Acetylated analog of ACTH(4-10). The N-acetyl group protects against peptidase degradation, giving a longer half-life and more sustained CNS exposure than Semax. Primary mechanism is BDNF upregulation and TrkB receptor sensitization, with secondary monoamine modulation across dopamine, serotonin, and norepinephrine systems. The TrkB upregulation is the key synergy with ACD-856: more receptor gives the pan-Trk PAM more to work with.
Subjectively a mild but meaningful focus boost, nothing like a stimulant. Enhances Lisdexamfetamine effects mildly and without adding jitteriness, consistent with BDNF supporting healthy dopaminergic tone. Neurogenic effects accumulate over weeks rather than hours. Mild irritability occasionally on first few days (transient).
Dose: 400mcg intranasal Cycling: 2-4 weeks on, 1-2 weeks off Stacks: N-Acetylselank (cognitive + anxiolytic pairing), ACD-856 (Semax sensitizes TrkB expression, ACD-856 amplifies signaling at it), Lisdexamfetamine (mild stimulant synergy) Notes: Strictly better than Semax via longer half-life and stability. Cycle to maintain efficacy.