Harmaline

Harmaline
Product Name Harmaline
CAS No.: 304-21-2
Catalog No.: CFN98385
Molecular Formula: C13H14N2O
Molecular Weight: 214.3 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Targets: NOS | cAMP | Calcium Channel | PKC | Antifection | AChR | alpha1-adrenorecepteor
Source: The herbs of Peganum harmala L.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $40/20mg
Harmaline is a central nervous system stimulant and an acetylcholinesterase (AChR) inhibitor; also inhibits histamine N-methyltransferase. Harmaline has antileishmanial, bioinsecticidal, and vasorelaxant effects. It has antagonist effects on alpha1-adrenorecepteors in non-competitive manner, it also exerts an antioxidant activity by scavenging the free radical generated by DPPH.Harmaline may prevent dopamine-induced mitochondrial damage and PC12 cell death through a scavenging action on reactive oxygen species and inhibition of monoamine oxidase and thiol oxidation.
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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.

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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.
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    Exp Parasitol. 2004 Mar-Apr;106(3-4):67-74.
    In vitro activity of the beta-carboline alkaloids harmane, harmine, and harmaline toward parasites of the species Leishmania infantum.[Pubmed: 15172213 ]
    Harmane, harmine, and Harmaline were investigated for their in vitro antileishmanial activity toward parasites of the species Leishmania infantum.
    METHODS AND RESULTS:
    Harmane and Harmine displayed a moderate antiproliferative activity toward human monocytes and exerted a weak antileishmanial activity toward both the promastigote and the amastigote forms of the parasite. Their mechanism of action on the promastigote form of the parasite involved interactions with DNA metabolism leading to an accumulation of parasites in the S-G(2)M phases of the cell-cycle. Harmaline, at the contrary, was deprived from toxicity toward human cells and Leishmania promastigotes, however it exerted a strong antileishmanial activity toward the intracellular amastigote form of the parasite.
    CONCLUSIONS:
    This property was shown to partly result from the capacity of the molecule to prevent parasite internalization within macrophages by inhibiting Leishmania PKC activity.
    Pesticide Biochemistry & Physiology, 2007, 89(2):137-145.
    Bioinsecticidal effect of harmaline on Plodia interpunctella development (Lepidoptera: Pyralidae).[Reference: WebLink]
    We have investigated the effects of Harmaline, a plant secondary metabolic compound belonging to β-carboline alkaloids, on the 4th instar larvae of Plodia interpunctella (Lepidoptera).
    METHODS AND RESULTS:
    When incorporated into the diet, Harmaline caused weight loss of larvae with a reduction in protein and glycogen contents and an inhibition of α-amylase activity. Using electron microscopy, we showed that Harmaline provoked a severe cytotoxicity on the epithelial cells of the midgut resulting in marked vacuolization of the cytoplasm, appearance of numerous autophagic vesicles and lysosomic structures, fragmentation of rough endoplasmic reticulum cisternae, disruption of microvilli, rupture of the plasma membrane leading to shedding of the cytoplasm contents into the midgut lumen.
    CONCLUSIONS:
    The development of larvae to the pupal and adult stages was prevented and high mortality was recorded.
    J Neurochem. 2000 Aug;75(2):521-31.
    Protective effect of harmalol and harmaline on MPTP neurotoxicity in the mouse and dopamine-induced damage of brain mitochondria and PC12 cells.[Pubmed: 10899927]
    The present study elucidated the protective effect of beta-carbolines (Harmaline, harmalol, and harmine) on oxidative neuronal damage.
    METHODS AND RESULTS:
    MPTP treatment increased activities of total superoxide dismutase, catalase, and glutathione peroxidase and levels of malondialdehyde and carbonyls in the basal ganglia, diencephalon plus midbrain of brain compared with control mouse brain. Coadministration of harmalol (48 mg/kg) attenuated the MPTP effect on the enzyme activities and formation of tissue peroxidation products. Harmaline, harmalol, and harmine attenuated both the 500 microM MPP(+)-induced inhibition of electron flow and membrane potential formation and the 100 microM dopamine-induced thiol oxidation and carbonyl formation in mitochondria. The scavenging action of beta-carbolines on hydroxyl radicals was represented by inhibition of 2-deoxy-D-ribose degradation. Harmaline and harmalol (100 microM) attenuated 200 microM dopamine-induced viability loss in PC12 cells. The beta-carbolines (50 microM) attenuated 50 microM dopamine-induced apoptosis in PC12 cells. The compounds alone did not exhibit significant cytotoxic effects. The results indicate that beta-carbolines attenuate brain damage in mice treated with MPTP and MPP(+)-induced mitochondrial damage.
    CONCLUSIONS:
    The compounds may prevent dopamine-induced mitochondrial damage and PC12 cell death through a scavenging action on reactive oxygen species and inhibition of monoamine oxidase and thiol oxidation.
    Pharmacol Res. 2006 Aug;54(2):150-7.
    Vasorelaxant effects of harmine and harmaline extracted from Peganum harmala L. seeds in isolated rat aorta.[Pubmed: 16750635 ]
    The present work describes the mechanisms involved in the vasorelaxant effect of harmine and Harmaline.
    METHODS AND RESULTS:
    These alkaloids induce in a dose-dependent manner the relaxation in the aorta precontracted with noradrenaline or KCl. However, the removal of endothelium or pre-treatment of intact aortic ring with L-NAME (inhibitor of NOSe synthetase) or with indomethacin (non-specific inhibitor of cyclo-oxygenase), reduces significantly the vasorelaxant response of Harmaline but not harmine. According to their IC50 values, prazosin (inhibitor of alpha-adrenorecepteors) reduces the vasorelaxant effect only of Harmaline, whereas, pre-treatment with IBMX (non-specific inhibitor of phosphodiesterase) affects both the Harmaline and harmine-responses. Inhibitions of L-type voltage-dependent Ca2+ channels (VOCs) in endothelium-intact aortic rings with diltiazem depress the relaxation evoked by Harmaline as well as by harmine. Pre-treatment with Harmaline or harmine (3, 10 or 30 microM) shifted the phenylephrine-induced dose response curves to the right and the maximum response was attenuated indicating that the antagonist effect of both alkaloids on alpha1-adrenorecepteors was non-competitive. These two alkaloids also exert an antioxidant activity by scavenging the free radical generated by DPPH.
    CONCLUSIONS:
    Therefore, the present results suggest that the vasorelaxant effect of Harmaline but not harmine is related to its action on the prostacyclin pathway and on the endothelial cells to release NO. However, both alkaloids can act as blockers VOCs, as inhibitors of phosphodiesterase resulting in an increase of the second messenger (cAMP and cGMP) levels and finally reduce the levels of free radicals in tissues.
    Mov Disord. 2005 Mar;20(3):298-305.
    Harmaline-induced tremor as a potential preclinical screening method for essential tremor medications.[Pubmed: 15580562]
    No preclinical method to evaluate potential new medications for essential tremor (ET) is available currently. Although Harmaline tremor is a well known animal model of ET, it has not found utility as a preclinical drug screen and has not been validated with anti-ET medications.
    METHODS AND RESULTS:
    We measured Harmaline tremor in rats (10 mg/kg s.c.) and mice (20 mg/kg s.c.) with a load sensor under the cage floor and performed spectral analysis on 20-minute epochs. The motion power over the tremor frequency bandwidth (8-12 Hz in rats; 10-16 Hz in mice) was divided by the motion power over the full motion frequency range (0-15 Hz in rats; 0-34 Hz in mice). The use of these measures greatly reduced data variability, permitting experiments with small sample sizes.
    CONCLUSIONS:
    Three drugs that suppress ET (propranolol, ethanol, and octanol) all significantly suppressed Harmaline-induced tremor. We propose that, with this methodology, Harmaline-induced tremor may be useful as a preclinical method to identify potential medications for ET.
    Brain Res., 1973, 53(1):81-95.
    Rhythmic activity induced by harmaline in the olivo-cerebello-bulbar system of the cat.[Reference: WebLink]

    METHODS AND RESULTS:
    Unitary extracellular recordings were obtained from brain stem and cerebellar neurons following administration of Harmaline in decerebrate paralyzed cats. Rhythmic discharges at 8鈥12/sec in the inferior olive generated synchronous climbing fiber responses in Purkinje cells associated with an almost complete suppression of simple spike activity. Rhythmic bursting was also recorded from neurons of the fastigial, the bulbar reticular and the lateral vestibular nuclei. This central rhythmic activity was not modified by spinal section at the C 2 level. After total cerebellectomy the rhythmic activity persisted in the inferior olive but not in the other bulbar nuclei. These data indicate that the rhythmicity induced by Harmaline in the inferior olive is not generated within loops involving the cerebellum or the bulbar nuclei and that the olivo-cerebellar system is responsible for the rhythmic activation of the bulbar reticular and vestibular nuclei.
    CONCLUSIONS:
    From simultaneous recordings along the olivo-cerebello-bulbar system, it appears very likely that the bulbar reticular and vestibular rhythmic activity is primarily the consequence of the periodic interruption of fastigial cells firing by the rhythmic climbing fiber responses.
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