Peptides›Cognitive›9-Me-BC

9-Me-BC

/ β-carboline alkaloid (small molecule); proposed dopamine system upregulator

SPECULATIVEN = 0 · TESTING PENDINGMW 182.22 g·mol⁻¹

ALIAS · 9-Methyl-β-carboline · 9-Methyl-beta-carboline

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Research use onlyAny dose figures below describe what specific cited studies used, reported factually. Nothing on this page is guidance for human use.READ FIRST →

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§ A · Identity

Primary sequence— sequence not captured —

MW · 182.22CLASS · β-carboline alkaloid (small molecule); proposed dopamine system upregulatorCATEGORY · Cognitive

Tier 4. Sparse rodent and in-vitro literature on dopaminergic effects from a single research group line (Polanski, Gruss, Hamann, et al., principally based at the Leibniz Institute and German university collaborators). No human dosing studies. Vendor-marketed as a nootropic on the strength of these preclinical signals.

§ B · Mechanism of action

9-Methyl-β-carboline is a tricyclic small-molecule alkaloid related to the broader β-carboline family (which includes harmine, harmane, and other endogenous indoleamine derivatives). The principal published mechanistic claim is that exposure increases the appearance and dendritic complexity of dopaminergic neurons in primary mesencephalic culture, with associated elevations in striatal and hippocampal dopamine in rodent administration studies. The molecular target driving the dopaminergic signal has not been definitively assigned.

§ C · Human clinical evidence

Tier 4. The published evidence base is rodent and in-vitro from a small set of collaborating groups, principally between 2007 and 2012. No Phase 1 or later human trials have been published.

§ D · Primary literature

PubMed17913302Hamann J et al. — 9-Methyl-beta-carboline up-regulates the appearance of differentiated dopaminergic neurones in primary mesencephalic culture · Neurochemistry International · in-vitro9-Me-BC exposure increased the number of tyrosine hydroxylase-positive dopaminergic neurons and dendritic complexity in rat primary mesencephalic culture.Limitations: In vitro only; mechanism not assigned to a defined molecular target.2008

PubMed20374418Polanski W et al. — Stimulation, protection and regeneration of dopaminergic neurons by 9-methyl-β-carboline: a new anti-Parkinson drug? · Journal of Neurochemistry · in-vitroReview and original data on dopaminergic-neuron protective effects of 9-Me-BC in cell culture and rodent models.Limitations: Single-group programmatic review; no human data; selection bias toward positive findings.2010

PubMed21651332Polanski W et al. — Stimulation, protection and regeneration of dopaminergic neurons by 9-methyl-β-carboline: a new anti-Parkinson drug? · Expert Review of Neurotherapeutics · reviewNarrative review of 9-Me-BC dopaminergic effects positing potential as anti-Parkinson candidate.Limitations: Review by the originating group; no independent translational data.2011

PubMed22380576Gruss M et al. — 9-Methyl-β-carboline-induced cognitive enhancement is associated with elevated hippocampal dopamine levels and dendritic and synaptic proliferation · Journal of Neurochemistry · rodentRodent administration of 9-Me-BC produced spatial-learning improvements with elevated hippocampal dopamine and increased dendritic spine density.Limitations: Single rodent study; hippocampal-dopamine causal chain inferred rather than established.2012

§ F · Safety signal

No formal human safety database. Class-level concerns about β-carboline alkaloids include monoamine oxidase inhibition (better characterised for harmine and harmaline) and theoretical neurotoxicity at sustained high exposure; specific data for 9-Me-BC are absent.

§ H · Regulatory status

Regulatory status

FDA status:: Not FDA-approved

§ I · Notable gaps and controversies

The published preclinical literature concentrates in a small number of laboratories. Independent replication outside the originating group is limited. Vendor sales of 9-Me-BC presume a translational effect that the published animal data alone cannot establish.