DeCure's autonomous Metabolic AI scientist is researching a drug-repurposing hypothesis for metabolic disease — screening already-approved drugs against its 43-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleMetabolic disease maps to a 43-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 metabolic disease 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.
Molecular view
lipoprotein(a) (LPA) — LPA is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet 2sdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8TCE · 1.07 Å · ligand (2S)-3-phenyl-2-[(3R)-pyrrolidin-3-yl]propanoic acid (HWF). Experimental structure, not a prediction.
What the evidence adds up to
A 1989 paper on investigating suspected inherited metabolic disease describes a multi-disciplinary approach and a standardised application form to collect clinical information. The authors argue that running a full metabolic investigation programme for every new patient is not feasible or efficient, and they propose selection criteria to decide which laboratory programme to perform. Diagnostic results from a two-year period are presented, but the abstract gives no specific numbers for detection rates or patient outcomes.
A 2020 thesis on hepatic lipid metabolism states that obesity has contributed to a rise in chronic metabolic disorders such as fatty liver disease and cardiovascular disease. The research focus was to identify new proteins and pathways that could be targeted by drug therapy or act as biomarkers. No drugs, clinical results, or patient data are reported in the abstract.
A 2024 paper defines metabolic disease as a disorder comprising insulin resistance, glucose intolerance, dyslipidemia, hypertension and obesity, particularly abdominal obesity. It notes that prevalence is increasing worldwide due to changes in diet and lifestyle, and that people with metabolic disease have a higher risk of developing diabetes and cardiovascular disease. No interventions, trials, or quantitative results are described.
What is still missing is any clinical trial data, any tested drug, any patient stratification strategy, and any funding for translational work that would move from identifying pathways to testing a repurposed compound in humans.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Cochrane Database of Systematic Reviews · 2021 · 12 citations · open access
Tyrosine supplementation for phenylketonuria
AbstractBACKGROUND: Phenylketonuria is an inherited disease for which the main treatment is the dietary restriction of the amino acid phenylalanine. The diet has to be initiated in the neonatal period to prevent or reduce mental handicap. However, the diet is very restrictive and unpalatable and can be difficult to follow. A deficiency of the amino acid tyrosine has been suggested as a cause of some of the neuropsychological problems exhibited in phenylketonuria. Therefore, this review aims to assess the efficacy of tyrosine supplementation for phenylketonuria. This is an update of previously published versions of this review. OBJECTIVES: To assess the effects of tyrosine supplementation alongside or instead of a phenylalanine-restricted diet for people with phenylketonuria, who commenced on diet at diagnosis and either continued on the diet or relaxed the diet later in life. To assess the evidence that tyrosine supplementation alongside, or instead of a phenylalanine-restricted diet improves intelligence, neuropsychological performance, growth and nutritional status, mortality rate and quality of life. SEARCH METHODS: We searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Trials Register which is comprised of references identified from comprehensive electronic database searches, handsearches of relevant journals and abstract books of conference proceedings. Additional studies were identified from handsearches of the Journal of Inherited Metabolic Disease (from inception in 1978 to 1998). The manufacturers of prescribable dietary products used in the treatment of phenylketonuria were also contacted for further references. Date of the most recent search of the Group's Inborn Errors of Metabolism Trials Register: 07 December 2020. SELECTION CRITERIA: All randomised or quasi-randomised trials investigating the use of tyrosine supplementation versus placebo in people with phenylketonuria in addition to, or instead of, a phenylalanine-restricted diet. People treated for maternal phenylketonuria were excluded. DATA COLLECTION AND ANALYSIS: Two authors independently assessed the trial eligibility, methodological quality and extracted the data. MAIN RESULTS: Six trials were found, of which three trials reporting the results of a total of 56 participants, were suitable for inclusion in the review. The blood tyrosine concentrations were significantly higher in the participants receiving tyrosine supplements than those in the placebo group, mean difference 23.46 (95% confidence interval 12.87 to 34.05). No significant differences were found between any of the other outcomes measured. The trials were assessed as having a low to moderate risk of bias across several domains. AUTHORS' CONCLUSIONS: From the available evidence no recommendations can be made about whether tyrosine supplementation should be introduced into routine clinical practice. Further randomised controlled studies are required to provide more evidence. However, given this is not an active area of research, we have no plans to update this review in the future.
Journal of Inherited Metabolic Disease · 1989 · 7 citations
A clinical biochemist's view of the investigation of suspected inherited metabolic disease
AbstractSummary The necessity for a multi‐disciplinary approach to the study of genetic disease is discussed. The progress of laboratory investigation programmes made it not feasible and inefficient to run a full metabolic investigation programme in every new patient suspected of inherited metabolic disease. An application form for metabolic investigation is described, which can be used to collect clinical information relevant to metabolic disease. On the basis of the patient's clinical information, selection criteria are given to decide which laboratory investigation programme has to be performed in the individual patient. A full metabolic laboratory investigation programme is described and illustrated with some examples of abnormal metabolite patterns. Diagnostic results over a 2‐year period are presented.
An Integrated Systems Biology Approach to the Discovery and Characterisation of Novel Regulators of Hepatic Lipid Metabolism
AbstractThe epidemic of obesity worldwide has contributed to the meteoric rise in the chronic metabolic disorders such as fatty liver disease and cardiovascular disease. Underlying these chronic conditions is a disruption to the metabolism of fat, which predominately occurs in the liver. Given this, the research focus of this thesis was to identify new proteins and pathways that have the potential to be targeted by drug therapy, or act as biomarkers of metabolic disease, through a cutting-edge discovery platform.
Zenodo (CERN European Organization for Nuclear Research) · 2024 · 0 citations · open access
Metabolic Disease Models
AbstractMetabolic disease is a disorder comprising insulin resistance, glucose intolerance, dyslipidemia, hypertension and obesity, in particular abdominal obesity. Metabolic disease is one of the most important challenges facing public health and biomedical research, the prevalence of which is increasing worldwide as a result of changes in diet and lifestyle. People with metabolic disease have a higher risk of developing diabetes and cardiovascular disease.
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.
