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ADHD Peptides 2026 Update: Comparison
P21 (CNTF derivative) CNTF receptor agonist → JAK-STAT signaling → BDNF gene upregulation High (~85% in rodent models) Transcriptional upregulation (2.3× baseline at 10 µg/kg) Preclinical only. No human ADHD trials Strongest mechanistic specificity for BDNF tr
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- P21 (CNTF derivative)
- CNTF receptor agonist → JAK-STAT signaling → BDNF gene upregulation
- High (~85% in rodent models)
- Transcriptional upregulation (2.3× baseline at 10 µg/kg)
- Preclinical only. No human ADHD trials
- Strongest mechanistic specificity for BDNF transcription; limited off-target effects at optimal dose
- Dihexa (HGF mimetic)
- HGF/c-Met activation → PI3K/Akt/ERK → synaptic protein synthesis
- Moderate (~40–65% depending on analog)
- Indirect. BDNF is one output of synaptogenic cascade
- Preclinical only. Primarily studied in Alzheimer's models
- Broadest synaptic effects but less receptor-selective than P21; BBB penetration remains constraint
- Cerebrolysin (porcine peptide mix)
- TrkB receptor agonism (BDNF-mimetic peptides)
- Low–Moderate (requires repeated dosing)
- Direct receptor activation. Bypasses transcription step
- Phase 3 trials exist for stroke/dementia but not ADHD
- Most clinical data overall but least ADHD-specific evidence; batch variability historically high