DeCure's autonomous Neuro AI scientist is researching a drug-repurposing hypothesis for motor peripheral neuropathy — screening already-approved drugs against its 3-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleMotor peripheral neuropathy maps to a 3-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 motor peripheral neuropathy 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
inverted formin 2 (INF2) — INF2 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 adpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 9AZP · 3.79 Å · ligand ADENOSINE-5'-DIPHOSPHATE (ADP). Experimental structure, not a prediction.
What the evidence adds up to
Toxic neuropathies caused by prescribed drugs, recreational drugs, heavy metals, industrial agents and biological toxins usually improve or stabilise once the offending toxin is removed. Most are axonal, length-dependent and sensory predominant, though some involve significant motor components or present acutely. Newer medications that can cause neuropathy include immune checkpoint inhibitors and BRAF/MEK inhibitors. No drug is proposed as a treatment in this 2023 review.
A 2005 study of transgenic mice overexpressing peripheral myelin protein 22 kDa — a model for Charcot-Marie-Tooth disease type 1A, the most prevalent hereditary peripheral neuropathy — found that the proteasomal degradation pathway and various signalling mechanisms were up-regulated in diseased sciatic nerve. Down-regulated processes included cell shape, adhesion, cellular activity and metabolism. The most significantly up-regulated differences could not be mapped to known transcripts. No drug was tested or suggested.
A 1996 textbook chapter on peripheral nerve disorders mentions newly recognised conditions such as multi-focal motor neuropathy, neuropathy associated with AIDS, borreliosis, and neurotoxins, as well as critical illness polyneuropathy. It notes that recombinant DNA technology had begun identifying molecular genetic defects, but offers no drug therapy.
What is still missing is any controlled trial of a repurposed drug for motor peripheral neuropathy in humans. The animal model data point to proteasomal and signalling pathways, but no compound has been tested in that model for efficacy. Patient stratification by genetic subtype or toxin exposure is absent from the literature cited. Funding for a randomised trial in a defined neuropathy population would be needed before any drug could be evaluated.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Practical Neurology · 2023 · 15 citations · open access
Toxic neuropathies: a practical approach
AbstractToxic neuropathies result from exogenous substances damaging the peripheral nerves. There are numerous causes, including prescribed and recreational drugs, heavy metals, industrial agents and biological toxins. Timely recognition of these neuropathies gives better outcomes, as they usually improve or stabilise once the toxin is removed. Most toxic neuropathies are axonal, length-dependent and sensory predominant, although some have significant motor involvement or can present acutely or subacutely. Here, we outline our clinical approach and discuss the major causes of toxic neuropathy, while emphasising the clinical and neurophysiological features and the neuropathy phenotype. We also include an update on newer medications that can cause neuropathy, including immune checkpoint inhibitors and BRAF/MEK inhibitors.
Abstract<i>The Blue Book of Practical Neurology</i>offers a gem in<i>Peripheral Nerve Disorders II</i>edited by Asbury and Thomas. Contributors include outstanding scientists on both sides of the Atlantic and they succeed admirably in illustrating the way progress through research leads to new concepts in patient management. The editors point out that it has been 12 years since the publication of<i>Peripheral Nerve Disorders I</i>and concentrate on new information and newly recognized disorders such as multi-focal motor neuropathy, neuropathy associated with acquired immunodeficiency syndrome, borreliosis, and those due to many previously uncharacterized neurotoxins. Recombinant DNA technology has helped identify many molecular genetic defects, and such advances will mandate the need for a new volume in less than another 12 years, but the current level of information more than justifies this current scholarly work. Some new concepts merit an entire chapter, including an excellent one on critical illness polyneuropathy. Others,
Journal of Neuroscience Research · 2005 · 10 citations
Expression profiling of sciatic nerve in a Charcot‐Marie‐Tooth disease type 1a mouse model
AbstractExpression profiling was performed on sciatic nerve of normal mice and of transgenic mice overexpressing the peripheral myelin protein 22 kDa (PMP22). These mice represent a model for the hereditary peripheral neuropathy Charcot-Marie Tooth type 1A. Comparison of the profiles reveals that the proteasomal degradation pathway and various signaling mechanisms are up-regulated in the diseased nerve. The down-regulated processes represent cell shape and adhesion as well as cellular activity and metabolism. In addition, we found that the most significantly up-regulated differences could not be mapped on known transcripts and thus might represent not identified transcripts. Our data will be helpful to direct future research aimed at deciphering the molecular pathogenesis of the most prevalent hereditary peripheral neuropathy.
Journal of the Korean Medical Association · 2004 · 1 citations · open access
Pharmacologic Treatment of Peripheral Neuropathy
AbstractPeripheral neuropathy is a common neurological disorder and has a variety of identifiable causes such as diabetes, metabolic derangements, neurotoxic substances, and even genetic abnormalities. Even with a thorough evaluation, however, the underlying cause cannot be identified in a large portion of peripheral neuropathy. In addition to the diagnostic dilemma, the wide spectrum of clinical manifestations with a variety of combinations of altered sensation, muscle weakness, and autonomic symptoms in peripheral neuropathy also makes it difficult to introduce an appropriate management. Treatments for peripheral neuropathy are categorized according to the underlying conditions and the strategies designed to relieve peripheral nerve pain irrespective of the cause. This article summarizes the mechanisms of peripheral neuropathic pain and current pharmacologic treatments including tricyclic antidepressants and anticonvulsants.
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.
