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

✓ Approved

AbbVie, Inc. · AGTR1 · 小分子

什么是 eprosartan mesylate + HCTZ？

eprosartan mesylate + HCTZ 是一种小分子，由AbbVie, Inc.研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Teveten Combi, Teveten HCT, Teveten Plus
公司AbbVie, Inc.
药物类别小分子
分子靶点AGTR1, SLC12A3
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, AbbVie, Inc.

作用机制

分子靶点

eprosartan mesylate + HCTZ 作用于 2 个分子靶点：

AGTR1angiotensin II receptor type 1 (HAT1R, AT1)
SLC12A3solute carrier family 12 member 3 (NCCT, NCC)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

eprosartan mesylate + HCTZ 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersHypertension✓ Approved

相关研究文献

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.

PMID 42714782
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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.

PMID 42716792
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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.

PMID 42707612
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PubMedASAIO journal (American Society for Artificial Internal Organs : 1992)2026-09-07

Circuit Change, Peri-Change Anticoagulation and Transfusion, and Survival in Pediatric Postcardiotomy Extracorporeal Membrane Oxygenation.

Nishida Keisuke K, Yanai Takanori T, Takeda Chikashi C, Takeuchi Muneyuki M et al.

Circuit and oxygenator changes during pediatric postcardiotomy extracorporeal membrane oxygenation (PC-ECMO) are clinically significant; however, their timing and management are poorly described. Moreover, outcomes beyond discharge remain unclear. We describe circuit changes, temporal trends in anticoagulant use and transfusion, and mid- to long-term survival in pediatric PC-ECMO. This study used a Japanese administrative database spanning 2014-2024. Cardiac surgery cases in patients aged <18 years with congenital heart disease were classified into PC-ECMO and non-ECMO groups. For the PC-ECMO group, we assessed the cumulative incidence of the first circuit change, temporal trends in anticoagulant use and transfusion around each change, and postoperative and post-discharge 1 year survival. Among 4,395 cases, 73 involved PC-ECMO. Of these, 24 (32.9%) required at least one circuit change, with a cumulative incidence of 33.1% (95% confidence interval [CI], 19.4-46.7) within 3 days. Anticoagulants were switched from heparin to nafamostat mesylate alone or no anticoagulation (p = 0.001), and fresh-frozen plasma transfusion increased on the day of change (p = 0.016). Postoperative 1 year survival was 0.566 (95% CI, 0.449-0.713); among those discharged alive, 1 year post-discharge survival was 0.967 (95% CI, 0.901-1.000). Circuit changes were common and occurred early after PC-ECMO initiation. Post-discharge survival was favorable among patients discharged alive.

PMID 42704884
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PubMedBioImpacts : BI2026-08-29

Correction to: Sustained release microneedle patch for pronounced systemic delivery of doxazosin mesylate.

Anwar Imran I, Zafar Nadiah N, Mahmood Asif A, Zulcaif

[This corrects the article DOI: 10.15171/bi.30257.].

PMID 42666976
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PubMedIndian journal of surgical oncology2026-08-28

Dermatofibroasarcoma Protuberans (DFSP) of the Breast: An Eight Case Series From A Single Institution.

Surendra Shreya S, Sahu Shalini S, Raj Santhosh S, Daniel Nirmal N et al.

Dermatofibrosarcoma protuberans (DFSP) is a rare, slow-growing soft tissue sarcoma arising from dermal fibroblasts. Breast involvement is extremely rare, posing diagnostic and therapeutic challenges. We retrospectively reviewed eight cases of breast DFSP managed at our center over a 10-year period. The cohort included seven females and one male with a median age of 39.1 years. Clinical presentations were diverse: one patient had multiple areolar nodules, five presented with breast lumps including three with recurrent lumps, which is an uncommon presentation for DFSP, one had an ulceroproliferative growth with bleeding, and one presented following excision of a recurrent lump elsewhere with histopathology showing positive margins. Histological diagnosis was confirmed via core biopsy or block review. Four patients had classic DFSP, while three had fibrosarcomatous transformation. All cases of DFSP showed CD34 positivity. Wide local excision was performed in seven patients, and one underwent mastectomy. Two patients received adjuvant radiotherapy. No recurrence was observed within six months. Breast DFSP is rare and requires histopathological confirmation. Core biopsy with appropriate histologic features and CD34 immunostaining aids in diagnosis. Wide local excision remains the primary treatment approach. Radiotherapy is recommended in cases with close or positive margins, recurrence, metastatic disease, or when surgery is not feasible. Targeted therapy with Imatinib Mesylate, a tyrosine kinase inhibitor, is reserved for unresectable or metastatic lesions, provided the COL1A1::PDGFB translocation involving chromosomes 17 and 22 [t (17; 22)] is confirmed. Long term stringent follow up is required as recurrence in breast has been noted 26 years following primary treatment in literature.

PMID 42661834
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