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for educational and safety purposes
class, effects, and the receptor fingerprint, side by side; add up to four, then source the whole stack
Popular head-to-heads →MAO-A / MAO-Binhibits
BDNF / GDNFupregulates
Dopamine synthesis (TH, AADC)boosts
Hippocampal neurogenesispromotes
Monoamine oxidase A (MAO-A)Inhibition; the most potent measured activity of this compound
Monoamine oxidase B (MAO-B)Inhibition; weaker than at MAO-A
Dopamine transporter (DAT, SLC6A3)Uptake route into dopaminergic neurons, not an inhibitor; DAT blockade abolished the increase in TH-positive neuron number
Organic cation transporters (OCT1/2/3, SLC22A1-3)Uptake route into astrocytes; the OCT inhibitor disprocynium 24 at 50 nM blocked roughly half the anti-proliferative effect
PI3K/Akt signalling pathwayRequired downstream pathway rather than a direct binding target; the PI3K inhibitor LY294002 at 10 µM completely abolished the increase in TH-positive neurons
Tyrosine hydroxylase and its transcription factor programme (Gata2, Gata3, Creb1, Crebbp, Nurr1, Pitx3, En1/En2)Upregulation of gene and protein expression in pre-existing DOPA-decarboxylase-positive neurons
Brain β-carboline-2-N-methyltransferase / phenylethanolamine N-methyltransferase (PNMT)9-Me-BC is a SUBSTRATE, not an inhibitor; these enzymes 2N-methylate it into the neurotoxic quaternary cation 2,9-dimethyl-β-carbolinium
Dopamine D2 and D3 receptorsNo detectable involvement; this is a negative result worth recording because 9-Me-BC is often loosely described as dopaminergic
Dopamine synthesis (TH, AADC)upregulates
Stress response (actoprotector)lowers overdrive
Serotoninmodulates
D2R signaling on indirect-pathway MSNs (iMSNs)stabilizes
HDAC1inhibits
checking 9-Me-BC and Bromantane: no adverse interactions were flagged (1 compatible pair); the pairs read as compatible at the class level.
9-Me-BC and Bromantane are both dopaminergic; no adverse class-level interaction flagged.
General educational info, not medical advice.
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