Source comparison
Adamax vs Selank Amidate: Research Application Comparison
Primary Mechanism BDNF/NGF upregulation via MC4R activation Enkephalin metabolism inhibition → GABAergic modulation Adamax for neuroplasticity; Selank for anxiolysis Receptor Targets Melanocortin receptors (MC4R), TrkB (indirectly via BDNF) Enkephalin-degradin
This comparison does not assign a generated winner or score.
- Primary Mechanism
- BDNF/NGF upregulation via MC4R activation
- Enkephalin metabolism inhibition → GABAergic modulation
- Adamax for neuroplasticity; Selank for anxiolysis
- Receptor Targets
- Melanocortin receptors (MC4R), TrkB (indirectly via BDNF)
- Enkephalin-degrading enzymes, indirect GABA modulation
- Non-overlapping pathways. Suitable for combination in multi-target designs
- Experimental Models
- Morris water maze, novel object recognition, ischaemic stroke, neurodegeneration
- Elevated plus maze, open field, fear conditioning, stress biomarkers
- Choose based on behavioural vs cognitive endpoints
- Onset of Action
- Cumulative (7–14 days for structural changes)
- Acute (30–90 minutes for anxiolytic effects)
- Selank for acute studies; Adamax for chronic protocols
- Half-Life (Serum)
- ~90 minutes (CNS effects 6–8 hours)
- ~2 hours (behavioural effects 4–6 hours)
- Both require daily dosing; Selank timing is critical
- Typical Dose Range (Rodent)
- 50–500 µg/kg intranasal or subcutaneous
- 100–300 µg/kg intranasal or subcutaneous
- Dose-response curves are steep. Pilot titration recommended
- Storage Requirements
- Lyophilised: −20°C; reconstituted: 2–8°C, 28 days
- Identical stability profiles. Handle both identically
- Tolerance/Dependency
- None documented in preclinical models
- Both lack benzodiazepine-like dependency markers