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Harmol (hydrochloride)

Harmol hydrochloride is an orally active β-carboline alkaloid. Harmol hydrochloride is a TFEB activator and monoamine oxidase inhibitor. Harmol hydrochloride can induce cell mitosis, Autophagy and Apoptosis. Harmol hydrochloride promotes the degradation of α-synuclein by regulating the autophagy-lysosomal pathway. Harmol hydrochloride has anti-tumor, anti-depressant and anti-aging activities. Harmol hydrochloride improves motor impairment in a mouse Parkinson's disease model[1][2][3][4].

Product Specifications

CAS Number

40580-83-4

UNSPSC

12352005

Hazard Statement

H302-H312-H332

Target

Apoptosis; Autophagy; Mitosis; Monoamine Oxidase; α-synuclein

Type

Reference compound

Related Pathways

Apoptosis; Autophagy; Neuronal Signaling

Applications

Neuroscience-Neuromodulation

Field of Research

Cancer; Neurological Disease

Assay Protocol

https://www.medchemexpress.com/harmol-hydrochloride.html

Solubility

10 mM in DMSO

Smiles

OC1=CC2=C(C=C1)C3=C(C(C)=NC=C3)N2.[H]Cl

Molecular Formula

C12H11ClN2O

Molecular Weight

234.68

Precautions

P261-P264-P270-P271-P280-P302+P352-P304+P340-P330-P363-P501

References & Citations

[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.|[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. |[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.|[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.

Shipping Conditions

Room temperature

Scientific Category

Reference compound1

Clinical Information

No Development Reported

Frequently Asked Questions

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