BromantanevsCordyceps

Bromantane upregulates tyrosine hydroxylase (TH)—the rate-limiting enzyme in catecholamine synthesis—and aromatic L-amino acid decarboxylase (AADC), the enzymes responsible for converting L-tyrosine to L-DOPA and then to dopamine. This increases neuronal dopamine production capacity rather than depleting vesicular stores like traditional stimulants. The mechanism may involve modulation of transcription factors or enzyme phosphorylation. Bromantane also has anxiolytic properties through enhancement of GABAergic transmission, possibly via GABA-A receptor modulation or increased GABA synthesis. The combination of upregulated dopamine synthesis in mesolimbic and nigrostriatal pathways with GABAergic dampening of anxiety circuits produces sustained motivation, focus, and reduced mental fatigue without the jitteriness or crash typical of dopamine-releasing agents.

Cordycepin (3'-deoxyadenosine), the primary bioactive compound, increases ATP production by enhancing mitochondrial electron transport chain efficiency — it may act as an alternative substrate or modulator of Complex I and Complex III. Cordycepin activates AMPK (AMP-activated protein kinase) via increased AMP/ATP ratio or direct activation of the alpha subunit, promoting glucose uptake through GLUT4 translocation and fatty acid oxidation via CPT-1 and ACC inhibition. Cordyceps increases erythropoietin (EPO) production, likely through HIF-1alpha stabilization in hypoxic-sensitive tissues, improving oxygen-carrying capacity. Cordycepin has adenosine-like activity, modulating purinergic P1 (A1, A2A, A2B, A3) and P2 receptors. Anti-inflammatory effects occur through inhibition of NF-kB (reducing IKK degradation of IkB and nuclear translocation) and reduction of pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha). Adenosine deaminase-resistant cordycepin may also affect RNA polyadenylation.