DeCure's autonomous Dermatology AI scientist is researching a drug-repurposing hypothesis for drug-Induced dyskinesia — screening already-approved drugs against its 2-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleDrug-Induced dyskinesia maps to a 2-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 drug-induced dyskinesia 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
xylosyltransferase 1 (XYLT1) — XYLT1 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 udxdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6EJ7 · 2.0 Å · ligand URIDINE-5'-DIPHOSPHATE-XYLOPYRANOSE (UDX). Experimental structure, not a prediction.
What the evidence adds up to
Dyskinesia developed in four patients soon after therapeutic doses of dextroamphetamine sulfate, with tic-like and dystonic movements similar to those produced by phenothiazines; the movements disappeared when the drug was stopped. The authors considered these idiosyncratic reactions rather than an extension of amphetamine pharmacology, possibly unmasking a subclinical extrapyramidal disorder. A single low dose of oral flupentixol also produced acute-onset orofacial dyskinesia in one reported case, though tardive dyskinesia is more commonly associated with prolonged neuroleptic use.
Reversible choreoathetoid dyskinesias have been observed with tricyclic antidepressants, trazodone, amoxapine, and serotonin reuptake inhibitors, and unlike neuroleptic-induced tardive dyskinesias they tend to remit after drug discontinuation. One case report describes reversible dyskinesia with the atypical antidepressant bupropion. The anticholinergic antiparkinsonism agent benztropine mesylate aggravated dyskinesia to a significant degree in a six-month study of thiopropazate hydrochloride for tardive dyskinesia.
In that same six-month blind evaluation, thiopropazate hydrochloride up to 30 mg daily reduced the severity of tardive dyskinesia in most patients, but overall improvement was not significant after one or three months; it became significant only after six months. The drug did not appear to aggravate the underlying pathophysiology over that period. For tardive dyskinesia specifically, the VMAT2 inhibitor deutetrabenazine at 24 and 36 mg/day showed efficacy over placebo in a 12-week Phase 3 trial, and these results supported FDA approval for that indication. Valbenazine, clonazepam, and vitamin E are also described as adjunctive treatments after optimising causative drugs.
What remains missing are head-to-head comparisons of these agents, long-term safety data beyond six months for thiopropazate, and trials that stratify patients by underlying cause or duration of dyskinesia. No study here addresses drug-induced dyskinesia from modern antipsychotics or Parkinson’s disease treatments, and the evidence for most interventions rests on small case series or single trials.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
JAMA · 1968 · 82 citations
Dextroamphetamine-Sulfate-Induced Dyskinesias
AbstractDyskinesia developed in four patients soon after the administration of therapeutic doses of dextroamphetamine sulfate. The movements were tic-like, dystonic, and similar to those occasionally produced by phenothiazines, and they promptly disappeared when the use of the drug ceased. They probably represented idiosyncratic reactions rather than extension of the pharmacologic effects of amphetamines. It is possible that the dextroamphetamine unmasked a subclinical extrapyramidal disorder in these patients.
The Journal of Clinical Psychiatry · 1997 · 17 citations · open access
Reversible Dyskinesia During Bupropion Therapy
AbstractArticle AbstractLetter to the Editor Sir: Rare instances of choreoathetoid dyskinesias have been observed with tricyclic antidepressants, trazodone, amoxapine, and serotonin reuptake inhibitors, but unlike neurolepticinduced tardive dyskinesias, those associated with antidepressants tend to remit after drug discontinuation. Reversible dyskinesia may also occur with the atypical antidepressant bupropion, as the following case illustrates.
Journal of Neurology Neurosurgery & Psychiatry · 1979 · 14 citations · open access
Six month evaluation of thiopropazate hydrochloride in tardive dyskinesia.
AbstractUsing a blind evaluation of cinematographic films of patients suffering from tardive dyskinesia we found that thiopropazate hydrochloride in a dosage up to 30 mg daily was effective in reducing the severity of the dyskinesia in most patients. The overall improvement in the group of patients studied was not significant after one or three months of therapy but was significant after six months of treatment. The administration of thiopropazate hydrochloride over a six month period did not appear to aggravate the underlying pathophysiology so that the drug could be considered likely to be safe for long-term use. The anticholinergic antiparkinsonism agent benztropine mesylate aggravated the dyskinesia to a significant degree.
AbstractDyskinesia developed in four patients soon after the administration of therapeutic doses of dextroamphetamine sulfate. The movements were tic-like, dystonic, and similar to those occasionally produced by phenothiazines, and they promptly disappeared when the use of the drug ceased. They probably represented idiosyncratic reactions rather than extension of the pharmacologic effects of amphetamines. It is possible that the dextroamphetamine unmasked a subclinical extrapyramidal disorder in these patients.
Indian Journal of Psychological Medicine · 2018 · 4 citations · open access
Acute-onset Orofacial Dyskinesia with a Single Low Dose of Oral Flupentixol: A Case Report
AbstractTardive dyskinesia are known to occur commonly among patients receiving neuroleptic drugs for prolonged periods. But, few reports of acute onset dyskinesia have also been reported in the literature. This report highlights one such case where the patient had dyskinetic movements with a single low dose of oral Flupentixol. Further, we examine the potential nosological status of acute onset dyskinesia associated with neuroleptic use.
The Brown University Psychopharmacology Update · 2017 · 0 citations
Two doses of deutetrabenazine show efficacy over placebo in treating tardive dyskinesia
AbstractThe vesicular monoamine transporter‐2 (VMAT2) inhibitor deutetrabenazine at doses of 24 and 36 mg/day demonstrated efficacy compared with placebo in a 12‐week Phase 3 trial in patients with tardive dyskinesia (TD). The results of this study and another trial were instrumental in the Food and Drug Administration's (FDA's) recent decision to approve deutetrabenazine for the TD indication.
[Pharmacological Treatment of Tardive Dyskinesia].
AbstractTardive dyskinesia (TD) is a serious, intractable, and potentially disabling side effect. Adjunctive drug treatment is used after optimizing the causative drugs. This article describes valbenazine, the first drug for treating TD that was recently approved in Japan, clonazepam, and vitamin E.
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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