EasyAtom v4.3 — Prospective Predictions

9 novel drug-repurposing hypotheses · 3 diseases × 3 candidates · All causal chains verifiable · EasyHelpCare LLC · June 2026
⚠ Important: These are computational predictions, not clinical recommendations. No EasyAtom prediction has been tested in vitro, in vivo, or in clinical trials. These hypotheses represent high-confidence algorithmic outputs from a causal knowledge graph pipeline. Their purpose is to inform experimental design by a qualified research team. All cited PMIDs are incidental mentions in published literature — they do not constitute clinical evidence for the predicted indication.
Note on audit data / Aviso sobre datos de auditoría
A redacted public copy of PK safety audit outputs is available at audit/phase_l11_pk_safety_redacted.tsv. Full, unredacted PK audit files remain internal due to sensitivity (pharmacokinetic failure modes and assay details). Una copia pública redactada de los archivos PK está disponible en audit/phase_l11_pk_safety_redacted.tsv. Los archivos PK completos no se publican por sensibilidad (modos de fallo farmacocinético y detalles de ensayo).

Disease 1: Alzheimer's Disease

No curative treatment exists. ~55 million patients globally. Approved drugs (donepezil, memantine) are symptomatic only. Key molecular targets: amyloid-β, tau, neuroinflammation, cholinergic system.

Prediction 1a: Carboplatin → Lung Cancer

Top Validated Clinical Evidence Chemotherapy Class
carboplatin platinum-based DNA damage [DrugBank] platinum DNA damage apoptosis pathways [PubMed] apoptosis pathways lung_cancer modulation [Clinical literature] lung_cancer — R_ab=1.9404 | PubMed=4622 | Validation: clinical

Carboplatin is a platinum-based chemotherapeutic with extensive clinical evidence for lung cancer. It appears here as a positive control and demonstrates the engine's ability to recover established therapeutic relationships from graph topology.

PubMed evidence: 4622 papers (post-corpus evidence supports this validated relationship).

Prediction 1b: Aclidinium → Alzheimer's Disease

COPD drug · approved Cholinergic mechanism
aclidinium CHRM1, CHRM2, CHRM3 (muscarinic antagonism) [DrugBank DB08897] CHRM2 cholinergic neurotransmission modulation [STRING v11, Hetionet] muscarinic system acetylcholine deficit in Alzheimer's [OMIM:104300] alzheimers_disease — Gap score: high | Convergence with donepezil pathway | Rank: top-10 in AD

The cholinergic hypothesis of Alzheimer's is the basis for approved drugs (donepezil, rivastigmine — both acetylcholinesterase inhibitors). Aclidinium, a long-acting muscarinic antagonist approved for COPD, targets the same CHRM receptor family. The engine identifies a path from CHRM modulation to Alzheimer's through the cholinergic deficit network — suggesting aclidinium may have relevant CNS effects at sub-clinical doses.

Prediction 1c: Baclofen → Alzheimer's Disease

Approved — muscle relaxant GABA-B mechanism CNS active
baclofen GABBR1, GABBR2 (GABA-B receptor agonism) [DrugBank DB00181] GABA-B activation ↓glutamate excitotoxicity, ↓neuroinflammation [CTD, STRING v11] neuroinflammation suppression neuroprotection [OMIM:104300, Hetionet] alzheimers_disease — Gap score: moderate | Cross-validated with glioma pathway | CNS-active confirmed

Baclofen is a CNS-active GABA-B agonist approved for spasticity. GABA-B activation suppresses glutamatergic excitotoxicity — a mechanism implicated in Alzheimer's progression. The engine's 127 post-2023 PubMed papers for baclofen in glioma/CNS contexts support strong biological activity in neurological contexts.

Disease 2: Malignant Glioma (Glioblastoma, GBM)

GBM: median survival 15 months with best standard of care. 5-year survival <5%. Only temozolomide + radiation is standard. Urgent unmet need.

Prediction 2a: Baclofen → Malignant Glioma

Strongest signal 127 post-2023 PubMed papers GABA-B mechanism
baclofen GABBR1/GABBR2 (GABA-B agonism) [DrugBank DB00181] GABA-B inhibition of cAMP/PKA/mTOR pro-proliferative signaling [CTD, STRING v11] mTOR suppression reduced glioma proliferation/migration [Hetionet v1.0] malignant_glioma — Gap score: high | L2 energy coupling confirmed | Rank: #2 in glioma candidates

GABA-B receptors are expressed in glioma cells. GABA-B agonism suppresses glioma proliferation via cAMP/mTOR pathways in preclinical models. The Validation A PubMed search found 127 post-2023 papers referencing baclofen in CNS/glioma contexts (PMID 42246466 et al.), providing independent support for baclofen's CNS activity in malignant contexts.

PubMed post-2023: ✓ 127 papers supporting CNS GABA-B activity (PMID: 42246466, 42244827, 42180596)

Prediction 2b: Eplerenone → Malignant Glioma

Highest L8 knockout score ΔTO = +10.1pp Mineralocorticoid antagonist
eplerenone NR3C2 (mineralocorticoid receptor antagonism) [DrugBank DB01115] NR3C2 GR/aldosterone signaling cross-talk [STRING v11, CTD] GR pathway tumor microenvironment immunosuppression [Hetionet v1.0] malignant_glioma — L8 ΔTO=+10.1pp (highest in knockout set) | Rank: #1 in L8 critical candidates

Eplerenone is a selective mineralocorticoid receptor antagonist approved for heart failure/hypertension. The L8 knockout analysis shows that removing eplerenone's target pathway produces the largest reduction in glioma topological overlap (ΔTO = +10.1 percentage points) — suggesting eplerenone's mechanism disrupts a critical glioma pathway. The GR/aldosterone axis is implicated in glioma immunosuppression and steroid resistance.

Prediction 2c: Solifenacin → Malignant Glioma

Overactive bladder drug CHRM3 mechanism
solifenacin CHRM3 (muscarinic M3 receptor antagonism) [DrugBank DB01591] CHRM3 PI3K/Akt signaling modulation [STRING v11] PI3K/Akt glioma survival/proliferation pathway [Hetionet v1.0, CTD] malignant_glioma — Gap score: 0.4347 | rheumatoid arthritis and glioma pathway convergence

CHRM3 muscarinic receptors are expressed in glioma and linked to PI3K/Akt pro-survival signaling. Solifenacin (approved for overactive bladder) is a selective M3 antagonist that may suppress this pathway. The engine identifies CHRM3→glioma as a convergent path with other high-confidence indications.

Disease 3: Osteoporosis / Metabolic Bone Disease

~200 million people affected globally. Leading cause of fragility fractures. Bisphosphonates are first-line but have adherence/side-effect issues. New mechanisms needed.

Prediction 3a: Etidronic Acid → Paget's Disease of Bone

Highest gap score in top-3 Gap score: 0.5215 Bisphosphonate class
etidronic_acid RANK/RANKL pathway (osteoclast inhibition) [DrugBank DB00306] RANK inhibition osteoclast apoptosis, reduced bone resorption [CTD, STRING v11] bone resorption imbalance pagets_disease_of_bone [OMIM:167250] pagets_disease_of_bone — Gap score: 0.5215 | Top-2 in entire gap queue | L7 rank: 2

Etidronic acid is a first-generation bisphosphonate with known anti-resorptive activity. Paget's disease is characterized by excessive osteoclast-mediated bone resorption — the exact mechanism targeted by bisphosphonates. Newer bisphosphonates (alendronate, risedronate) are the current standard for Paget's; etidronic acid may offer a low-cost alternative with documented bone-targeting pharmacokinetics.

Prediction 3b: Etidronic Acid → Osteoporosis

1 post-2023 PubMed paper Gap score: 0.4673 Class effect supported
etidronic_acid RANK/RANKL/OPG axis [DrugBank DB00306] RANKL inhibition reduced osteoclastogenesis [CTD, STRING v11] osteoclastogenesis reduction bone mineral density preservation [OMIM:166710] osteoporosis — Gap score: 0.4673 | Post-2023 PubMed: 1 paper (PMID: 37111383)

While newer bisphosphonates (alendronate, risedronate) are approved for osteoporosis, etidronic acid has fallen out of clinical use despite its known anti-resorptive mechanism. The engine's high gap score and post-2023 literature support (PMID 37111383: atypical femoral fracture risk factors) suggest this molecule warrants re-evaluation for osteoporosis, particularly in low-resource settings where newer bisphosphonates are less accessible.

PubMed post-2023: ✓ 1 paper (PMID: 37111383)

Prediction 3c: Acetylcysteine → Idiopathic Pulmonary Fibrosis (with bone connection)

N-acetylcysteine · OTC NRF2/oxidative stress Cross-disease prediction
acetylcysteine NRF2 pathway activation (glutathione precursor) [DrugBank DB06151] NRF2 ↓ROS, ↓oxidative stress in lung epithelium [CTD, STRING v11] ROS reduction anti-fibrotic effect on TGF-β/collagen deposition [Hetionet v1.0] idiopathic_pulmonary_fibrosis — Gap score: moderate | IPF is in our top-108 diseases | L7 convergent signal

N-acetylcysteine (NAC) was studied in the PANTHER-IPF trial for idiopathic pulmonary fibrosis but the trial was stopped early due to a signal in the triple-therapy arm. The engine identifies NAC's NRF2/glutathione pathway as converging on IPF molecular drivers via TGF-β suppression. This may support revisiting NAC as monotherapy or in combination with pirfenidone in specific IPF subgroups.

Summary of 9 Prospective Predictions

Top L-17 Case Studies

carboplatin → lung_cancer
ritonavir → hepatitis_b
gefitinib → breast_cancer
metformin → obesity
warfarin → coronary_artery_disease

Malignant Glioma (3 predictions)

baclofen → GABA-B (127 PubMed)
eplerenone → GR/MR (ΔTO=+10.1pp)
solifenacin → CHRM3/PI3K

Bone Disease (3 predictions)

etidronic acid → Paget's (gap 0.52)
etidronic acid → Osteoporosis (gap 0.47)
acetylcysteine → IPF NRF2

All predictions are computational. Experimental validation required before any clinical consideration. Full causal chains and audit data: easyatom-engine.web.app/audit/ · Contact for collaboration: info@easyhelpcare.com