N-Methylserotonin is found in plants, animals, and fungi. These include the plants, Actaea racemosa (black cohosh)[1] and Zanthoxylum piperitum,[2] the Green and Golden Bell Frog, Litoria aurea,[3] and Amanita mushrooms.[4] The compound binds to several serotonin receptors, including the 5-HT7 and 5-HT1A receptors, with high affinity (IC50 ≤ 2 nM) and selectivity, and displays agonist activity; besides its direct interaction with the serotonin receptors, N-methylserotonin also acts as a selective serotonin reuptake inhibitor.[1]

United States
N-Methylserotonin is not scheduled at the federal level in the United States,[5] but could be considered an analog (of Bufotenin), in which case, sales or possession intended for human consumption could be prosecuted under the Federal Analog Act.

Florida
N-Methylserotonin is a Schedule I controlled substance in the state of Florida making it illegal to buy, sell, or possess in Florida.[6]

Constituents: Constituents of black cohosh with proposed or demonstrated pharmacological activity include triterpine glycosides (23-epi-26-deoxyactein, actein, 27-deoxyactein, cimicifugoside A, cimicifugoside M, cimiracemoside A-H)21,45,46,47,48,12,49,50,51, cyclolanostanol xylosides 52, isoflavonone formononetin 53, hydroxytyrosol 54, actaeaeposcide 55, phenylpropanoids (cimiracemate A, cimiracemate B)8,56, organic acids (caffeic acid, cimicifugic acid A, cimicifugic acid B, cimicifugic acid E, cimicifugic acid F, cinnamic acid ester dehydrocimicifugic A, dehydrocimicifugic acid B, dihydroxyphenyl lactic acid, ferulic acid, fukinolic acid, isoferulic acid, methyl caffeate acid, salicylic acid)8,57,54,58, phenols57, quinoid metabolites of caffeic acid, cimiracemate B, fukinolic acid, fukiic acid, and.hydroxytyrosol54. Actaea racemosa specifically contains lignans (e.g., actaealactone), phenylpropanoid ester derivatives (e.g., cimicifugic acid), polyphenols (0.36-2.92% (w/w) in dried root and rhizome), protocatechuic acid, protocatechualdehyde, p-coumaric acid, caffeic acid, methyl caffeate, ferulic acid, ferulate-1-methyl ester, isoferulic acid, 1-isoferuloyl-beta-d-glucopyranoside, fukinolic acid, and cimicifugic acids A, B, and D-F

Neuropharmacologic effects: Black cohosh has been shown to exhibit an action on the central endogenous opioid system in postmenopausal women as evidenced by suppression of mean luteinizing hormone pulse frequency following opioid receptor blockade.

Black cohosh extract showed inhibitory potential for histamine release

Black Cohosh behaves as a mixed competitive ligand and partial agonist at the human mu opiate receptor

The first medicinal use of black cohosh is generally attributed to Native Americans, who used black cohosh for the treatment of a variety of disorders, including various conditions unique to women such as amenorrhea and menopause, rheumatism, kidney disorders, malaise, and pain during menses and childbirth

Dr. John King claimed that Macrotys was a remedy of “abnormal conditions of the principal organs of reproduction in the female”, and the roots “very efficacious in the treatment of chronic ovaritis, endometriosis, and menstrual derangements, such as amenorrhea, dysmenorrhea”

Dopaminergic activity in the CR extract BNO 1055 could be demonstrated with the D(2)-receptor assay. A countercurrent chromatography resulted in a separation of estrogenic and dopaminergic activity in two distinct fractions.

N-Methylserotonin. 5-Hydroxy-N-methyltryptamine.

NMT has been found in the bark, shoots and leaves of several plant species, including Virola, Acacia, Mimosa and Desmanthus

Orally administered NMT appears to produce no psychoactive effects, likely as a result of extensive first-pass metabolism.[3] However, it may become active upon combination with a MAOA inhibitor (MAOI).[3] By vaporization NMT shows activity at 50–100 mg, with a duration of 45–70 minutes; duration of visual effects 15–30 seconds. Effects are primarily non-visual.

Compound 53 had an elemental composition containing two hydrogens less than 58 and 59 (C12H12N2O), suggesting a dihydro-β-carboline structure. The ready loss of a methyl radical (m/z 186), along with the fragment ion of m/z 170, [MH-CH3NH2]+, indicated that the N(2) nitrogen on the β-carboline ring was methylated. Biosynthetic considerations were used to deduce the position of the double bond on the β-carboline ring. Accordingly, the most likely position of the double bond is 1,2 which was confirmed by comparison of retention time and fragmentation pattern with authentic N(2)-methyl-6-hydroxy-3,4-dihydro-β-carboline. Biosynthetically, this compound is likely formed by dehydrogenation of 58 and represents a new natural product. It should be noted that dihydro-β-carbolines are often by-products of Pictet-Spengler condensation [58]. Thus, it is possible that 58 is an isolation artifact.

The product ion spectrum of compound 46 eluting at 10.6 min during LC-MS of fraction 4 was dominated by an ion of m/z 144 with the elemental composition (C10H13N2), corresponding to protonated tryptamine. In-source fragmentation followed by MS-MS product ion analysis of m/z 144 showed a fragmentation pattern identical to authentic tryptamine, suggesting that this compound is a tryptamine derivative. The neutral loss of iminoacetic acid (C2H3NO2) combined with database searching suggested that 46 might be a tetrahydro-β-carboline carboxylic acid. Since two positional isomers (1 and 3-substituted) are known, both analogs were synthesized and compared with 46. These experiments identified 46 as 1,2,3,4-tetrahydro-β-carboline-3-carboxylic acid,

Aporphine and its related alkaloids bulbocapnine, boldine, glaucine and corytuberine are antipsychotic, exert naloxone-reversible antinociceptive (reducing sensitivity to painful stimuli) activity and with the exception of corytuberine are anticonvulsant.

In a rodent model, it was found that higenamine (norcoclaurine) produced cardiotonic, vascular relaxation, and bronchodilator effects.[8][9] In particular, higenamine, via a beta-adrenoceptor mechanism, induced relaxation in rat corpus cavernosum, leading to improved vasodilation and erectile function.

Related to improved vasodilatory signals, higenamine has been shown in animal models to possess antiplatelet and antithrombotic activity via a cAMP-dependent pathway, suggesting higenamine may contribute to enhanced vasodilation and arterial integrity.[2][7][9][10]

Reticuline is one of the alkaloids found in opium, and experiments in rodents suggest it possesses potent central nervous system depressing effects.[3] It is the precursor of morphine and many other alkaloids.

So I popped one pill, and awaited its effects. The effects came on relatively quickly. I felt slightly sedated, so I plopped on my bed for a nap.

I looked at the ceiling and the walls seem to be moving slightly, and it looked like my rods and cones were more visible than usual. Just minor benadryl-like hallucinations.

It reminded me of kava kava herb which is a sedative and mild psychedelic.