DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for acute myeloid leukemia — screening already-approved drugs against its 47-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleAcute myeloid leukemia maps to a 47-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
approvedSunitinibApproved drug
Structures already discussed alongside acute myeloid leukemia in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
KIT kinase domain — Sunitinib has a real, experimentally solved structure in complex with this target (PDB 3G0E, 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 b49drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 3G0E · 1.6 Å · ligand Sunitinib (B49). Experimental structure, not a prediction.
What the evidence adds up to
A 2008 review of phase II and III studies in relapsed or refractory acute myeloid leukemia found that no single regimen could be identified as standard of care. The authors concluded that outcomes remained inadequate and that balancing treatment-related mortality, response rates, and the likelihood of long-term disease-free survival was critical for individual patients. No comparative data were available to guide treatment choices.
A 2012 commentary noted that the overall remission rate for adult patients with acute myeloid leukemia was only approximately 40%. The commentary discussed a study seeking evidence that a drug with a novel mechanism of action might be effective for these patients.
A 2016 laboratory study examined sunitinib, a multi-target tyrosine kinase inhibitor approved for renal cell carcinoma and imatinib-resistant gastrointestinal tumours. In AML-derived cell lines, sunitinib induced growth arrest and apoptosis. At 7 µM, sunitinib reduced AML patient-derived clonogenic cells by 75% compared to DMSO control (n=4). In umbilical cord blood derived normal CD34+ cells, the same concentration caused a 29% reduction (n=5). Treatment of ALDH+ cells sorted from two AML cases and CD34+ CD133+ cells from one patient also showed reduced clonogenic growth. The study highlighted a potent anti-proliferative and proapoptotic effect in vitro, but noted that early clinical trials of sunitinib in AML had shown limited success, with more promising results only in patients carrying FLT3 mutations.
A 2016 review of gene mutations in AML stated that reproducible gene mutations are critical for diagnostic typing, risk stratification, and prognostic evaluation, and that agents targeting these mutations have been applied in clinical research. What remains missing are adequately powered randomised trials that can establish whether any specific targeted agent improves survival in defined molecular subtypes, and the funding to conduct such trials in relapsed or refractory disease where outcomes remain poor.
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 · 2008 · 26 citations
Novel strategies for relapsed and refractory acute myeloid leukemia
AbstractPURPOSE OF REVIEW: Treatment for relapsed or refractory acute myeloid leukemia remains a major challenge for the leukemia community. Although several approaches have been tested in phase II study designs, few comparative data exist to guide treatment choices. We searched the recent literature in Medline, EMBASE and BIOSIS, and abstracts from the American Society of Hematology and American Society of Clinical Oncology published between 2005 and 2007. We reviewed each report to identify studies that used a phase II or III design and that included a majority of adults with non-M3 acute myeloid leukemia described as 'relapsed' or 'refractory'. RECENT FINDINGS: Several studies utilized novel cytotoxic chemotherapies, immunotherapies, epigenetic agents, and small molecule inhibitors. It is not possible to identify a single regimen or approach as the standard of care in relapsed and refractory acute myeloid leukemia. New and promising approaches are being explored, however. SUMMARY: Outcomes in patients treated for relapsed or refractory acute myeloid leukemia remain inadequate. Striking a balance between the treatment-related mortality associated with salvage therapies, response rates of salvage regimens, and the likelihood of long-term disease-free survival are critical in planning a treatment approach for the individual patient with relapsed or refractory acute myeloid leukemia.
Humana Press eBooks · 2007 · 2 citations · open access
Acute Myelogenous Leukemia
AbstractThe contributors herein have carefully checked to ensure that the drug selections and dosages set forth in this text are accurate in accord with the standards accepted at the time of publication. Notwithstanding, as new research. changes in government regulations, and knowledge from clinical experience relating to drug therapy and drug reactions constantly occurs, the reader is advised to check the product information provided by the manufacturer of each drug for any change in dosages or for additional warnings and contraindications. This is of utmost importance when the recommended drug herein is a new or infrequently used drug. It is the responsibility of the health care provider to ascertain the Food and Drug Administration status of each drug or device used in their clinical practice. The publisher, editors, and authors are not responsible for errors or omissions or for any consequences from the application of the information presented in this book and make no warranty, express or implied, with respect to the contents in this publication.
AbstractIn this issue of Blood , Ranganathan et al seek a holy grail: evidence that a drug with a novel mechanism of action may be effective for acute myeloid leukemia patients.[1][1]
Unfortunately, the overall remission rate for adult patients with acute myeloid leukemia (AML) is only approximately 40%,
Open Journal of Blood Diseases · 2016 · 1 citations · open access
Sunitinib Reduces Acute Myeloid Leukemia Clonogenic Cells <i>in Vitro</i> and Has Potent Inhibitory Effect on Sorted AML ALDH+ Cells
AbstractSunitinib is an orally administered, multi-target tyrosine kinase inhibitor that has been approved by the FDA for the treatment of renal cell carcinoma and imatinib resistant gastro-intestinal tumors. Anti-leukemic activity of sunitinib has been examined in early clinical trials with limited success. However, recent trials on acute myeloid leukemia (AML) patients carrying FLT3 mutations have shown promising results. Effects of sunitinib on leukemic clonogenic cells and potential leukemic stem cells have not been examined so far. We analyzed the anti-proliferative and apoptotic properties of sunitinib on AML-derived cell lines. We also tested the effect of sunitinib on AML patient derived clonogenic cells (AML-CFC), as well as flow-sorted potential leukemic progenitors. Peripheral blood or bone marrow samples were obtained from newly diagnosed AML patients and flow sorted for CD34+ CD133+ or ALDH+ cells. Umbilical cord blood derived CD34+ cells were used as normal controls. Sunitinib induced growth arrest and apoptosis in AML derived cell lines. In addition, 7 μM sunitinib induced 75% reduction of AML-CFC as compared to DMSO treated control (±6.79%; n = 4). In contrast, 7 μM sunitinib treatment of umbilical cord blood derived normal CD34+ cells showed 29% reduction in AML-CFC (±6.77%; n = 5). Treatment of ALDH+ cells sorted from 2 AML cases and CD34+ CD133+ cells from one patient showed reduction of AML-CFC on treatment with sunitinib. Our study highlighted a potent anti-proliferative and proapoptotic effect of sunitinib on AML cell lines, AML patient derived clonogenic cells and potential leukemic stem cells.
Guoji shuxue ji xueyexue zazhi · 2016 · 0 citations
Research of gene mutation in acute myeloid leukemia: development and prospect
AbstractAcute myeloid leukemia (AML) is a range of clonal diseases with high heterogeneity. It characterized by typical morphology, immunology, cytogenetic and molecular genetic. Available evidence supports reproducible gene mutation is critical in AML, especially in diagnostic typing, risk stratification and prognostic evaluation. Moreover, agents targeted mutantions also have been applied in clinical research. We review these gene mutantions closely related to the prognosis of AML, thereby helping to understand and explore the pathogenesis of AML better.
Key words:
Leukemia, myeloid, acute; Mutation; Molecular targeted therapy
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.
