DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for myelodysplastic syndrome — screening already-approved drugs against its 40-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleMyelodysplastic syndrome maps to a 40-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 myelodysplastic syndrome 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
BCR activator of RhoGEF and GTPase (BCR) — BCR 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 ip2drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 5OC7 · 1.652 Å · ligand D-MYO-INOSITOL-4,5-BISPHOSPHATE (IP2). 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.
Current Opinion in Hematology · 2009 · 41 citations
Advancements in the molecular pathogenesis of myelodysplastic syndrome
AbstractPURPOSE OF REVIEW: Myelodysplastic syndrome is an important hematological malignancy affecting the expanding aged population. Our understanding of the biology of this disease has been limited by the heterogeneous clinicopathological features, difficulty in creating animal models, and paucity of evidence linking molecular abnormalities to disease pathogenesis. The importance of new advances in myelodysplastic syndrome will be discussed in this review. RECENT FINDINGS: Heightened awareness of the myelodysplastic syndrome burden has garnered rising interest in the development of new treatment strategies and investigation of the molecular basis of this complex disease. A multistep process explains the heterogeneity observed in myelodysplastic syndrome better than a single event, whereby multiple biological forces culminate in telomere erosion and genomic instability. Intrinsic genetic factors within myeloid progenitors along with extrinsic factors in the microenvironment may foster clonal selection. Specific targeted intervention at critical stages along this multistep pathway, prior to acute myeloid leukemia transformation, may produce the best clinical outcome. SUMMARY: Newly identified molecular defects, the creation of animal models, and several advancements in our understanding of the molecular pathogenesis have dramatically improved diagnostic and therapeutic potential of myelodysplastic syndrome.
The Genomics of Myelodysplastic Syndromes: Origins of Disease Evolution, Biological Pathways, and Prognostic Implications
AbstractThe molecular pathogenesis of myelodysplastic syndrome (MDS) is complex due to the high rate of genomic heterogeneity. Significant advances have been made in the last decade which elucidated the landscape of molecular alterations (cytogenetic abnormalities, gene mutations) in MDS. Seminal experimental studies have clarified the role of diverse gene mutations in the context of disease phenotypes, but the lack of faithful murine models and/or cell lines spontaneously carrying certain gene mutations have hampered the knowledge on how and why specific pathways are associated with MDS pathogenesis. Here, we summarize the genomics of MDS and provide an overview on the deregulation of pathways and the latest molecular targeted therapeutics.
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.
