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calcium carbonate + vitamin D3 (Ideos)

✓ Approved

Innothera · VDR · 小分子

什么是 calcium carbonate + vitamin D3？

calcium carbonate + vitamin D3 是一种小分子，由Innothera研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Ideos
公司Innothera
药物类别小分子
分子靶点VDR
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Innothera

作用机制

分子靶点

calcium carbonate + vitamin D3 作用于 1 个分子靶点：

VDRvitamin D receptor (NR1I1, PPP1R163)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

calcium carbonate + vitamin D3 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
Musculoskeletal and connective tissue disordersOsteoporosis✓ Approved

相关研究文献

PubMedMetabolites2026-10-27

Linking Stone Mineral Composition to 24-Hour Urinary Metabolic Profiles: An Episode-Based Cohort Study.

Sun Shiwei S, Liu Jiang J, Qiao Yi Y, Wang Dong D et al.

Stone composition reflects the urinary environment in which calculi form, whereas 24 h urine testing identifies modifiable lithogenic abnormalities. This study examined component-specific urinary metabolic profiles and evaluated whether routine clinical and urinary variables could distinguish common stone minerals. This retrospective study included 256 patients undergoing 297 stone surgeries, consolidated into 256 treatment episodes. Fourier-transform infrared spectroscopy identified stone minerals, which were linked to preoperative 24 h urine profiles. Calcium oxalate monohydrate (COM), calcium oxalate dihydrate (COD), carbonate apatite, and anhydrous uric acid were evaluated using multivariable logistic regression. Mutually exclusive calcium oxalate-calcium phosphate phenotypes, nested cross-validated prediction models, and unsupervised clustering were also examined. COM, COD, carbonate apatite, and anhydrous uric acid were present in 78.5%, 73.0%, 39.5%, and 9.8% of episodes, respectively. Higher urine pH was associated with carbonate apatite (odds ratio [OR] per standard deviation, 1.78; 95% confidence interval [CI], 1.33-2.38), whereas lower pH was associated with anhydrous uric acid (OR, 0.26; 95% CI, 0.11-0.58). Higher urinary citrate was associated with COM, but phenotype analysis showed that hypocitraturia increased from 45.3% in calcium oxalate-only episodes to 60.7% in mixed calcium oxalate-calcium phosphate episodes and 89.5% in calcium phosphate episodes without calcium oxalate. Lower urine volume was associated with COD. Cross-validated areas under the curve ranged from 0.654 to 0.712, and metabolic clusters showed substantial mineral overlap. Urine pH provided the clearest component-specific signal, whereas citrate associations depended on accompanying minerals. Routine 24 h urine testing complemented but did not replace direct stone analysis.

PMID 42941187
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PubMedJournal of clinical medicine2026-10-27

Serum sLOX-1 and 25-Hydroxyvitamin D3 Across the Glycemic Spectrum: Associations with Metabolic and Microvascular Parameters in Prediabetes and Type 2 Diabetes.

Alagoz Maide Hacer MH, Adas Mine M, Gokden Yasemin Y, Guntas Gulcan G

Background/Objectives: Oxidative endothelial injury and vitamin D deficiency have independently been implicated in diabetic vascular complications, yet their distribution across the glycemic spectrum, from normoglycemia through prediabetes to established type 2 diabetes, has not been systematically characterised. This study aimed to evaluate serum soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) and 25-hydroxyvitamin D3 [25(OH)D3] levels across the glycemic spectrum and to examine their associations with microvascular complications and metabolic parameters in prediabetic individuals and patients with type 2 diabetes mellitus (T2DM). Methods: In this prospectively recruited cross-sectional study, 80 adults were enrolled: 26 healthy controls, 27 prediabetic individuals, and 27 T2DM patients. Serum sLOX-1 was quantified by enzyme-linked immunosorbent assay (ELISA) and 25(OH)D3 by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Between-group comparisons were performed using the Kruskal-Wallis test with Dunn's post hoc correction. Spearman's rank correlation and binary logistic regression were applied to examine associations with metabolic and microvascular parameters. Results: Serum sLOX-1 was significantly elevated in both prediabetic (median 10.75 ng/mL; p = 0.0397) and T2DM (8.83 ng/mL; p = 0.0209) groups compared to controls (3.50 ng/mL) in unadjusted analyses. After adjustment for age and body mass index (BMI) by quantile regression, the elevation persisted in the prediabetic group (adjusted ratio of medians = 2.91, p = 0.040) but was substantially attenuated and no longer significant in the T2DM group (ratio = 1.81, p = 0.265). Serum 25(OH)D3 was significantly lower in the T2DM group than in prediabetic individuals (12.11 vs. 22.69 ng/mL; p = 0.0024) but did not decline progressively across the glycemic spectrum; vitamin D deficiency (<20 ng/mL) was present in 78% of T2DM patients. In binary logistic regression (five predictors, events per variable (EPV) = 5.4), 25(OH)D3 (odds ratio (OR) = 0.922, p = 0.020) and log-transformed urinary albumin-to-creatinine ratio (logUACR; OR = 4.014, p = 0.001) were independently associated with T2DM status after adjustment for age and waist circumference, while sLOX-1 was not significant (OR = 1.058, p = 0.136). In unadjusted analyses, sLOX-1 correlated positively with waist circumference and glycated hemoglobin (HbA1c); both associations were no longer statistically significant after age adjustment. Conclusions: These findings show that sLOX-1 is elevated at the prediabetic stage independently of age and BMI, whereas the elevation in established T2DM was not robust to covariate adjustment. Lower 25(OH)D3 concentrations were associated with T2DM status in logistic regression, but this association was not significant when the reference group was restricted to normoglycaemic controls, indicating that the finding reflects the contrast between T2DM and prediabetic groups rather than a generalised pattern across the glycaemic spectrum. The two biomarkers were not significantly correlated with one another. Given the cross-sectional design, low EPV, and exploratory nature of all analyses, prospective validation in larger age-matched cohorts is required.

PMID 42941502
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PubMedNutrients2026-10-27

Cord Blood 3-Epi-25-Hydroxyvitamin D3 and Autism-Related Cognitive Traits at Age 10 Years: An Exploratory Secondary Analysis of the KLOTHO Birth Cohort.

Karras Spyridon N SN, Goulis Dimitrios G DG, Dalamaga Maria M, Kypraiou Maria M et al.

The C3 epimer of 25-hydroxyvitamin D3 [3-epi-25(OH)D3] can be measured in maternal and umbilical cord circulation, but whether it is related to later neurodevelopment is unknown. To explore associations between cord 3-epi-25(OH)D3 and parent-reported autism-related trait domains at 10 years in the KLOTHO birth cohort. This secondary analysis used prospectively collected perinatal samples and 10-year questionnaire data. Vitamin D metabolites were quantified by liquid chromatography-tandem mass spectrometry with epimer separation. The Australian Scale for Asperger's Syndrome was used dimensionally, not diagnostically. Spearman correlations, false-discovery-rate (FDR) correction across 13 unique bivariate comparisons, supportive linear regressions, sex-stratified analyses, and a stricter record-linkage sensitivity analysis were conducted. Data were available for 87 offspring (41 boys and 46 girls). Cord 3-epi-25(OH)D3 was inversely associated with cognitive-domain score (Spearman ρ = -0.412; p < 0.001; Benjamini-Hochberg q = 0.001). The crude regression estimate was also inverse (B = -0.285; 95% CI, -0.458 to -0.112; p = 0.002), but the association attenuated after covariate adjustment and all adjusted confidence intervals included the null. A stricter linkage analysis remained significant (n = 84; ρ = -0.350; p = 0.001). The correlation was numerically stronger in boys than girls, but the between-sex comparison was not significant (p = 0.075). A positive correlation was also observed for social and emotional traits (ρ = 0.302; q = 0.023), indicating inconsistent directions across domains; the tertile analysis was non-significant. Cord 3-epi-25(OH)D3 was associated with lower cognitive-domain scores in unadjusted rank analyses, but the lack of stable adjusted linear evidence, inconsistent domain pattern, and small sample restrict interpretation. These findings are hypothesis-generating and do not imply causality, sex-specific effects, or clinical utility.

PMID 42942932
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PubMedNutrients2026-10-27

Role of Osteocalcin in the Regulation of Glucose Metabolism in Children and Adolescents with Obesity.

Sbilordo Serena S, Drago Selene Francesca Anna SFA, Catalano Antonino A, Zirilli Giuseppina G et al.

Osteocalcin (OC) is a bone-derived hormone increasingly implicated in glucose and lipid metabolism. Although its metabolic role has been extensively investigated in adults, evidence in pediatric populations remains limited. This exploratory study aimed to evaluate the relationship between serum OC levels and glucose metabolism in children and adolescents with obesity. A single-center, retrospective study was conducted in a cohort of pediatric patients with essential obesity. Auxological and biochemical parameters were assessed, including fasting glucose, insulin, lipid profile, liver enzymes, thyroid function, calcium-phosphorus metabolism, vitamin D3, parathormone (PTH), C-terminal telopeptide of type I collagen (CTX), and OC. Insulin resistance was evaluated using the HOMA-IR index (>2.5 considered positive). Correlation analyses were performed to assess the associations between serum OC levels and metabolic, biochemical, and clinical parameters. Twenty-two of 33 patients (66.7%) had insulin resistance (HOMA-IR > 2.5) despite preserved glucose tolerance. Mean fasting glucose was 88.1 ± 10.83 mg/dL, fasting insulin 24.9 ± 13 μU/mL, and mean serum OC 112.1 ± 56.1 ng/mL. Serum OC levels were positively correlated with fasting insulin (r = 0.41, p = 0.023) and HOMA-IR (r = 0.46, p = 0.013). In children with obesity and preserved glucose tolerance, higher serum OC levels were associated with insulin resistance. Further studies in larger pediatric cohorts are needed to clarify this association and evaluate the potential role of OC as a biomarker of early metabolic dysregulation.

PMID 42942989
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PubMedBiomolecules2026-10-27

Vitamin D-VDR Signaling Across Thyroid Disorders: A Systematic Review of Molecular Mechanisms, Autoimmunity, Genetic Susceptibility, Experimental Evidence and Therapeutic Translation.

Satyam Shakta Mani SM, Paryani Murk Jai Pal MJP, Shameer Ilmia I, Al-Dawoodi Shams S et al.

Vitamin D-Vitamin D receptor (VDR) signaling extends beyond calcium-phosphate homeostasis and regulates immune tolerance, inflammation, cellular differentiation, oxidative stress, and endocrine physiology. This systematic review evaluated the relationship between vitamin D-VDR signaling and thyroid disorders, including hypothyroidism, hyperthyroidism, Hashimoto's thyroiditis, Graves' disease, thyroid autoimmunity, genetic susceptibility, experimental mechanisms, and therapeutic implications. This study was conducted and reported in accordance with the PRISMA 2020 statement. PubMed/MEDLINE and Scopus were searched for studies published from January 2005 through June 2026, supplemented by backward and forward citation screening of relevant studies and reviews. Eligible evidence included human observational and interventional studies, genetic investigations, and relevant animal and in vitro studies addressing vitamin D status, vitamin D exposure or supplementation, VDR variation, vitamin D metabolism, or vitamin D-VDR mechanisms in relation to thyroid function, thyroid disease, thyroid autoantibodies, or related biological outcomes. A total of 13,623 records were identified, of which 11,730 unique records underwent title and abstract screening, 449 reports were assessed at the full-text stage, and 118 primary studies were included in the final synthesis. Because of substantial heterogeneity in populations, study designs, vitamin D exposures, outcomes, genetic backgrounds, and experimental models, findings were synthesized narratively rather than by quantitative meta-analysis. Lower circulating 25-hydroxyvitamin D [25(OH)D] concentrations were frequently associated with thyroid disease, particularly autoimmune phenotypes, and increased thyroid peroxidase and thyroglobulin antibodies in Hashimoto's thyroiditis. Interventional evidence suggests that vitamin D supplementation may reduce thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) concentrations in some patients with autoimmune thyroid disease. However, these laboratory changes represent immunological surrogate outcomes and should not be interpreted as evidence of restored thyroid function, prevention of progression to overt hypothyroidism, reduced dependence on thyroid hormone replacement, or sustained clinical remission. Randomized evidence does not establish a general preventive effect of vitamin D supplementation on incident hypothyroidism. Associations between VDR polymorphisms, including FokI/rs2228570, rs1544410, rs731236, and rs7975232, and thyroid autoimmunity were inconsistent across populations. Experimental evidence implicates immune regulation, Th17/Treg balance, inflammatory signaling, vitamin D metabolism, and calcium-phosphate homeostasis. The evidence was limited by substantial clinical, methodological, and biological heterogeneity, frequent reliance on observational studies, population-specific genetic findings, and differences between experimental models and human thyroid physiology. Overall, vitamin D-VDR signaling represents a biologically plausible modifier of thyroid disease, but current evidence does not establish universal causality or therapeutic efficacy.

PMID 42939785
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PubMedInternational journal of molecular sciences2026-10-27

Vitamin D in Digestive Neoplasms: Molecular Mechanisms and Clinical Evidence.

Treteanu Andreea-Ramona AR, Stănescu Ana Maria Alexandra AMA, Constantinescu Alexandru A, Băjenaru Ovidiu Lucian OL et al.

Digestive neoplasms represent a major global health burden, accounting for a substantial proportion of cancer incidence and mortality. Increasing attention has been directed toward modifiable factors that may influence both the onset and progression of these malignancies. Among them, vitamin D has emerged as a potential protective factor, with deficiency frequently associated with elevated risk and unfavorable prognosis in gastrointestinal cancers. This review critically examines the current evidence regarding the role of vitamin D and its receptor (VDR) in digestive tumorigenesis. Beyond its classical function in calcium and bone homeostasis, vitamin D exerts pleiotropic effects on cellular processes fundamental to carcinogenesis, including regulation of proliferation, differentiation, apoptosis, angiogenesis, immune modulation and genomic stability. Experimental studies demonstrate that adequate vitamin D status or administration of its analogues may suppress tumor growth and enhance responsiveness to conventional therapies. Epidemiological and clinical data, however, remain inconsistent across cancer subtypes, geographic populations and methods of vitamin D assessment. The analysis underscores the need for standardized evaluation of vitamin D levels, elucidation of dose-response relationships and clarification of interactions with genetic polymorphisms and environmental exposures. Future large-scale, randomized controlled trials are essential to establish causality and to define the optimal role of vitamin D in prevention and treatment strategies. Taken together, current findings support the hypothesis that vitamin D may serve not only as a biomarker of prognosis but also as a promising adjunctive approach in the management of digestive neoplasms.

PMID 42942110
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