DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for pulmonary embolism — screening already-approved drugs against its 44-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease modulePulmonary embolism maps to a 44-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 pulmonary embolism 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
ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase (ABO) — ABO 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 6-deoxy-alpha-l-galactopyranosyldrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4Y63 · 1.3 Å · ligand octyl 2-O-(6-deoxy-alpha-L-galactopyranosyl)-beta-D-galactopyranoside (BHE). Experimental structure, not a prediction.
What the evidence adds up to
A 1999 review of pulmonary embolism management summarises diagnostic and therapeutic strategies from the literature between 1967 and 1998, presenting algorithms for diagnosis and treatment but providing no new patient data or outcome numbers. A 2017 prospective cohort study of 38 patients with massive or submassive pulmonary embolism treated with ultrasound-accelerated catheter-directed thrombolysis (UACDT) using the EKOS EkoSonic system reported a median tissue plasminogen activator dose of 21.0 mg and a median infusion time of 15 hours. The median right ventricular to left ventricular diameter ratio fell from 0.9 at baseline to 0.7 at six-month follow-up (P=0.001), and mean pulmonary artery pressure dropped from 61.4 to 37.2 mmHg (P=0.001). Median BNP level decreased from 169 pg/mL at baseline to 45.5 pg/mL at six months (P=0.001). Among the 38 patients, one intracranial haemorrhage, one gastrointestinal bleed, and two puncture site bleeds occurred. The authors describe UACDT as an alternative treatment option but do not compare it against standard therapy in a randomised design.
A 2015 case-control study of 100 patients with isolated pulmonary embolism and 100 controls screened the prothrombin gene’s last intron, last exon, 3’UTR, and part of the 3’FR region by DNA sequencing. Heterozygous carriers of the FII G20210A variant had a significantly higher risk of isolated pulmonary embolism (odds ratio 4.83, 95% CI 1.33–17.52, P=0.02). Carriers of the FII 19911GG genotype (OR 1.41, 95% CI 0.72–2.73, P=0.31) and the FII 20068CT genotype (OR 3.06, 95% CI 0.31–29.95, P=0.34) were more frequent among patients than controls, but these differences did not reach statistical significance. Two novel variants, FIIc.*64_*66del and FIIc.*303T>C, were detected in two patients. A 2017 review of severe thrombophilia in idiopathic fatal pulmonary embolism notes that when sudden death occurs in young decedents without common risk factors, thrombophilia testing is typically limited to factor V Leiden and prothrombin G20210A sequencing.
What remains missing is a randomised controlled trial comparing ultrasound-accelerated catheter-directed thrombolysis against standard anticoagulation or systemic thrombolysis in a larger, stratified patient population. The genetic studies are small and lack replication in independent cohorts. No data exist on whether screening for the novel prothrombin variants alters clinical outcomes or guides management. Funding for adequately powered trials and prospective genetic registries is absent.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
British journal of surgery · 1999 · 40 citations · open access
Modern management of pulmonary embolism
AbstractBACKGROUND: Pulmonary embolism is a significant cause of morbidity and death after operation. The introduction of new technologies in the diagnosis, and thrombolysis in the treatment, of pulmonary embolism has led to a need to reappraise the management of this condition. METHODS: This review encompasses a comprehensive discussion of diagnostic modalities and therapeutic strategies used in the current management of pulmonary embolism. Relevant papers on the diagnosis and treatment of pulmonary embolism were identified from a Medline search for the period 1967-1998. Additional papers were derived from the reference lists of retrieved articles. Articles presenting prospectively gathered data have been referenced preferentially. RESULTS AND CONCLUSION: Algorithms for the diagnosis and treatment of pulmonary embolism are presented.
Thrombus resolution and right ventricular functional recovery using ultrasound-accelerated thrombolysis in acute massive and submassive pulmonary embolism
AbstractBACKGROUND: This study aims to evaluate the efficacy and safety of ultrasound-accelerated catheter-directed thrombolysis (UACDT) in the treatment of massive and submassive pulmonary embolism (PE). METHODS: We conducted a prospective, observational cohort study of consequtive patients with massive or submassive PE treated with low-dose UACDT using EKOS EkoSonic® system at single center from May 2014 until April 2015. Overall, thirty-eight patients (median age, 64.5 years) were included. The primary safety outcomes were change in right ventricular (RV) to left ventricular (LV) diameter ratio within 24 hours of procedure initiation, at 1- and 6-month follow-up and major bleeding within 96 hours of the procedure initiation. BNP, troponin and D-dimer levels were also measured. RESULTS: The ultrasound-accelerated thrombolytic catheters were bilaterally placed in 25 (65.8%) patients. The median tissue plasminogen activator (tPA) dose for all patients in our study was 21.0 mg and the median infusion time was 15 hours. Measurements before and after treatment showed a decrease in pulmonary artery pressure. The median value of RV/LV diameter ratio decreased from 0.9 (0.7-1.1) at baseline to 0.7 (0-0.97) at 6-month follow-up (P=0.001) and pulmonary artery pressure from 61.4 ±16.7 to 37.2±9.1 mmHg (P=0.001). The median BNP level at baseline was 169 (29-721) pg/mL and 45.5 (0-328) pg/mL at 6 month follow-up (P=0.001). Of 38 patients with PE, one had intracranial hemorrage, one gastrointestinal bleeding and two developed puncture site bleeding. CONCLUSIONS: This prospective study provides alternative treatment option and an addition to the treatment algorithm for the management of pulmonary embolism.
Prothrombin 3’ end gene variants in isolated pulmonary embolism – The first report of FIIc.*64_*66del and FIIc.*303T gt C variants
AbstractObjective Pulmonary embolism is usually considered as a complication of deep vein thrombosis, but there are still a number of cases of isolated pulmonary embolism. We aimed to investigate whether prothrombin 3’ end gene variants might play a signifi cant role in the pathogenesis of isolated pulmonary embolism. Methods and results In this study 100 patients with isolated pulmonary embolism and 100 controls were screened by DNA sequencing. Screening included last intron, last exon, 3’UTR and part of the 3’FR region of the prothrombin gene. Our results have shown that heterozygous carriers of the FII G20210A variant have a signifi cantly higher risk of isolated pulmonary embolism (OR 4.83; 95%CI 1.33-17.52; P = 0.02). Carriers of the FII 19911GG genotype (OR 1.41; 95%CI 0.72-2.73; P = 0.31) and FII 20068CT genotype (OR 3.06; 95%CI 0.31-29.95; P = 0.34) were more frequent in patients with isolated pulmonary embolism compared to controls. We also detected the novel gene variants, FIIc.*64_*66del and FII c.*303T gt C, in two patients. Conclusions Our results suggest that FII G20210A represents a signifi cant risk factor for isolated pulmonary embolism. The FII G19911A and FII C20068T are potentially associated with an increased risk for the occurrence of isolated pulmonary embolism, but the results did not reach statistical signifi cance. This is the fi rst study in which the two novel 3’ end prothrombin gene variants, FIIc.*64_*66del and FII c.*303T gt C, were reported.
Severe Thrombophilia in Idiopathic Fatal Pulmonary Embolism
AbstractPulmonary embolism is caused by blockage of an artery in the lung due to a clot that travels from elsewhere in the body. The main causes are stasis, surgery and cancer, but older age, use of oral contraceptives, and prior unprovoked venous thromboembolism in non-anticoagulated patients are also clear risk factors for pulmonary embolism (Kline and Kabrhel, 2015). When pulmonary embolism causes sudden death and common risk factors are not identified in young decedents, thrombophilia tests are requested, but only factor V Leiden and prothrombin G20210A are sequenced.
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.
