DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for cancer — screening already-approved drugs against its 50-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleCancer maps to a 50-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
approvedSorafenibApproved drugapprovedVandetanibApproved drug
Structures already discussed alongside cancer in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
Human P38 MAP kinase — Sorafenib has a real, experimentally solved structure in complex with this target (PDB 3GCS, 2.1 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 baxdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 3GCS · 2.1 Å · ligand Sorafenib (BAX). Experimental structure, not a prediction.
What the evidence adds up to
Only 5% of cancer drugs entering Phase I clinical trials are ultimately approved for routine care. Drug repurposing — using established drugs for new indications — is proposed as a way to reduce cost and speed up development, especially for cancers that do not respond to standard therapies. At MD Anderson Cancer Center, early phase trials with repurposed drug combinations showed promising outcomes in patients with treatment-refractory advanced cancers, both rare and common. However, advancing these strategies beyond early phase studies has been difficult, primarily because of a lack of funding and pharmaceutical industry interest.
Cancer is not a single disease but a collection of diseases sharing unregulated cell growth, impaired differentiation, invasiveness, and metastatic potential. It is a disease of abnormal gene expression, involving loss, mutation, or dysregulation of proto-oncogenes and tumour suppressor genes. Molecular-targeted therapy, including mono-targeted and multi-targeted agents, has become an important approach, but patients who initially respond often later progress. Resistance mechanisms include second mutations in the targeted gene, activation of alternative signalling pathways, and effects of cellular factors.
Some targeted agents have shown success in specific tumour types: trastuzumab against HER2 in breast cancer, bevacizumab against VEGF, cetuximab against EGFR, and sorafenib against B-RAF. These examples come from an era of genomic medicine where understanding tumour biology has produced some spectacular cures and major improvements in patient well-being. Yet the same review notes that cancer cells undergo perpetual mutations and clonal evolution, and that pathways targeted in cancer are usually those incompatible with normal development if altered in the germline — meaning non-neoplastic disorders tend to affect more regulatory, peripheral pathways.
What remains missing is not biological insight but the funding and industry partnership needed to move repurposed drug combinations through later-phase trials. Patient stratification — matching the right repurposed drug to the right tumour genetics and resistance profile — is also not yet standardised in this approach. Without these, promising early signals cannot be converted into approved treatments.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Oncoscience · 2015 · 57 citations · open access
Challenges and perspective of drug repurposing strategies in early phase clinical trials
AbstractDespite significant investments in the development of new agents only 5% of cancer drugs entering Phase I clinical trials are ultimately approved for routine clinical cancer care. Drug repurposing strategies using novel combinations of previously tested anticancer agents could reduce the cost and improve treatment outcomes. At MD Anderson Cancer Center, early phase clinical trials with drug repurposing strategies demonstrated promising outcomes in patients with both rare and common treatment refractory advanced cancers. Despite clinical efficacy advancing drug repurposing strategies in the clinical trial trajectory beyond early phase studies has been challenging mainly due to lack of funding and interest from the pharmaceutical industry. In this review, we delineate our experience and challenges with drug repurposing strategies.
The Journal of Clinical Endocrinology & Metabolism · 2012 · 47 citations · open access
Risk of Rash in Cancer Patients Treated with Vandetanib: Systematic Review and Meta-Analysis
AbstractBACKGROUND: Vandetanib is an oral inhibitor of vascular endothelial growth factor receptor, epidermal growth factor receptor, and rearranged during transfection tyrosine kinases. It is approved for the treatment of unresectable or metastatic medullary thyroid cancer. Its use may be hindered due to adverse events, including rash. The reported incidence and risk of rash to vandetanib varies widely and has not been more closely investigated. Therefore, we conducted a systematic review and meta-analysis of the literature to determine the incidence and risk of developing a rash. DATA SOURCES: Databases from PubMed from 1996 through July 2011 and abstracts presented at the American Society of Clinical Oncology annual meetings from 2004 through July 2011 were searched for relevant studies. STUDY SELECTION: Eligible studies were prospective trials that described side effects of all-grade or high-grade rash for patients who received vandetanib 300 mg as a single agent. The incidence of all-grade and high-grade rash and relative risk were calculated using random-effects or fixed-effects models. RESULTS: Of 63 studies initially identified, nine met the selection criteria and were included for the study. A total of 2961 patients were included for analysis. The summary incidences of all-grade and high-grade rash were 46.1% [95% confidence interval (CI), 40.6-51.8%] and 3.5% (95% CI, 2.5-4.7%), respectively. From randomized controlled trials, patients who received vandetanib 300 mg had a significantly increased risk of developing all-grade rash in comparison with controls, with a relative risk of 2.43 (95% CI, 1.37-4.29; P = 0.002). CONCLUSION: There is a significant risk of developing rash in cancer patients receiving vandetanib. Awareness and treatment of this adverse event is critical to ensure adherence and maximize dosing, guaranteeing the best possible clinical benefit.
ecancermedicalscience · 2016 · 14 citations · open access
ecancermedicalscience
AbstractCancer is one of the leading causes of death today and is only set to worsen as its incidence continues to rise worldwide. The development of novel and effective anti-cancer drugs is a lengthy, extremely costly and inefficient process and many potential compounds are eliminated at the preclinical stages and thereafter many still never make it to the market. The cancer medical community, probably more than any other, understands the urgent need for more effective therapies as the current high cost of cancer care is unsustainable. Drug repurposing or drug repositioning is the application of established drugs to new indications and represents an increasingly promising way to speed up the development of treatments for diseases that do not respond well to standard therapies.
Progress in drug-resistance mechanisms of molecular targeted agents
AbstractMolecular-targeted therapy is a newly developed approach for cancer therapy. Molecular-targeted drugs include mono- targeted and multi-targeted agents. Both of them play an important role in cancer therapy. However,patients who initially respond to targeted-drugs may result in disease progress. Therefore,it is of significance to study drug-resistance mechanisms in the application of molecular targeted agents. We summarize in this review that these mechanisms may include second mutation of targeted gene, the activation of other signal pathway and the effect of some cellular factors.
Key words:
Carcinoma; Molecular-targeted therapy; Drug-resistance mechanism
AbstractCancer does not represent a single disease. Rather, cancer is a myriad collection of diseases with as many different manifestations as there are tissues and cell types in the human body, involving innumerable endogenous or exogenous carcinogenic agents, and various etiological mechanisms. What all of these disease states share in common are certain biological properties of the cells that compose the tumors, including unregulated (clonal) cell growth, impaired cellular differentiation, invasiveness, and metastatic potential. It is now recognized that cancer, in its simplest form, is a genetic disease, or more precisely, a disease of abnormal gene expression. Recent research efforts have revealed that different forms of cancer share common molecular mechanisms governing uncontrolled cellular proliferation, involving loss, mutation, or dysregulation of genes that positively and negatively regulate cell proliferation, migration, and differentiation (generally classified as protooncogenes and tumor suppressor genes). Essential to any discussion of the molecular mechanisms that govern disease pathogenesis for specific cancers is an appreciation for the distribution of these diseases among world populations, with consideration of specific risk factors and etiologic agents involved in disease causation. This introduction will describe cancer incidence and mortality for the major forms of human cancer, and will briefly review some of the known risk factors and/or causes of these cancers for specific at-risk populations.
Journal of Developing Drugs · 2012 · 1 citations · open access
Development of Cures in the Era of Genomic Medicine
AbstractCancer, in contrast to many other somatic disorders of mankind, is a semi-autonomous from its human host deregulation of cells where complex genetic, epigenetic and metabolic changes lead to a cancer phenotype- incessant growth, resistance to apoptosis, and perpetual mutations and clonal evolution. In depth understanding of biology of tumors has lead not only to spectacular cures and major advancements in the well-being of cancer patients, but it also propelled forward other fields of Medicine where similar pathological processes are at play. In fact, genetic and regulatory changes in cancer cells tend to involve pathways that are usually spared from germline alterations due to incompatibility with normal tissue and organ development [1]. Conversely, non-neoplastic disorders tend to affect genes and metabolic pathways that are more regulatory in nature and more peripheral to the life-sustaining pathways in mammalian cells [2]. Despite these differences, cancer medicine has been offering itself as a unique testing ground for manipulation of these core biological processes in humans. From perturbation of DNA replication with chemotherapy DNA poisons, the field of oncology moved on to develop a new class of anticancer agents targeting components of cellular signaling systems, usually a kinase of a cell surface receptor that are functionally upregulated or are products of an amplified gene. This approach is meeting with some success in specific tumor types: for example, trastuzumab against human epidermal growth factor receptor 2 (HER2) in breast cancer cells, bevacizumab against vascular endothelial growth factor (VEGF), cetuximab against epidermal growth factor receptor (EGFR), sorafenib against B-RAF. The lessons and challenges are instructive to other areas of drug development in several ways.
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.
