BromantanevsCaffeine

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.

Caffeine is a non-selective adenosine receptor antagonist with highest affinity for A1 and A2A subtypes. Adenosine accumulates during wakefulness and promotes sleepiness by binding to A1 receptors (inhibiting adenylyl cyclase and reducing neuronal excitability) and A2A receptors (modulating dopamine D2 receptor signaling in striatum). Caffeine competitively blocks these receptors, preventing the drowsiness signal. This disinhibition indirectly increases dopamine, norepinephrine, and acetylcholine neurotransmission via downstream pathways. Caffeine also inhibits phosphodiesterase (PDE) enzymes—particularly PDE4 in the brain—reducing cAMP degradation. Elevated intracellular cAMP amplifies catecholamine signaling through PKA-mediated phosphorylation of CREB and other transcription factors, enhancing alertness and cognitive performance.