9-Me-BC (9-methyl-beta-carboline)

updated

9-Me-BC (9-methyl-beta-carboline) is a research compound sold for dopaminergic enhancement, motivation and protection against dopamine downregulation from stimulants. Its published work is cell culture, enzyme assays and two rat studies, nearly all from one network of authors, and no controlled human study exists: a PubMed query on 10 October 2026 found no record of 9-Me-BC given to a person. No study tested the stimulant use, and the motivation wording has no support in the records reviewed.

N-methylated beta-carboline (monoamine oxidase inhibitor in vitro)

  • 9-Me-BC is PubChem CID 164979, C12H10N2, molecular weight 182.22, CAS 2521-07-5, and is also called 9-methylnorharman or 9-methylnorharmane.
  • In rats given MPP+ for 28 days, 9-Me-BC infused into the brain ventricle for 14 days reversed striatal dopamine lowering and brought tyrosine hydroxylase-positive substantia nigra cell counts back to normal values.
  • In rats, 10 days but not 5 days of treatment improved radial maze spatial learning; the abstract gives no dose or route.
  • In cell and enzyme work 9-Me-BC inhibited MAO-A with an IC50 of 1 micromolar and MAO-B with an IC50 of 15.5 micromolar.
  • Three 9-methyl-beta-carbolines damaged DNA under UVA light in solution, and no study tested skin, eyes or phototoxicity in an animal or a person.
  • A PubMed query on 10 October 2026 found no record of 9-Me-BC given to a person, and none testing the stimulant claim.

What is 9-Me-BC, and what is its regulatory status?

9-Me-BC is 9-methyl-beta-carboline, also called 9-methylnorharman, a defined molecule (PubChem CID 164979). It has no label, no application and no registered study in the records reviewed, and it is a separate molecule from other methylated beta-carbolines such as 9-methyl-harmane.

9-Me-BC is PubChem CID 164979, C12H10N2, 182.22 g/mol, CAS 2521-07-5 (listed among the PubChem synonyms), IUPAC name 9-methylpyrido[3,4-b]indole. The literature also calls it 9-methylnorharman or 9-methylnorharmane, after its unmethylated parent norharmane.

It is one of several N-methylated beta-carbolines that behave differently. 9-methyl-harmane and 9-methyl-harmine are separate molecules, and the 2-methyl and 2,9-dimethyl beta-carbolinium cations are separate again; the 2,9-dimethyl cation is the toxin used in some of the cell work described below. No public record ties any vendor material to the studied compound.

On 10 October 2026 DailyMed returned no label for 9-methyl-beta-carboline, an openFDA Drugs@FDA query returned no match, and ClinicalTrials.gov queries for the exact phrase and for 9-methylnorharmane and methylcarboline returned no studies. Status outside the United States is not covered here.

PubChem: 9-Me-BC identity, CID 164979

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 164979, 9-methylpyrido[3,4-b]indole (9-methyl-beta-carboline, 9-methylnorharmane).

9-Me-BC is PubChem CID 164979, C12H10N2, 182.22 g/mol, CAS 2521-07-5 (listed among the PubChem synonyms), IUPAC name 9-methylpyrido[3,4-b]indole. The literature also calls it 9-methylnorharman or 9-methylnorharmane, after its unmethylated parent norharmane. It is one of several N-methylated beta-carbolines that behave differently: 9-methyl-harmane and 9-methyl-harmine are separate molecules, and the 2-methyl and 2,9-dimethyl beta-carbolinium cations are separate again.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

Identity record only. No public record ties any vendor material to the studied compound.

Read the original source
Label and registry searches, 10 October 2026: no label, no match, no study

Regulatory record

U.S. Food and Drug Administration (DailyMed label search; openFDA Drugs@FDA query) and ClinicalTrials.gov. Searches for 9-methyl-beta-carboline and name variants, run 10 October 2026.

DailyMed returned no label for 9-methyl-beta-carboline, the openFDA Drugs@FDA query returned no match, and ClinicalTrials.gov queries for the exact phrase 9-methyl-beta-carboline and for 9-methyl-beta-carboline OR 9-methylnorharmane OR methylcarboline returned no studies.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026. It covers United States label, application and registry records only.

Read the original source

What did the cell and rat studies find?

In cultured dopaminergic cells 9-Me-BC lowered cell death markers and raised dopaminergic differentiation, and in rats it reversed MPP+-induced dopamine and nigral cell loss when infused into the brain ventricle and improved radial maze learning. All of it is cell or rat work, mostly from one network of authors, and no controlled human study exists.

In primary mesencephalic dopaminergic cultures (species not stated in the abstract), 9-Me-BC lowered lactate dehydrogenase release, propidium iodide staining and caspase-3 activity, raised ATP content, reduced inflammation-related gene expression and increased the number of differentiated dopaminergic neurons and the expression of dopaminergic differentiation genes. Dopamine uptake capacity rose, while dopamine content rose only slightly and not significantly. The compound was anti-proliferative in human SH-SY5Y neuroblastoma cells.

A 2010 follow-up from the same group reported raised TH expression and neurite outgrowth, protection of TH-immunoreactive neurons against lipopolysaccharide and against 2,9-dimethyl-beta-carbolinium toxicity, regeneration after chronic rotenone, fewer microglia, lower inflammatory cytokine expression and lower alpha-synuclein protein. Concentrations are not in either abstract, and neither reports behavior or any whole-animal result.

In rats, 28 days of MPP+ infusion lowered dopamine by about 50%. 9-Me-BC delivered for 14 days into the left cerebral ventricle reversed the dopamine lowering in the left striatum and brought the stereological count of tyrosine hydroxylase-positive substantia nigra cells back to normal values. Striatal mitochondrial complex I activity rose by about 80% and the neurotrophins BDNF, conserved dopamine neurotrophic factor, cerebellin 1 precursor protein and CNTF were induced. This is a neurotoxin model of Parkinson's disease with direct delivery into the brain ventricle, so it shows neither oral activity nor any effect in a healthy brain. The abstract does not state the dose.

The only behavioral result found is in rats: 10 days, but not 5 days, of treatment improved spatial learning in the radial maze, raised dopamine in the hippocampal formation and gave longer, more complex dendritic trees and higher spine numbers on dentate gyrus granule neurons. The authors call it a cognitive enhancer in a hippocampus-dependent task. The abstract gives no dose or route and names no disease model, and motivation, reward, effort and attention were not measured. This paper comes from the same author network as the cell work.

Dopaminergic cell cultures: less cell death, more differentiation

Cell study

Hamann J et al. Neurochem Int. 2008;52(4-5):688-700. PMID 17913302.

In primary mesencephalic dopaminergic cultures (species not stated in the abstract), 9-Me-BC lowered lactate dehydrogenase release, propidium iodide staining and caspase-3 activity, raised ATP content, reduced inflammation-related gene expression, and increased the number of differentiated dopaminergic neurons and the expression of dopaminergic differentiation genes (Shh, Wnt1, Wnt5a, En1, En2, Nurr1, Pitx3, Th, Dat, Aldh1a1). Dopamine uptake capacity rose, while dopamine content rose only slightly and not significantly. It was anti-proliferative in human SH-SY5Y neuroblastoma cells. A 2010 follow-up from the same group (PMID 20374418) reported raised TH expression and neurite outgrowth, protection of TH-immunoreactive neurons against lipopolysaccharide and against 2,9-dimethyl-beta-carbolinium toxicity, regeneration after chronic rotenone, fewer microglia and lower inflammatory cytokine expression, and lower alpha-synuclein protein.

Participants / model
Primary mesencephalic cell cultures; SH-SY5Y human neuroblastoma cells
Treatment
9-Me-BC added to cell culture; concentrations not stated in either abstract
Follow-up
not stated in the source
Study design
Original preclinical studies in cell culture, from one research network
Funding
not stated in the source

Neither abstract reports behavior or any whole-animal result.

Read the original source
MPP+ rat model: dopamine and nigral cell counts restored

Animal study

Wernicke C et al. Pharmacol Rep. 2010;62(1):35-53. PMID 20360614.

After 28 days of MPP+ infusion, which lowered dopamine by about 50%, 9-Me-BC delivered for 14 days into the left cerebral ventricle reversed the dopamine lowering in the left striatum and brought the stereological count of tyrosine hydroxylase-positive substantia nigra cells back to normal values. Complex I activity in striatal mitochondria was raised by about 80% and the neurotrophins BDNF, conserved dopamine neurotrophic factor, cerebellin 1 precursor protein and CNTF were induced.

Participants / model
Rats pretreated with MPP+
Treatment
9-Me-BC by infusion into the left cerebral ventricle for 14 days; dose not stated in the abstract
Follow-up
28 days of MPP+ infusion, then 14 days of 9-Me-BC
Study design
Original preclinical study in a neurotoxin model of Parkinson's disease
Funding
not stated in the source

Direct delivery into the brain ventricle in a toxin model, so it shows neither oral activity nor any effect in a healthy brain.

Read the original source
Rat radial maze: 10 days of treatment improved spatial learning

Animal study

Gruss M et al. J Neurochem. 2012;121(6):924-31. PMID 22380576.

In rats, 10 days (but not 5 days) of pharmacological treatment with 9-Me-BC improved spatial learning in the radial maze, raised dopamine levels in the hippocampal formation, and gave longer, more complex dendritic trees and higher spine numbers on dentate gyrus granule neurons. The authors call it a cognitive enhancer in a hippocampus-dependent task.

Participants / model
Rats
Treatment
9-Me-BC for 5 or 10 days; dose and route not stated in the abstract
Follow-up
5 and 10 days of treatment
Study design
Original preclinical study
Funding
not stated in the source

The only behavioral result found. The abstract names no disease model. Motivation, reward, effort and attention were not measured. The paper comes from the same research network as the cell culture work.

Read the original source

How does 9-Me-BC act on dopamine neurons?

In cultures 9-Me-BC raised dopaminergic differentiation and neurotrophic factor expression and inhibited monoamine oxidase, with an IC50 of 1 micromolar for MAO-A and 15.5 micromolar for MAO-B. These are cell and enzyme results, and no source says what concentration 9-Me-BC reaches in a living brain.

In dopaminergic midbrain and cortical astrocyte cultures, 9-Me-BC was anti-proliferative without toxic properties and raised gene expression of Artn, Bdnf, Egln1, Tgfb2 and Ncam1 through the PI3K pathway, with the organic cation transporter but not the dopamine transporter mediating part of the effect. A correction notice for this 2020 paper was published in 2022, and the notice record does not state what was corrected.

9-Me-BC inhibited monoamine oxidase activity with an IC50 of 1 micromolar for MAO-A and 15.5 micromolar for MAO-B, which the authors suggest may contribute to the raised dopamine content and anti-apoptotic effects seen in cell culture. An independent 2011 study from Madrid found that 9-methylnorharman inhibited oxidation of the neurotoxin MPTP by human mitochondria (IC50 7.3 micromolar) and inhibited human MAO-B.

These are enzyme and cell results. No source says what concentration 9-Me-BC reaches in a living brain, so the link from these assays to the rat findings is not established.

Astrocyte cultures and MAO: IC50 1 micromolar for MAO-A, 15.5 micromolar for MAO-B

Cell study

Keller S et al. J Neural Transm (Vienna). 2020;127(7):999-1012. PMID 32285253.

In dopaminergic midbrain and cortical astrocyte cultures, 9-Me-BC was anti-proliferative without toxic properties and raised gene expression of Artn, Bdnf, Egln1, Tgfb2 and Ncam1 through the PI3K pathway, with the organic cation transporter but not the dopamine transporter mediating part of the effect. It inhibited monoamine oxidase activity with an IC50 of 1 micromolar for MAO-A and 15.5 micromolar for MAO-B, which the authors suggest may contribute to the raised dopamine content and anti-apoptotic effects seen in cell culture. A correction notice for this paper was published in 2022 (PMID 34779915), and the notice record does not state what was corrected. An independent 2011 study from Madrid (PMID 21554916) found 9-methylnorharman inhibited oxidation of the neurotoxin MPTP by human mitochondria (IC50 7.3 micromolar) and inhibited human MAO-B.

Participants / model
Midbrain and cortical astrocyte cultures; human mitochondria and recombinant MAO preparations
Treatment
9-Me-BC in cell culture and enzyme assays
Follow-up
not stated in the source
Study design
Original preclinical studies, cell culture and enzyme assays
Funding
not stated in the source

Enzyme and cell results. No source says what concentration 9-Me-BC reaches in a living brain. The paper has a published correction whose content is not stated.

Read the original source
Dopaminergic cell cultures: less cell death, more differentiation

Cell study

Hamann J et al. Neurochem Int. 2008;52(4-5):688-700. PMID 17913302.

In primary mesencephalic dopaminergic cultures (species not stated in the abstract), 9-Me-BC lowered lactate dehydrogenase release, propidium iodide staining and caspase-3 activity, raised ATP content, reduced inflammation-related gene expression, and increased the number of differentiated dopaminergic neurons and the expression of dopaminergic differentiation genes (Shh, Wnt1, Wnt5a, En1, En2, Nurr1, Pitx3, Th, Dat, Aldh1a1). Dopamine uptake capacity rose, while dopamine content rose only slightly and not significantly. It was anti-proliferative in human SH-SY5Y neuroblastoma cells. A 2010 follow-up from the same group (PMID 20374418) reported raised TH expression and neurite outgrowth, protection of TH-immunoreactive neurons against lipopolysaccharide and against 2,9-dimethyl-beta-carbolinium toxicity, regeneration after chronic rotenone, fewer microglia and lower inflammatory cytokine expression, and lower alpha-synuclein protein.

Participants / model
Primary mesencephalic cell cultures; SH-SY5Y human neuroblastoma cells
Treatment
9-Me-BC added to cell culture; concentrations not stated in either abstract
Follow-up
not stated in the source
Study design
Original preclinical studies in cell culture, from one research network
Funding
not stated in the source

Neither abstract reports behavior or any whole-animal result.

Read the original source

Does 9-Me-BC damage DNA under light?

In test-tube experiments with UVA light, three 9-methyl-beta-carbolines including 9-methylnorharmane damaged DNA, mostly through oxidized purine residues. These are cell-free chemistry results, and no study tested skin, eyes or phototoxicity in an animal or a person.

A 2013 paper opens by saying beta-carboline alkaloids, particularly the 9-methyl derivatives, are efficient photosensitizers. It tested three 9-methyl-beta-carbolines (9-methyl-norharmane, 9-methyl-harmane and 9-methyl-harmine) with UVA excitation at physiological pH and found DNA damage: mostly oxidized purine residues in a type-I reaction from the protonated excited form, plus single-strand breaks, base-loss sites and cyclobutane pyrimidine dimers from the excited neutral form. A 2018 study measured singlet oxygen quantum yields for N-methyl-beta-carboline derivatives including 9-methyl compounds, and its abstract gives no values.

These are cell-free DNA and photochemistry experiments. A PubMed query on 10 October 2026 combining the 9-methyl-beta-carboline names with skin, photosensitivity, phototoxicity, photodynamic, UVA or light returned 2 records, this paper and a fluorescence spectroscopy study of protonation in solvent mixtures, and neither tested skin, eyes or phototoxicity in an animal or a person. Whether photosensitivity occurs in living tissue after dosing is unstudied in the records reviewed.

UVA experiments: three 9-methyl-beta-carbolines damaged DNA in solution

Cell study

Vignoni M et al. Org Biomol Chem. 2013;11(32):5300-9. PMID 23842892.

The 2013 paper opens by saying beta-carboline alkaloids, particularly the 9-methyl derivatives, are efficient photosensitizers. It tested three 9-methyl-beta-carbolines (9-methyl-norharmane, 9-methyl-harmane, 9-methyl-harmine) with UVA excitation at physiological pH and found DNA damage, mostly oxidized purine residues in a type-I reaction from the protonated excited form, plus single-strand breaks, base-loss sites and cyclobutane pyrimidine dimers from the excited neutral form. A 2018 study (PMID 28741707) measured singlet oxygen quantum yields for N-methyl-beta-carboline derivatives including 9-methyl compounds, and its abstract gives no values. A PubMed query on 10 October 2026 combining the 9-methyl-beta-carboline names with skin, photosensitivity, phototoxicity, photodynamic, UVA or light returned 2 records, this paper and a fluorescence spectroscopy study of protonation in solvent mixtures (PMID 19536642), and neither tested skin, eyes or phototoxicity in an animal or a person.

Participants / model
DNA in solution; aqueous chemical solutions
Treatment
In vitro irradiation experiments with UVA light
Follow-up
not stated in the source
Study design
Original chemistry and photobiology studies, cell-free
Funding
not stated in the source

A chemistry result. It does not show skin damage in people, and photosensitivity in living tissue after dosing is unstudied in the records reviewed.

Read the original source

Has 9-Me-BC been tested in people?

No. A PubMed query on 10 October 2026 for the names with human, patients, volunteers or clinical returned 4 records, and none reports 9-Me-BC given to a person. No pharmacokinetic, bioavailability, half-life or toxicology result appears in the records reviewed.

A PubMed query on 10 October 2026 for the 9-methyl-beta-carboline names with human, patients, volunteers or clinical returned 4 records: two reviews, the 2008 cell paper and the 2011 MPTP paper. None reports 9-Me-BC given to a person.

A query pairing the names with pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice returned 5 records, and none reports plasma levels, bioavailability, half-life or toxicology. ClinicalTrials.gov queries returned no studies. No controlled human trial exists in the records reviewed.

PubMed, 10 October 2026: 4 records with human terms, none gives 9-Me-BC to a person

PubMed search record

PubMed search run 10 October 2026 for the 9-methyl-beta-carboline names AND (human OR patients OR volunteers OR clinical), with a follow-up query adding pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice.

A search for the names with human, patients, volunteers or clinical returned 4 records (two reviews, the 2008 cell paper and the 2011 MPTP paper), and none reports 9-Me-BC given to a person. A query pairing the names with pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice returned 5 records (the cell, astrocyte, MPP+ rat and radial maze papers among them), and none reports plasma levels, bioavailability, half-life or toxicology. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished or unindexed work exists.

Read the original source
Label and registry searches, 10 October 2026: no label, no match, no study

Regulatory record

U.S. Food and Drug Administration (DailyMed label search; openFDA Drugs@FDA query) and ClinicalTrials.gov. Searches for 9-methyl-beta-carboline and name variants, run 10 October 2026.

DailyMed returned no label for 9-methyl-beta-carboline, the openFDA Drugs@FDA query returned no match, and ClinicalTrials.gov queries for the exact phrase 9-methyl-beta-carboline and for 9-methyl-beta-carboline OR 9-methylnorharmane OR methylcarboline returned no studies.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026. It covers United States label, application and registry records only.

Read the original source

Does 9-Me-BC enhance motivation or counter stimulant downregulation?

Only in part, and only in cells and rats. Dopaminergic enhancement and neuroprotection describe cell and rat findings, while motivation and use against dopamine downregulation from stimulants have no supporting study in the records reviewed.

Sellers describe dopaminergic enhancement, motivation and possible neuroprotection, and use against dopamine downregulation from stimulants. Dopaminergic enhancement and neuroprotection describe the cell culture findings and the rat MPP+ and radial maze results described above, none of them in people.

Motivation has no support here: the rat cognition paper measured spatial learning, and motivation, reward, effort and attention were not measured. For the stimulant claim, a PubMed query on 10 October 2026 for the name variants with methamphetamine, amphetamine, cocaine, stimulant, addiction, drug abuse, downregulation or desensitization returned 2 records, the rat cognition paper and a 2012 commentary on it, and neither involves a stimulant drug or receptor or transporter downregulation. A broader beta-carboline query returned 1 record, a 1989 paper on an unrelated tetrahydro-beta-carbolinone antidepressant candidate, and a query pairing the names with motivation, reward, depression, attention or effort returned 0 records. The nearest animal evidence is the MPP+ neurotoxin model, which is not a stimulant exposure model.

PubMed, 10 October 2026: 2 records, neither involves a stimulant

PubMed search record

PubMed search run 10 October 2026 for the 9-methyl-beta-carboline name variants AND (methamphetamine OR amphetamine OR cocaine OR stimulant OR stimulants OR addiction OR "drug abuse" OR downregulation OR down-regulation OR desensitization), with follow-up queries.

The search returned 2 records: the rat cognition paper and a 2012 commentary on it (PMID 22372749, no abstract). Neither involves a stimulant drug or receptor or transporter downregulation. A broader query for beta-carboline with methamphetamine, amphetamine or cocaine, dopamine and neuroprotection or restoration returned 1 record, a 1989 paper on an unrelated tetrahydro-beta-carbolinone antidepressant candidate (PMID 2636891). A query pairing the names with motivation, reward, depression, attention or effort returned 0 records. The nearest animal evidence is the MPP+ neurotoxin model, which is not a stimulant exposure model.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished or unindexed work exists.

Read the original source
Rat radial maze: 10 days of treatment improved spatial learning

Animal study

Gruss M et al. J Neurochem. 2012;121(6):924-31. PMID 22380576.

In rats, 10 days (but not 5 days) of pharmacological treatment with 9-Me-BC improved spatial learning in the radial maze, raised dopamine levels in the hippocampal formation, and gave longer, more complex dendritic trees and higher spine numbers on dentate gyrus granule neurons. The authors call it a cognitive enhancer in a hippocampus-dependent task.

Participants / model
Rats
Treatment
9-Me-BC for 5 or 10 days; dose and route not stated in the abstract
Follow-up
5 and 10 days of treatment
Study design
Original preclinical study
Funding
not stated in the source

The only behavioral result found. The abstract names no disease model. Motivation, reward, effort and attention were not measured. The paper comes from the same research network as the cell culture work.

Read the original source
MPP+ rat model: dopamine and nigral cell counts restored

Animal study

Wernicke C et al. Pharmacol Rep. 2010;62(1):35-53. PMID 20360614.

After 28 days of MPP+ infusion, which lowered dopamine by about 50%, 9-Me-BC delivered for 14 days into the left cerebral ventricle reversed the dopamine lowering in the left striatum and brought the stereological count of tyrosine hydroxylase-positive substantia nigra cells back to normal values. Complex I activity in striatal mitochondria was raised by about 80% and the neurotrophins BDNF, conserved dopamine neurotrophic factor, cerebellin 1 precursor protein and CNTF were induced.

Participants / model
Rats pretreated with MPP+
Treatment
9-Me-BC by infusion into the left cerebral ventricle for 14 days; dose not stated in the abstract
Follow-up
28 days of MPP+ infusion, then 14 days of 9-Me-BC
Study design
Original preclinical study in a neurotoxin model of Parkinson's disease
Funding
not stated in the source

Direct delivery into the brain ventricle in a toxin model, so it shows neither oral activity nor any effect in a healthy brain.

Read the original source

What is known about the safety of 9-Me-BC?

No human safety, pharmacokinetic or toxicology data exist for 9-Me-BC. Three concerns remain open: DNA damage under UVA light in test-tube work, a class caution about beta-carboline neurotoxicity, and MAO inhibition in vitro that raises interaction questions no source addresses.

No record reports 9-Me-BC given to a person, so no human adverse event, tolerability or interaction information exists, and no pharmacokinetic or toxicology result appears in the records reviewed.

The photochemistry work shows DNA damage under UVA light in solution. That is a chemistry result and not a finding of skin damage in people, and whether photosensitivity occurs in living tissue after dosing is unstudied.

The 2010 cell paper opens by describing beta-carbolines as potential endogenous and exogenous neurotoxins that may contribute to Parkinson's disease. A 2002 enzymology paper reports that mammalian brain converts beta-carbolines into 2N-methylated beta-carbolinium cations, described as analogs of the Parkinsonian toxin MPP+, and that purified phenylethanolamine N-methyltransferase 2N-methylates 9-methylnorharman, with the activity present in human adrenal medulla. The abstract does not name the product, and the authors present the toxic-cation role as a hypothesis. Whether 9-Me-BC forms a toxic cation in animals or people was not tested in any record reviewed, and no source states that it does.

Because 9-Me-BC inhibited MAO-A with an IC50 of 1 micromolar in vitro, interactions with medicines are an open question that no source addresses, and nothing here supports calling it compatible with any medicine. Product identity is a separate concern, because no public record ties any vendor material to the studied compound.

PubMed, 10 October 2026: 4 records with human terms, none gives 9-Me-BC to a person

PubMed search record

PubMed search run 10 October 2026 for the 9-methyl-beta-carboline names AND (human OR patients OR volunteers OR clinical), with a follow-up query adding pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice.

A search for the names with human, patients, volunteers or clinical returned 4 records (two reviews, the 2008 cell paper and the 2011 MPTP paper), and none reports 9-Me-BC given to a person. A query pairing the names with pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice returned 5 records (the cell, astrocyte, MPP+ rat and radial maze papers among them), and none reports plasma levels, bioavailability, half-life or toxicology. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished or unindexed work exists.

Read the original source
UVA experiments: three 9-methyl-beta-carbolines damaged DNA in solution

Cell study

Vignoni M et al. Org Biomol Chem. 2013;11(32):5300-9. PMID 23842892.

The 2013 paper opens by saying beta-carboline alkaloids, particularly the 9-methyl derivatives, are efficient photosensitizers. It tested three 9-methyl-beta-carbolines (9-methyl-norharmane, 9-methyl-harmane, 9-methyl-harmine) with UVA excitation at physiological pH and found DNA damage, mostly oxidized purine residues in a type-I reaction from the protonated excited form, plus single-strand breaks, base-loss sites and cyclobutane pyrimidine dimers from the excited neutral form. A 2018 study (PMID 28741707) measured singlet oxygen quantum yields for N-methyl-beta-carboline derivatives including 9-methyl compounds, and its abstract gives no values. A PubMed query on 10 October 2026 combining the 9-methyl-beta-carboline names with skin, photosensitivity, phototoxicity, photodynamic, UVA or light returned 2 records, this paper and a fluorescence spectroscopy study of protonation in solvent mixtures (PMID 19536642), and neither tested skin, eyes or phototoxicity in an animal or a person.

Participants / model
DNA in solution; aqueous chemical solutions
Treatment
In vitro irradiation experiments with UVA light
Follow-up
not stated in the source
Study design
Original chemistry and photobiology studies, cell-free
Funding
not stated in the source

A chemistry result. It does not show skin damage in people, and photosensitivity in living tissue after dosing is unstudied in the records reviewed.

Read the original source
Enzyme study: PNMT 2N-methylates 9-methylnorharman

Cell study

Gearhart DA et al. Neurochem Int. 2002;40(7):611-20. PMID 11900856.

A 2002 enzymology paper reports that mammalian brain converts beta-carbolines into 2N-methylated beta-carbolinium cations, described as analogs in structure and function of the Parkinsonian toxin MPP+, and that purified phenylethanolamine N-methyltransferase 2N-methylates 9-methylnorharman (21.1 pmol/h per unit PNMT), with the activity present in human adrenal medulla (43.7 pmol/h/mg protein). The abstract does not name the product. The authors present the toxic-cation role as a hypothesis. The 2010 cell paper also opens by describing beta-carbolines as potential endogenous and exogenous neurotoxins that may contribute to Parkinson's disease.

Participants / model
Purified enzyme and human adrenal medulla tissue (in vitro)
Treatment
Enzyme assays
Follow-up
not stated in the source
Study design
Original enzymology study
Funding
not stated in the source

No source in the records reviewed tested whether 9-Me-BC forms a toxic cation in animals or people, and no source states that it does.

Read the original source
Astrocyte cultures and MAO: IC50 1 micromolar for MAO-A, 15.5 micromolar for MAO-B

Cell study

Keller S et al. J Neural Transm (Vienna). 2020;127(7):999-1012. PMID 32285253.

In dopaminergic midbrain and cortical astrocyte cultures, 9-Me-BC was anti-proliferative without toxic properties and raised gene expression of Artn, Bdnf, Egln1, Tgfb2 and Ncam1 through the PI3K pathway, with the organic cation transporter but not the dopamine transporter mediating part of the effect. It inhibited monoamine oxidase activity with an IC50 of 1 micromolar for MAO-A and 15.5 micromolar for MAO-B, which the authors suggest may contribute to the raised dopamine content and anti-apoptotic effects seen in cell culture. A correction notice for this paper was published in 2022 (PMID 34779915), and the notice record does not state what was corrected. An independent 2011 study from Madrid (PMID 21554916) found 9-methylnorharman inhibited oxidation of the neurotoxin MPTP by human mitochondria (IC50 7.3 micromolar) and inhibited human MAO-B.

Participants / model
Midbrain and cortical astrocyte cultures; human mitochondria and recombinant MAO preparations
Treatment
9-Me-BC in cell culture and enzyme assays
Follow-up
not stated in the source
Study design
Original preclinical studies, cell culture and enzyme assays
Funding
not stated in the source

Enzyme and cell results. No source says what concentration 9-Me-BC reaches in a living brain. The paper has a published correction whose content is not stated.

Read the original source
PubChem: 9-Me-BC identity, CID 164979

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 164979, 9-methylpyrido[3,4-b]indole (9-methyl-beta-carboline, 9-methylnorharmane).

9-Me-BC is PubChem CID 164979, C12H10N2, 182.22 g/mol, CAS 2521-07-5 (listed among the PubChem synonyms), IUPAC name 9-methylpyrido[3,4-b]indole. The literature also calls it 9-methylnorharman or 9-methylnorharmane, after its unmethylated parent norharmane. It is one of several N-methylated beta-carbolines that behave differently: 9-methyl-harmane and 9-methyl-harmine are separate molecules, and the 2-methyl and 2,9-dimethyl beta-carbolinium cations are separate again.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

Identity record only. No public record ties any vendor material to the studied compound.

Read the original source

Why does 9-Me-BC sit in D tier?

The mechanism is interesting on paper, but the outcome evidence is one rat cognition study and one rat toxin-model study, nearly all from one author network, with no human data and no study of the stimulant use. A published phototoxicity concern and a class neurotoxicity caution add to that.

The mechanism looks plausible: dopaminergic neuron differentiation and protection in culture, MAO inhibition, and restoration of nigral TH cells after MPP+ in rats. The outcome evidence is thin, with one cognition study and one toxin-model study in rats. Nearly every paper comes from one network of authors, and the independent papers are the MPTP-oxidation assay and the photochemistry.

There is no human exposure, no pharmacokinetics, no toxicology and no study of the stimulant use sellers cite. Against that stand a specific published phototoxicity concern, a class warning about beta-carboline neurotoxicity and an unanswered metabolism question. That puts it with other D-tier research chemicals such as J147 and dihexa, because the seller use case has no data behind it at all.

Dopaminergic cell cultures: less cell death, more differentiation

Cell study

Hamann J et al. Neurochem Int. 2008;52(4-5):688-700. PMID 17913302.

In primary mesencephalic dopaminergic cultures (species not stated in the abstract), 9-Me-BC lowered lactate dehydrogenase release, propidium iodide staining and caspase-3 activity, raised ATP content, reduced inflammation-related gene expression, and increased the number of differentiated dopaminergic neurons and the expression of dopaminergic differentiation genes (Shh, Wnt1, Wnt5a, En1, En2, Nurr1, Pitx3, Th, Dat, Aldh1a1). Dopamine uptake capacity rose, while dopamine content rose only slightly and not significantly. It was anti-proliferative in human SH-SY5Y neuroblastoma cells. A 2010 follow-up from the same group (PMID 20374418) reported raised TH expression and neurite outgrowth, protection of TH-immunoreactive neurons against lipopolysaccharide and against 2,9-dimethyl-beta-carbolinium toxicity, regeneration after chronic rotenone, fewer microglia and lower inflammatory cytokine expression, and lower alpha-synuclein protein.

Participants / model
Primary mesencephalic cell cultures; SH-SY5Y human neuroblastoma cells
Treatment
9-Me-BC added to cell culture; concentrations not stated in either abstract
Follow-up
not stated in the source
Study design
Original preclinical studies in cell culture, from one research network
Funding
not stated in the source

Neither abstract reports behavior or any whole-animal result.

Read the original source
MPP+ rat model: dopamine and nigral cell counts restored

Animal study

Wernicke C et al. Pharmacol Rep. 2010;62(1):35-53. PMID 20360614.

After 28 days of MPP+ infusion, which lowered dopamine by about 50%, 9-Me-BC delivered for 14 days into the left cerebral ventricle reversed the dopamine lowering in the left striatum and brought the stereological count of tyrosine hydroxylase-positive substantia nigra cells back to normal values. Complex I activity in striatal mitochondria was raised by about 80% and the neurotrophins BDNF, conserved dopamine neurotrophic factor, cerebellin 1 precursor protein and CNTF were induced.

Participants / model
Rats pretreated with MPP+
Treatment
9-Me-BC by infusion into the left cerebral ventricle for 14 days; dose not stated in the abstract
Follow-up
28 days of MPP+ infusion, then 14 days of 9-Me-BC
Study design
Original preclinical study in a neurotoxin model of Parkinson's disease
Funding
not stated in the source

Direct delivery into the brain ventricle in a toxin model, so it shows neither oral activity nor any effect in a healthy brain.

Read the original source
Rat radial maze: 10 days of treatment improved spatial learning

Animal study

Gruss M et al. J Neurochem. 2012;121(6):924-31. PMID 22380576.

In rats, 10 days (but not 5 days) of pharmacological treatment with 9-Me-BC improved spatial learning in the radial maze, raised dopamine levels in the hippocampal formation, and gave longer, more complex dendritic trees and higher spine numbers on dentate gyrus granule neurons. The authors call it a cognitive enhancer in a hippocampus-dependent task.

Participants / model
Rats
Treatment
9-Me-BC for 5 or 10 days; dose and route not stated in the abstract
Follow-up
5 and 10 days of treatment
Study design
Original preclinical study
Funding
not stated in the source

The only behavioral result found. The abstract names no disease model. Motivation, reward, effort and attention were not measured. The paper comes from the same research network as the cell culture work.

Read the original source
UVA experiments: three 9-methyl-beta-carbolines damaged DNA in solution

Cell study

Vignoni M et al. Org Biomol Chem. 2013;11(32):5300-9. PMID 23842892.

The 2013 paper opens by saying beta-carboline alkaloids, particularly the 9-methyl derivatives, are efficient photosensitizers. It tested three 9-methyl-beta-carbolines (9-methyl-norharmane, 9-methyl-harmane, 9-methyl-harmine) with UVA excitation at physiological pH and found DNA damage, mostly oxidized purine residues in a type-I reaction from the protonated excited form, plus single-strand breaks, base-loss sites and cyclobutane pyrimidine dimers from the excited neutral form. A 2018 study (PMID 28741707) measured singlet oxygen quantum yields for N-methyl-beta-carboline derivatives including 9-methyl compounds, and its abstract gives no values. A PubMed query on 10 October 2026 combining the 9-methyl-beta-carboline names with skin, photosensitivity, phototoxicity, photodynamic, UVA or light returned 2 records, this paper and a fluorescence spectroscopy study of protonation in solvent mixtures (PMID 19536642), and neither tested skin, eyes or phototoxicity in an animal or a person.

Participants / model
DNA in solution; aqueous chemical solutions
Treatment
In vitro irradiation experiments with UVA light
Follow-up
not stated in the source
Study design
Original chemistry and photobiology studies, cell-free
Funding
not stated in the source

A chemistry result. It does not show skin damage in people, and photosensitivity in living tissue after dosing is unstudied in the records reviewed.

Read the original source
PubMed, 10 October 2026: 4 records with human terms, none gives 9-Me-BC to a person

PubMed search record

PubMed search run 10 October 2026 for the 9-methyl-beta-carboline names AND (human OR patients OR volunteers OR clinical), with a follow-up query adding pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice.

A search for the names with human, patients, volunteers or clinical returned 4 records (two reviews, the 2008 cell paper and the 2011 MPTP paper), and none reports 9-Me-BC given to a person. A query pairing the names with pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice returned 5 records (the cell, astrocyte, MPP+ rat and radial maze papers among them), and none reports plasma levels, bioavailability, half-life or toxicology. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished or unindexed work exists.

Read the original source

Studies and sources

PubChem: 9-Me-BC identity, CID 164979

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 164979, 9-methylpyrido[3,4-b]indole (9-methyl-beta-carboline, 9-methylnorharmane).

9-Me-BC is PubChem CID 164979, C12H10N2, 182.22 g/mol, CAS 2521-07-5 (listed among the PubChem synonyms), IUPAC name 9-methylpyrido[3,4-b]indole. The literature also calls it 9-methylnorharman or 9-methylnorharmane, after its unmethylated parent norharmane. It is one of several N-methylated beta-carbolines that behave differently: 9-methyl-harmane and 9-methyl-harmine are separate molecules, and the 2-methyl and 2,9-dimethyl beta-carbolinium cations are separate again.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

Identity record only. No public record ties any vendor material to the studied compound.

Read the original source
Dopaminergic cell cultures: less cell death, more differentiation

Cell study

Hamann J et al. Neurochem Int. 2008;52(4-5):688-700. PMID 17913302.

In primary mesencephalic dopaminergic cultures (species not stated in the abstract), 9-Me-BC lowered lactate dehydrogenase release, propidium iodide staining and caspase-3 activity, raised ATP content, reduced inflammation-related gene expression, and increased the number of differentiated dopaminergic neurons and the expression of dopaminergic differentiation genes (Shh, Wnt1, Wnt5a, En1, En2, Nurr1, Pitx3, Th, Dat, Aldh1a1). Dopamine uptake capacity rose, while dopamine content rose only slightly and not significantly. It was anti-proliferative in human SH-SY5Y neuroblastoma cells. A 2010 follow-up from the same group (PMID 20374418) reported raised TH expression and neurite outgrowth, protection of TH-immunoreactive neurons against lipopolysaccharide and against 2,9-dimethyl-beta-carbolinium toxicity, regeneration after chronic rotenone, fewer microglia and lower inflammatory cytokine expression, and lower alpha-synuclein protein.

Participants / model
Primary mesencephalic cell cultures; SH-SY5Y human neuroblastoma cells
Treatment
9-Me-BC added to cell culture; concentrations not stated in either abstract
Follow-up
not stated in the source
Study design
Original preclinical studies in cell culture, from one research network
Funding
not stated in the source

Neither abstract reports behavior or any whole-animal result.

Read the original source
Astrocyte cultures and MAO: IC50 1 micromolar for MAO-A, 15.5 micromolar for MAO-B

Cell study

Keller S et al. J Neural Transm (Vienna). 2020;127(7):999-1012. PMID 32285253.

In dopaminergic midbrain and cortical astrocyte cultures, 9-Me-BC was anti-proliferative without toxic properties and raised gene expression of Artn, Bdnf, Egln1, Tgfb2 and Ncam1 through the PI3K pathway, with the organic cation transporter but not the dopamine transporter mediating part of the effect. It inhibited monoamine oxidase activity with an IC50 of 1 micromolar for MAO-A and 15.5 micromolar for MAO-B, which the authors suggest may contribute to the raised dopamine content and anti-apoptotic effects seen in cell culture. A correction notice for this paper was published in 2022 (PMID 34779915), and the notice record does not state what was corrected. An independent 2011 study from Madrid (PMID 21554916) found 9-methylnorharman inhibited oxidation of the neurotoxin MPTP by human mitochondria (IC50 7.3 micromolar) and inhibited human MAO-B.

Participants / model
Midbrain and cortical astrocyte cultures; human mitochondria and recombinant MAO preparations
Treatment
9-Me-BC in cell culture and enzyme assays
Follow-up
not stated in the source
Study design
Original preclinical studies, cell culture and enzyme assays
Funding
not stated in the source

Enzyme and cell results. No source says what concentration 9-Me-BC reaches in a living brain. The paper has a published correction whose content is not stated.

Read the original source
MPP+ rat model: dopamine and nigral cell counts restored

Animal study

Wernicke C et al. Pharmacol Rep. 2010;62(1):35-53. PMID 20360614.

After 28 days of MPP+ infusion, which lowered dopamine by about 50%, 9-Me-BC delivered for 14 days into the left cerebral ventricle reversed the dopamine lowering in the left striatum and brought the stereological count of tyrosine hydroxylase-positive substantia nigra cells back to normal values. Complex I activity in striatal mitochondria was raised by about 80% and the neurotrophins BDNF, conserved dopamine neurotrophic factor, cerebellin 1 precursor protein and CNTF were induced.

Participants / model
Rats pretreated with MPP+
Treatment
9-Me-BC by infusion into the left cerebral ventricle for 14 days; dose not stated in the abstract
Follow-up
28 days of MPP+ infusion, then 14 days of 9-Me-BC
Study design
Original preclinical study in a neurotoxin model of Parkinson's disease
Funding
not stated in the source

Direct delivery into the brain ventricle in a toxin model, so it shows neither oral activity nor any effect in a healthy brain.

Read the original source
Rat radial maze: 10 days of treatment improved spatial learning

Animal study

Gruss M et al. J Neurochem. 2012;121(6):924-31. PMID 22380576.

In rats, 10 days (but not 5 days) of pharmacological treatment with 9-Me-BC improved spatial learning in the radial maze, raised dopamine levels in the hippocampal formation, and gave longer, more complex dendritic trees and higher spine numbers on dentate gyrus granule neurons. The authors call it a cognitive enhancer in a hippocampus-dependent task.

Participants / model
Rats
Treatment
9-Me-BC for 5 or 10 days; dose and route not stated in the abstract
Follow-up
5 and 10 days of treatment
Study design
Original preclinical study
Funding
not stated in the source

The only behavioral result found. The abstract names no disease model. Motivation, reward, effort and attention were not measured. The paper comes from the same research network as the cell culture work.

Read the original source
UVA experiments: three 9-methyl-beta-carbolines damaged DNA in solution

Cell study

Vignoni M et al. Org Biomol Chem. 2013;11(32):5300-9. PMID 23842892.

The 2013 paper opens by saying beta-carboline alkaloids, particularly the 9-methyl derivatives, are efficient photosensitizers. It tested three 9-methyl-beta-carbolines (9-methyl-norharmane, 9-methyl-harmane, 9-methyl-harmine) with UVA excitation at physiological pH and found DNA damage, mostly oxidized purine residues in a type-I reaction from the protonated excited form, plus single-strand breaks, base-loss sites and cyclobutane pyrimidine dimers from the excited neutral form. A 2018 study (PMID 28741707) measured singlet oxygen quantum yields for N-methyl-beta-carboline derivatives including 9-methyl compounds, and its abstract gives no values. A PubMed query on 10 October 2026 combining the 9-methyl-beta-carboline names with skin, photosensitivity, phototoxicity, photodynamic, UVA or light returned 2 records, this paper and a fluorescence spectroscopy study of protonation in solvent mixtures (PMID 19536642), and neither tested skin, eyes or phototoxicity in an animal or a person.

Participants / model
DNA in solution; aqueous chemical solutions
Treatment
In vitro irradiation experiments with UVA light
Follow-up
not stated in the source
Study design
Original chemistry and photobiology studies, cell-free
Funding
not stated in the source

A chemistry result. It does not show skin damage in people, and photosensitivity in living tissue after dosing is unstudied in the records reviewed.

Read the original source
Enzyme study: PNMT 2N-methylates 9-methylnorharman

Cell study

Gearhart DA et al. Neurochem Int. 2002;40(7):611-20. PMID 11900856.

A 2002 enzymology paper reports that mammalian brain converts beta-carbolines into 2N-methylated beta-carbolinium cations, described as analogs in structure and function of the Parkinsonian toxin MPP+, and that purified phenylethanolamine N-methyltransferase 2N-methylates 9-methylnorharman (21.1 pmol/h per unit PNMT), with the activity present in human adrenal medulla (43.7 pmol/h/mg protein). The abstract does not name the product. The authors present the toxic-cation role as a hypothesis. The 2010 cell paper also opens by describing beta-carbolines as potential endogenous and exogenous neurotoxins that may contribute to Parkinson's disease.

Participants / model
Purified enzyme and human adrenal medulla tissue (in vitro)
Treatment
Enzyme assays
Follow-up
not stated in the source
Study design
Original enzymology study
Funding
not stated in the source

No source in the records reviewed tested whether 9-Me-BC forms a toxic cation in animals or people, and no source states that it does.

Read the original source
PubMed, 10 October 2026: 2 records, neither involves a stimulant

PubMed search record

PubMed search run 10 October 2026 for the 9-methyl-beta-carboline name variants AND (methamphetamine OR amphetamine OR cocaine OR stimulant OR stimulants OR addiction OR "drug abuse" OR downregulation OR down-regulation OR desensitization), with follow-up queries.

The search returned 2 records: the rat cognition paper and a 2012 commentary on it (PMID 22372749, no abstract). Neither involves a stimulant drug or receptor or transporter downregulation. A broader query for beta-carboline with methamphetamine, amphetamine or cocaine, dopamine and neuroprotection or restoration returned 1 record, a 1989 paper on an unrelated tetrahydro-beta-carbolinone antidepressant candidate (PMID 2636891). A query pairing the names with motivation, reward, depression, attention or effort returned 0 records. The nearest animal evidence is the MPP+ neurotoxin model, which is not a stimulant exposure model.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished or unindexed work exists.

Read the original source
PubMed, 10 October 2026: 4 records with human terms, none gives 9-Me-BC to a person

PubMed search record

PubMed search run 10 October 2026 for the 9-methyl-beta-carboline names AND (human OR patients OR volunteers OR clinical), with a follow-up query adding pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice.

A search for the names with human, patients, volunteers or clinical returned 4 records (two reviews, the 2008 cell paper and the 2011 MPTP paper), and none reports 9-Me-BC given to a person. A query pairing the names with pharmacokinetic, bioavailability, half-life, toxicology, LD50, in vivo, rats or mice returned 5 records (the cell, astrocyte, MPP+ rat and radial maze papers among them), and none reports plasma levels, bioavailability, half-life or toxicology. No controlled human trial exists in the records reviewed.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished or unindexed work exists.

Read the original source
Label and registry searches, 10 October 2026: no label, no match, no study

Regulatory record

U.S. Food and Drug Administration (DailyMed label search; openFDA Drugs@FDA query) and ClinicalTrials.gov. Searches for 9-methyl-beta-carboline and name variants, run 10 October 2026.

DailyMed returned no label for 9-methyl-beta-carboline, the openFDA Drugs@FDA query returned no match, and ClinicalTrials.gov queries for the exact phrase 9-methyl-beta-carboline and for 9-methyl-beta-carboline OR 9-methylnorharmane OR methylcarboline returned no studies.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026. It covers United States label, application and registry records only.

Read the original source

Why is 9-Me-BC (9-methyl-beta-carboline) in D tier?

D fits a compound whose mechanism looks interesting on paper but whose outcome evidence is one rat cognition study and one rat toxin-model study, mostly from one author network. There are no human, pharmacokinetic or toxicology data, nothing tests the stimulant use, and a phototoxicity finding in vitro and a class neurotoxicity caution are unanswered.