DeCure's autonomous Nephrology AI scientist is researching a drug-repurposing hypothesis for impaired renal function disease — screening already-approved drugs against its 11-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleImpaired renal function disease maps to a 11-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 impaired renal function disease 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
apolipoprotein L1 (APOL1) — APOL1 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 eohdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7LF7 · 2.026 Å · ligand ETHANOL (EOH). Experimental structure, not a prediction.
What the evidence adds up to
A 2018 review identified 193 endogenous factors with renoprotective properties from the GeneRIF database, based on literature on nephroprotection and renal repair. Many of these factors are secretory molecules or plasma membrane receptors, and they show elevated expression not only in renal tissue but also in connective tissue and pancreas. The factors fall into broad functional categories including cell proliferation and signalling, inflammatory response, apoptosis, blood pressure regulation, and cellular response to hypoxia, heat, or mechanical stimulus. Eight of these factors are already being studied in clinical trials, and additional factors are targeted by compounds. The review does not report any clinical outcomes such as survival or response rates, and no specific drug is named.
Two 2024 abstracts on intrinsic kidney pathology describe the range of disorders from glomerular diseases to tubulointerstitial nephritis and vascular disorders, and note that understanding renal dysfunction involves genetic predisposition, environmental factors, and immune dysregulation. These abstracts are overviews and provide no concrete data on treatments, survival, or response rates. No drug is mentioned.
The 2018 review does not test any drug in patients, and the 2024 abstracts offer no experimental results. There is no evidence from these abstracts that any specific compound improves renal function in humans. What is missing is clinical trial data that tests these renoprotective factors as therapies, funding for such trials, and patient stratification to identify who might benefit.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Renal Failure · 2010 · 33 citations
Acute Renal Failure under Dasatinib Therapy
AbstractDasatinib is a second-generation tyrosine kinase inhibitor that is approved for the treatment of imatinib-resistant or imatinib-intolerant chronic myeloid leukemia. It has a 325 times stronger in vitro activity against to native BCR-ABL when comparing with imatinib. Little is known about the effects of dasatinib on renal function. A literature review revealed only one case with imatinib-resistant chronic myeloid leukemia that developed renal failure after being placed on dasatinib therapy. Here we report a patient with imatinib-resistant chronic myeloid leukemia who developed gastroenteritis and acute renal failure after a short time from the initiation of dasatinib therapy. After dasatinib interruption, these side effects resolved completely in days. In summary, dasatinib is a potent drug in the treatment of chronic myeloid leukemia, but close clinical monitoring and the timely interruption of the therapy in patients who developed acute renal failure are warranted.
European Journal of Clinical Investigation · 2018 · 6 citations · open access
Endogenous factors and mechanisms of renoprotection and renal repair
AbstractBACKGROUND: An imbalance between renal damaging molecules and nephroprotective factors contributes to the development and progression of kidney diseases. Molecules with renoprotective properties might serve as biomarkers, drug targets as well as therapeutic options themselves. MATERIALS AND METHODS: For this review, we generated a set of renoprotective factors based on GeneRIF (Gene Reference Into Function) information available at NCBI's PubMed. The final set of manually curated renoprotective factors was investigated with respect to tissue-specific expression, subcellular location distribution and involvement in biological processes using information from gene ontology as well as information from protein-protein interaction databases. We furthermore investigated the factors in the context of clinical trials of renal disease and diabetes. RESULTS: One hundred and ninety-three factors could be retrieved from the set of GeneRIFs on nephroprotection and renal repair. A large number of factors were either secretory molecules or plasma membrane receptors. Next to the elevated expression in renal tissue, also higher expression in connective tissue and pancreas was observed. The proteins could be assigned to the broad functional categories of cell proliferation and signalling, inflammatory response, apoptosis, blood pressure regulation as well as cellular response to different kinds of insults such as hypoxia, heat or mechanical stimulus. Eight factors are studied in clinical trials with additional ones being targeted by compounds. CONCLUSIONS: We have generated a set of renoprotective factors based on the literature information, which was functionally annotated and evaluated with respect to tested compounds in kidney disease and diabetes clinical trials.
International Journal of Hematology · 2025 · 3 citations · open access
Stopping bosutinib reverses bosutinib-induced elevation of serum creatinine in patients with chronic myeloid leukemia
AbstractBosutinib is known to increase serum creatinine levels, and its mechanism of action is believed to involve a decrease in tubular creatinine excretion due to inhibition of tubular transporters and organic cation transporter 2. This study aimed to determine whether discontinuation of bosutinib could reverse bosutinib-induced elevation of serum creatinine levels. Serum creatinine levels were compared immediately before and after bosutinib administration and after bosutinib discontinuation in 11 patients with chronic myeloid leukemia. The median serum creatinine concentration significantly increased from 0.66 mg/dL before bosutinib to 0.76 mg/dL after bosutinib (P = 0.003) and decreased from 0.79 mg/dL before discontinuation of bosutinib to 0.66 mg/dL after discontinuation of bosutinib at 3 months (P = 0.005). This study revealed that bosutinib-induced elevation of serum creatinine, which was more pronounced in patients with the SLC22A2 808G/G genotype, does not indicate chronic kidney disease, but rather is simply a laboratory abnormality. If bosutinib-induced chronic kidney disease is suspected, renal function should be assessed by urinalysis and cystatin C levels to differentiate from simple elevation of serum creatinine.
Zenodo (CERN European Organization for Nuclear Research) · 2024 · 0 citations · open access
Intrinsic kidney pathology: Exploring the inner landscape of renal disorders
AbstractThe kidneys play a vital role in maintaining homeostasis within the body, filtering waste products and regulating electrolyte balance. Intrinsic kidney pathology encompasses a diverse array of disorders, ranging from glomerular diseases to tubulointerstitial nephritis and vascular disorders. Understanding the intricate inner landscape of renal disorders involves unraveling the complex interactions between genetic predisposition, environmental factors and immune dysregulation. This abstract provides a brief overview of intrinsic kidney pathology, highlighting key mechanisms underlying renal dysfunction and paving the way for targeted therapeutic interventions.
Zenodo (CERN European Organization for Nuclear Research) · 2024 · 0 citations · open access
Intrinsic kidney pathology: Exploring the inner landscape of renal disorders
AbstractThe kidneys play a vital role in maintaining homeostasis within the body, filtering waste products and regulating electrolyte balance. Intrinsic kidney pathology encompasses a diverse array of disorders, ranging from glomerular diseases to tubulointerstitial nephritis and vascular disorders. Understanding the intricate inner landscape of renal disorders involves unraveling the complex interactions between genetic predisposition, environmental factors and immune dysregulation. This abstract provides a brief overview of intrinsic kidney pathology, highlighting key mechanisms underlying renal dysfunction and paving the way for targeted therapeutic interventions.
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.
