| Size | Price | Stock | Qty |
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| 500mg |
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| 1g |
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| 2g |
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| 5g |
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| Other Sizes |
Purity: ≥98%
| Targets |
5-HT2A Receptor (Ki = 397 nM); DYRK1A
Harmine primarily targets monoamine oxidase A (MAO-A), an enzyme responsible for the oxidative deamination of neurotransmitters such as serotonin, dopamine, and norepinephrine. By inhibiting MAO-A, harmine increases the levels of these monoamines in the brain. It is also a potent inhibitor of DYRK1A, a kinase involved in various cellular processes including neurodevelopment and cell cycle regulation. Additionally, harmine has been reported to interact with other targets including the 5-HT2A receptor, the imidazoline I₂ receptor, and various ion channels. |
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| ln Vitro |
Harmine inhibits tau phosphorylation by DYRK1A by specific DANDYs, with an IC50 of 190 nM[2]. Harmine causes extreme cytotoxicity in hepatoma cells by disrupting Rad51 recruitment, which is how it negatively regulates homologous recombination (HR). Moreover, Hep3B cells are significantly more susceptible to the anti-proliferative effects of harmine when exposed to the NHEJ inhibitor Nu7441[3].
In vitro, harmine demonstrates potent MAO-A inhibitory activity with an IC₅₀ in the low micromolar range. It also inhibits DYRK1A with an IC₅₀ in the nanomolar range. The compound shows cytotoxic activity against various cancer cell lines, including those of the breast, colon, and lung. Harmine induces apoptosis in cancer cells through the mitochondrial pathway and by activating caspases. It also exhibits neuroprotective effects in cellular models of neurodegenerative diseases by reducing oxidative stress and inflammation. |
| ln Vivo |
It has been demonstrated that the TBI group has a noticeably higher brain water content. In comparison to the TBI group, treatment with harmine dramatically lowers the tissue water content at 1, 3, and 5 days. When comparing the escape latency at 3 and 5 days to the TBI group, the use of ammine treatment significantly lowers it. When compared to the TBI group that did not receive Harmine treatment, the motor function recovery of the rats is significantly improved by the administration of Harmine post-TBI at 1, 3, and 5 days post-TBI. In comparison with the TBI group, the neuronal survival rate is markedly higher in the group treated with harmine. When Harmine is administered, compared to the TBI group, there is a noticeable increase in GLT-1 expression. In contrast to the TBI group, the administration of harmine dramatically lowers caspase 3 expression[4].
In vivo, harmine has been shown to produce psychoactive effects in animal models, consistent with its MAO-A inhibitory activity. It increases brain levels of serotonin, dopamine, and norepinephrine. In rodent models of depression, harmine exhibits antidepressant-like effects in the forced swim test and tail suspension test. In models of Parkinson's disease, harmine shows neuroprotective effects. Harmine has also demonstrated antitumor activity in xenograft models, with tumor growth inhibition observed in various cancer types. |
| Enzyme Assay |
Cell-free enzyme assays for harmine typically involve measuring its inhibition of MAO-A and DYRK1A activities. For MAO-A, the enzyme is incubated with a substrate (such as kynuramine or serotonin) and various concentrations of harmine. The production of the oxidized metabolite is measured spectrophotometrically or fluorometrically. For DYRK1A, kinase activity is measured using a peptide substrate and ATP, with phosphorylation detected by radioactive or fluorescence-based methods. IC₅₀ values are calculated from dose-response curves.
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| Cell Assay |
Experiments on DNA damage, cell death, and proliferation are carried out using the High Content Screening (HCS) format. A multiwell 384 µClear plate coated with 100 µg/mL Poly-L-ornithine and 10 µg/mL laminin is used to plate the hNPCs (1,500 cells/per well). Following a 24-hour period, cells are treated with harmine, INDY, and pargyline in quintuplicate (five wells per condition) for four days in N2B27 medium supplemented with bFGF and EGF. Day 4: 30 minutes before fixation or image acquisition, cells are labeled with 10 µM EdU for cell proliferation or BOBO™ -3 for cell death.
In vitro cellular assays for harmine involve treating cultured cells with the compound to assess its effects on cell viability, proliferation, and signaling pathways. For cancer studies, various cancer cell lines are treated with harmine at different concentrations, and cell viability is measured using MTT or CCK-8 assays. Apoptosis is assessed by flow cytometry or by measuring caspase activity. For neuroprotection studies, neuronal cell lines are treated with harmine prior to exposure to neurotoxic insults such as oxidative stress or excitotoxicity. |
| Animal Protocol |
Rats: The study uses 150 male Sprague-Dawley rats, weighing between 280 and 320 g and aged between 10 and 12 weeks. Three groups of rats are randomly assigned: the TBI group (n=35); the TBI + Harmine-treated group (n=35); and the Sham-operated group (n= 15). Immediately after traumatic brain injury, heroine (i.p., 30 mg/kg daily) is given for a maximum of five days. Equal volumes of 0.9% saline solution are given to the TBI and sham groups (i.p.). For the purpose of examining behavioral recovery, the rats are divided into three groups: Sham (n = 3), TBI (n = 7), and Harmine (n = 7). The NSS is assessed 1, 3, and 5 days after a traumatic brain injury. An observer who is blind to the animal treatment evaluates each rat individually[4].
In vivo animal studies for harmine typically use rodent models. For antidepressant studies, mice or rats are treated with harmine via intraperitoneal or oral administration, and behavioral tests such as the forced swim test and tail suspension test are performed. For neuroprotection studies, animal models of Parkinson's disease or Alzheimer's disease are used. For cancer studies, tumor-bearing mice are treated with harmine, and tumor growth inhibition is monitored. Dosing regimens and treatment durations vary depending on the specific experimental model. |
| ADME/Pharmacokinetics |
Metabolism / Metabolites
Harmine's known human metabolites include 6-hydroxyHarmine and harmoll. Harmine has a molecular formula of C₁₃H₁₂N₂O and a molecular weight of 212.25. It is a beta-carboline alkaloid with a planar structure that allows it to intercalate with DNA. The compound is metabolized primarily by the liver, and its pharmacokinetic profile includes good oral bioavailability. Harmine crosses the blood-brain barrier, which is important for its central nervous system effects. Its half-life is relatively short, and it is excreted primarily in urine. |
| References |
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| Additional Infomation |
Harmine is a Harmine alkaloid, with its Harmine skeleton substituted with a methoxy group at the C-7 position. It is a metabolite, an anti-HIV drug, and an EC 1.4.3.4 (monoamine oxidase) inhibitor. It is derived from the hydride of Harmine. Harmine has been reported in passionflower (Passiflora phoenicia), Sichuan aster (Symplocos setchuensis), and several other organisms with relevant data. Harmine is an alkaloid isolated from the seeds of Peganum harmala, a plant in the Zygophyllaceae family. It is identical to banisterine or telepathine found in Banisteria caapi, and is one of the active ingredients in hallucinogenic drinks made from related plants in the western Amazon. It has no therapeutic use, but (like banisterine) it was touted as a treatment for post-encephalitis Parkinson's disease in the 1920s.
Harmine is a naturally occurring compound found in various plants, including Peganum harmala and Banisteriopsis caapi. It is used in research to study neurological disorders, cancer, and psychiatric conditions. Harmine is also one of the active components in the traditional Amazonian brew ayahuasca, where it acts as an MAO-A inhibitor to allow the oral activity of DMT. The compound is for research use only and not for human therapeutic use. Harmine has been studied for its potential in treating depression, Alzheimer's disease, Parkinson's disease, and cancer. |
| Molecular Formula |
C13H12N2O
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|---|---|
| Molecular Weight |
212.2472
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| Exact Mass |
212.094
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| Elemental Analysis |
C, 73.56; H, 5.70; N, 13.20; O, 7.54
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| CAS # |
442-51-3
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| Related CAS # |
Harmine hydrochloride;343-27-1
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| PubChem CID |
5280953
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| Appearance |
White to yellow solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
421.4±40.0 °C at 760 mmHg
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| Melting Point |
264 - 265 °C
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| Flash Point |
139.8±17.0 °C
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| Vapour Pressure |
0.0±1.0 mmHg at 25°C
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| Index of Refraction |
1.706
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| LogP |
3.17
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
1
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| Heavy Atom Count |
16
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| Complexity |
258
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| Defined Atom Stereocenter Count |
0
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| SMILES |
O(C([H])([H])[H])C1C([H])=C([H])C2=C(C=1[H])N([H])C1C(C([H])([H])[H])=NC([H])=C([H])C2=1
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| InChi Key |
BXNJHAXVSOCGBA-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C13H12N2O/c1-8-13-11(5-6-14-8)10-4-3-9(16-2)7-12(10)15-13/h3-7,15H,1-2H3
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| Chemical Name |
7-methoxy-1-methyl-9H-pyrido[3,4-b]indole
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| Synonyms |
Harmine; telepathine; Yageine; 7-Methoxy-1-methyl-9H-pyrido[3,4-b]indole; Banisterine; Telepathine; Leucoharmine; Yajeine; Banisterine; Leucoharmine
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO: ≥ 30 mg/mL (~141.3 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (11.78 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (11.78 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.7114 mL | 23.5571 mL | 47.1143 mL | |
| 5 mM | 0.9423 mL | 4.7114 mL | 9.4229 mL | |
| 10 mM | 0.4711 mL | 2.3557 mL | 4.7114 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Link: https://clinicaltrials.gov/ct2/show/NCT06252506
Conditions:Neuropharmacological Investigation of Ayahuasca Constituents DMT and HarmineLink: https://clinicaltrials.gov/ct2/show/NCT05780216
Conditions:Healthy ParticipantsLink: https://clinicaltrials.gov/ct2/show/NCT04716335
Conditions:Emotions|Mood|Cognitive Function 1, Social|Empathy
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