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| 100mg |
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| 250mg |
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| 500mg |
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Harmine (telepathine) is a naturally occuring beta-carboline and fluorescent harmala alkaloid found in a number of different plants, most notably the Middle Eastern plant harmal or Syrian rue (Peganum harmala) and the South American vine Banisteriopsis caapi (formerly known as 'yage' or 'ayahuasca'). Harmine reversibly inhibits monoamine oxidase A (MAO-A), an enzyme which breaks down monoamines, making it a RIMA. Harmine selectively binds to MAO-A but does not inhibit the variant MAO-B. It is also a tyrosine phosphorylation-regulated kinase (DYRK) inhibitor with anticancer and anti-inflammatory activities. Harmine has a high affinity of 5-HT2A serotonin receptor, with an Ki of 397 nM.
| Targets |
DYRK1A; 5-HT2A Receptor (Ki = 397 nM)
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|---|---|
| ln Vitro |
Harmine has an IC50 of 190 nM and inhibits tau phosphorylation of DYRK1A through specific DANDY [2]. Harmine causes severe cytotoxicity in liver cancer cells by obstructing Rad51 recruitment, which negatively regulates homologous recombination (HR). Furthermore, Hep3B cells were considerably more sensitive to the anti-proliferative effects of Harmine when Nu7441, an NHEJ inhibitor, was used [3].
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| ln Vivo |
The TBI group's brain water content increased dramatically, according to the results. When compared to the TBI group, the hormone treatment considerably decreased the amount of water in the tissue on days 1, 3, and 5. When compared to the TBI group, the escape delay on days 3 and 5 was dramatically reduced by dehydrokine therapy. Rats given harmine 1, 3, and 5 days post-trauma showed a markedly better recovery in motor function than the group of rats given no treatment. When comparing the TBI group to the Harmine-treated group, there was a significant increase in the rates of neural survival. GLT-1 expression was much higher after receiving harmine than it was in the TBI group. When Harmine was administered, the expression of caspase 3 was considerably lower than in the TBI group [4].
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| Cell Assay |
To avoid cell cycle arrest or apoptosis, rapidly proliferating cancer cells have to promote DNA double strand break (DSB) repair to fix replication stress induced DSBs. Therefore, developing drugs blocking homologous recombination (HR) and nonhomologous end joining (NHEJ) - 2 major DSB repair pathways - holds great potential for cancer therapy. Over the last few decades, much attention has been paid to explore drugs targeting DSB repair pathways for cancer therapy. Here, using 2 well-established reporters for analyzing HR and NHEJ efficiency, we found that both HR and NHEJ are elevated in hepatoma cell lines Hep3B and HuH7 compared with normal liver cell lines Chang liver and QSG-7701. Our further study found that Harmine, a natural compound, negatively regulates HR but not NHEJ by interfering Rad51 recruitment, resulting in severe cytotoxicity in hepatoma cells. Furthermore, NHEJ inhibitor Nu7441 markedly sensitizes Hep3B cells to the anti-proliferative effects of Harmine. Taken together, our study suggested that Harmine holds great promise as an oncologic drug and combination of Harmine with a NHEJ inhibitor might be an effective strategy for anti-cancer treatment.[3]
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| 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].
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| ADME/Pharmacokinetics |
Metabolism / Metabolites
Harmine has known human metabolites that include 6-Hydroxy-harmaline and Harmol. |
| References |
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| Additional Infomation |
Harmine is a harmala alkaloid in which the harman skeleton is methoxy-substituted at C-7. It has a role as a metabolite, an anti-HIV agent and an EC 1.4.3.4 (monoamine oxidase) inhibitor. It derives from a hydride of a harman.
Harmine has been reported in Passiflora phoenicia, Symplocos setchuensis, and other organisms with data available. Alkaloid isolated from seeds of PEGANUM HARMALA; ZYGOPHYLLACEAE. It is identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic PARKINSON DISEASE in the 1920's. |
| Molecular Formula |
C13H12N2O
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|---|---|
| Molecular Weight |
212.2472
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| Exact Mass |
248.071
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| Elemental Analysis |
C, 62.78; H, 5.27; Cl, 14.25; N, 11.26; O, 6.43
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| CAS # |
343-27-1
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| Related CAS # |
Harmine; 442-51-3
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| PubChem CID |
5280953
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| Appearance |
Off-white to light yellow solid
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| Boiling Point |
421.4ºC at 760mmHg
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| Melting Point |
265-270°C
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| Flash Point |
139.8ºC
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| LogP |
3.835
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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 |
VNPLYCKZIUTKJM-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C13H12N2O.ClH/c1-8-13-11(5-6-14-8)10-4-3-9(16-2)7-12(10)15-13;/h3-7,15H,1-2H3;1H
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| Chemical Name |
7-methoxy-1-methyl-9H-pyrido[3,4-b]indole;hydrochloride
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| Synonyms |
Harmine Hydrochloride; 343-27-1; 7-Methoxy-1-methyl-9H-pyrido[3,4-b]indole hydrochloride; HARMINE HCl; Harmine monohydrochloride; Harmine (hydrochloride); Telepathine (hydrochloride); T89I34ODAA;
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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 Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| 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) |
H2O : ~10 mg/mL (~40.21 mM)
DMSO : ~5 mg/mL (~20.10 mM) |
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (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.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT05526430 | Completed | Drug: Harmine Hydrochloride Capsules |
Diabetes Mellitus | James Murrough | September 13, 2022 | Phase 1 |
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