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calcium hopantothenate (Hopate / hopantenate calcium)

✓ Approved

Mitsubishi Tanabe Pharma Corporation · 小分子 · 小分子

什么是 calcium hopantothenate？

calcium hopantothenate 是一种小分子，由Mitsubishi Tanabe Pharma Corporation研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名Hopate, hopantenate calcium
公司Mitsubishi Tanabe Pharma Corporation
药物类别小分子
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, Mitsubishi Tanabe Pharma Corporation

治疗适应症

calcium hopantothenate 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
Psychiatric disordersAttention deficit hyperactivity disorder✓ Approved

相关研究文献

PubMedCardiovascular research2026-10-26

NOR-1 is an upstream regulator of Ca2+ homeostasis and calmodulin kinase II-dependent arrhythmogenesis.

Vázquez-Sufuentes Paula P, Jiménez-Sábado Verónica V, Ballester-Servera Carme C, Casabella-Ramón Sergi S et al.

Dysregulation of NOR-1 has been reported in cardiovascular diseases associated with altered calcium handling. We therefore investigated how NOR-1 affects calcium homeostasis and arrhythmogenesis to identify the underlying mechanisms. We assessed the expression of NOR-1 and calcium regulatory proteins in myocardial samples from humans and mice that overexpress human NOR-1 in the heart (TgNOR-1). Gene promoter activity was determined by transient co-transfection assays. Calcium imaging, patch-clamp recordings and immunofluorescent labeling was performed in mouse cardiomyocytes. Experimental data were used for mathematical modeling. Arrhythmias were induced in vivo by an epinephrine/caffeine challenge. In human cardiac samples, mRNA levels of genes coding for SERCA2a, CASQ2, TN-C1 and PLB correlated with those of NOR-1, while TgNOR-1 mice exhibited higher cardiac levels of these calcium regulatory proteins than wild-type animals (WT). NOR-1 increased luciferase activity driven by the proximal promoter of both human and mouse genes. Calcium transients were smaller in TgNOR-1 cardiomyocytes while L-type calcium current and SR calcium content were unchanged. Mathematical modeling revealed that more calcium binds to CASQ2 and is released from the SR in TgNOR-1 cardiomyocytes, but the resulting calcium transient is smaller because more calcium is buffered by TN-C1. Furthermore, NOR-1 transgenesis increased the level of reactive oxygen species and CAMKII oxidation, as well as RyR2 phosphorylation at Ser-2814, which led to a higher incidence of calcium waves and afterdepolarizations in resting TgNOR-1 cardiomyocytes. In electrically paced myocytes, NOR-1 transgenesis promoted extra-transients at low frequencies and calcium alternans at high frequencies. Importantly, these derangements in intracellular calcium handling concurred with a dramatic increase in epinephrine/caffeine-induced bidirectional ventricular tachycardia in TgNOR-1 mice. Moreover, the antioxidant N-acetylcysteine and the CAMKII inhibitor KN-93 attenuated arrythmia in TgNOR-1 mice and arrhythmogenic calcium release in isolated myocytes. Our findings highlight NOR-1 as an upstream regulator of CAMKII-oxidation underlying arrhythmia induced by defective calcium homeostasis, pointing to therapies targeting CAMKII as a means to attenuate arrhythmia triggered by pathological upregulation of NOR-1.

PMID 42929040
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PubMedTraffic (Copenhagen, Denmark)2026-10-26

TMEM55B Maintains Lysosomal Homeostasis and Promotes ER-Lysosome Calcium Signaling.

Mukae Nagi N, Maki Honoka H, Shirane Michiko M

At membrane contact sites (MCSs) between the endoplasmic reticulum (ER) and endolysosomal compartments, the Protrudin-PDZD8 complex promotes the maturation of endosomes into lysosomes, a process accompanied by acidification. Endosomal maturation is closely associated with both lysosomal acidification and calcium signaling; however, the molecular mechanisms linking the Protrudin-PDZD8 complex to these processes remain unclear. Here, we identified TMEM55B, a lysosome-localized protein, as a binding partner of the Protrudin-PDZD8 complex. TMEM55B has been reported to interact with the v-ATPase complex, suggesting a role in lysosomal function. Suppression of TMEM55B expression reduced the fluorescence of a lysosomal acidification probe, suggesting impaired lysosomal acidification. In addition, TMEM55B depletion attenuated lysosomal Ca2+ release and reuptake and reduced ATP-induced Ca2+ responses in the ER. These findings suggest impaired calcium-induced calcium release (CICR) at ER-lysosome MCSs. By contrast, mitochondrial Ca2+ dynamics were unaffected. Together, these results identify TMEM55B as a factor involved in maintaining lysosomal homeostasis and regulating calcium dynamics. Our findings suggest that TMEM55B cooperates with the Protrudin-PDZD8 complex to contribute to the regulation of lysosomal function at ER-lysosome MCSs.

PMID 42928446
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PubMedJournal of medical case reports2026-10-26

High-dose regular insulin as a potential rescue therapy in severe aluminum phosphide poisoning: a case report.

Sedaghattalab Moslem M, Akbari Ghaidafeh G

Aluminum phosphide (rice tablet) can cause cardiocirculatory collapse and has negative cardiac inotropic effect. Positive inotropic effect of insulin on the cardiac myocytes is through calcium flux. Insulin increases the intramyocytes calcium concentration by increasing conductance of calcium through the L-type calcium channels and by increasing intramyocytes concentration of cyclic adenosine monophosphate. In addition to increasing the intramyocytes calcium level, insulin also enhances the responsiveness of the cardiac cells to calcium. High-dose insulin is a potential therapy for hypodynamic and hypotensive septic shock due to its positive inotropic qualities. In this paper, a critical aluminum phosphide poisoning patient (a 25-year-old Iranian young woman), presented with mixed severe metabolic acidosis and respiratory alkalosis, tachypnea, tachycardia, and hypotension. In contrast to our previous experiences that ingestion of aluminum phosphide tablets associated with multiple organ failure and severe shock in approximately all critical poisoning patients, early initiation of high-dose intravenous regular insulin for this patient prevented multiorgan dysfunction and death. Treatment with high-dose intravenous insulin associated with IV fluids, sodium bicarbonate, hydrocortisone, potassium, dextrose therapy and supportive care resolved completely signs and symptoms of patient after 3 days in ICU. High-dose intravenous regular insulin may be act as a rescue therapy for aluminum phosphide poisoning patients. While this single case suggests a potential benefit, further studies are required to confirm these findings.

PMID 42928247
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PubMedCells2026-10-26

RapC Is Involved in the Development of Dictyostelium Through the Regulation of Autophagy and Calcium Signaling.

Han Nara N, Han Uri U, Kim Dahyeon D, Kim Wonbum W et al.

RapC is a Rap-subfamily small GTPase in Dictyostelium whose developmental function remains largely uncharacterized. Upon starvation, individual amoebae aggregate and undergo morphogenetic transitions to ultimately produce a fruiting body, a process requiring precise spatiotemporal regulation of a single apical tip as the primary organizing center. Here, we report that RapC is required for tip organizer formation during multicellular development by modulating autophagy and intracellular calcium signaling. rapC null cells develop normally through aggregation but consistently form three to four apical tips per aggregate rather than the single organizer tip characteristic of wild-type cells. Pharmacological phenocopy experiments revealed that caffeine and the selective TORC1 inhibitor rapamycin recapitulate the multi-tip phenotype, whereas the PI3K inhibitor LY294002 and the pan-TOR inhibitor Torin2 do not, implicating TORC1 signaling as the relevant downstream effector. In line with this, rapC null cells exhibit normal GFP-PH:CRAC translocation kinetics and slightly elevated PKB/PKBR1 phosphorylation, ruling out defects in the PI3K-TORC2-PKB signaling axis. Instead, rapC null cells display markedly elevated autophagic flux as assessed by the tandem RFP-GFP-Atg8 reporter assay, consistent with attenuated TORC1-mediated autophagy suppression. Furthermore, aggregation-competent rapC null cells show increased intracellular calcium ([Ca2+]i) upon external calcium stimulation, a response absent in wild-type cells and not reproduced by rapamycin, indicating a TORC1-independent role for RapC in calcium homeostasis. Together, our findings establish that RapC promotes normal Dictyostelium development by supporting TORC1 activity to suppress excessive autophagic flux and by maintaining [Ca2+]i homeostasis through a TORC1-independent mechanism.

PMID 42929849
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PubMedBiochemical Society transactions2026-10-26

Novel chemogenetic approaches in modulating calcium signaling.

Price Anna A, Lan Tien-Hung TH, Zhou Yubin Y

Calcium (Ca2+) signals regulate diverse processes ranging from neurotransmission and muscle contraction to gene expression, immune response, and cell death. Conventional pharmacological agents are readily applied but often lack molecular and cell-type specificity, whereas genetic perturbations offer greater precision but are typically slow and difficult to reverse. Chemogenetic systems bridge these approaches by combining genetically encoded protein actuators with exogenous chemical ligands. The present review summarizes emerging chemogenetic strategies that modulate Ca2+ signaling at distinct steps of the signaling cascade. These include engineered G protein-coupled receptors, chemically inducible receptor tyrosine kinases, direct actuators and inhibitors of STIM-ORAI coupling, genetically encoded blockers of voltage-gated Ca2+ channels, and engineered ligand-gated ion channels. We also discuss prospective designs targeting the phospholipase C signaling axis. Collectively, these approaches enable reversible and cell-specific modulation of Ca2+ dynamics.

PMID 42929082
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PubMedMolecular medicine (Cambridge, Mass.)2026-10-26

Renal tubular injury-repair imbalance in calcium oxalate nephrolithiasis: mechanisms and therapeutic implications.

Yang Shushuai S, Qi Yuanjiong Y, Zhang Shichao S, Zhang Longchao L et al.

Calcium oxalate (CaOx) nephrolithiasis is a globally prevalent disease with complex pathogenesis and limited targeted therapies. The imbalance between renal tubular epithelial cell (RTEC) injury and repair serves as a key driver of stone formation. Under hyperoxaluric or crystal-induced stress, RTECs undergo multiple regulated cell death pathways including apoptosis, pyroptosis, ferroptosis, and necroptosis, alongside autophagic dysfunction. These processes trigger the release of damage-associated molecular patterns and inflammatory mediators that amplify local inflammation and enhance crystal adhesion. Importantly, tubular repair after injury is not a uniform process but diverges into three distinct outcomes, including adaptive tubular regeneration, repair failure, and fibrogenic maladaptive repair. Persistent RTEC injury-repair imbalance disrupts tubular barrier integrity, perpetuates self-sustaining inflammatory cascades, and upregulates epithelial crystal adhesion molecules, collectively remodeling the renal microenvironment into a stable pro-stone niche that facilitates CaOx crystal deposition and stone formation. This review systematically summarizes the types of RTEC injury, the compromised repair pathways and their regulatory networks. It also discusses emerging therapeutic strategies aimed at correcting the injury-repair imbalance axis to provide new directions for the prevention and treatment of CaOx nephrolithiasis.

PMID 42928125
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