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Peptides for Shift Work Sleep Disorder: Mechanism Comparison
Semax (N-acetyl-Semax) BDNF upregulation, MAO modulation, circadian entrainment signaling Strengthens SCN-peripheral clock synchronization, increases monoamine availability during circadian low points 60–90 minutes (intranasal) 6–8 hours (cognitive), 12–24 hou
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- Semax (N-acetyl-Semax)
- BDNF upregulation, MAO modulation, circadian entrainment signaling
- Strengthens SCN-peripheral clock synchronization, increases monoamine availability during circadian low points
- 60–90 minutes (intranasal)
- 6–8 hours (cognitive), 12–24 hours (BDNF elevation)
- Transition weeks when switching shift patterns; repeated rapid rotations
- Most effective for adaptation speed. Doesn't directly induce sleep but makes the new schedule feel coherent faster
- Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro)
- Enkephalin-degrading enzyme inhibition, anxiolytic without sedation
- Reduces anticipatory anxiety that disrupts sleep onset; no direct circadian modulation
- 20–30 minutes (intranasal)
- 3–4 hours (anxiolytic effect)
- High-stress shifts with pre-sleep anxiety; rotating schedules with unpredictable demands
- Breaks the anxiety-insomnia loop without next-shift cognitive impairment. Reactive intervention, not maintenance
- DSIP (delta sleep-inducing peptide)
- Delta-opioid receptor agonism, GABAergic neuron activation, HPA axis suppression
- Directly induces stage 3–4 NREM sleep, suppresses cortisol release during inappropriate wake phases
- 30–45 minutes (subcutaneous)
- 4–6 hours (deep sleep induction), 8–12 hours (cortisol suppression)
- Daytime sleep windows post-night-shift; chronic SWSD with documented delta-wave deficiency
- Strongest direct sleep architecture effect. Increases objectively measured deep sleep and suppresses cortisol that fragments sleep