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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

PubMedRSC advances2026-08-25

Electronic and magnetic properties of ZnO:Er(Ga) thin films.

Das Shivani S, Mishra D K DK, Chen K-H KH, Chhotaray Tapaswini T et al.

Er- and Ga-substituted ZnO diluted magnetic semiconductor polycrystalline thin films were deposited on sapphire substrates via DC sputtering at 700 °C under an oxygen plasma atmosphere. The electronic structure, local coordination, and magnetic behavior of these materials were systematically examined. While pure ZnO is diamagnetic, the substitution of Er3+ (Ga3+) at the Zn2+ site introduces donor states, increases the carrier concentration, and distorts the lattice owing to ionic size mismatch. These structural modifications promote room-temperature ferromagnetism while preserving the lattice structure, with a slight change in the lattice parameter. The substitution of Er(Ga) in ZnO increases structural disorder and intrinsic defects, including zinc vacancies (VZn), and oxygen vacancies (VO). Combined X-ray diffraction, Raman spectroscopy, X-ray photoelectron spectroscopy, and X-ray absorption near-edge structure spectroscopy confirmed the substitutional incorporation of Er(Ga) in the ZnO system. The spectroscopic results indicate hybridization and charge transfer within Er(Ga)-O-Zn bonds. In ZnO:Er, VO trap electrons and enhance magnetic exchange interactions; whereas ZnO:Ga does not. Consequently, the ZnO:Er system shows a stronger ferromagnetic response than ZnO:Ga. These findings highlight Er(Ga)-substituted ZnO as a promising material for optoelectronic applications.

PMID 42639534
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PubMedAging cell2026-08-25

DHCR24 Alleviates DNA Damage in Senescent Vascular Endothelial Cells via ENKUR/Ca2+ Signaling.

Li Han H, Yang Zhen Z, Liang Wukaiyang W, Huang Jie J et al.

DNA damage is considered one of the major contributors to aging. DHCR24, a multifunctional enzyme located within the endoplasmic reticulum (ER), is closely related to DNA damage. Our previous study showed that DHCR24 could delay vascular endothelial cells (ECs) senescence. The relationship between DHCR24 and DNA damage during ECs senescence requires further investigation. Here, we demonstrate that aging activates ATM-mediated DNA damage response (DDR) in human umbilical vein endothelial cells (HUVECs) and mouse pulmonary microvascular endothelial cells (PMVECs), and DHCR24 expression is downregulated. Knocking down DHCR24 in young HUVECs induces the activation of ATM-mediated DDR, which has been confirmed in PMVECs of DHCR24 endothelial-specific knockout mice. Consistently, RNAseq indicated that DHCR24 was essential for cell cycle regulation. Further investigations revealed that both replicatively senescent HUVECs and young HUVECs with DHCR24 knockout exhibited ER stress and mitochondrial dysfunction, which might be attributable to calcium overload resulting from DHCR24 deficiency. In this pathological process, the DHCR24-deficiency-induced upregulation of ENKUR markedly exacerbates calcium overload. Conversely, ENKUR knockdown not only alleviates the ER stress and mitochondrial dysfunction caused by DHCR24 inhibition, but also suppresses the ATM-mediated DDR. Moreover, DHCR24 overexpression reduces the elevated ENKUR levels and simultaneously mitigates DOX-induced calcium overload in HUVECs. Collectively, these findings identify DHCR24-ENKUR-dependent Ca2+ signaling as a mechanism linking ER-mitochondrial homeostasis to endothelial DNA damage and senescence. Accordingly, restoring DHCR24 function or regulating calcium signal transduction through this pathway may hold therapeutic potential for delaying vascular ECs senescence and preventing age-related diseases.

PMID 42639736
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PubMedCase reports in oncological medicine2026-08-25

Synchronous Multicentric Breast Cancer With Opposite Molecular Phenotypes: A Case Report and Therapeutic Considerations.

Buelvas Nelson N, Acevedo Zully Z

Multifocal and multicentric breast cancers are increasingly diagnosed due to advances in imaging. Although some degree of molecular heterogeneity between tumor foci is recognized, most multicentric tumors share similar biological profiles. The presence of synchronous multicentric breast cancer with completely opposing molecular phenotypes remains exceptional. We report the case of a 67-year-old woman diagnosed with synchronous multicentric breast cancer of the left breast. One tumor focus showed a HER2-enriched phenotype (ER-negative, PR-negative, HER2-amplified, and Ki67 60%), whereas a second spatially distinct focus (both confirmed on the surgical specimen) exhibited a luminal A phenotype (ER 100%, PR 1%, HER2-negative, and Ki67 15%). Both lesions were confirmed by magnetic resonance imaging and independently biopsied. The patient underwent modified radical mastectomy and received adjuvant anti-HER2 targeted therapy and endocrine therapy. At 22 months of follow-up, she remains disease-free. This case highlights the importance of comprehensive imaging assessment and independent molecular characterization of all suspicious tumor foci in multicentric breast cancer, as molecular discordance may have significant prognostic and therapeutic implications.

PMID 42639293
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PubMedFrontiers in molecular neuroscience2026-08-25

HGSNAT alleviates oxygen-glucose deprivation- induced endothelial injury by suppressing ER stress: implications for Moyamoya disease.

Wen Zhonghui Z, Hu Bin B, Wang Hai H, Chen Ziyu Z et al.

Moyamoya disease (MMD) is a progressive cerebrovascular disorder characterized by chronic cerebral hypoperfusion and ischemic microenvironments that critically impact brain microvascular endothelial cells. Oxygen-glucose deprivation (OGD) models have been extensively employed in MMD research to recapitulate the ischemic conditions relevant to MMD pathophysiology. This study aims to explore the functional involvement and molecular basis of HGSNAT in human brain microvascular endothelial cells (HBMECs) following OGD-induced injury, to establish a theoretical foundation for elucidating the pathogenesis of vascular endothelial injury associated with MMD. An in vitro model of hypoxic-ischemic injury was established by subjecting HBMECs to OGD. After HGSNAT overexpression, endoplasmic reticulum stress (ERS) activator Tunicamycin treatment, and GPX8 silencing, cell viability, angiogenic capacity, and migratory ability were evaluated using the CCK-8 assay, tube formation assay, and scratch wound healing assay, respectively. Enzyme-linked immunosorbent assay (ELISA) was employed to evaluate the secretion of inflammatory cytokines, while intracytoplasmic reactive oxygen species (ROS) levels were examined using DCFH-DA staining. Additionally, Western blotting was performed to assess the abundance of factors linked to the ERS cascade. OGD exposure significantly downregulated HGSNAT mRNA expression and enzymatic activity. HGSNAT overexpression markedly enhanced the viability of OGD-treated HBMECs and improved angiogenic and migratory capacities, while reducing the secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Functional studies uncovered that HGSNAT overexpression reduced ROS accumulation and suppressed activation of the PERK-eIF2α-ATF4 cascade; these effects were abrogated by Tunicamycin treatment. Furthermore, the study found that GPX8 knockout could weaken the protective effect mediated by HGSNAT, resulting in decreased cell survival, impaired angiogenesis and migratory ability, elevated inflammatory levels, and reactivation of the ERS pathway. This indicates that the efficacy of HGSNAT required for maintaining endothelial homeostasis depends on the function of GPX8. Overexpression of HGSNAT is associated with maintaining or enhancing GPX8 levels under OGD stress, thereby protecting HBMECs from OGD-induced endoplasmic reticulum stress and endothelial damage. GPX8 knockdown partially abolished these protective effects, suggesting that GPX8 contributes to HGSNAT-mediated inhibition of the PERK-eIF2α-ATF4 ER stress pathway, oxidative stress, and inflammation.

PMID 42639067
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PubMedAngewandte Chemie (International ed. in English)2026-08-25

Theranostic Potential of an NAD(P)H-Activatable Fluorophore: Assessing Cancer Aggressiveness and Triggering Apoptosis.

Cha Yujin Y, Oh Taehoon T, Kim Hui Joo HJ, Kang Minju M et al.

Molecular theranostics, integrating precise diagnosis with targeted therapy, represents a cornerstone of personalized medicine. As a pivotal metabolic cofactor, reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) is intrinsically linked to cancer progression and survival when dysregulated. In this study, we report DE-CQ, an NAD(P)H-activatable fluorophore that enables both cancer imaging and apoptosis. DE-CQ allows the real-time quantification and visualization of intracellular NAD(P)H, serving as a robust molecular indicator of cancer malignancy. Beyond its diagnostic utility, DE-CQ preferentially induces mitochondria- and ER stress-dependent, caspase-mediated apoptosis in aggressive MDA-MB-231 cancer cells while maintaining minimal toxicity toward normal cells. Our findings demonstrate that DE-CQ functions as a potent theranostic agent, simultaneously providing diagnostic insights into cancer aggressiveness and triggering cell death. Given its dual functionality and high selectivity, DE-CQ holds significant potential as a next-generation platform for advanced, personalized cancer treatment.

PMID 42639950
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PubMedActa pharmacologica Sinica2026-08-25

Berberrubine alleviates PCS-induced tubular injury via HNRNPF/NR4A1/ER stress axis.

Liu Ying Y, Wang Yong-Song YS, Jin Shu-Fan SF, Yuan Meng-Ting MT et al.

The key uremic toxin p-cresyl sulfate (PCS) has been shown to induce renal tubule injury-mediated chronic kidney disease via endoplasmic reticulum stress (ERS). Berberine offers renoprotective benefits and attenuates ERS-driven apoptosis. Owing to the low oral bioavailability of berberine, its primary metabolite, berberrubine (BRB), here considered a direct bioactive-agent responsible for its effects. However, the protective effects of BRB against nephritic damage and its regulatory function involving ERS or underlying molecular targets remain poorly understood. In this work, biochemical, cellular assays and animal studies revealed that BRB alleviates PCS-induced renal dysfunction, pathological damage, ERS and apoptosis. Additionally, transcriptomics, biochemical and cellular assays revealed that BRB effectively inhibited the PCS-mediated phosphorylation and nuclear translocation of NR4A1, which in turn suppressed the GRP78/IRE1α/XBP1s/CHOP signaling pathway. Mechanistically, DARTS, CETSA, SPR and mutant plasmids identified HNRNPF as the functional target of BRB, with key binding sites TYR306 and ASN313, further revealing its role as a critical regulator of the NR4A1/GRP78/IRE1α/XBP1s/CHOP signaling pathway in HNRNPF-knockdown/overexpressing HK-2 cells and AAV9-saCAS9-sgRNA knockdown C57BL/6 mice. Our findings reveal a previously unrecognized HNRNPF/NR4A1/ERS pathway in which BRB targets HNRNPF as a newly identified small-molecule ligand, and these results offer valuable insights into the potential targeting of HNRNPF for the treatment of tubule lesions.

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