DeCure's autonomous Metabolic AI scientist is researching a drug-repurposing hypothesis for vitamin metabolic disorder — screening already-approved drugs against its 2-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleVitamin metabolic disorder maps to a 2-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for vitamin metabolic disorder is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
What the evidence adds up to
A 2014 dose-response meta-analysis of observational studies found that each 25 nmol/L increase in blood 25-hydroxyvitamin D was associated with a pooled odds ratio for metabolic syndrome of 0.87 (95% CI 0.83–0.92) across 16 cross-sectional studies, but a null result (OR 1.00, 95% CI 0.98–1.02) in two longitudinal cohort and nested case-control studies. The authors concluded that the association seen in cross-sectional data was not confirmed in longitudinal studies, and that randomised trials are needed to establish causality.
A 2015 propensity-score matched cohort study of 335 nonalcoholic fatty liver disease patients with metabolic syndrome in South Korea compared 58 patients who received vitamin E with 58 matched controls. After six months, mean ALT levels decreased significantly in the vitamin E group compared with controls (P < 0.01), but changes in body weight, lipids, and glucose did not differ between groups. The study reported a short-term effect on a liver enzyme without corresponding improvement in metabolic profiles.
A 2025 systematic review and meta-analysis of vitamin interventions in autism spectrum disorder and attention-deficit/hyperactivity disorder reported that vitamin supplementation improved symptoms overall, but effects varied by vitamin type and disorder. Vitamin B supplementation was associated with reduced ASD-related symptoms, while vitamin D supplementation showed greater efficacy for ADHD symptoms. The review did not provide specific effect sizes, sample sizes, or numbers of studies included for each comparison.
What remains missing are randomised controlled trials that test vitamin D supplementation for preventing metabolic syndrome in the general population, longer-term data on whether vitamin E’s ALT reduction in NAFLD translates to histological or clinical outcomes, and adequately powered, blinded trials in ASD and ADHD that report standardised effect sizes and account for baseline vitamin status, dietary intake, and genetic variation in vitamin metabolism.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
The Journal of Clinical Endocrinology & Metabolism · 2014 · 123 citations
Blood Vitamin D Status and Metabolic Syndrome in the General Adult Population: A Dose-Response Meta-Analysis
AbstractCONTEXT: Increasing evidence has suggested an association between blood vitamin D levels and metabolic syndrome. OBJECTIVE: Our objective was to determine the relationship between blood vitamin D status and metabolic syndrome in the general adult population, using a dose-response meta-analysis. DATA SOURCE: We searched the PubMed, EMBASE, Web of Science, and Cochrane Library databases through July 2013 to identify relevant studies. STUDY SELECTION: Observational studies, reporting risk ratios with a 95% confidence interval (CI) for metabolic syndrome in ≥3 categories of blood 25-hydroxyvitamin D [25(OH)D] levels, were selected. DATA EXTRACTION: Data extraction was performed independently by 2 authors, and the quality of the studies was evaluated using the risk of bias assessment tool for nonrandomized studies. DATA SYNTHESIS: The pooled odds ratio of metabolic syndrome per 25 nmol/L increment in the serum/plasma 25(OH)D concentration was 0.87 (95% CI = 0.83-0.92, I(2) = 85%), based on 16 "cross-sectional studies" and 1.00 (95% CI = 0.98-1.02, I(2) = 0%) for 2 "cohort and nested case-control studies." The dose-response meta-analysis showed a generally linear, inverse relationship between 25(OH)D levels and metabolic syndrome in the cross-sectional studies (P for linear trend < .001). CONCLUSIONS: Blood vitamin D levels were associated with a risk of metabolic syndrome in cross-sectional studies but not in longitudinal studies. Randomized, clinical trials will be necessary to address the issue of causality and to determine whether vitamin D supplementation is effective for the prevention of metabolic syndrome.
Vitamin D intoxication causes hypercalcaemia by increased bone resorption which responds to pamidronate
AbstractOBJECTIVE: Vitamin D intoxication is a relatively rare but treatable cause of hypercalcaemia. In the past this has been undertaken using corticosteroids. Previous observations have suggested that there is increased bone resorption in hypervitaminosis D. If this were to be the case, specific inhibitors of bone resorption might provide more effective treatment. We have therefore studied the mechanisms of hypercalcaemia and response to therapy in a group of patients with vitamin D intoxication. DESIGN: Vitamin D metabolites were measured in six patients with vitamin D intoxication; in five of these the components of hypercalcaemia were calculated. These measurements were repeated following treatment with corticosteroids (two patients) or the bisphosphonate, pamidronate (three patients). RESULTS: In each case the serum 25-hydroxyvitamin D was grossly elevated and there was a more modest elevation in serum 1,25-dihydroxyvitamin D. The components of hypercalcaemia suggest that there was a significant degree of bone resorption in all six patients and that this is the major determinant of hypercalcaemia. Pamidronate treatment resulted in a brisk reduction in plasma calcium concentration. Following corticosteroids the return of calcium to normal was more delayed. CONCLUSION: The hypercalcaemia of vitamin D intoxication is mediated by increased bone resorption and bisphosphonates have a role in its management.
Clinical and Molecular Hepatology · 2015 · 23 citations · open access
Effect of vitamin E in nonalcoholic fatty liver disease with metabolic syndrome: A propensity score-matched cohort study
AbstractBACKGROUND/AIMS: Vitamin E improves the biochemical profiles and liver histology in nonalcoholic steatohepatitis, but the role of vitamin E is not clearly defined in the management of nonalcoholic fatty liver disease (NAFLD) which includes both simple steatosis and steatohepatitis. Co-morbid metabolic syndrome increases the probability of steatohepatitis in NAFLD. In this study, we aimed to determine the short-term effects of vitamin E and off-treatment durability of response in a propensity-score matched cohort of NAFLD patients with metabolic syndrome. METHODS: A retrospective cohort was constructed by retrieving 526 consecutive NAFLD patients from the electronic medical record data warehouse of a tertiary referral hospital in South Korea. Among them, 335 patients (63.7%) had metabolic syndrome and were eligible for vitamin E therapy. In order to assess the effect of vitamin E, propensity score matching was used by matching covariates between control patients (n=250) and patients who received vitamin E (n=85). RESULTS: The PS-matched vitamin E group (n=58) and control group (n=58) exhibited similar baseline metabolic profiles. After 6 months of vitamin E therapy, the mean ALT levels decreased significantly compared to PS-matched control (P<0.01). The changes in metabolic profiles (body weight, lipid and glucose levels) did not differ between control and vitamin E groups during the study period. CONCLUSIONS: Short-term vitamin E treatment significantly reduces ALT levels in NAFLD patients with metabolic syndrome, but metabolic profiles are not affected by vitamin E.
Annals of Clinical Microbiology and Antimicrobials · 2008 · 16 citations · open access
Osteomalacia in an HIV-infected man receiving rifabutin, a cytochrome P450 enzyme inducer: a case report
AbstractINTRODUCTION: People infected with human immunodeficiency virus are frequently treated with medications that can induce or inhibit cytochrome P450 enzymes. CASE PRESENTATION: A 59 year old man treated with zidovudine, lamivudine, indinavir, and ritonavir for infection with human immunodeficiency virus volunteered to take part in a study of bone loss. He was found to have vitamin D insufficiency with secondary hyperparathyroidism and received vitamin D and calcium supplementation. He suffered a recurrence of infection with Mycobacterium avium intracellulare for which he received treatment with ciprofloxacin, rifabutin, and ethambutol. Subsequently, he developed worsening vitamin D deficiency with hypocalcaemia, secondary hyperparathyroidism and elevated markers of bone turnover culminating in an osteomalacic vertebral fracture. Correction of the vitamin D deficiency required 100,000 IU of cholecalciferol monthly. Rifabutin is a cytochrome P450 inducer, and vitamin D and its metabolites are catabolised by cytochrome P450 enzymes. We therefore propose that treatment with rifabutin led to the induction of cytochrome P450 enzymes catabolising vitamin D, thereby causing vitamin D deficiency and osteomalacia. This process might be mediated through the steroid and xenobiotic receptor (SXR). CONCLUSION: Treatment with rifabutin induces the cytochrome P450 enzymes that metabolise vitamin D and patients treated with rifabutin might be at increased risk of vitamin D deficiency. In complex medication regimens involving agents that induce or inhibit cytochrome P450 enzmyes, consultation with a clinical pharmacist or pharmacologist may be helpful in predicting and/or preventing potentially harmful interactions.
Neuropsychiatric Disease and Treatment · 2025 · 2 citations · open access
Vitamin Interventions in ASD and ADHD: Systematic Review and Meta-Analysis
AbstractBackground: Vitamin interventions have emerged as a cost-effective and accessible approach to managing Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD), primarily for alleviating gastrointestinal symptoms such as constipation. Recent studies suggest vitamins may also improve core symptoms, yet most existing research focuses on comparisons between patients and healthy controls, lacking clinically relevant, evidence-based insights. Methods: A meta-analysis was conducted using studies retrieved from PubMed, Web of Science, and the Cochrane Library, focusing on vitamin interventions in ASD and ADHD populations. Results: The findings indicate that vitamin supplementation significantly improves symptoms in both ASD and ADHD. However, the effects vary by vitamin type and disorder. Vitamin B supplementation was particularly effective in reducing ASD-related symptoms, while vitamin D supplementation showed greater efficacy in improving ADHD symptoms. Conclusion: Different vitamins exert disorder-specific therapeutic effects, suggesting their potential role in guiding tailored clinical interventions for ASD and ADHD.
The American Journal of Emergency Medicine · 2006 · 0 citations
Un esponente dell'Opera dei Congressi milanese: il nobile Alberto de Mojana
AbstractMethylene blue is the first-choice treatment of methemoglobinemia, but it is not readily available in most Korean emergency departments because of an import suspension. An 84-year-old woman with dapsone-induced massive methemoglobinemia visited our emergency department for unclear mentality and cyanosis. Because methylene blue was not available, we intravenously administrated vitamin C (VC) for symptomatic methemoglobinemia, although VC is not a universally accepted treatment. Vitamin C (10 g intravenously) administered 6 hourly successfully treated the dapsone-induced methemoglobinemia and did not adversely affect renal functions. Thus,we recommend that if methylene blue is unavailable, 6 hourly intravenous administrations of 10 g of VC should be considered for dapsone-induced methemoglobinemia.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
