DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for deficiency anemia — screening already-approved drugs against its 36-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleDeficiency anemia maps to a 36-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
approvedCyanocobalaminApproved drug
Structures already discussed alongside deficiency anemia in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
STRUCTURE OF THE COENZYME B12 DEPENDENT ENZYME GLUTAMATE MUTASE FROM CLOSTRIDIUM COCHLEARIUM — Cyanocobalamin has a real, experimentally solved structure in complex with this target (PDB 1CCW, 1.6 Å). This is the drug's own deposited structure, not a prediction, and confirms it is a structurally characterised molecule rather than an untested guess.
Loading structure…
helix sheet cncdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 1CCW · 1.6 Å · ligand Cyanocobalamin (CNC). Experimental structure, not a prediction.
What the evidence adds up to
The 2002 review notes that oral cyanocobalamin is underused for vitamin B12–deficiency anaemia, largely because a 1959 US advisory board warned against oral therapy for pernicious anaemia due to unpredictable efficacy. The review states that subsequent studies have shown that this caution is not always justified, but it does not provide its own trial data, response rates, or survival figures. The 1986 commentary observes that deficiency anaemias—cobalamin, folic acid, or iron—are curable with small doses of the missing nutrient and minimal side effects, and that patients feel better before the anaemia is corrected. It criticises the standard practice of giving large, frequent intramuscular injections of cyanocobalamin (1,000 µg per injection, ten to 20 injections initially, then monthly), noting that Minot and Murphy achieved remissions by feeding 240 g of liver per day.
A 2021 case report describes a 59-year-old man with chronic myelogenous leukaemia who developed iron deficiency anaemia and colitis after seven years on dasatinib 100 mg daily. His haemoglobin fell from 13.8 g/dL to 12.3 g/dL, and iron saturation dropped to 11%. Colonoscopy showed patchy colitis with rectosigmoid sparing. After dasatinib was withdrawn, repeat colonoscopy five months later showed no colitis, haemoglobin improved to 13.4 g/dL, iron saturation rose to 31%, and ferritin normalised. The authors state that dasatinib-induced colitis and iron deficiency anaemia are very rare, and that the exact pathogenesis is unclear.
A 2025 overview describes iron deficiency anaemia and vitamin B12 deficiency anaemia as prevalent nutritional disorders that impair oxygen transport and increase morbidity, but it offers no new data, no sample sizes, and no treatment outcomes. Across these abstracts, no controlled trial compares oral versus injectable B12 with modern endpoints, no study addresses optimal dosing for iron deficiency, and no data exist on patient stratification by absorption capacity or genetic factors. The evidence base remains limited to small case series, opinion pieces, and single case reports, with no adequately funded randomised trials that could settle the oral-versus-injectable question or define which patients need parenteral therapy.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Annals of Pharmacotherapy · 2002 · 10 citations
Treatment of Vitamin B12–Deficiency Anemia: Oral Versus Parenteral Therapy
AbstractCobalamin deficiency is commonly observed in olderpeople, with an estimated prevalence of nearly 40%.1 Oral cyanocobalamin can be a pharmacotherapeutic option for the treatment of cobalamin (vitamin B12) – deficient anemia of various etiologies, although it is underused. This is most likely a result of the 1959 US Pharmacopeia Anti-Anemia Preparations Advisory Board, which cautioned against the use of oral therapy for pernicious anemia be-cause of its unpredictable efficacy.2 Historically, oral cyanocobalamin therapy was perceived as inadequate due to reported low serum cobalamin concentrations in patients taking 100–250 µg/d.3 Over the course of many years, var-ious published studies4-9 have shown that this is not always the case. This article reviews the data supporting the use of oral cyanocobalamin for the treatment of all forms of vita-min B12-deficient anemia. Pathophysiology Cobalamin is an important cofactor for synthase and mutase enzymes maintaining methylation reactions in the brain.10 Its deficiency can result in failure of myelin syn-thesis and other neurotoxic processes. Cobalamin deficien-cy classically presents as macrocytic megaloblastic ane-mia.11 Patients may have a smooth and beefy red tongue from atrophic glossitis and possible neurologic complica-tions. Frequently, neurologic signs and symptoms precede hematologic abnormalities and include peripheral neuropa-thy, ataxia, imbalance, upper motor neuronal signs, behav-ioral abnormalities, and dementia. A patient presenting with these neurologic manifestations may already have ir-reversible damage to the spinal cord and cerebrum.12, 13 The consequences range from mild paresthesias and numbness to memory loss and frank psychosis. The daily cobalamin requirement is 2.4 µg/d.14 Absorp-tion depends on intrinsic factor, which is secreted by the gastric mucosa. Intrinsic factor then binds cobalamin,
Archives of Internal Medicine · 1986 · 7 citations
Overtreating the Deficiency Anemias
AbstractOne great pleasure of hematologic practice is the predictable response to specific therapy of a patient with deficiency anemia. The deficiency anemias, caused by lack of cobalamin, folic acid, or iron, are curable with an optimal response to small doses of the missing nutrient and minimal risk of side effects. Not only that, but before the anemia is corrected the patient begins to feel better. With such information in the public domain, why is overtreatment of deficiency anemia the standard practice? <h3>COBALAMIN DEFICIENCY</h3> Pernicious anemia (PA) and other cobalamin deficiencies are always treated with large, frequent intramuscular injections of cyanocobalamin: 1,000 μg per injection until ten or 20 injections have been given and, after that, one a month.<sup>1</sup>When Minot and Murphy<sup>2</sup>described their method of treating PA by feeding 240 g of liver per day, they achieved remissions in all patients. Such daily doses of liver contain
The American Journal of Gastroenterology · 2021 · 1 citations
S1703 Dasatinib-Induced Colitis Presenting as Iron Deficiency Anemia in a Patient With CML
AbstractIntroduction: Dasatinib, a BCR-ABL Tyrosine Kinase inhibitor (TKI), is a commonly utilized agent in the treatment of chronic myelogenous leukemia (CML). Dasatinib can result in gastrointestinal (GI) adverse effects although uncommon, including diarrhea, abdominal pain, GI bleeding, and colitis. We present a rare case of colitis secondary to Dasatinib therapy investigated during workup of iron deficiency anemia (IDA). Case Description/Methods: A 59 year old male with CML treated with Dasatinib 100 mg daily, was referred for evaluation of IDA. He had been prescribed Dasatinib seven years prior, with no significant adverse effects. On presentation patient had a hemoglobin of 12.3 g/dL (normal 13-17 g/dL), with baseline hemoglobin of 13.8 g/dL and an iron saturation of 11% (normal 16-55%). He denied any GI symptoms. Had no family history of inflammatory bowel disease or colorectal cancer. Upper endoscopy was normal. Colonoscopy showed patchy areas of erosions and inflammation throughout the colon with rectosigmoid sparing and normal terminal ileum. Biopsies showed mild to moderate active and chronic colitis. Given the possibility of GI injury from Dasatinib use, the medication was withdrawn after informed discussion with patient and oncologist. Repeat colonoscopy, five months off Dasatinib, showed no evidence of colitis and random biopsies were negative for inflammation. Repeat hemoglobin improved to 13.4g/dl, iron was 111 ug/dL, ferriten was 42 ng/ml, and iron saturation was 31%. Patient was started on alternative therapy, in setting of Dasatinib induced IDA and colitis. Discussion: Patients with CML can present with anemia, but iron deficiency in setting of Dasatanib therapy in absence of overt GI symptoms warrants endoscopic workup. Dasatinib is a highly potent TKI and mediates its effects by affecting various kinase pathways and other receptors including SRC and PDGFR. IDA and colitis as presenting side effects of Dasatinib therapy are very rare. The exact pathogenesis of Dasatinib induced colitis is unclear, however it is hypothesized that it may induce an immune reaction by T cell infiltration of the colonic mucosa. Establishing diagnosis can be challenging, as it may need to be distinguished from other conditions that may have a similar presentation such as inflammatory bowel disease or infection. This case shows the resolution colitis and IDA upon cessation of Dasatinib.Figure 1.: Figure 1A: shows patchy areas of erosions and inflammation that were seen throughout the colon, with rectosigmoid sparing, consistent with colitis. Endoscopic appearance not consistent with any infectious etiology, such as CMV, with negative H&E stain findings. Figure 1B: shows resolution of erosions and inflammation. Five months after withdrawal of Dasatinib therapy.
Zenodo (CERN European Organization for Nuclear Research) · 2025 · 0 citations · open access
Iron and B12 deficiency anemia,
AbstractAnemia is a common hematological disorder characterized by a decrease in the total number of red blood cells (RBCs), hemoglobin concentration, or hematocrit below the normal range. Iron deficiency anemia (IDA) and Vitamin B12 deficiency anemia are among the most prevalent forms of nutritional anemia worldwide. Both conditions impair oxygen transport, reduce work capacity, and contribute to increased morbidity. Understanding their etiology, diagnosis, and treatment is essential for rational pharmacotherapy.
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.
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