Drug Database
BU

bunazosin (bunazosin retard / Detantol R / bunazosin, ER, Esai)

✓ Approved

Eisai Co., Ltd. · ADRA1A · Small Molecule

What is bunazosin?

bunazosin is a small molecule developed by Eisai Co., Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namesbunazosin retard, Detantol R, bunazosin, ER, Esai
CompanyEisai Co., Ltd.
Drug ClassSmall Molecule
Molecular TargetADRA1A
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Eisai Co., Ltd.

Mechanism of Action

Molecular Targets

bunazosin acts on 1 molecular target:

ADRA1Aadrenoceptor alpha 1A (ALPHA1AAR, ADRA1C)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

bunazosin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedFrontiers in oncology2026-10-22

Integrated CDK4/6 inhibitor resistance and primary-metastatic discordance in hormone receptor-positive/HER2-negative metastatic breast cancer: a translational framework focused on invasive ductal carcinoma with gastric metastasis.

Cheng Minyi M, Wang Dongqing D, Lin Yingyi Y, Wu Cangui C et al.

CDK4/6 inhibitors have reshaped treatment for hormone receptor-positive (HR+)/HER2-negative metastatic breast cancer, but resistance frequently emerges and may interact with metastatic phenotypic evolution. We developed an integrated resistance-discordance framework and explored its clinical interpretability in invasive ductal carcinoma (IDC) with gastric metastasis. Public MSK-INK4 (cBioPortal study ID: breast_ink4_msk_2021) and MBCproject (brca_mbcproject_wagle_2017) cohorts were curated for HR+/HER2-negative disease. A five-module CDK4/6 inhibitor resistance score (0-5) was constructed from predefined mutation and copy-number events. In MBCproject RNA-seq samples, single-sample gene-set enrichment analysis quantified proliferation and estrogen-response activity. Discordance burden was defined as z(proliferation score) minus z(ER score), using primary tumors as the reference. Three institutional IDC gastric-metastasis cases were projected onto the framework for interpretability but not inferential testing. Seventy HR+/HER2-negative MBCproject samples and 1116 deduplicated MSK-INK4 metastatic samples were analyzed. MBCproject metastases had higher resistance scores than primary tumors (P = 0.001), whereas metastatic scores were similar between MBCproject and MSK-INK4 (P = 0.202). Metastases showed higher proliferation activity (P = 0.014) and a trend toward lower ER activity (P = 0.071). The high-resistance/high-discordance quadrant was enriched for PI3K-axis events (OR = 16.52; P = 0.034), chromatin-remodeling loss-of-function events (OR = 12.47; P = 0.001), and cell-cycle/RB-axis events (OR = 9.03; P = 0.001). Among the three IDC gastric-metastasis cases, two available gastric NGS profiles mapped to predefined resistance modules, and the case with increased gastric Ki-67 showed the strongest IHC-adapted discordance and projected toward the high-resistance/high-discordance phenotype. Coupling resistance-associated genomic events with metastatic phenotype discordance may provide a clinically interpretable lens for HR+/HER2-negative metastatic breast cancer and for rare IDC gastric-metastasis presentations.

PMID 42903090
Read full article →
PubMedEye and vision (London, England)2026-10-21

Blocking IL-6 trans-signaling mitigates benzalkonium chloride-induced inflammation, oxidative imbalance, ER stress, and barrier disruption in human corneal epithelial cells.

Lax Karina K, Glass Joshua J, Aliste Antonella A, Sharma Ashok A et al.

Benzalkonium chloride (BAC), a commonly used preservative in ophthalmic formulations, elicits a pro-inflammatory cytokine response and cytotoxic effects in corneal epithelial cells, contributing to ocular surface injuries associated with dry eye disease (DED). Interleukin-6 (IL-6) trans-signaling is a well-established pro-inflammatory pathway that contributes to endothelial and epithelial barrier dysfunction. Thus, this study investigated whether targeted inhibition of IL-6 trans-signaling with sgp130Fc could attenuate BAC-induced cytotoxic injury in corneal epithelial cells. Human telomerase-immortalized corneal epithelial (hTCEpi) cells were exposed to 0.001% BAC for 30 min in the presence or absence of 10 μg/mL sgp130Fc. Markers of inflammation, oxidative imbalance, endoplasmic reticulum (ER) stress, and epithelial barrier disruption were assessed using enzyme-linked immunosorbent assay, reverse transcriptase polymerase chain reaction, and western blot analyses. Reactive oxygen species (ROS), antioxidant capacity, and intracellular calcium flux were quantified using colorimetric, fluorescence-based, and luminescence-based assays. Epithelial barrier function was assessed using electric cell-substrate impedance sensing. Statistical analyses were performed using one-way analysis of variance followed by Tukey's or Holm-Šídák multiple-comparison tests, with P < 0.05 considered statistically significant. BAC exposure activated IL-6 trans-signaling as indicated by an increased sIL-6R/sgp130 ratio, reduced mIL-6R levels, and unchanged gp130 levels. BAC also increased secreted IL6 levels, IL6RA expression, and downstream inflammatory mediators MCP1 and ICAM1, all of which were attenuated by sgp130Fc. BAC-induced oxidative imbalance was characterized by increased ROS and hydrogen peroxide production, reduced antioxidant enzymes, and diminished total antioxidant capacity, whereas sgp130Fc mitigated these effects. In addition, BAC increased intracellular calcium levels and ER stress markers, including HSP72, BiP, PERK, and Ero1α, and impaired epithelial barrier function as observed by reduced trans-epithelial electrical resistance and decreased β-catenin, occludin, and claudin-1 levels. sgp130Fc mitigated increases in intracellular calcium, partially alleviated ER stress responses, and preserved epithelial barrier integrity and junctional protein levels. These findings indicate that IL-6 trans-signaling contributes to BAC-induced corneal epithelial injury, suggesting that targeting this pathway may have therapeutic potential for DED and related ocular surface inflammatory disorders.

PMID 42902348
Read full article →
PubMedBMC public health2026-10-21

Comorbidity patterns and inpatient expenditure among patients with coronary heart disease in China.

Chen Xiali X, Liu Zhixin Z, Han Pan P, Dong Rui R et al.

Coronary heart disease (CHD) often co-occurs with other chronic conditions. This increases care complexity and hospital costs. Most previous studies have relied on single diseases or simple comorbidity counts. Less is known about whether different multimorbidity patterns are associated with different levels and structures of inpatient expenditure. We aimed to identify comorbidity patterns among middle-aged and older inpatients with CHD and to examine their associations with hospital costs. We conducted a retrospective study using electronic health record data from a tertiary hospital in Shanxi Province, China, from 2020 to 2024. Patients aged 45 years or older with a principal discharge diagnosis of CHD (ICD-10: I20-I25) were included. The outcome was total inpatient expenditure per admission. Latent class analysis was applied to 14 comorbidities with prevalence of at least 1%. We then used generalised linear models with a gamma family and log link to examine the association between latent classes and inpatient expenditure, adjusting for sociodemographic and clinical covariates. Among 33,044 patients used for pattern identification, 85.16% (28,140) had at least one included comorbidity. Five classes were identified: low comorbidity (39.89%), vascular disease (5.20%), hypertension-dominant (42.27%), diabetes-renal (3.16%), and cardiac dysfunction (9.48%). Compared with the low-comorbidity class, all other classes were associated with higher inpatient expenditure, with the largest increases observed in the cardiac dysfunction class (ER = 1.33, 95% CI: 1.30-1.36) and the diabetes-renal class (ER = 1.27, 95% CI: 1.23-1.32). Predicted mean expenditure was highest in the cardiac dysfunction class ($2,615.77; 95% CI: 2,562.30-2,669.24) and the diabetes-renal class ($2,502.99; 95% CI: 2,421.49-2,584.49), compared with $1,964.85 (95% CI: 1,943.54-1,986.16) in the low-comorbidity class. Medical consumables accounted for the largest share of expenditure in all groups, while the cardiac dysfunction class had the highest proportions of diagnostic and medication costs. Multimorbidity was highly prevalent among middle-aged and older inpatients with CHD. Distinct comorbidity patterns were associated with different levels and structures of inpatient expenditure. These findings may help inform more tailored care planning and more refined payment adjustment in tertiary inpatient settings.

PMID 42902291
Read full article →
PubMedCell reports2026-10-20

Polycystin-2 functions as a calcium leak channel under endoplasmic reticulum stress to protect against myocardial ischemia.

Vuchkovska Virdjinija V, Paluru Sanjeet S, Knutila Ryne M RM, Simoens Djamilla D et al.

Endoplasmic reticulum (ER) stress activates the unfolded protein response (UPR) to enhance metabolism and restore homeostasis by increasing mitochondrial calcium at mitochondrial-endoplasmic reticulum contact sites (MERCs). Unresolved ER stress is deleterious and contributes to the severity of diseases such as myocardial infarction (MI). The identity of the MERC calcium source and its interplay with the UPR is unclear. We find that ER-localized polycystin-2 (PC2), a calcium channel, is upregulated in cardiomyocytes with MI. Cardiomyocyte PC2-knockout mice with MI exhibit worsened heart function and decreased PERK. ER stress induces a PC2-facilitated adaptive ER calcium leak and PC2 localization to MERCs. PC2 requires PERK phosphorylation for mitochondrial calcium transfer. PC2 mutations impair ER calcium leak, restored by full-length PC2 expression. Thus, PC2 functions in a PERK-dependent manner under ER stress to provide mitochondrial calcium, and its upregulation is cardioprotective in MI.

PMID 42900588
Read full article →
PubMedACS nano2026-10-20

Erlotinib Engineering Programs Tumor Targeting in an Atomically Precise Au8 Cluster.

Wang Shuai-Bo SB, Ge Xue-Yu XY, Xu Wen-Hao WH, Zhao Xueli X et al.

Atomically precise metal clusters hold great promise for cancer theranostics, yet current strategies for introducing tumor-targeting functionality often compromise their structural precision. Herein, an erlotinib (Er)-functionalized gold cluster, Au8-Er, is constructed through ligand engineering for targeted non-small-cell lung cancer (NSCLC) theranostics. The Er ligands endow Au8-Er with high affinity toward the epidermal growth factor receptor (EGFR), enabling selective tumor targeting and preferential accumulation at lung tumor sites. Under the glutathione-rich tumor microenvironment, Au8-Er releases Er to achieve chemotherapy. Simultaneously, the cluster exhibits strong X-ray attenuation and oxygen-sensitive phosphorescence, allowing it to function as both an X-ray scintillator and a photosensitizer for efficient X-ray-induced photodynamic therapy (X-PDT) under low-dose irradiation. Moreover, its X-ray-excited luminescence enables high-contrast imaging. The synergistic integration of targeted chemotherapy, X-PDT, and imaging within a structurally precise nanoplatform results in enhanced therapeutic efficacy against NSCLC. This work highlights ligand engineering as an effective strategy for imparting biological functionality to atomically precise metal clusters and advances their application in precision cancer theranostics.

PMID 42899760
Read full article →
PubMedFrontiers in oncology2026-10-20

ER-/PR+ breast cancer: from diagnostic discordance to precision therapy.

Shao Yuanhao Y, Zhou Meng M, Hu Zhenwei Z, Wu Bin B et al.

Estrogen receptor-negative/progesterone receptor-positive/human epidermal growth factor receptor 2-negative (ER-/PR+/HER2-)breast cancer is a rare, controversial type that makes up about 0. 3% of all breast cancer cases and does not follow the traditional ER→PR regulatory hierarchy. This review synthesizes the available evidence on the diagnostic evaluation, clinicopathological characteristics, molecular mechanisms, prognosis, and treatment of ER-/PR+/HER2-(ER-/PR+) breast cancer. Although there are false-negative ER staining results and pre-analytical/analytical factors, a number of clinical and transcriptomic data support the existence of a reproducible ER-/PR+subgroup with molecular heterogeneity. These tumors often have a high histological grade, elevated Ki-67 expression, TP53 alterations, and basal-like features, and are closer to triple-negative breast cancer than luminal disease. Potential drivers include ER-independent non-canonical PR activation, epigenetic dysregulation, kinase-mediated receptor phosphorylation, membrane-associated progesterone signaling and receptor network reprogramming. Direct subtype-specific evidence remains limited, and the effectiveness of conventional endocrine therapy is unknown. Current guidelines classify these tumors as hormone receptor-positive/HER2-negative, obscuring clinically relevant heterogeneity. Standardized repeat testing and multi-omic characterization are thus required. Future studies should prioritize prospective multicenter cohorts with paired pre-treatment and post-treatment receptor testing, spatial or single-cell characterization, biomarker-guided stratification and adaptive clinical trials. A PR-oriented precision-medicine framework may improve diagnostic classification and help identify therapeutic vulnerabilities in biologically distinct patient subsets. In addition, this rare phenotype may serve as a useful model for investigating lineage plasticity and endocrine resistance.

PMID 42898714
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about bunazosin