DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for Horner syndrome — screening already-approved drugs against its 9-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleHorner syndrome maps to a 9-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 horner syndrome 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
adrenoceptor beta 3 (ADRB3) — ADRB3 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 aledrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 9IJE · 2.34 Å · ligand L-EPINEPHRINE (ALE). Experimental structure, not a prediction.
What the evidence adds up to
Horner syndrome is defined by unilateral ptosis, an ipsilateral miotic but normally reactive pupil, and sometimes ipsilateral facial anhidrosis, all from damage to the oculosympathetic pathway. The syndrome is classified into central, preganglionic, and postganglionic types depending on where the interruption occurs. Pharmacologic testing, including the more recent use of apraclonidine, can confirm the presence of Horner syndrome and guide further investigation.
Causes range from benign to life-threatening. A 2009 retrospective review of six cases (five women, one man, aged 37 to 79) found that neck procedures — coronary artery bypass surgery with neck catheter, carotid endarterectomy, cervical and thoracic sympathectomy, parathyroid surgery, and two cervical spine fusion surgeries — can produce Horner syndrome. The authors note that while central nervous system lesions, lung and sympathetic chain tumours, and carotid dissection are better-known causes, clinicians should ask about prior neck surgeries when evaluating a new case.
One 2006 case report describes a 24-year-old man with acquired Horner syndrome and heterochromia, a feature usually seen only in congenital cases. His main complaint was hypochromia on the affected side. After 19 months of latanoprost treatment, the hypochromia was obviously improved. In a 2007 report, a patient with SUNA (short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms) developed permanent partial Horner syndrome. Indomethacin at doses up to 200 mg/day for three weeks produced no response. Gabapentin at 900 mg/day brought the headache attacks under control within about one month, but the partial Horner syndrome persisted unchanged over four years of follow-up.
No randomised trial has tested any drug specifically for treating the ptosis or miosis of Horner syndrome. The evidence for latanoprost is a single case of heterochromia, not the core signs. What is missing is any controlled trial of a pharmacological intervention for the syndrome itself, along with funding for such work and a clear patient stratification that distinguishes congenital from acquired cases and accounts for the underlying cause.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Eye and Brain · 2015 · 131 citations · open access
Horner syndrome: clinical perspectives
AbstractHorner syndrome consists of unilateral ptosis, an ipsilateral miotic but normally reactive pupil, and in some cases, ipsilateral facial anhidrosis, all resulting from damage to the ipsilateral oculosympathetic pathway. Herein, we review the clinical signs and symptoms that can aid in the diagnosis and localization of a Horner syndrome as well as the causes of the condition. We emphasize that pharmacologic testing can confirm its presence and direct further testing and management.
American Journal of Roentgenology · 2006 · 80 citations
Neuroimaging Strategies for Three Types of Horner Syndrome with Emphasis on Anatomic Location
AbstractOBJECTIVE: The purposes of this study were to review the anatomy of the oculosympathetic pathway, to describe the clinical characteristics of the three types of Horner syndrome, and to illustrate underlying pathologic features with an emphasis on neuroimaging strategies based on three symptom complexes. CONCLUSION: Horner syndrome results from interruption of the oculosympathetic pathway and is usually associated with unique clinical features classified into central, preganglionic, and postganglionic types according to the anatomic location of the underlying pathologic process.
Ophthalmic Plastic and Reconstructive Surgery · 2006 · 33 citations
Effect of 0.5% Apraclonidine on Ptosis in Horner Syndrome
AbstractIn Brief To demonstrate the effect of apraclonidine on anisocoria and ptosis in Horner syndrome, one drop of 0.5% apraclonidine was instilled in both eyes of 3 patients who presented with acute Horner syndrome, and the effect on ptosis and anisocoria was documented. As reported in the literature, one drop of 0.5% apraclonidine reverses the anisocoria of Horner syndrome. In addition, 0.5% apraclonidine leads to a complete resolution of the ptosis associated with Horner syndrome, a finding reported once in the literature. Apraclonidine is a safe and readily available alternative to cocaine for the diagnosis of Horner syndrome. Apraclonidine (0.5%) readily reverses the anisocoria of Horner syndrome and leads to the resolution of ptosis, making it a safe and reliable alternative to cocaine for diagnostic testing in Horner syndrome.
Ophthalmic Plastic and Reconstructive Surgery · 2009 · 25 citations
Neck Procedures Resulting in Horner Syndrome
AbstractIn Brief Purpose: To report cases of Horner syndrome caused by interventions in the neck region. Methods: Retrospective chart review and focused literature search. Results: Six cases of Horner syndrome caused by neck procedures were identified. The study included 5 women and 1 man, ranging in age from 37 to 79 years old. Procedures included coronary artery bypass surgery with neck catheter, carotid endarterectomy, cervical and thoracic sympathectomy, parathyroid surgery, and 2 cases of cervical spine fusion surgery. Conclusions: Physicians should be aware that procedures involving the neck, even relatively minor ones, may be a cause of Horner syndrome. In the evaluation of patients with newly diagnosed Horner syndrome, it is important to obtain the history of prior surgeries or procedures involving the neck that may identify a cause of sympathetic denervation and etiology of Horner syndrome. Although the more well-known causes of Horner syndrome are central nervous system, lung and sympathetic chain tumors, and carotid dissection, the authors report a series of cases in which oculosympathetic paresis resulted from interventional procedures in the neck.
Asia-Pacific Journal of Ophthalmology · 2012 · 8 citations
Horner Syndrome
AbstractHorner syndrome is typically described by the classic triad of blepharoptosis, miosis, and anhydrosis resulting from disruption along the oculosympathetic pathway. Because of the complex and extensive course of this pathway, there are a large number of causes of Horner syndrome ranging from benign to life-threatening diseases. This review article aims to provide a practical approach to investigation and management, including evaluation of the more recent use of apraclonidine for pharmacological testing.
Latanaprost Treatment of the Heterochromia in a Patient with Acquired Horner Syndrome
AbstractHorner syndrome results from either congenital or acquired causes of sympathetic denervation. Heterochromia, a clinical feature of congenital Horner syndrome, is quite rare in acquired Horner syndrome, especially after the age of two. There were only a few cases reported previously. We reported a 24-year-old man who was diagnosed up on pharmacological tests and clinical findings as acquired Horner syndrome with heterochromia. The main complaint of the patient was hypochromia on the affected side, which was obviously improved after 19 months of latanoprost treatment.
European Neurology · 2007 · 0 citations · open access
Permanent Partial Horner Syndrome due to SUNA
Abstractsweating were detected during the pain period. Indomethacin was administered for approximately 3 weeks at 75 mg/day in the 1st, 150 mg/day in the 2nd, and 200 mg/day in the 3rd week. There was no response. Gabapentin was then administered at 900 mg/day and the attacks came under control within approximately 1 month. The first attack continued for approximately 13 weeks. Partial Horner syndrome was still present following full recovery from the attack ( fig. 1 ), although no pupillary or eyelid abnormalities were seen on his photo at 23 years of age ( fig. 2 ). All probable causes of Horner syndrome, including topical drugs, were ruled out. All laboratory and imaging tests were normal. No topical medications which might have caused this syndrome had been administered. No change in the Horner syndrome was evident during the entire follow-up period of 4 years. His attacks lasted 2–3 weeks, occurring at least twice a year. The onset of attacks led to immediate admission to our headache polyclinic and to the administration of gabapentin 900 mg/ day. To date, medication has been administered regularly without considering spontaneous remission. The patient has been followed up for 4 years. No changes have been observed in his findings during periodic checkups.
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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