DeCure for Autoimmune disease, multisystem, infantile-onset, 2
DeCure's autonomous Immuno AI scientist is researching a drug-repurposing hypothesis for autoimmune disease, multisystem, infantile-onset, 2 — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleAutoimmune disease, multisystem, infantile-onset, 2 maps to a 1-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 autoimmune disease, multisystem, infantile-onset, 2 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
zeta chain of T cell receptor associated protein kinase 70 (ZAP70) — ZAP70 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 anpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 2OZO · 2.6 Å · ligand PHOSPHOAMINOPHOSPHONIC ACID-ADENYLATE ESTER (ANP). 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.
Brain Behavior and Immunity · 2025 · 10 citations · open access
Childhood adversity as a risk factor for autoimmune disease: A systematic review and meta-analysis with implications for psychiatry
AbstractBACKGROUND: Autoimmune diseases are a heterogeneous category of disorders caused by an interaction between genetic and environmental factors which lead to a dysregulated immune response. Childhood adversity is an environmental risk factor with enduring effects on the immune system and may therefore be implicated in the aetiology of autoimmune disorders. This systematic review and meta-analysis sought to examine the association between childhood adversity and autoimmune disease in adulthood. METHODS: Electronic databases (MEDLINE, PsycINFO, Embase, and Web of Science) were searched for peer-reviewed studies in English, examining rates of childhood adversity in adults with a diagnosis of any autoimmune disease. This study was registered with PROSPERO, CRD42023439745. FINDINGS: The meta-analysis included 45 effect sizes from 27 studies (Ncases = 8,728, Ncontrol = 3,298,392). Results revealed a small effect (SMD = 0.30, 95 % CI [0.20-0.40], p < 0.001) of exposure to childhood adversity on autoimmune disease in adulthood. Heterogeneity was very high, and Egger's test and funnel plot inspection suggested that publication bias may be present. Rheumatoid arthritis (SMD = 0.48, 95 % CI [0.20-0.76], p < 0.001), psoriasis (SMD = 0.30, 95 % CI [0.17-0.43], p < 0.001), multiple sclerosis (SMD = 0.20, 95 % CI [0.01-0.38], p = 0.008), and inflammatory bowel disease (SMD = 0.31, 95 % CI [0.04-0.58], p = 0.024) were each associated with childhood adversity. Systemic lupus erythematosus was not (SMD = 0.17, 95 % CI [-0.06-0.41], p = 0.141). Twenty-one studies were assessed as being at high risk of bias. INTERPRETATION: There is evidence of an association between a history of childhood adversity and autoimmune disorders. This exposure may contribute to the elevated comorbidity between autoimmune diseases and severe mental illnesses. Due to the heterogeneity of the evidence and the high risk of bias in numerous studies, however, results should be treated with caution. Possible mechanisms underlying the relationship and implications for treatment and prevention of autoimmune diseases are discussed.
[Chronic autoimmune urticaria: treatment with omalizumab].
AbstractUNLABELLED: We report the case of a child with diagnosis of chronic urticaria/angioedema and its evolution upon omalizumab treatment. CASE REPORT: Our patient is a 12-years-old female who suffered for 14 months severe chronic urticaria/angioedema. She had a poor response to the highest doses of combined therapy with 3 antihistamines, steroids and anti-leukotrienes and great impairment of her quality of life. An autologous serum skin test was positive until 1:100 dilutions, leading to the diagnosis of chronic autoimmune urticaria. Due to the lack of response to treatment, therapy with omalizumab was administered. A notable reduction in symptoms toward the third dose was observed. After 12 months of this treatment, the patient is asymptomatic and has a negative autologous serum test. CONCLUSION: Omalizumab could be a therapeutic option for patients with autoimmune urticaria unresponsive to other treatments.
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.
