DeCure for Hyper-IgE recurrent infection syndrome 1, autosomal dominant
DeCure's autonomous AMR AI scientist is researching a drug-repurposing hypothesis for hyper-IgE recurrent infection syndrome 1, autosomal dominant — screening already-approved drugs against its 3-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleHyper-IgE recurrent infection syndrome 1, autosomal dominant maps to a 3-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 hyper-ige recurrent infection syndrome 1, autosomal dominant 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
signal transducer and activator of transcription 3 (STAT3) — STAT3 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 2-{[(5s,8s,10ardrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6NJS · 2.7 Å · ligand [(2-{[(5S,8S,10aR)-3-acetyl-8-({(2S)-5-amino-1-[(diphenylmethyl)amino]-1,5-dioxopentan-2-yl}carbamoyl)-6-oxodecahydropyrrolo[1,2-a][1,5]diazocin-5-yl]carbamoyl}-1H-indol-5-yl)(difluoro)methyl]phosphonic acid (non-preferred name) (KQV). Experimental structure, not a prediction.
What the evidence adds up to
Two case reports from 2005 describe girls aged six and twelve with recurrent cutaneous and respiratory infections and moderately elevated serum IgE. The authors note that therapy should include prolonged antibiotics and early surgery, and that non-specific agents like levamisole and ascorbic acid may reduce recurrent infections. No controlled trial data are provided for those agents, and the sample is two patients.
A 2018 report describes a four-year-old girl with autosomal-recessive hyper-IgE syndrome, caused by mutations in tyrosine kinase 2 or dedicator of cytokinesis 8 genes, and notes that this form features recurrent bacterial and viral infections, atopic eczema, and raised IgE. The abstract offers no treatment outcomes.
A 2013 chapter on hyper-IgE recurrent infection syndromes lists therapeutic options from prophylactic anti-infective measures to haematopoietic stem cell transplantation and gene therapy, but provides no efficacy data from trials. A 2009 lecture traces the history from Job’s syndrome to the discovery of STAT3 mutations in the autosomal dominant form in 2007, but again gives no quantitative results for any intervention.
No abstract reports a randomised trial, a survival rate, or a response rate for any drug in hyper-IgE recurrent infection syndrome. What is missing is any controlled clinical evidence for levamisole, ascorbic acid, or any other repurposed agent; adequate sample sizes; and patient stratification by genetic subtype.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Indian Journal of Dermatology Venereology and Leprology · 2005 · 15 citations · open access
Hyper IgE syndrome: Report of two cases with moderate elevation of IgE
AbstractHyper IgE syndrome with recurrent infection (Job's syndrome) is a rare idiopathic primary immunodeficiency disease characterized by the triad of elevated serum IgE (>2000 IU/ml), recurrent cutaneous abscesses and recurrent sinopulmonary infections. The bacteria which commonly infect these patients are Staphylococcus aureus and Haemophilus influenzae. Therapy should include prolonged antibiotic therapy and early surgery. Non-specific agents like levamisole and ascorbic acid may reduce recurrent infections. We are reporting two girls, six and twelve years of age, presented with recurrent cutaneous and respiratory infections and moderately elevated levels of serum IgE.
Autosomal Recessive Hyperimmunoglobulin E Syndrome: A Distinct Disease Entity
AbstractRenner ED, Puck JM, Holland SM, et al. J Pediatr . 2004;144:93–99
To describe the clinical and immunologic features of a distinct subgroup of patients with hyper-IgE syndrome (HIES) having autosomal recessive inheritance (AR-HIES) as distinct from the form having autosomal dominant inheritance (AD-HIES).
Thirteen patients from 6 families having AR-HIES and 68 of their relatives.
Patients were identified based on exhibiting a classic triad of features of HIES: recurrent skin abscesses, recurrent pneumonias, and elevated serum IgE. Medical records were reviewed, and patients and family members underwent uniform immunologic evaluations.
All families were consanguineous. Five are from Turkey and 1 is …
Indian Journal of Dermatology · 2018 · 12 citations · open access
Autosomal-Recessive Hyper-IgE syndrome
AbstractThe hyper-IgE syndrome (HIES) is a rare group of primary immunodeficiency characterised by recurrent infections, eczema, and elevated serum levels of IgE. Autosomal dominant HIES is caused by mutations in transcription factor - signal transducer and activator of transcription-3. Autosomal-recessive (AR) HIES was described in 2004 due to mutation of tyrosine kinase 2 gene, and subsequently, another mutation in dedicator of cytokinesis 8 gene was discovered in 2009. Although both the forms have many common clinical features, few characteristic findings help in differentiating them. AR-HIES is characterized by recurrent bacterial and viral infections, atopic eczema, and raised serum IgE levels. We report a case of a 4-year-old girl presenting with the features of AR-HIES to highlight the presentation of this rare disease.
Oxford University Press eBooks · 2013 · 4 citations
Hyper-IgE Recurrent Infection Syndromes
AbstractPrimary immunodeficiency diseases are inherited disorders that affect human adaptive and innate immunity. In most cases, affected individuals experience recurrent infections, but they may also suffer from autoimmune diseases and malignancies. This chapter focuses on Hyper-IgE Recurrent Infection Syndromes,including the historic and scientific background, clinical presentations, immunologic characteristics, and the molecular/genetic underpinnings. Where appropriate, diagnostic tools and therapeutic options are outlined -- from prophylactic anti-infective measures to hematopoietic stem cell transplantation and gene therapy.
Hyper-IgE syndrome. The history of disease (from Job's syndrome to defect STAT3 gene)
AbstractThe lecture is devoted to hyper-IgE recurrent infections syndrome and is based both upon the literature survey and numerous personal observations for more than 25 years. Initial description of this disease by Davis et al (1966) under the name «Job's syndrome: recurrent «cold» staphylococcal abscesses» was followed by remarkable rinding of Buckley et al (1972) connecting this disease with extreme hyper-immunoglobulinemia E. Later on the two district forms of the disease were described: an autosomal dominant and autosomal recessive. Recently (2007) the nature of the most typical autosomal dominant form of the syndrome was discovered as mutations in STAT3. The discovery explains multiple disorders seen in this multisystem syndrome.
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.
