DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for peptic esophagitis — screening already-approved drugs against its 6-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease modulePeptic esophagitis maps to a 6-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 peptic esophagitis 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
adhesion G protein-coupled receptor F1 (ADGRF1) — ADGRF1 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 clrdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7WU5 · 3.0 Å · ligand CHOLESTEROL (CLR). Experimental structure, not a prediction.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Archives of Surgery · 1954 · 17 citations
PEPTIC ESOPHAGITIS
AbstractTHE PATIENT with peptic esophagitis has long been neglected, allowing progression of the disease to chronic ulceration, fibrosis, and stricture. This neglect has been due to a failure of appreciation of the pathogenesis and clinical course of the disease and an ineffective therapeutic program. Peptic esophagitis is an inflammatory process of the esophagus which occurs when there is a persistent association of gastric or intestinal secretions with the nonresistant squamous mucosa of the esophagus.<sup>1</sup>The reflux of these secretions into the esophagus is due to nonfunction or failure of the cardiac sphincter mechanism. This is usually caused by an associated sliding hiatus hernia, persistent vomiting, or the surgical excision or disruption of the cardiac sphincter (Table 1). The major factors involved in the prevention of regurgitation into the esophagus by the cardiac sphincter can be identified. The inferior constrictor muscle of the esophagus and the oblique gastric muscles about
Zeitschrift für Gastroenterologie · 2007 · 2 citations
The Elucidation of Peptic Esophagitis: from Hamperl to Heartburn
AbstractAlthough the esophagus was initially considered as the "humble" organ, it has in recent times evoked both substantial interest and considerable controversy as esophagitis becomes a global pandemic and the debate over the causes of esophagitis and the management of Barrett's has escalated. The esophagus has always defied easy understanding and the origins of its name and its symptomatology continue to confound those who address them. Esophagitis is increasing relentlessly on a global scale and the challenge of defining its symptomatology remains today as great a problem as when initially identified by Herwig Hamperl and Asher Winkelstein. Their identification of the entity they called "peptic esophagitis" in 1934, while initially for the most part overlooked, has today become one of the centers of gastroenterological focus. Although the initial symptomatology of esophagitis was limited to heartburn, it has more recently become apparent that a diverse group of symptoms is produced by the inflammation associated with intermittent reflux of gastric acid. Of interest is the nature of the original observations that led to the identification of the physiopathology of esophagitis and the elucidation of the relationship between symptomatology, acid reflux and inflammation. Although Asher Winkelstein of New York has long been considered the first to define the relationship of acid peptic reflux, esophageal ulceration and reflux symptomatology, it is of note to consider the seminal role of Herwig Hamperl, an Austrian pathologist in the elucidation of acid peptic esophagitis. Indeed, a careful consideration of the relative contributions of these two pioneers suggests that both deserve credit for identifying a disease process that, although initially for the most part ignored by clinicians, has now become one of the most fundamental problems faced by both gastroenterologists and pathologists.
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.
