DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for erectile dysfunction — screening already-approved drugs against its 38-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleErectile dysfunction maps to a 38-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 erectile dysfunction 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
aldo-keto reductase family 1 member B (AKR1B1) — AKR1B1 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 ndpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 1US0 · 0.66 Å · ligand NADPH DIHYDRO-NICOTINAMIDE-ADENINE-DINUCLEOTIDE PHOSPHATE (NDP). Experimental structure, not a prediction.
What the evidence adds up to
Phosphodiesterase type 5 inhibitors are the largest segment of the erectile dysfunction market and are highly efficacious for many men, but a relatively large subset of patients do not respond to them. A 2004 study notes that moderate or severe erectile dysfunction occurs in up to 26% of the male population, and the percentage rises under conditions such as diabetes, hypertension, cardiovascular disease, depression, and renal or cancer disease. The same paper proposes analysing non-responders with respect to drug target mechanisms and suggests a rationale for PDE5 inhibitor combination therapy.
Emerging drugs under development for erectile dysfunction include compounds that act centrally, such as clavulanic acid, dopamine receptor agonists, and melanocortin receptor agonists, and peripherally acting agents including novel PDE5 inhibitors, soluble and particulate guanylyl cyclase activators, rho-kinase inhibitors, and maxi-K channel openers. A 2010 review expects that emerging drugs may allow treatment protocols tailored to individual patients, possibly including combinations of various emerging drugs to enhance efficacy in difficult-to-treat patients. No concrete response rates or survival data are reported for any of these compounds in the abstracts provided.
The molecular pathogenesis of erectile dysfunction is not known and may vary between different forms of the condition. A 2003 review notes that most knowledge of gene expression and penile erection has come from experimental models, and that altered expression or activities of smooth muscle regulatory components have been reported in ischaemic, diabetic, or ageing penile tissue. A 2023 chapter states that deficits in psychologic, neurologic, vascular, and endocrine function can all lead to erectile dysfunction, and that the condition is strongly associated with aging, comorbid conditions, poor lifestyle, and adverse cardiovascular health.
What is still missing are large population-based studies that could disclose whether particular gene mutations or variants predispose to erectile dysfunction, and integrated genetic, molecular, and functional investigations to identify targets for preventive or pharmacological measures. No trial data comparing any emerging drug against placebo or existing PDE5 inhibitors in non-responders are presented in these abstracts, and no patient stratification strategy has been validated in a clinical trial.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Expert Opinion on Emerging Drugs · 2010 · 93 citations
The future is today: emerging drugs for the treatment of erectile dysfunction
AbstractIMPORTANCE OF THE FIELD: Erectile dysfunction (ED) is the most common male sexual dysfunction presented for treatment affecting between 10 and 20% of men. PDE type 5 inhibitors (PDE5I) now account for the largest segment of the ED market. While these drugs are highly efficacious for many men, a relatively large subset of ED patients who do not respond to PDE5I is increasingly recognized. AREAS COVERED IN THIS REVIEW: In this review, we discuss clinical and preclinical evidence supporting various emerging compounds that regulate penile erection both centrally (clavulanic acid, dopamine and melanocortin receptor agonists) and peripherally (novel PDE5I, soluble and particulate guanylil cyclase activators, rho-kinase inhibitors and maxi-K channel openers). WHAT THE READER WILL GAIN: The reader will gain a broad understanding of erectile (patho-)physiology and gain insights in the mechanisms of action, efficacy and adverse events of various compounds under development for the treatment of ED. TAKE HOME MESSAGE: We expect emerging drugs to allow treatment protocols tailored to the specific needs of each individual patient, taking into consideration the efficacy of erectile performance enhancement and the potential for adverse events. This tailored approach may include combination of various emerging drugs to enhance efficacy in difficult-to-treat patients.
AbstractPURPOSE OF REVIEW: Few human studies have been performed with specific genetic endpoints coupled with erectile function or dysfunction. Most knowledge of gene expression and the function thereof on penile erection has been acquired in experimental models. The purpose of the present review is to give an overview of the available information obtained in studies of genes or genetic products versus erectile function or dysfunction. RECENT FINDINGS: The association of, for example, systemic vascular disease with diminished erectile function has brought attention to investigations of the distribution, in men with erectile dysfunction, of some genotype variants proposed to be involved in cardiovascular disease. Altered expression or activities of some smooth muscle regulatory components of the ischaemic, diabetic, or ageing penis have been reported. SUMMARY: Although penile erection can be considered a polygenic trait, some key effectors for normal erectile function within, for example, the nitric oxide/cyclic guanosine monophosphate pathway may be identified. Findings in future population-based studies may disclose the presence of a particular mutation of a gene or gene variants that may predispose to the development of erectile dysfunction. The exact molecular pathogenesis of erectile dysfunction is not known, and may vary between different forms of erectile dysfunction. With integrated approaches in genetic, molecular, and functional investigations, we can learn more of the impact of a particular genotype on erectile function, and also identify targets for preventive, pharmacological, or molecular measures.
Cambridge University Press eBooks · 2023 · 1 citations
Molecular Biology and Physiology of Erectile Function and Dysfunction
AbstractMale erectile dysfunction is a common condition that can significantly impact quality of life and interpersonal relationships. It is strongly associated with aging, comorbid conditions, poor lifestyle, and adverse cardiovascular health. Deficits in psychologic, neurologic, vascular, and endocrine function can all lead to erectile dysfunction. The aim of this chapter is to review the molecular biology required for erectile function as well as delve into the clinical pathophysiology that leads to erectile dysfunction.
The phosphodiesterase V inhibitor low responder study (PILRS) in patients with erectile dysfunction — A rationale for a PDE5 inhibitor combination therapy
AbstractPopulation-based surveys have shwon that erectile dysfunction (ED) is a constant and common condition in aging men [1–3]. The majority experiences mild ED, while moderate or severe ED occurs in up to 26% of the male population [2]. Under pathological situations, such as diabetes, hypertension, cardiovascular diseases, depression, renal and cancer diseases the percentage of occurrence may increase [2, 4–6]. Multiple psychological and organic conditions are involved in the etiology of ED. The current focus on the molecular mechanisms of penile erection is leading to new treatment approaches and analysing the failure of non-responders with respect to drug target mechanisms.
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.
