Rare & Orphan Lab · DeCure for X

DeCure for Hypochromic anemia

DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for hypochromic anemia — 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 module1 genesLead labRare & Orphan
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Rare & OrphanDOID:11759$DeCureRare

The disease map

Disease moduleHypochromic anemia 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 hypochromic 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

STEAP3 metalloreductase (STEAP3)STEAP3 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 napdrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 2VQ3 · 2.0 Å · ligand NADP NICOTINAMIDE-ADENINE-DINUCLEOTIDE PHOSPHATE (NAP). 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.

Science · 1966 · 52 citations

Sex-Linked Anemia: A Hypochromic Anemia of Mice

AbstractThis hereditary anemia is most severe in young mice and tends to diminish with increasing age. Erythrocytes show great variation in size and form, with hypochromia and formation of target cells. Though the anemia occurs on a normal diet, it responds rapidly to iron-dextran injection. It may represent an unusual primary disturbance of iron metabolism.

https://doi.org/10.1126/science.151.3710.581
Zenodo (CERN European Organization for Nuclear Research) · 2018 · 0 citations · open access

THALASSEMIA IN MICROCYTIC HYPOCHROMIC ANEMIA PATIENTS

Abstract<strong><em>Objective:</em></strong><em> The purpose of this study is to assess the regularity of </em><em>α</em><em>-gene, ß-gene, and hemoglobin different facts in patients with Microcytic hypochromic anemia.</em> <strong><em>Methodology:</em></strong><em> 340 patients (out of 850) with microcytic hypochromic anemia [MCV&lt;80fl; MCH&lt;27pg] were study in Mayo Hospital Lahore. This study includes a total of 325 individuals out of which 88 patients were of Alpha-thalassemia trait, 171 patients of Beta-thalassemia trait, 42 with iron-deficiency anemia, 13 with thalassemia major and 11 with hemoglobin variants (HbS, HbC, and HbD). Remaining 15 out of 340 patients not diagnosed with any certain etiology. </em> <strong><em>Results: </em></strong><em>With gap-PCR, Genotyping for -</em><em>α </em><em><sup>3.7</sup></em><em>, -</em><em>α </em><em><sup>4.2</sup></em><em>, –</em><em> α </em><em><sup>PA</sup></em><em>, -</em><em> α </em><em><sup>5NT</sup></em><em> and - - <sup>MED</sup> was done. The overall ratio of deletion of -</em><em> α </em><em><sup>3.7 </sup></em><em>is 20% in 325 individuals. 23 most acknowledge ß-gene mutations Genotyping completed through absolute transformation investigation thru Amplification Refractory Mutation System (ARMS). The most recurrent transformations were CD 36/37, IVS I-110 and IVS II-I in 340 patients with 9.7%, 3.5% and 11.7% respected rates. Statistically noteworthy dissimilarity exist among Beta-thalassemia Major and Beta-thalassemia trait in case of MCH (P–value =0.23) and MCV (p- value = 0.25) indications, and similarly MCH indicator among Hb Variants and Beta-thalassemia trait (P-value = 0.04).</em> <strong><em>Conclusion: </em></strong><em>In the province of Punjab </em><em>α</em><em>-gene and ß-gene alteration is fairly communal.</em> <em>Baffling micro cytosis diagnosed with the help of molecular genotyping of </em><em>α </em><em>-thalassemia and ß-thalassemia, and resultantly preclude needless iron incrimination.</em>

https://doi.org/10.5281/zenodo.1492847

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.