The Science
From a phenotype to human-relevant mechanism
Every BioSēq run returns the genes, pathways, and candidate endpoints behind your ingredient's effect — mapped from C. elegans to human biology.
How it works
The BioSēq workflow
Bioactive exposure
C. elegans + your ingredient→
HT RNA-seq
3 technical replicates→
Worm → human
DEGs to human orthologs→
Pathways & insights
Enriched pathways, endpointsWhat you get
A complete, publication-ready readout
- Differentially expressed genes — full up/down-regulated list across ~20,000 protein-coding genes.
- Human orthologs — worm DEGs mapped to human homologs, with a homology score.
- Enriched pathways — the dominant human-relevant pathways your ingredient engages.
- Gene-level roles — annotated by health area.
- Candidate clinical endpoints — pathways translated to functional outcomes and biomarkers.
- 3 technical replicates · 8-week turnaround.
2,087Total DEGs
3,641Human homologs
1.74Homology score
Example output. Every run reports total DEGs, total human homologs, and a homology score = human homologs ÷ worm DEGs — a measure of translatability (here 3,641 ÷ 2,087 = 1.74; higher means more of the worm response maps to human biology). More homologs than DEGs is expected, since one worm gene can map to several human orthologs (e.g., gst-20 → GSTA1/2/3/4).
Actionable bio-intelligence · Part 1
Which human pathways does your ingredient drive?
Top enriched human pathways
Highest significanceHighModerate
Representative example output.
Human orthologs behind the dominant pathways
| Worm gene | Human ortholog | Expr (log2FC) | Role |
|---|---|---|---|
| Oxidative stress resilience | |||
| gst-1 | GSTM4 | +1.31 ▲ | ROS detoxification via glutathione conjugation |
| gst-20 | GSTA1/2/3/4 | +6.40 ▲ | Glutathione transferases; neutralise lipid peroxides & xenobiotics |
| gst-39 | HPGDS | +6.40 ▲ | Prostaglandin D2 synthesis; anti-inflammatory / antioxidative |
| gcs-1 | GCLC | +1.10 ▲ | Rate-limiting step in glutathione biosynthesis |
| ugt-61 | UGT1A1 | +3.61 ▲ | Conjugates bilirubin & xenobiotics for detoxification |
| Mitochondrial health | |||
| acs-5 | ACSL1/2/3/4/5 | +0.80 ▲ | Fatty-acid activation for β-oxidation |
| ogdh-1 | OGDHL | +0.56 ▲ | TCA cycle (α-ketoglutarate → succinyl-CoA) |
| aco-2 | ACO-2 | +1.89 ▲ | Aconitase 2; TCA enzyme; oxidative-stress sensitive |
| cdc-48.2 | VCP | +1.20 ▲ | Mitophagy & mitochondrial protein quality control |
| Muscle health | |||
| hum-1 | MYO | +1.16 ▲ | Myosin heavy chain; sarcomere integrity |
| nmy-1 | MYH | +1.02 ▲ | Myosin heavy chains; skeletal-muscle contractility |
| Cognitive health | |||
| hlh-14 | ASCL1 | +7.20 ▲ | Proneural transcription factor; neurogenesis |
| unc-63 | CHRNA1/2/3 | +4.09 ▲ | Nicotinic ACh receptor subunits; synaptic transmission |
| goa-1 | GNAO1, GNAI3 | −0.80 ▼ | G-protein α-subunits; modulate neurotransmission |
Expression as log2 fold change · ▲ upregulated, ▼ downregulated.
Actionable bio-intelligence · Part 2
Which health benefits does the intervention support?
Health-benefit areas supported by the signature
▲ Driven by upregulation▼ Protective downregulation
Representative example output.
From mechanism to the clinic
Design your trial with endpoints already in hand
| Key pathway | Functional outcome | Candidate clinical endpoint |
|---|---|---|
| Muscle & performance ▲ | ||
| Striated muscle contraction | Improved contractile function in skeletal muscle | Grip strength, gait speed, endurance capacity |
| Myogenesis | Enhanced muscle regeneration & development | Muscle-mass maintenance/gain; recovery from atrophy |
| Muscle contraction | Increased muscle function & endurance | Performance in fatigue/endurance tests |
| Myosin filament | Myofibril alignment & force generation | Higher strength output |
| Collagen-containing ECM | Strengthened barrier & ECM organisation | Muscle integrity; reduced fibrosis |
| Cardiovascular (protective) ▼ | ||
| Cardiac hypertrophy / remodeling | Suppression of stress-induced enlargement/fibrosis | ↓ LV mass; improved ejection fraction |
| Cardiac muscle contraction | Reduced cardiac workload | Improved cardiac efficiency; lower resting HR |
| Endothelin signaling | Vasodilation; reduced vascular resistance | Lower systolic/diastolic BP |
| MAPK in cardiomyocytes | Suppression of pathological remodeling | Reduced troponin; improved HRV |
▲ upregulated (beneficial) · ▼ downregulated (protective). Endpoints are hypotheses generated from the transcriptomic signature.
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