Understand the source comparison
Chronic Fatigue Peptide Comparison — Mechanisms and Research Context
Thymalin Thymic immune modulation. Restores T-regulatory cell output and reduces IL-6 signalling Immune dysregulation with elevated cytokines or reduced NK cell function 5–10 mg subcutaneous 3× weekly for 4–6 weeks Russian immunology research; limited Western
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- Thymalin
- Thymic immune modulation. Restores T-regulatory cell output and reduces IL-6 signalling
- Immune dysregulation with elevated cytokines or reduced NK cell function
- 5–10 mg subcutaneous 3× weekly for 4–6 weeks
- Russian immunology research; limited Western clinical trials but consistent mechanism plausibility
- Best first-line option for fatigue with documented immune markers; thymic restoration takes 6–8 weeks to show subjective improvement
- MK 677 (Ibutamoren)
- Growth hormone secretagogue. Increases IGF-1 and supports mitochondrial biogenesis during sleep
- Mitochondrial dysfunction with low VO2 max or poor sleep recovery
- 12.5–25 mg oral once daily in evening
- Phase 2 trials for muscle wasting show 30–40% increase in IGF-1; improves sleep architecture (Stage 3/4 duration)
- Effective for fatigue tied to poor recovery or low baseline GH; requires 8–12 weeks; watch for insulin resistance at higher doses
- Cerebrolysin
- Neurotrophic peptide blend. Supports BDNF signalling and synaptic repair in prefrontal cortex
- Cognitive fatigue with brain fog, executive dysfunction, or post-viral neuroinflammation
- 5–10 mL IV or IM 5 days/week for 4 weeks
- European stroke recovery trials; used off-label for CFS brain fog in integrative clinics
- Strongest evidence for neurological fatigue symptoms; requires medical supervision for IV administration
- Dihexa
- BDNF mimetic. Potent neuroplasticity enhancer (7 orders of magnitude stronger than BDNF in receptor binding)
- Severe cognitive fatigue resistant to other interventions
- 1–5 mg subcutaneous or oral 2–3× weekly
- Preclinical only; no human RCTs; anecdotal reports from research communities
- Extremely potent but untested in humans; reserve for refractory cases where risk tolerance is high
- SLU PP 332
- Mitochondrial uncoupler. Increases basal metabolic rate and mitochondrial biogenesis without thyroid suppression
- Metabolic fatigue with low basal temperature or blunted thermogenesis
- Research-phase compound; no established human dosing
- Preclinical rodent data shows fat oxidation increase without cardiac stress
- Promising mechanism but human safety data absent; not recommended outside supervised research contexts