Anonymous
ID: InlzV82f
7/14/2025, 6:15:07 PM No.510368083
Why aren't you biohacking? There's new research chemicals that have recently come out that are confirmed to make you smarter
>ACD856 is a selective TrkB positive allosteric modulator (PAM) and enhances signaling of neurotrophic factors like BDNF and NGF by increasing binding at TrkA, TrkB, and TrkC receptors
>Mechanism overlaps with many antidepressants and psychedelics, which also act as TrkB PAMs (e.g., psilocin, LSD, ketamine metabolite, fluoxetine)
>Supports the theory that TrkB/BDNF activation underlies antidepressant and plasticity effects
ACD856 may enhance cognition similarly to AMPA PAMs like TAK-653, due to shared downstream effects involving BDNF and mTOR
>In animal studies, ACD856 reversed cognitive deficits induced by NMDA antagonists (MK-801), indicating potential neuroprotective and procognitive effects
>Also shown to increase endogenous BDNF in a possible feed-forward mechanism
>Passes early clinical trials with good pharmacokinetics and no significant side effects; 20-hour half-life improves over ACD855โs impractical 68-day half-life
>ACD856 can potentiate other BDNF-linked compounds, making it a strong candidate for stacking
>Usmarapride is a 5-HT4 partial agonist, structurally related to Prucalopride but designed for CNS selectivity to avoid peripheral side effects
>Demonstrated improvements in hippocampus-dependent memory in healthy humans in tasks like RAVLT and PILT
>ACD856 is a selective TrkB positive allosteric modulator (PAM) and enhances signaling of neurotrophic factors like BDNF and NGF by increasing binding at TrkA, TrkB, and TrkC receptors
>Mechanism overlaps with many antidepressants and psychedelics, which also act as TrkB PAMs (e.g., psilocin, LSD, ketamine metabolite, fluoxetine)
>Supports the theory that TrkB/BDNF activation underlies antidepressant and plasticity effects
ACD856 may enhance cognition similarly to AMPA PAMs like TAK-653, due to shared downstream effects involving BDNF and mTOR
>In animal studies, ACD856 reversed cognitive deficits induced by NMDA antagonists (MK-801), indicating potential neuroprotective and procognitive effects
>Also shown to increase endogenous BDNF in a possible feed-forward mechanism
>Passes early clinical trials with good pharmacokinetics and no significant side effects; 20-hour half-life improves over ACD855โs impractical 68-day half-life
>ACD856 can potentiate other BDNF-linked compounds, making it a strong candidate for stacking
>Usmarapride is a 5-HT4 partial agonist, structurally related to Prucalopride but designed for CNS selectivity to avoid peripheral side effects
>Demonstrated improvements in hippocampus-dependent memory in healthy humans in tasks like RAVLT and PILT
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