DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for hemangioma — screening already-approved drugs against its 25-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleHemangioma maps to a 25-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 hemangioma 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
isocitrate dehydrogenase (NADP(+)) 2 (IDH2) — IDH2 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 ndpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 5I96 · 1.55 Å · ligand NADPH DIHYDRO-NICOTINAMIDE-ADENINE-DINUCLEOTIDE PHOSPHATE (NDP). Experimental structure, not a prediction.
What the evidence adds up to
Fifteen infants with infantile hemangioma, mean age 7.1 months, received propranolol at 2–3 mg/kg. Thirteen responded to treatment. Baseline serum VEGF was 0.234 ± 0.059 and TIMP-2 was 1.338 ± 0.679. Over six monthly samples, the sequential VEGF and TIMP-2 values did not show statistically significant change from baseline overall. In subgroup analysis, VEGF was significantly different only in the excellent-response category at month six and in the good-response category at month one; TIMP-2 showed significant change from sample two through sample six in the excellent-response group, but without a consistent increasing or decreasing trend. The authors conclude that despite propranolol’s clinical benefit in shrinking hemangiomas, its mechanism remains unknown and the optimal treatment duration is not established.
A 2012 review of vascular anomaly genetics notes that infantile hemangioma shows familial clustering and association with atopic disease, and that gene expression varies during proliferation and involution. Inherited forms of venous malformation are linked to TIE2/TEK mutations, and somatic TIE2 mutations are found in about half of sporadic venous malformations. Capillary malformation-arteriovenous malformation is caused by RASA1 mutation, and some inherited lymphedema by VEGFR3 mutation. The review suggests that variable gene expression during hemangioma phases may offer future therapeutic targets.
A single case report describes a mixed intercostal hemangioma treated surgically; no drug therapy was involved.
What is still missing: larger prospective trials with standardised timing and duration of propranolol treatment, direct measurement of drug concentration at the tissue level, and patient stratification by genetic subtype or proliferation phase. No trial has yet linked the genetic markers described in the 2012 review to propranolol response or to any other drug.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Current Opinion in Otolaryngology & Head & Neck Surgery · 2012 · 22 citations
The genetics of vascular anomalies
AbstractPURPOSE OF REVIEW: To summarize clinically relevant findings in the genetic cause and gene expression of vascular anomalies. RECENT FINDINGS: Infantile hemangioma demonstrates familial clustering and is associated with atopic disease. Variable gene expression is seen in infantile hemangioma during proliferation and involution. Capillary malformation may be sporadic or inherited in an autosomal dominant pattern. Capillary malformation-arteriovenous malformation is caused by mutation in RASA1. Some inherited forms of lymphedema are due to mutation in VEGFR3. Venous malformation may be sporadic, paradominant, or autosomal dominant inheritance. Autosomal dominantly inherited forms of venous malformation are due to mutations in TIE2/TEK. Additionally, TIE2 somatic mutations have been identified in about half of sporadic venous malformations. SUMMARY: Multiple genes have been identified causing inherited forms of vascular anomalies including capillary malformations, venous malformations and lymphedema. Variable gene expression of infantile hemangioma during proliferation and involution may offer new therapeutic targets for treatment.
Journal of Indian Association of Pediatric Surgeons · 2020 · 6 citations · open access
Evaluation of effect of propranolol on serum vascular endothelial growth factor and tissue inhibitor of metalloproteinase-2 levels in infantile hemangioma
Abstract<br><b>Background:</b> Infantile hemangioma is the most common tumor of infancy. Currently, propranolol is a preferred drug for treating hemangioma. The exact mechanism of action of propranolol is not known. In this study, we attempted to assess whether propranolol has any effect on vascular endothelial growth factor (VEGF) and tissue inhibitor of metalloproteinase-2 (TIMP-2) over a period of time, and if it is there, how long it affects it.<br><b>Materials and Methods:</b> Propranolol was administered in the dosage of 2–3 mg/kg. The first serum sample was collected before starting the propranolol treatment. Thereafter, samples were collected at monthly intervals up to a total of six samples. The samples were assessed for TIMP-2 and VEGF using enzyme-linked immunosorbent assay kit.<br><b>Results:</b> The duration of this study was from June 2016 to November 2017. The total number of patients in this study was 15. Thirteen patients responded to treatment. The mean age of patients was 7.1 months. The mean value of baseline VEGF was 0.234 ± 0.059 and that of TIMP-2 was 1.338 ± 0.679. As compared to baseline value, the <i>P</i> value was statistically not significant in any of sequential values. In category-wise analysis, apart from statistically significant value in the 6<sup>th</sup> month in excellent category and good response category in the 1<sup>st</sup> month, all other values did not reveal any significant change in VEGF analysis. The analysis of TIMP-2 revealed a significant change in the levels from Sample 2 to Sample 6 in the excellent response group; however, the levels did not show a specific trend either increasing or decreasing.<br><b>Conclusion:</b> Despite its beneficial action in regression of hemangioma, the exact mechanism is yet to be identified. The exact duration of treatment needs further evaluation.<br>
International Journal of Cardiovascular and Thoracic Surgery · 2017 · 2 citations · open access
A Very Rare Case of Mixed Intercostal Hemangioma and Literature Review
AbstractHemangiomas affecting the chest wall are rare. The literature suggests sporadic cases of these chest wall tumors. We report in this paper a very rare subtype of intercostal hemangiomas (mixed subtype). We describe the physical, clinical, imaging and pathology findings as well as the surgical therapeuthic procedure. In addition we review the literature for similar cases reported.
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.
