DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for low grade glioma — screening already-approved drugs against its 48-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleLow grade glioma maps to a 48-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
approvedVinblastineApproved drug
Structures already discussed alongside low grade glioma 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 Calmodulin — Vinblastine has a real, experimentally solved structure in complex with this target (PDB 1XA5, 2.12 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 kardrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 1XA5 · 2.12 Å · ligand Vinblastine (KAR). Experimental structure, not a prediction.
What the evidence adds up to
A 2002 review of low-grade glioma treatment notes that local recurrence and conversion to malignant glioma are the expected outcome within 4–8 years from diagnosis, and that the correct timing and dosage of radiotherapy, as well as the indications for cytotoxic drugs, remain controversial due to low incidence and a paucity of randomised trials. A 2010 review of high-grade glioma states that prognosis is poor despite multimodality therapy with surgery, radiation, and/or chemotherapy. A 2007 review of targeted therapy for malignant glioma confirms that prognosis for most patients remains very poor despite technical advances.
A 1996 German study protocol for children with malignant gliomas (glioblastoma, grade 3 astrocytoma, diffuse pons glioma) planned conventional fractionated radiotherapy (54 Gy) after surgery, with an experimental treatment arm starting with oral trofosfamide 100 mg/m2/d and VP16 25 mg/m2/d. No results from this protocol are reported in the abstract.
A 2014 retrospective analysis of 30 patients with recurrent or progressive high-grade glioma treated with sorafenib monotherapy under a named patient programme reported a median progression-free survival of 3 months (95% CI 1.9–4.1) for glioblastoma patients and 3.1 months (95% CI 1.4–4.8) for patients with grade 3 gliomas. The progression-free survival at 6 months for the whole cohort was 23%. Median overall survival was 6 months (95% CI 3.9–8.0) for glioblastoma and 10 months (95% CI 3.1–16.9) for other high-grade gliomas. Sixteen patients reported adverse events, mostly moderate; hypertension was the most common (seven patients), and one patient died of cerebral bleeding (grade 5 toxicity). The authors concluded that sorafenib was associated with tumour stabilisation in a small subset of heavily pretreated patients.
A 2018 case report describes a 5-year-old girl with a highly vascularised pilocytic astrocytoma (a low-grade glioma) who received neoadjuvant single-agent vinblastine. Over 10 months, progressive reduction of tumour vascularity was demonstrated on MRI, and the tumour was surgically removed after 14 months of therapy. The authors state this is the first report of vinblastine used in low-grade glioma to obtain tumour shrinkage prior to total resection. No data on response rates in larger cohorts, long-term outcomes, or comparison with standard care are provided.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Klinische Pädiatrie · 1996 · 14 citations
HIT-GBM: Multizentrische Studie zur Behandlung von Kindern mit malignen Gliomen
AbstractThe German society for paediatric oncology and hematology starts a clinical study for the treatment of children with glioblastoma, multifocal astrocytoma grade 3, brain stem grade 3 astrocytoma and typical diffuse ponsglioma. Conventional fractionated radiotherapy (54 Gy) will follow surgery. Simultaneously an additional experimental treatment will be given. The experimental treatment study will change every second year and starts with oral trofosfamide 100 mg/m2/d and VP16 25 mg/m2/d.
Sorafenib for patients with pretreated recurrent or progressive high-grade glioma
AbstractTherapeutic options for patients with pretreated advanced high-grade glioma (HGG) are limited. Sorafenib, a small molecule with multiple potential beneficial actions, appears particularly promising. We reviewed the outcomes of 30 patients with recurrent or progressive HGG treated with sorafenib within a named patient program. Overall, 16 patients suffered from recurrent or progressive glioblastoma multiforme and 14 patients had grade 3 gliomas. All but four patients had previously undergone surgical debulking; all but one patient had received previous standard multimodal treatment; and 18 patients (60%) had received more than one line of chemotherapy, in median three. Progression-free survival (PFS), defined as the time from initiation of sorafenib to treatment discontinuation because of tumor progression or death, was selected as the endpoint. The use of sorafenib resulted in a median PFS of 3 months [95% confidence interval (CI) 1.9-4.1 months] in patients with glioblastoma and of 3.1 months (95% CI 1.4-4.8 months) in patients with other HGG. The PFS-6 for the whole cohort was 23%. Sixteen patients reported adverse events, mostly moderate, with hypertension as the most frequently reported toxicity (seven patients). One patient died of cerebral bleeding (grade 5 toxicity). The overall survival after initiation of sorafenib was 6 months (95% CI 3.9-8.0 months) for patients with glioblastoma multiforme and 10 months (95% CI 3.1-16.9 months) for patients with HGG. In this retrospective analysis of heavily pretreated patients with HGG, sorafenib monotherapy was associated with tumor stabilization in a small subset of patients. The risk-benefit ratio was acceptable in the context of an apparent clinical benefit in patients with a fatal disease.
British Journal of Neurosurgery · 2018 · 7 citations
The use of neo adjuvant single-agent vinblastine for tumour shrinkage in a highly vascular paediatric low-grade glioma
AbstractVinblastine has shown activity as second line treatment in Low Grade Glioma (LGG) in children as well as anti-angiogenic activity in vitro.A 5 year old girl presented with 6 week history of headaches. MRI demonstrated a right temporo-parietal mass with abnormal pathological vasculature including aneurysmal vessels. Biopsy showed a pilocytic astrocytoma. Due to increased risk from surgery, first line treatment with vinblastine was given.Over 10 months, progressive reduction of tumour vascularity was demonstrated. The tumour was then surgically removed after 14 months of therapy.To our knowledge, this is the first report in which vinblastine has been successfully used in LGG to obtain tumour shrinkage prior to total tumor resection in a high vascularized LGG.
Expert Review of Anticancer Therapy · 2002 · 4 citations
Controversies in the therapy of low-grade glioma: when and how to treat
AbstractTreatment of low-grade gliomas is one of the most challenging management dilemmas in neuro-oncology. Young age of onset and low rate of growth theoretically favor minimally invasive treatments. Yet, local recurrence and conversion to malignant glioma are the expected outcome within 4-8 years from diagnosis and impose the use of additional therapies, such as radiotherapy and chemotherapy. Due to low incidence and paucity of randomized trials, the correct timing and dosage of radiotherapy are still controversial, as well as the indications and possible benefits of the administration of cytotoxic drugs. Current concepts and future perspectives in the treatment of low-grade gliomas drawn from recent scientific literature are here summarized and discussed.
touchREVIEWS in Neurology · 2010 · 2 citations · open access
Advances in Treatment Options for High-grade Glioma—Current Status and Future Perspectives
AbstractHigh-grade gliomas, including glioblastoma, anaplastic astrocytoma, anaplatic oligodendroglioma, and anaplastic oligoastrocytoma, account for the majority of malignant primary brain tumors diagnosed in adults. The prognosis for these tumors is poor despite multimodality therapy with surgery, radiation, and/or chemotherapy. This article summarizes treatment options for high-grade glioma, including standard regimens, targeted agents, and novel therapies.
DOAJ (DOAJ: Directory of Open Access Journals) · 2007 · 0 citations
TARGETED THERAPY – A HOPE FOR MALIGNANT GLIOMA TREATMENT
AbstractMalignant glioma therapy represent one of the greatest challenges in neuro-oncology. Despite technical advances in neurosurgery, radiotherapy and chemotherapy the prognosis of most patients remains very poor. Advances in understanding the molecular mechanisms involved in malignant glioma pathogenesis helped researchers to develop new agents that target the genetic and cellular alterations. This review presents the targeted agents used in research and clinical trials for malignant glioma treatment.
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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