trials. PDV offers comparable short-term efficacy to TDF, with longer-term data now available; continued follow-up will define its role among nucleotide prodrugs.

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