DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for hemolytic anemia — screening already-approved drugs against its 41-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleHemolytic anemia maps to a 41-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 hemolytic anemia 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
polypeptide N-acetylgalactosaminyltransferase 2 (GALNT2) — GALNT2 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 a2gdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 5AJO · 1.48 Å · ligand 2-acetamido-2-deoxy-alpha-D-galactopyranose (A2G). Experimental structure, not a prediction.
What the evidence adds up to
In a Danish nationwide register study covering 1980 to 2016, 5868 patients with acquired haemolytic disorders were identified: 2715 with autoimmune haemolytic anaemia (AIHA), 112 with cold agglutinin disease (CAD), 397 with drug-induced haemolysis (DIHA), 116 with paroxysmal nocturnal haemoglobinuria (PNH), and 2154 with acquired haemolysis not otherwise specified. The incidence of AIHA rose from 0.81 per 100 000 person-years in 1980–1993 to 1.77 in 2008–2016, while DIHA incidence fell from 0.31 to 0.12 over the same periods. PNH incidence increased from 0.04 to 0.08. CAD incidence in 2008–2016 was 0.18 per 100 000 person-years. Prevalence per 100 000 persons rose from 2.52 to 17.01 for AIHA, from 0.80 to 1.50 for DIHA, and from 0.18 to 1.04 for PNH between 1980 and 2015. CAD prevalence in 2015 was 1.04 per 100 000. All incidence rates increased with age. The authors conclude that, except for DIHA, incidence and prevalence of acquired haemolytic anaemias are markedly increasing.
A 1963 review defines haemolytic anaemia as conditions where red-cell lifespan is shortened and the rate of destruction exceeds twice normal, sometimes reaching ten to twelve times normal. Anaemia results when destruction outpaces bone marrow compensation. Therapy is directed at restoring the balance between destruction and production, either by slowing destruction or increasing production. No specific drug or treatment is evaluated in this review.
A 2023 case report describes a 28-year-old man with jaundice, bile duct stone, and splenomegaly but no anaemia. Gene sequencing revealed a novel heterozygous SPTB variant (c.1801C>T, p.Q601X) not present in his parents or child. Splenectomy normalised his bilirubin. The authors note that the absence of typical haemolysis made diagnosis challenging, and that this variant may truncate β-spectrin, causing loss of normal function and leading to jaundice and haemolytic anaemia. No drug treatment was tested.
What remains missing for acquired haemolytic anaemias are prospective studies that explain the rising incidence and prevalence, and trials that test specific interventions beyond splenectomy or supportive care. For hereditary spherocytosis, the case report identifies a single novel mutation but provides no data on drug repurposing, no trial design, and no patient stratification strategy. Funding for large-scale, multi-centre trials of existing drugs in defined haemolytic anaemia subtypes is absent.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Clinical Epidemiology · 2020 · 64 citations · open access
<p>Increasing Incidence and Prevalence of Acquired Hemolytic Anemias in Denmark, 1980–2016</p>
AbstractBACKGROUND: Acquired hemolytic disorders-autoimmune hemolytic anemia (AIHA), cold agglutinin disease (CAD), paroxysmal nocturnal hemoglobinuria (PNH), drug-induced hemolysis (DIHA), and acquired hemolysis not otherwise specified (AHNOS)-are considered rare. Despite their potentially major health implications, data regarding their incidence and prevalence are scarce. METHODS: To fill this gap we collected data regarding all patients with acquired hemolytic disorder diagnoses in 1977-2016 from the Danish National Patient Register. These data were linked with vital and migration status information from the Danish Civil Registration System. From these data combined with annual demographic data for the background population, we calculated age- and sex-specific incidence rates and prevalence proportions of acquired hemolytic disorders for specified time periods. RESULTS: Our analysis included 5868 patients with acquired hemolytic disorders (2715 with AIHA, 112 CAD, 397 DIHA, 116 PNH, and 2154 AHNOS). The incidence rates per 100 000 person-years in 1980-1993 and 2008-2016 were 0.81 and 1.77 for AIHA, 0.31 and 0.12 for DIHA, and 0.04 and 0.08 for PNH, respectively. The 2008-2016 CAD incidence rate was 0.18/100 000 person-years, CAD diagnosis code was not defined before 1994. All incidence rates increased with age. The prevalence proportion per 100 000 persons in 1980 and 2015 was 2.52 and 17.01 for AIHA, 0.80 and 1.50 for DIHA, and 0.18 and 1.04 for PNH. CAD prevalence in 2015 was 1.04/100 000 persons. CONCLUSION: Acquired hemolytic anemia incidence rates and prevalence proportions with the exception of DIHA are markedly increasing.
New England Journal of Medicine · 1963 · 9 citations
Hemolytic Anemia
AbstractIF one defines hemolytic anemias as those in which the life-span of the red cell is diminished, most anemias are hemolytic. Practically, however, it is useful to confine the term to anemias in which shortening of the red-cell life-span is the principal cause of the anemia. The rate of red-cell destruction in such anemias ordinarily exceeds twice the normal and may be ten or twelve times the normal rate. When this rate exceeds the compensatory efforts of the bone marrow anemia ensues. Accordingly, therapy is directed toward restoring the equilibrium between the rates of destruction and production, either by slowing . . .
World Journal of Clinical Cases · 2023 · 4 citations · open access
Clinical manifestations of adult hereditary spherocytosis with novel <i>SPTB</i> gene mutations and hyperjaundice: A case report
AbstractBACKGROUND: The aim of the present study was to enhance understanding of the diagnosis and treatment of atypical hereditary spherocytosis (HS), and to broaden the diagnostic thoughts of physicians for patients with jaundice. CASE SUMMARY: A 28-year-old male presented with jaundice, bile duct stone, and splenomegaly, but without anemia. Other causes of jaundice were excluded, and gene sequencing revealed a novel heterozygous variant of c.1801C>T (p.Q601X) in exon 14 of the SPTB (NM_01355436) gene on chromosome 14 (chr14: 65260580) in the patient's blood; the biological parents and child of the patient did not have similar variants. A splenectomy was performed on the patient and his bilirubin levels returned to normal after surgery. Thus, a novel gene variant causing HS was identified. This variant may result in the truncation of β-hemoglobin in the erythrocyte membrane, leading to loss of normal function, jaundice, and hemolytic anemia. The clinical manifestations of the patient were hyperjaundice and an absence of typical hemolysis during the course of the disease, which caused challenges for diagnosis by the clinicians. CONCLUSION: Following a definitive diagnosis, genetic testing and response to treatment identified a gene variant site for a novel hemolytic anemia.
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.
