DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for coenzyme Q10 deficiency — screening already-approved drugs against its 7-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleCoenzyme Q10 deficiency maps to a 7-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 coenzyme q10 deficiency 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
coenzyme Q9 (COQ9) — COQ9 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 pefdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6AWL · 2.0 Å · ligand DI-PALMITOYL-3-SN-PHOSPHATIDYLETHANOLAMINE (PEF). Experimental structure, not a prediction.
What the evidence adds up to
Primary coenzyme Q10 deficiency results from mutations in at least ten genes involved in the CoQ10 biosynthetic pathway. Patients may respond well to oral CoQ10 supplementation, but only if the condition is recognised early, before irreversible tissue damage has occurred. A 2023 review of clinical studies up to March of that year attempted to resolve disparities between previous review articles regarding the usefulness of CoQ10 supplementation in these disorders, and highlighted unresolved issues that require further research.
CoQ10 deficiency has been implicated in the pathogenesis of a wide range of disorders, and is broadly divided into primary and secondary types. The compound has vital functions in all cells, including mitochondrial oxidative phosphorylation, acting as a lipid soluble antioxidant, and playing roles in fatty acid beta-oxidation, pyrimidine and lysosomal metabolism, and gene expression. A 2018 review analysed the role of CoQ10 in hypertension, ischemic heart disease, myocardial infarction, heart failure, viral myocarditis, cardiomyopathies, cardiac toxicity, dyslipidemia, obesity, type 2 diabetes mellitus, and metabolic syndrome.
A 2013 overview described CoQ10 as a vitamin-like substance that supplies all cells with energy, noting that tissues with high energy requirements, such as the heart, are particularly dependent on maintaining an adequate supply. Deficiency of CoQ10 was identified as a risk factor for cardiovascular and neurological diseases. The review focused on CoQ10's role in the prevention and treatment of cardiovascular disorders.
What is still missing is systematic clinical trial data for primary CoQ10 deficiency that resolves the disparities between existing reviews, and evidence on optimal timing of supplementation to prevent irreversible damage. The 2023 review explicitly identified unresolved issues requiring further research, but did not specify what funding or trial designs would be needed to address them. No patient stratification strategy has been validated for primary CoQ10 deficiency.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Current Cardiology Reviews · 2018 · 179 citations · open access
Coenzyme Q10 in Cardiovascular and Metabolic Diseases: Current State of the Problem
AbstractThe burden of cardiovascular and metabolic diseases is increasing with every year. Although the management of these conditions has improved greatly over the years, it is still far from perfect. With all of this in mind, there is a need for new methods of prophylaxis and treatment. Coenzyme Q10 (CoQ10) is an essential compound of the human body. There is growing evidence that CoQ10 is tightly linked to cardiometabolic disorders. Its supplementation can be useful in a variety of chronic and acute disorders. This review analyses the role of CoQ10 in hypertension, ischemic heart disease, myocardial infarction, heart failure, viral myocarditis, cardiomyopathies, cardiac toxicity, dyslipidemia, obesity, type 2 diabetes mellitus, metabolic syndrome, cardiac procedures and resuscitation. Keywords: Coenzyme Q10, hypertension, ischemic heart disease, myocardial infarction, heart failure, viral myocarditis, cardiomyopathies, cardiac toxicity, dyslipidemia, obesity, type 2 diabetes mellitus, metabolic syndrome, cardiac procedures and resuscitation.
AbstractCoenzyme Q10 (CoQ10) has a number of vital functions in all cells, both mitochondrial and extra-mitochondrial. In addition to its key role in mitochondrial oxidative phosphorylation, CoQ10 serves as a lipid soluble antioxidant and plays an important role in fatty acid beta-oxidation and pyrimidine and lysosomal metabolism, as well as directly mediating the expression of a number of genes, including those involved in inflammation. Due to the multiplicity of roles in cell function, it is not surprising that a deficiency in CoQ10 has been implicated in the pathogenesis of a wide range of disorders. CoQ10 deficiency is broadly divided into primary and secondary types. Primary CoQ10 deficiency results from mutations in genes involved in the CoQ10 biosynthetic pathway. In man, at least 10 genes are required for the biosynthesis of functional CoQ10, a mutation in any one of which can result in a deficit in CoQ10 status. Patients may respond well to oral CoQ10 supplementation, although the condition must be recognised sufficiently early, before irreversible tissue damage has occurred. In this article, we have reviewed clinical studies (up to March 2023) relating to the identification of these deficiencies, and the therapeutic outcomes of CoQ10 supplementation; we have attempted to resolve the disparities between previous review articles regarding the usefulness or otherwise of CoQ10 supplementation in these disorders. In addition, we have highlighted several of the potential problems relating to CoQ10 supplementation in primary CoQ10 deficiency, as well as identifying unresolved issues relating to these disorders that require further research.
British Journal of Cardiac Nursing · 2013 · 3 citations
The pharmacology of coenzyme Q<sub>10</sub>: its relevance to health
AbstractCoenzyme Q 10 (CoQ 10 ) is a vitamin-like substance that plays a key role in the metabolic process, supplying all cells with energy. Tissues with a high energy requirement, such as the heart, are particularly dependent on maintaining an adequate supply of CoQ 10 for normal functioning. Deficiency of CoQ 10 has been identified as a risk factor for a variety of disorders, including cardiovascular and neurological diseases. The objective of this article is therefore to provide a brief overview of the pharmacology of CoQ 10 , with particular emphasis on its role in the prevention and treatment of cardiovascular disorders.
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.
