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Benchmark validation hit Hypothesis #23443 Benchmark case

Fingolimod HMGB1 ALS

Cross-domain hypothesis: Multiple sclerosis drug → ALS outcome

Figure 1. Hypothesis chain: Fingolimod (downregulates) HMGB1 (correlates with) ALS.
Benchmark validation case
Outreach score
0.179
Evidence A → B
1
papers
Evidence B → C
2
papers
Direct A → C
0
papers

Evidence network

The full set of scientific papers supporting this hypothesis, visualized as a force-directed graph. Each gray node is one paper; hover for the extracted claim, click to open it on PubMed.

Figure 2. Evidence network for Fingolimod → HMGB1 → ALS. Each gray node represents a scientific paper from the Robertium extraction. A→B edges show Fingolimod → HMGB1 claims; B→C edges show HMGB1 → ALS claims. Hover for details, click a paper to open PubMed. Sparse evidence — 3 papers total. See Limitations section for context.
View as text list

A→B papers (1)

  • PMID 39207074 — Fingolimod Alleviates Inflammation after Cerebral Ischemia via HMGB1/TLR4/NF-κB Signaling Pathway (2024) · in hippocampus of MCAO/R rats conf 0.90

B→C papers (2)

  • PMID 35216298 — The Involvement of RAGE and Its Ligands during Progression of ALS in SOD1 G93A Transgenic Mice (2022) · at onset in SOD1 G93A mouse lumbar spinal cord conf 0.90
  • PMID 26733811 — Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis (2015) · in spinal cords of ALS patients conf 0.90

Clinical trials

0 registered trials for Fingolimod in ALS

Source: ClinicalTrials.gov

No registered trials found on ClinicalTrials.gov. This could indicate either an unexplored indication or a gap in registry coverage.

Search ClinicalTrials.gov →

Provenance trace

Full audit trail of how this hypothesis was generated: source papers, extracted claims, bridging logic, embedding model, and scoring. Every step is recorded and reproducible.

Provenance trace not available for hypothesis 23443.

The drug — Fingolimod

Source domain: Multiple sclerosis · entity type: drug

The mediator — HMGB1

Entity type: protein

The outcome — ALS

Target domain: ALS · entity type: disease

Evidence

Limited evidence base in our current extraction. Treat this hypothesis as a starting point for further literature review, not a settled conclusion.

A → B evidence: Fingolimod downregulates HMGB1

  • PMID 39207074 Fingolimod Alleviates Inflammation after Cerebral Ischemia via HMGB1/TLR4/NF-κB Signaling Pathway (2024)

B → C evidence: HMGB1 correlates with ALS

  • PMID 35216298 The Involvement of RAGE and Its Ligands during Progression of ALS in SOD1 G93A Transgenic Mice (2022)
  • PMID 26733811 Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis (2015)

References

All PMID-linked papers cited in the evidence network above, deduplicated and sorted by publication year.

  1. PMID 39207074 Fingolimod Alleviates Inflammation after Cerebral Ischemia via HMGB1/TLR4/NF-κB Signaling Pathway (2024) A→B
  2. PMID 35216298 The Involvement of RAGE and Its Ligands during Progression of ALS in SOD1 G93A Transgenic Mice (2022) B→C
  3. PMID 26733811 Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis (2015) B→C

Limitations & disclaimer

This hypothesis was generated algorithmically through cross-domain literature analysis and has not been experimentally validated. Treat it as a starting point for further investigation, not a therapeutic recommendation. For established knowledge about each entity, refer to the authoritative sources linked above (Wikipedia, DrugBank, UniProt, MeSH).