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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

PubMedCells2026-10-16

TRPs-NCX2 Axis Jointly Preserves Pancreatic Beta Cell Susceptibility/Sensitivity to Elevated Glucose.

Sagintayev Adlet A, Oflaz Furkan E FE, Kanlinuro Andra A, van Amsterdam Savina S et al.

Background: For appropriate glucose sensing, pancreatic beta-cells essentially establish a constant mitochondria-directed endoplasmic reticulum (ER) Ca2+ leak via phosphorylated presenilin-1 (PS1). In the current work, we investigated how cells maintain the ER Ca2+ content during this continuous Ca2+ leak. Methods: Ca2+ imaging for ER, cytosolic and subplasmalemmal Ca2+, high resolution respirometry, and ELISA for insulin secretion were used. Results: A novel ER Ca2+ refilling mechanism driven by reverse-mode NCX2, which is fueled by local Na+ influxes through TRPC3 and TRPV4 channels that are independent of STIM-ORAI1 was found in pancreatic rodent and human beta cell lines. Disrupting this TRPs-NCX2 axis reduces subplasmalemmal Ca2+ levels, abolishes glucose-induced cytosolic Ca2+ oscillations, suppresses glucose-triggered elevation in mitochondrial energetics, and impairs first-phase insulin secretion. Conclusions: We identified a novel, ORAI1-independent "TRPs-NCX2" relay that couples Na+ influx via TRPC3 and TRPV4 to NCX2 reverse mode to maintain ER Ca2+ stores during physiological basal ER Ca2+ leakage, which is fundamental to beta-cell responsiveness to elevated glucose.

PMID 42882464
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PubMedCells2026-10-16

Mitochondria-Endoplasmic Reticulum Crosstalk in Pancreatic β-Cell Stress: A Driver of Diabetes.

Niinuma Sara Anjum SA, Takemoto Ashleigh Suzu-Nishio AS, Khalil William Junior WJ, Butler Alexandra E AE et al.

Pancreatic β-cell failure is central to the pathogenesis of type 2 diabetes (T2D), developing when chronic metabolic stress overwhelms the adaptive capacity of these cells. Because insulin biosynthesis and glucose-stimulated secretion depend on tightly coordinated organelle function, crosstalk between the endoplasmic reticulum (ER) and mitochondria strongly influences β-cell fate. The two organelles are physically coupled at mitochondria-associated membranes (MAMs), contact sites that synchronize ER Ca2+ release with mitochondrial Ca2+ uptake and adenosine triphosphate (ATP) production, and that help regulate redox balance, autophagy, mitophagy and the unfolded protein response. This review draws together evidence on three questions. First, which stresses converge on the β-cell: ER stress, oxidative stress and dysregulated autophagy and mitophagy. Second, how ER-mitochondria crosstalk sustains β-cell health through Ca2+ handling and the proteins that maintain MAM integrity, including inositol 1,4,5-trisphosphate (IP3) receptors, voltage-dependent anion channel 1 (VDAC1), mitofusin 2 (Mfn2) and the ER stress sensors IRE1α and PERK. Third, how glucolipotoxic and inflammatory stress remodels these contacts and pushes communication towards a maladaptive state marked by mitochondrial Ca2+ overload, ROS accumulation, defective organelle quality control, cellular senescence and apoptosis. We contrast rodent and human data, where MAM composition and glucotoxic responses diverge, and consider therapeutic strategies, such as incretin-based agents and the mitochondrial-derived peptide MOTS-c, that target this interface to preserve β-cell function in diabetes.

PMID 42882431
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PubMedAnimals : an open access journal from MDPI2026-10-16

Chronic Energy Restriction Is Associated with Impaired Follicular Development and Hepatic Bile Acid Remodeling in Mice.

Zhu Wenjun W, Li Jiahao J, Cheng Xiaochan X, Zhang Hengyu H et al.

Chronic energy restriction (ER) can impair female reproductive function, but the peripheral metabolic mechanisms by which sustained energy deficiency disrupts follicular development remain poorly understood. This study aimed to determine whether hepatic bile acid (BA) remodeling contributes to the link between systemic energy availability and ovarian dysfunction. A chronic ER mouse model was established by reducing energy intake by 50% for 44 days. Multi-omics approaches, including hepatic transcriptomics, untargeted metabolomics, and targeted BA metabolomics, were integrated with ovarian functional analyses. ER significantly reduced ovarian weight, impaired follicular development, and decreased circulating concentrations of reproductive hormones. Hepatic transcriptomic and metabolomic analyses revealed extensive metabolic remodeling, with marked enrichment of BA-related pathways and increased expression of CYP7A1, suggesting increased hepatic BA synthetic capacity. Targeted BA profiling demonstrated elevated hepatic and circulating BA levels, including increased concentrations of several farnesoid X receptor (FXR)-activating BAs. Furthermore, ovarian FXR expression was increased, accompanied by decreased expression of key steroidogenic regulators, including SRB1, StAR, CYP11A1, and HSD3B1, consistent with reduced ovarian steroidogenic activity. These findings suggest that altered BA metabolism and increased ovarian FXR expression may contribute to reproductive dysfunction under chronic ER.

PMID 42882994
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PubMedInternational journal of molecular sciences2026-10-16

Diosgenin Alleviates Neuropathic Pain Associated with Alterations in Spinal Mitochondrial and ER Stress-Related Factors in CCI Mice.

Rahman Md Mahbubur MM, Yoon Taesu T, Yum Seung Hoon SH, Shim Ye Won YW et al.

Neuropathic pain is difficult to treat as current therapies are often insufficient and provide incomplete relief. However, the mechanisms of chronic nerve injury are poorly addressed. In the present study, we explored the therapeutic effects of natural steroidal saponin diosgenin and its possible spinal mechanisms in a mouse model of chronic constriction injury (CCI)-induced neuropathic pain. C57BL/6 mice underwent CCI and were orally administered diosgenin once daily from three days after surgery. Diosgenin significantly alleviated CCI-induced mechanical allodynia and thermal hyperalgesia and enhanced motor performance in paw withdrawal, open-field, and rotarod tests. These effects were associated with the restoration of mitochondrial homeostasis as evidenced by the increased mitochondrial fusion, decreased fission and activation of NRF2 signaling. Diosgenin also suppressed spinal endoplasmic reticulum (ER) stress, mitochondria apoptotic signaling and the expression of pro-inflammatory cytokines, and pain-related neuropeptides. Mechanistically, the inhibition of spinal NRF2 proteins and the pharmacological induction of ER stress reduced the analgesic effect of diosgenin, highlighting the critical involvement of these pathways in its therapeutic efficacy. Altogether, diosgenin alleviated neuropathic pain in CCI mice that were pharmacologically associated with the restoration of spinal mitochondrial function and ER stress suppression. Therefore, diosgenin could be a promising natural steroidal therapeutic candidate in alleviating neuropathic pain.

PMID 42883869
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PubMedBiology2026-10-16

Altered IRE1α-Dependent Decidual Programming Links Impaired Inflammation and Angiogenesis in Recurrent Implantation Failure.

Castagnola Lara L, Materazzi Lourdes L, Paparini Daniel D, Schafir Ana A et al.

Decidualization alters the endometrial stromal cells (EnSC) secretome, allowing sterile inflammation associated with embryo implantation, but mechanisms that lead to alterations in this process are still unknown. We evaluated whether impaired IRE1α-mediated endoplasmic reticulum (ER) stress signalling contributes to defective angiogenic decidual programming in patients with recurrent implantation failure (RIF). Candidate pathways were identified with bioinformatic analyses of endometrial arrays and validated in endometrial biopsies from fertile and RIF women (secretory phase) by RT-qPCR and in isolated EnSC by flow cytometry. Functional alterations were evaluated using trophoblast spheroid and endothelial cell migration assays. ER stress was pharmacologically induced in EnSC using thapsigargin. RIF endometria displayed impaired in vivo decidualization, with reduced expression of IGFBP1 and PGR, together with altered expression of molecules involved in blastocyst adhesion. Conditioned media from RIF-derived EnSC-impaired trophoblast outgrowth. RIF samples displayed an anti-angiogenic and altered inflammatory profile, characterized by reduced intracellular IL-1β accumulation, decreased VEGFA, and increased sFlt1 expression. Bioinformatic analyses identified IRE1α pathway as a central altered network associated with angiogenesis. Consistently, RIF samples showed reduced expression of IRE1α, sXBP1, and NLRP3. Moreover, ER stress induction in EnSC promoted endothelial cell migration. RIF is associated with defective angiogenic decidual programming linked to impaired IRE1α-mediated ER stress signalling. These findings identify the IRE1α axis as a potential pathway of interest for future therapeutic exploration in recurrent implantation failure.

PMID 42883366
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PubMedEnvironmental geochemistry and health2026-10-16

Spatial and campaign-scale dynamics of trace elements in lakes and ponds of the Iowa and Nebraska - Missouri River floodplain.

Adojoh Onema C OC, Trabal William W, Adewuyi Favour F, Ayinde Kayode K et al.

Trace-element contamination in small floodplain water bodies can vary sharply among neighboring catchments, and regional averages may conceal individual hotspots. Water from six lakes and ponds in western Iowa and eastern Nebraska were examined during three site-wide surveys: Summer 2024, Fall 2025, and Spring 2026, yielding 18 site-campaign observations. Eleven trace elements-aluminum (Al), arsenic (As), cadmium (Cd), cobalt (Co), copper (Cu), iron (Fe), manganese (Mn), nickel (Ni), lead (Pb), selenium (Se), and zinc (Zn) were retained after data verification, and concentrations were standardized to µg L-1. Site-specific exceedance ratios (ER = C/S) and Heavy Metal Pollution Index (HPI) values were calculated using the study screening benchmarks. Lake Manawa had the highest mean HPI (327.13) and the highest overall mean ER (1.85), driven principally by Co (mean ER = 7.19), Pb (5.16), Mn (1.99), Al (1.94), and Cd (1.49). Among the remaining sites, Pinky's Glen had the highest mean ER (1.57), dominated by Mn (5.31), Al (3.24), and Co (3.15), whereas Steinhart Park showed elevated Mn (5.61), Co (3.05), and Al (2.59). An additive two-factor variance partition indicated that water-body identity accounted for more than 90% of variation in Al, Co, Cu, Fe, Mn, Pb, and Zn during the sampled campaigns. The campaign accounted for 95.8% of As variation and 54.2% of Cd variation. An equal-weight score based on min-max-normalized mean HPI, exceedance frequency, and mean ER ranked Lake Manawa, Pinky's Glen, and Steinhart Park as the three highest priorities for confirmatory monitoring. A recovered physicochemical survey showed the highest mean TDS and EC at Carter Lake (264.67 mg L-1 and 529.33 µS cm-1), water temperatures of 3.03-6.57 °C, and circumneutral mean pH (6.95-7.62). Because the three surveys occurred in different years, temporal comparisons and benchmark exceedances are interpreted as screening-level evidence. The findings support site- and analyte-specific confirmatory monitoring rather than pooled regional assessment.

PMID 42881302
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