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Harmol

MCE China：Harmol

Brand：MedChemExpress (MCE)

Cat. No.HY-107811

CAS：487-03-6

Purity：99.77%

Storage：Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Harmol is a TFEB activator, an orally active monoamine oxidase inhibitor that has anti-tumor, anti-depressant, and anti-aging effects. Harmol can induce cell mitosis, autophagy and apoptosis. Harmol promotes the degradation of α-synuclein through the regulation of the autophagy-lysosomal pathway, improving motor deficits in mouse models of Parkinson's disease.

In Vitro：Harmol (3-30 μM, 6-24 h) reduces α-syn levels in PC12 cells in a dose- and time-dependent manner[1]. Harmol (30 μM, 24 h) promotes the nuclear translocation of exogenous TFEB (transcription factor EB) in HeLa cells and enhances the nuclear translocation of endogenous TFEB in N2a cells, along with a restoration of autophagic flux and lysosomal biogenesis[1]. Harmol (0-100 μM, 24 and 48 h) shows time- and dose-dependent inhibition of U251MG cell proliferation and induces cell death[2]. Harmol (0-100 μM, 0-48 h) inhibits the expression of survivin in U251MG cells and promotes the expression of LC3-I and LC3-II proteins, suppressing the Akt/mTOR pathway and inducing cell autophagy and apoptosis[2]. Harmol (0-100 μM, 0-24 h) exhibits slight cytotoxicity in A549 and H226 cells, but shows strong cytotoxicity in H596, inhibiting tumor proliferation[3]. Harmol (60 μM, 3-6 h) enhances the activity of caspase-3, caspase-6, caspase-8, and caspase-9, increases the cleavage of RAPA (an endogenous substrate for caspase-3), inducing apoptosis in H596 cells[3]. Harmol (1.3 μg/mL, 1-3 h) activates autophagy in C2C12 cells[4]. Harmol (1.3 μg/mL, 45-60 min) activates mitochondria-specific autophagy in C2C12 cells, occurring only in inactive TMRM-negative mitochondria[4]. Harmol (1.3 μg/mL, 16 h) upregulates the expression of markers for mitochondrial function in C2C12 cells[4]. Harmol (1.3 μg/mL, 0-20 h) has a specific inhibitory effect on MAO-B[4]. Harmol reduces GABAergic neurotransmission but does not completely inhibit the binding of GABA to GABAARs; GABAAR activity is crucial for Harmol-mediated mitochondrial depolarization and relies on mitochondrial function[4].

In Vivo：Harmol (10-40 mg/kg, orally, twice a day for one month) can improve motor deficits, including movement and coordination, in an α-syn transgenic mouse model. It reduces α-syn levels in the substantia nigra and prefrontal cortex and enhances autophagy-mediated degradation of protein aggregates[1]. Harmol (100 mg/kg, administered by gavage, once daily for three weeks) has a mild anxiety-reducing effect in mice[4]. Harmol (100 mg/kg, orally, for three months) improves insulin, glucose homeostasis, and metabolic adaptations in obese mice, with no impact on kidney function[4]. Harmol (15 μg/kg, orally, from day 0 to 50) extends the lifespan of invertebrates[4]. Harmol (100 mg/kg, orally, for two months) delays frailty in aging mice[4].

IC50 & Target：MAO-B

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References：

[1]. Jie Xu,et al. Harmol promotes α-synuclein degradation and improves motor impairment in Parkinson's models via regulating autophagy-lysosome pathway. NPJ Parkinsons Dis. 2022 Aug 6;8(1):100.  [Content Brief]

[2]. Akihisa Abe ,et al. Harmol induces autophagy and subsequent apoptosis in U251MG human glioma cells through the downregulation of surviving. Oncol Rep. 2013 Apr;29(4):1333-42.  [Content Brief]

[3]. Akihisa Abe,et al. Harmol induces apoptosis by caspase-8 activation independently of Fas/Fas ligand interaction in human lung carcinoma H596 cells. Anticancer Drugs. 009 Jun;20(5):373-81.  [Content Brief]

[4]. Luis Filipe Costa-Machado, et al. Peripheral modulation of antidepressant targets MAO-B and GABAAR by harmol induces mitohormesis and delays aging in preclinical models. Nat Commun. 2023 May 15;14(1):2779.  [Content Brief]