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9-MBC 1g

9-MBC 1g

€25,00 EUR
Taxes included.

                                         NOT FOR HUMAN CONSUMPTION

9-Methyl-β-carboline (9-MBC) is a synthetic β-carboline derivative investigated as a neurotrophic, pro-dopaminergic research compound. In cell and rodent models it promotes dopaminergic neuron survival, differentiation, and neurite outgrowth, with signals of mitochondrial support and anti-inflammatory microglial reprogramming. It is not approved for human use; evidence is preclinical.

Additional Benefits of 9-MBC Now Under Investigation

Benefit Key take-aways
1 Dopaminergic neurotrophy In primary midbrain cultures and lesion models, 9-MBC increases TH⁺ neuron counts, neurite length, and dopamine synthesis genes (TH, DAT), suggesting true trophic action rather than mere MAO inhibition. <br/><em>Journal of Neurochemistry; Molecular Neurobiology</em>
2 Protection in PD toxin models Attenuates loss of dopaminergic neurons and motor deficits after 6-OHDA or MPTP/MPP⁺, linked to mitochondrial preservation and oxidative-stress buffering. <br/><em>Neuropharmacology; Brain Research</em>
3 Mitochondrial support Improves complex I/III activity and membrane potential, raises PGC-1α/NRF1/TFAMsignaling, and lowers mtROS, pointing to a bioenergetic mechanism. <br/><em>Redox Biology; Journal of Neuroscience Research</em>
4 Microglial modulation Shifts microglia toward a pro-resolving phenotype, lowering TNF-α/IL-1β and increasing trophic cues (e.g., BDNF/GDNF signals) in injured striatum. <br/><em>Glia; Journal of Neuroinflammation</em>
5 Adult neurogenesis signals In hippocampal paradigms, increases DCX⁺/BrdU⁺ indices and dendritic maturation; behavioral readouts suggest memory consolidation benefits in stress models. <br/><em>Hippocampus; Neurobiology of Learning & Memory</em>
6 Synaptic plasticity Upregulates PSD-95, synapsin, and CREB/ERK pathways; improves LTP readouts ex vivo. <br/><em>Synapse; Neuroscience</em>
7 Anti-excitotoxicity Mitigates glutamate/NMDA injury via Ca²⁺ handling, antioxidant enzymes (SOD2, GPx), and maintenance of mitochondrial permeability thresholds. <br/><em>Experimental Neurology; Neurochemistry International</em>
8 Myelin/axon support (signals) Enhances neurite/axon elongation and may stabilize oligodendroglial support in mixed cultures—early evidence only. <br/><em>Cells; ASN Neuro</em>
9 Depression/anhedonia models Normalizes sucrose preference, novelty-suppressed feeding, and forced-swim immobility in stress rodents, paralleling increases in BDNF. <br/><em>Translational Psychiatry; Behavioural Brain Research</em>

2. Molecular Mechanism of Action

2.1 Pharmacodynamics (working model)

  • Pro-dopaminergic trophism: Upregulates TH, AADC, DAT expression, enhances dopaminergic differentiation and maintenance.

  • Mitochondrial preservation: Supports OXPHOS, reduces mtROS, and may activate AMPK→PGC-1αbiogenesis programs.

  • Neuroinflammation control: Microglial NF-κB restraint and increased neurotrophic factor milieu.

  • Enzyme targets: Unlike harmine/harmaline, strong MAO-A/B inhibition is not central to 9-MBC’s effects at trophic concentrations (some weak, context-dependent interactions reported).

2.2 Down-stream biology

Pathway Functional outcome Context
PGC-1α/NRF1/TFAM Mitochondrial biogenesis, ATP stability DA neurons
ERK/CREB/BDNF Synaptic plasticity, LTP Hippocampus/striatum
NF-κB restraint ↓ TNF-α/IL-1β, microglial shift Injury/inflammation
Antioxidant enzymes ↓ Oxidative damage Toxin models

3. Pharmacokinetics (preclinical only)

  • Route: Effective in systemic dosing in rodents (IP/PO in reports); good brain penetration inferred from CNS effects.

  • Half-life/exposure: Hours-scale in animals; human PK unknown.

  • Metabolism: Likely hepatic oxidative metabolism typical of β-carbolines; detailed metabolite map not standardized.

4. Evidence Summary

  • In vitro: Robust dopaminergic neuritogenesis and survival across primary cultures; synergy with GDNF/BDNFpathways.

  • In vivo: Neuroprotection and functional improvement in PD toxin and stress/depression models; hints of adult neurogenesis and cognitive gains.

  • No human trials to date; all efficacy claims are preclinical.

Evidence quality note: Convergent cellular and rodent data support dopaminergic trophism and mitochondrial protection. Translation to humans is unproven; dosing windows and long-term safety remain unknown.

5. Emerging Clinical Interests (conceptual)

Field Rationale Status
Parkinson’s disease (adjunct or prodrome) DA neuron protection/trophism + microglial control Preclinical
Post-toxin/trauma dopaminergic injury Regeneration/neurite outgrowth Preclinical
Cognitive impairment/aging Synaptic plasticity + hippocampal neurogenesis Preclinical
Depression/anhedonia Plasticity/BDNF angle Preclinical

6. Safety and Tolerability (unknowns & class cautions)

  • Human safety: Unknown. No phase-1 data.

  • Genotoxic/phototoxic potential (class): Planar β-carbolines can intercalate DNA and, at high doses or UV exposure, show phototoxic/genotoxic risks in some assays; 9-MBC-specific margins are not defined.

  • MAO interactions: Although not a strong MAO inhibitor at trophic doses, caution with MAOI/serotonergiccombinations is prudent until characterized.

  • Seizure threshold: High doses of some β-carbolines lower seizure threshold; relevance to 9-MBC is unclear—avoid in epilepsy risk.

  • Cardiac/mitochondrial: Excessive mitochondrial modulation could theoretically affect conductance/energetics—ECG and metabolic safety need formal study.

  • Reproductive/oncology: No data; avoid in pregnancy and in active malignancy until carcinogenicity is excluded.

  • Product quality: Grey-market “nootropic” supplies are unregulated and frequently misidentified—avoid human use outside regulated research.

Comparative snapshot (dopaminergic-trophic strategies)

Feature 9-MBC Selegiline/rasagiline GDNF (intracerebral)
Primary action Neurotrophic/mitochondrial β-carboline MAO-B inhibition (neuroprotection) Direct trophic signaling
Evidence Preclinical Human (symptomatic + some protection) Human surgical trials, mixed
Delivery Oral feasible (preclinical) Oral Neurosurgical infusion
Safety known No Yes (established) Procedure-heavy risks

7. Regulatory Landscape

  • Not approved by FDA/EMA/PMDA.

  • No registered IND-stage clinical program publicly available.

  • Any consumer sale is research-chemical market; identity and purity are not assured.

8. Practical Take & Future Directions

  • Do not self-experiment. Priorities are GLP toxicology, genotoxicity/phototoxicity screens, cardiovascular safety, and first-in-human SAD/MAD before any patient use.

  • Trial design ideas:

    • Phase 1: PK/PD with qEEG, oculomotor and motor battery, mitochondrial biomarkers (acyl-carnitines), and retinal/striatal MRI safety markers.

    • Phase 2a (PD or prodromal RBD): DAT-SPECT, MDS-UPDRS, gait/typing kinematics, and inflammatory/BDNF panels; exclude MAOI use.

  • Chemistry: Optimize photostability, selectivity, and mitochondrial-sparing while retaining dopaminergic trophism; explore prodrugs with CNS targeting.

Selected References

  • Journal of Neurochemistry; Molecular Neurobiology — Dopaminergic differentiation and neurite outgrowth under 9-MBC.

  • Neuropharmacology; Brain Research — Protection in MPTP/6-OHDA models; motor outcomes.

  • Redox Biology; Journal of Neuroscience Research — Mitochondrial function, PGC-1α signaling, and mtROS effects.

  • Glia; Journal of Neuroinflammation — Microglial phenotype shifts and cytokine modulation.

  • Hippocampus; Neurobiology of Learning & Memory — Adult neurogenesis and memory behaviors.

  • Synapse; Neuroscience — Synaptic proteins and LTP.

  • Experimental Neurology; Neurochemistry International — Anti-excitotoxic and antioxidant defenses.