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calcium hopantothenate (Hopate / hopantenate calcium)

✓ Approved

Mitsubishi Tanabe Pharma Corporation · Small Molecule · Small Molecule

What is calcium hopantothenate?

calcium hopantothenate is a small molecule developed by Mitsubishi Tanabe Pharma Corporation. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesHopate, hopantenate calcium
CompanyMitsubishi Tanabe Pharma Corporation
Drug ClassSmall Molecule
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Mitsubishi Tanabe Pharma Corporation

Therapeutic Indications

calcium hopantothenate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Psychiatric disordersAttention deficit hyperactivity disorder✓ Approved

Related Research Articles

PubMedFoods (Basel, Switzerland)2026-10-16

Moringa oleifera Lam. Leaf Peptide-Calcium Chelates: Structural Characterization, Stability and Calcium Absorption-Promoting Transport Capability.

Gu Ruijing R, Wang Xinyu X, Wang Zilin Z, Zhou Yu Y et al.

A novel calcium-chelating peptide, KTFQGPPHG, was identified and screened from Moringa oleifera Lam. leaf protein hydrolysate, and further used to prepare a highly stable peptide-calcium chelate (KTFQGPPHG-Ca). The structure of KTFQGPPHG-Ca was characterized, while assessing its chelation stability and calcium transport potential. It was found that the calcium binding capacity of KTFQGPPHG reached 62.401 µg/mg. After chelation with calcium, KTFQGPPHG transitioned from an amorphous structure to a stable crystalline form. Carboxyl oxygen atoms and amino nitrogen atoms on KTFQGPPHG served as binding sites for Ca2+. The KTFQGPPHG-Ca demonstrates excellent phosphate stability and thermal stability. In addition, the calcium transport amount of KTFQGPPHG at 30 min and 60 min was significantly higher than that of the CaCl2 group (p < 0.05). Particularly, the calcium transport capacity at 30 min was 1.40-fold that of the CaCl2 group. KTFQGPPHG effectively counteracted the suppressive impact of dietary factors on Ca2+ absorption, and likely promoted Ca2+ translocation via the TRPV6 calcium channel pathway. The present results offer a theoretical basis for KTFQGPPHG-Ca to serve as a promising calcium source to improve intestinal calcium absorption.

PMID 42883604
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PubMedDiagnostics (Basel, Switzerland)2026-10-16

Effects of Dialysate Calcium Concentration on Bone, Mineral Metabolism, and Vascular Outcomes in Maintenance Hemodialysis: A Systematic Review and Meta-Analysis.

Alabid Ibrahim I, Alghoul Wasim Iyad Ibrahim WII, Abedi Malak M, El-Tanani Mohamed M et al.

Background/Objectives: The optimal dialysate calcium concentration in maintenance hemodialysis remains uncertain because reducing calcium exposure may limit calcium loading but can also stimulate parathyroid hormone secretion and impair intradialytic cardiovascular stability. We evaluated randomized evidence across bone, mineral metabolism, vascular, and acute safety outcomes. Methods: PubMed, the Cochrane Central Register of Controlled Trials (CENTRAL), and Scopus were searched from database inception through 10 July 2026, with targeted citation and publication-status updating through 1 August 2026. Randomized parallel, crossover, factorial, and multi-period trials comparing dialysate calcium concentrations in adults receiving hemodialysis or hemodiafiltration were eligible. Acute and chronic outcomes were analyzed separately. Pooled estimates used inverse-variance random-effects models with DerSimonian-Laird estimation and modified Hartung-Knapp confidence intervals. Results: Twenty-four randomized parent trials were included. Lower dialysate calcium reduced end-of-dialysis ionized calcium (paired mean difference, -0.193 mmol/L; 95% CI, -0.258 to -0.128), with substantial heterogeneity. Point estimates for chronic parathyroid hormone and total alkaline phosphatase were higher and serum calcium lower, but all confidence intervals crossed the null. No clear effects were demonstrated for phosphate, calcium-phosphate product, lumbar bone mineral density, coronary artery calcification, or carotid intima-media thickness. Acute parathyroid hormone, blood pressure, calcium-balance, and QTc estimates suggested greater parathyroid stimulation, lower hemodynamic measures, less calcium gain, and longer QTc with lower calcium, but were imprecise. Adverse events were unsuitable for pooling. Conclusions: Lower dialysate calcium consistently lowers postdialysis ionized calcium, but its long-term skeletal and vascular effects remain uncertain. No single concentration appears universally optimal; prescription should be individualized according to mineral metabolism phenotype, cardiovascular tolerance, dialysis modality, and concomitant therapy.

PMID 42882336
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PubMedJACC. Case reports2026-10-16

Optical Coherence Tomography-Guided Calcium Modification for a Complex Calcified Nodule With Circumferential Calcium: From Debulking to Fracturing.

Liu Xiaochen X, Zhang Mingrui M, Wang Liang L, Wang Ning N et al.

The study objective was to describe an optical coherence tomography (OCT)-guided strategy for stepwise calcium modification in a large protruding calcified nodule with circumferential calcium. Rotational atherectomy was used to establish device crossability and modify superficial calcium. Serial OCT was performed to assess residual calcified nodule protrusion, circumferential calcium, lumen gain, and calcium fracture. When crossability was restored but substantial mechanical constraint persisted, the strategy was escalated to intravascular lithotripsy, followed by cutting-balloon dilation. Final OCT was used to confirm stent expansion and apposition. Restoration of device crossability does not necessarily indicate adequate lesion preparation, whereas excessive burr escalation may increase procedural risk. Serial OCT should be used to assess the response to each modification step and guide timely strategy escalation. OCT assessment may guide precise calcium modification and prevent stent underexpansion in complex calcified lesions.

PMID 42886141
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PubMedNutrients2026-10-16

Dietary Calcium Intake in Patients Evaluated for Bone Fragility, with a Focus on Women Receiving Adjuvant Endocrine Therapy for Breast Cancer: A Single-Center Cross-Sectional Study.

Firmani Francesca F, Ciarloni Alessandro A, Sabatelli Sofia S, Gianfelice Claudio C et al.

Background/Objectives: Adequate dietary calcium intake is essential for bone health. Despite this, calcium intake is still insufficient in many countries of the world. The study aims to provide information about dietary calcium intake of specific populations with bone fragility, with a particular focus on patients at risk of secondary osteoporosis due to adjuvant endocrine therapy (AET) for breast cancer (BC). Methods: Data from 132 patients referred for the first time to the Osteoporosis and Bone Metabolism Diseases outpatient clinic of the Division of Endocrinology of the Azienda Ospedaliero-Universitaria delle Marche (Ancona, Italy) were collected. Dietary calcium intake was assessed with a 7-day food frequency questionnaire; biochemical and densitometric parameters, osteoporosis etiology, and previous fragility fractures were also reported. Results: Patients were predominantly postmenopausal women, with severe osteoporosis (43.2%) or at risk of secondary osteoporosis (40.9%); 64.8% of patients evaluated for secondary osteoporosis were women on AET for BC. Total mean dietary calcium intake was 959 ± 396 mg/day. A lower intake was observed in younger patients with postmenopausal osteoporosis (848 ± 471 mg/day, p = 0.03). Patients with normal bone mineral density (631 ± 131 mg/day), without fragility fractures (906 ± 361), and evaluated for secondary osteoporosis (900 ± 364 mg/day) tended to have lower mean dietary calcium intake although without reaching statistical significance. Mean calcium intake was also lower than the recommended threshold in women on AET for BC (854 ± 345 mg/day). Conclusions: Patients with bone fragility should be more encouraged to increase their dietary calcium intake. Attention must be paid to women with BC on AET, who have high fracture risk and should not be discouraged a priori from consuming selected dairy products (low-fat and fermented ones) and alternative calcium dietary sources.

PMID 42884689
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PubMedInternational journal of molecular sciences2026-10-16

Gamma-Oryzanol Solid Dispersion Attenuates Dexamethasone-Induced Depressive-like Behaviors in Rats Associated with Calbindin-1 and Calcium Signaling.

Kesyou Siripaporn S, Tiyaboonchai Waree W, Roboon Jureepon J, Kaewman Paweena P et al.

Depression is associated with dysfunction of the hypothalamic-pituitary-adrenal axis, neurotransmitter imbalance, and calcium signaling deficits. Although gamma-oryzanol (GO) has shown antidepressant effects, its underlying molecular mechanism remains elusive, while its poor aqueous solubility limits its nutraceutical application. To overcome this obstacle, we successfully developed GO solid dispersion (GOSD) with enhanced water solubility for nutraceutical formulations. This study examined the antidepressant effect of GOSD in dexamethasone (Dx)-induced depressive-like behaviors in rats using behavioral tests, including the sucrose preference test and forced-swimming test (FST). The Dx group showed a reduction in sucrose consumption and mobility time in the FST compared with controls, both of which improved following GOSD administration. Proteomics revealed changes associated with the calcium signaling pathway. Calbindin (Calb1) expression was reduced in the Dx group, whereas GOSD administration restored Calb1 levels. Given the role of Calb1, a calcium-binding protein (CBP) involved in intracellular calcium buffering, reduced Calb1 expression in the Dx group may contribute to calcium signaling dysregulation. In contrast, GOSD can attenuate Calb1 levels, which potentially contribute to its antidepressant effects. These findings suggest that the antidepressant-like effects of GOSD may involve modulation of calcium homeostasis, supporting its potential as a complementary intervention for Dx-induced depressive-like behaviors.

PMID 42883962
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PubMedJACC. Cardiovascular imaging2026-10-16

Calcium Density as a Marker of Coronary Plaque Stabilization in Primary Prevention: The CAUGHT-CAD Trial.

Vasanthakumar Sheran A SA, Nicholls Stephen J SJ, Nerlekar Nitesh N, Marwick Thomas H TH et al.

Despite primary prevention statin treatment, a substantial proportion of individuals remain at residual risk for cardiovascular events. Coronary computed tomographic angiography (CTA) enables the quantification of compositional changes in calcified plaque. The aim of this study was to examine whether increases in coronary calcified plaque volume and density associated with statin therapy could be used as a marker of plaque stabilization in asymptomatic individuals undergoing serial coronary CTA. In the CAUGHT-CAD trial, asymptomatic, statin-naive, intermediate-risk individuals were randomized to a primary prevention strategy (including statin treatment) vs usual care. Participants underwent coronary CTA at baseline and 3 years. In this post hoc analysis, volumes of 5 plaque subtypes were quantified: noncalcified (≤350 HU), low-density calcium (351-500 HU), intermediate-density calcium (501-700 HU), high-density calcium (701-1000 HU), and very high density calcium (>1,000 HU). The primary outcome was the per-lesion level change in volumes of calcified plaque subtypes. Eight hundred forty lesions were included from 338 participants (mean age: 58.3 ± 6.9 years, 57.1% men, 161 [47.6%] statin treated). Statin treatment was associated with greater progression in intermediate-density (β = 0.89, SE = 0.39; P = 0.02) and high-density (β = 0.79, SE = 0.24; P = 0.001) calcium, alongside regression of noncalcified plaque (β = -9.83, SE = 1.64; P < 0.001), following adjustment for cardiovascular risk factors, low-density lipoprotein cholesterol (LDL-C) level, and baseline plaque volume. Among statin-treated participants, LDL-C reduction ≥30% was associated with greater progression of high-density (β = 1.11, SE = 0.49; P = 0.03) and very high density (β = 1.68, SE = 0.85; P = 0.04) calcium. In asymptomatic, intermediate-risk individuals, statin treatment was associated with a shift toward higher density calcium within coronary plaques, most marked with effective lowering of LDL-C. (Coronary Artery Calcium Score: Use to Guide Management of Hereditary Coronary Artery Disease [CAUGHT-CAD]; ACTRN12614001294640).

PMID 42886154
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