DeCure's autonomous Metabolic AI scientist is researching a drug-repurposing hypothesis for hyperthyroidism — screening already-approved drugs against its 39-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleHyperthyroidism maps to a 39-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
approvedSunitinibApproved drug
Structures already discussed alongside hyperthyroidism in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
KIT kinase domain — Sunitinib has a real, experimentally solved structure in complex with this target (PDB 3G0E, 1.6 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 b49drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 3G0E · 1.6 Å · ligand Sunitinib (B49). Experimental structure, not a prediction.
What the evidence adds up to
In a 2007 prospective cohort study of 24 patients with gastrointestinal stromal tumours given sunitinib (50 mg orally daily for four weeks followed by two weeks off), 46% developed hypothyroidism after one to six cycles. Thyroid-stimulating hormone rose at the end of the on-treatment periods and fell during the off periods, but the pattern worsened with successive cycles. Iodine-123 uptake was significantly reduced during on periods and partially or fully normalised during off periods. No changes were seen on ultrasound, and thyroglobulin and antithyroid antibodies did not rise. The authors concluded that sunitinib blocks iodine uptake and that the hypothyroidism is not autoimmune or destructive. One patient developed myxedematous coma.
A 1959 report on 194 hyperthyroid patients treated with radioactive iodine-131 at the Jules Bordet Institute found that 153 of 187 patients with diffuse goitre (81.8%) and 4 of 7 with nodular goitre were cured. Cure occurred in 59.5% of all cases within six months of the first dose and in 84.3% within one year. The 1953 paper notes that antithyroid drugs can control hyperthyroidism and maintain a euthyroid or hypothyroid state as long as treatment continues, but that reported remission rates after stopping therapy are inconsistent because follow-up periods vary widely and are often too short.
Two review papers from 2008 and 2014 summarise existing drug treatments for hyperthyroidism and the diagnosis and management of feline hyperthyroidism respectively, but provide no new trial data. The 2008 review covers current drug options for both hypo- and hyperthyroidism without reporting original results.
What is still missing is a prospective trial designed to test sunitinib specifically as a treatment for hyperthyroidism in humans, with appropriate dosing, monitoring for hypothyroidism, and long-term follow-up to assess remission durability. The 1953 paper’s criticism of short and uneven follow-up remains relevant to any future study. Patient stratification by goitre type, baseline thyroid function, and prior treatment history would be needed to interpret results. Funding for such a trial has not been reported.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
The Journal of Clinical Endocrinology & Metabolism · 2007 · 226 citations
A Novel Tyrosine-Kinase Selective Inhibitor, Sunitinib, Induces Transient Hypothyroidism by Blocking Iodine Uptake
AbstractCONTEXT: Sunitinib (sunitinib malate; SU11248; Sutent; Pfizer Inc., New York, NY) is a multitarget inhibitor of tyrosine kinases for the treatment of some human cancers. A myxedematous coma in a patient treated with sunitinib for a gastrointestinal stromal tumor was unexpectedly observed. OBJECTIVE: Our objective was to evaluate the effect of sunitinib on thyroid function in 24 patients with gastrointestinal stromal tumors. DESIGN: This was a prospective, observational cohort study. SETTING: The study was performed at two tertiary care hospitals. PATIENTS: A total of 24 patients receiving the following cycles of therapy were included in the study: 4-wk daily treatment at the dose of 50 mg orally (ON) and 2-wk withdrawal (OFF). INTERVENTIONS: Thyroid function tests, ultrasonography, and iodine-123 ((123)I) thyroidal uptake were performed at the end of several ON and OFF periods. RESULTS: After one to six cycles of treatment, 46% of patients developed hypothyroidism. Initially, TSH levels were elevated at the end of ON periods and normalized at the end of OFF periods, but a worsening in following cycles was always observed. Neither echographic alterations nor variations in thyroglobulin and antithyroid autoantibodies were found during the ON and OFF periods. On the contrary, (123)I uptake was significantly reduced at the end of ON periods, with partial or total normalization at the end of OFF periods. CONCLUSIONS: A high prevalence of hypothyroidism, very severe in some cases, was observed during sunitinib. Significant variations in (123)I uptake strongly suggest that the underlying mechanism is an impaired iodine uptake. The absence of thyroid autoimmunity, the lack of a preceding transient hyperthyroidism, and the normal echographic pattern exclude autoimmune and/or destructive mechanisms. Patients on sunitinib should be strictly monitored for the appearance of hypothyroidism and promptly treated.
PROGNOSIS OF HYPERTHYROIDISM TREATED BY ANTITHYROID DRUGS
AbstractHyperthyroidism can regularly be controlled by the administration of antithyroid drugs, and a euthyroid or hypothyroid state can be maintained for as long as treatment is continued. The optimal therapeutic schedules and the expected sequence of events during treatment have been determined.<sup>1</sup>There remains, however, considerable divergence of opinion on the incidence of prolonged remission after cessation of a course of therapy with an antithyroid compound.<sup>2</sup>This may in part be attributed to the many reports based on observation of patients for only a short time after the conclusion of treatment. Where this objection does not apply, the published rates of remission are nonetheless difficult to interpret, since they have been determined by giving equal weight to patients with a wide range of post-therapeutic periods of observation. This procedure introduces an obvious source of error into the data and also makes it impossible to derive the incidence of
Veterinary Medicine Research and Reports · 2014 · 17 citations · open access
Diagnosis and management of feline hyperthyroidism: current perspectives
AbstractPrevious and ongoing research has provided insights to the pathophysiology and diagnosis of hyperthyroidism as well as new treatment modalities. This paper reviews the etiology, clinical presentation, and clinicopathologic changes associated with hyperthyroidism, and provides a thorough explanation of confirmatory testing and treatment options.
Le Traitement De L'Hyperthyroidie Par L'I<sup>131</sup>
AbstractSummary194 hyperthyroid patients have been treated by I131 at the Jules Bordet Institute from 1952 to 1958. Diagnosis of hyperthyroidism has been made for each patient on the basis of clinical statuts, laboratory tests and functional investigation of the thyroid with I131. Results have been analyzed on the basis of the same criteria.153 hyperthyroid patients with or without diffuse goiter have been cured by the I131 treatment on a total of 187 (81,8 per cent); 4 hyperthyroid patients with a nodular goiter have been cured on a total of 7.Cure appeared in 59.5 per cent of all cases less than 6 months after the first administration of I131, and in 84.3 per cent less than one year after the beginning of I131 therapy.Data are briefly discussed with results of other forms of therapy.
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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