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    Harmaline
    Harmaline
    Information
    CAS No. 304-21-2 Price $100 / 20mg
    Catalog No.CFN98385Purity>=98%
    Molecular Weight214.3 Type of CompoundAlkaloids
    FormulaC13H14N2OPhysical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Harmaline Description
    Source: The herbs of Peganum harmala L.
    Biological Activity or Inhibitors: 1. The highest concentration of Harmaline treatment inhibited S3QB(-) charge recombination but promoted formation of QA(-)YD(+) charge pairs.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.6664 mL 23.3318 mL 46.6636 mL 93.3271 mL 116.6589 mL
    5 mM 0.9333 mL 4.6664 mL 9.3327 mL 18.6654 mL 23.3318 mL
    10 mM 0.4666 mL 2.3332 mL 4.6664 mL 9.3327 mL 11.6659 mL
    50 mM 0.0933 mL 0.4666 mL 0.9333 mL 1.8665 mL 2.3332 mL
    100 mM 0.0467 mL 0.2333 mL 0.4666 mL 0.9333 mL 1.1666 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Harmaline References Information
    Citation [1]

    Pestic Biochem Physiol. 2014 Oct;115:23-31.

    Herbicidal effects of harmaline from Peganum harmala on photosynthesis of Chlorella pyrenoidosa: probed by chlorophyll fluorescence and thermoluminescence.[Pubmed: 25307462]
    The herbicidal effects of Harmaline extracted from Peganum harmala seed on cell growth and photosynthesis of green algae Chlorella pyrenoidosa were investigated using chlorophyll a fluorescence and thermoluminescence techniques. Exposure to Harmaline inhibited cell growth, pigments contents and oxygen evolution of C. pyrenoidosa. Oxygen evolution was more sensitive to Harmaline toxicity than cell growth or the whole photosystem II (PSII) activity, maybe it was the first target site of Harmaline. The JIP-test parameters showed that Harmaline inhibited the donor side of PSII. Harmaline decreased photochemical efficiency and electron transport flow of PSII but increased the energy dissipation. The charge recombination was also affected by Harmaline. Amplitude of the fast phase decreased and the slow phase increased at the highest level of Harmaline. Electron transfer from QA(-) to QB was inhibited and backward electron transport flow from QA(-) to oxygen evolution complex was enhanced at 10 μg mL(-1) Harmaline. Exposure to 10 μg mL(-1) Harmaline caused appearance of C band in thermoluminescence. Exposure to 5 μg mL(-1) Harmaline inhibited the formation of proton gradient. The highest concentration of Harmaline treatment inhibited S3QB(-) charge recombination but promoted formation of QA(-)YD(+) charge pairs. P. harmala Harmaline may be a promising herbicide because of its inhibition of cell growth, pigments synthesis, oxygen evolution and PSII activities.
    Citation [2]

    Neuropharmacology. 2014 Aug;83:28-35.

    Lu AF21934, a positive allosteric modulator of mGlu4 receptors, reduces the harmaline-induced hyperactivity but not tremor in rats.[Pubmed: 24726309]
    Harmaline induces tremor in animals resembling essential tremor which has been suggested to result from activation of the glutamatergic olivo-cerebellar projection.On the Harmaline-induced tremor and other forms of motor activity in rats using fully automated Force Plate Actimeters. The influence of Harmaline on the mGlu4 mRNA expression in the cerebellum and inferior olive was analysed by in situ hybridization. Harmaline at a dose of 15 mg/kg (ip) triggered tremor which was manifested by an increase in the power within 9-15 Hz band and in the tremor index (a difference in power between bands 9-15 Hz and 0-8 Hz). Harmaline induced a biphasic effect on mobility, initially inhibiting the exploratory locomotor activity of rats (0-30 min after administration), followed by an increase in their basic activity. Lu AF21934 (0.5-5 mg/kg sc) did not influence tremor but at doses of 0.5 and 2.5 mg/kg reversed Harmaline-induced hyperactivity. MGlu4 mRNA expression was high in the cerebellar cortex and low in the inferior olive. Repeated Harmaline (15 mg/kg ip once a day for 5 days] decreased mGlu4 mRNA in the cerebellum and inferior olive. The present study indicates that the mGlu4 stimulation counteracts hyperactivity induced by Harmaline which suggests the involvement of cerebellar glutamatergic transmission in this process. In contrast, neuronal mechanisms involved in tremor seem to be insensitive to the stimulation of mGlu4.
    Citation [3]

    Brain Res. 2013 Nov 6;1537:303-11.

    A partial lesion of the substantia nigra pars compacta and retrorubral field decreases the harmaline-induced glutamate release in the rat cerebellum.[Pubmed: 24012623]
    Harmaline was administered in a dose of 30 mg/kg ip on the 8th day after the operation and the extracellular level of glutamate was measured by microdialysis in vivo in the cerebellar vermis. Harmaline induced glutamate release in the cerebellum. The lesion which encompassed 23-37% neurons in the anterior SNC, 52-54% in the posterior SNC and 47-55% in the RRF did not influence the basal extracellular glutamate level but decreased the Harmaline-induced release of this neurotransmitter. Tremor evoked by Harmaline was also visibly inhibited by the above lesion. The results of the present study seem to indicate that midbrain dopaminergic neurons influence glutamatergic transmission in the cerebellum which may be important for generation of the tremor induced by Harmaline.
    Citation [4]

    J Neurosci Res. 2013 Oct;91(10):1328-37.

    Effects of unilateral stereotactic posterior striatotomy on harmaline-induced tremor in rats.[Pubmed: 23873746]
    Harmaline-induced tremor in rats. Fifty-four male Wistar rats were randomly distributed into three groups: experimental (EG), surgical control (SCG), and pharmacological control (PCG) groups. EG animals underwent stereotactic unilateral posterior striatotomy. SCG rats underwent sham lesion at the same target. PCG served exclusively as controls for Harmaline effects. All animals received, postoperatively, intraperitoneal Harmaline, and the induced tremor was video-recorded for later evaluation by a blind observer. Thirteen animals were excluded from the study. Limb tremor was reduced ipsilaterally to the operation in 20 of 21 rats of EG and in two of nine of SCG, being asymmetric in one of 10 of PCG rats. Comparisons between EG × SCG and EG × PCG were statistically significant, but not between SCG × PCG. Limb tremor reduction was greater in anterior than in posterior paws. Lateral lesions yielded better results than medial lesions. These results suggest that the posterior striatum is involved with Harmaline-induced tremor in rats and support the hypothesis presented.
    Citation [5]

    Drug Metab Dispos. 2013 May;41(5):975-86.

    Pharmacokinetic interactions between monoamine oxidase A inhibitor harmaline and 5-methoxy-N,N-dimethyltryptamine, and the impact of CYP2D6 status.[Pubmed: 23393220 ]
    This study is aimed at delineating Harmaline and 5-MeO-DMT pharmacokinetic (PK) interactions at multiple dose levels, as well as the impact of CYP2D6 that affects Harmaline PK and determines 5-MeO-DMT O-demethylation to produce bufotenine. Our data revealed that inhibition of MAO-A-mediated metabolic elimination by Harmaline (2, 5, and 15 mg/kg) led to a sharp increase in systemic and cerebral exposure to 5-MeO-DMT (2 and 10 mg/kg) at all dose combinations. A more pronounced effect on 5-MeO-DMT PK was associated with greater exposure to Harmaline in wild-type mice than CYP2D6-humanized (Tg-CYP2D6) mice. Harmaline (5 mg/kg) also increased blood and brain bufotenine concentrations that were generally higher in Tg-CYP2D6 mice. Surprisingly, greater Harmaline dose (15 mg/kg) reduced bufotenine levels. The in vivo inhibitory effect of Harmaline on CYP2D6-catalyzed bufotenine formation was confirmed by in vitro study using purified CYP2D6. Given these findings, a unified PK model including the inhibition of MAO-A- and CYP2D6-catalyzed 5-MeO-DMT metabolism by Harmaline was developed to describe blood Harmaline, 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models. This PK model may be further employed to predict Harmaline and 5-MeO-DMT PK interactions at various doses, define the impact of CYP2D6 status, and drive Harmaline-5-MeO-DMT pharmacodynamics.