Tranylcypromine hemisulfate is an inhibitor of monoamine oxidase (MAO) and prostacyclin synthase, potently suppresses the enzymatic activity of Lysine-Specific Demethylase 1 (LSD1) (IC50 < 2 μM for BHC110/LSD1).
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Tranylcypromine hemisulfate is an irreversible, nonselective monoamine oxidase (MAO) inhibitor used in the treatment of depression. TCP (Tranylcypromine) significantly prevented Aβ-induced neuronal death in a concentration-dependent fashion and was maximally protective only at 10 µM. TCP-But was maximally protective in mixed neuronal cultures at 1 µM, a lower concentration compared to TCP, whereas the new derivative, TCP-Ac(TCP acetamide), was more efficacious than TCP and TCP-But (TCP butyramide) and significantly protected cortical neurons against Aβ toxicity at nanomolar concentrations (100 nM)[3]. TC (tranylcypromine) treatment significantly and substantially reduced the lesion size and improved generalized hyperalgesia in a dose-dependent fashion in mice with induced endometriosis. In addition, TC treatment resulted in reduced immunoreactivity to biomarkers of proliferation, angiogenesis, and H3K4 methylation, leading to arrested EMT (epithelial-mesenchymal transition) and lesion growth[4]. Tranylcypromine (100 μM) significantly protects RGCs (retinal ganglion cell) from glutamate neurotoxicity-induced apoptosis as well as apoptosis induced by oxidative stress. Tranylcypromine promotes mitogen-activated protein kinase 12 (p38 MAPKγ) expression under conditions of glutamate (Glu)-induced stress. Besides, tranylcypromine contributes to RGC survival via alterations of p38 MAPKγ activity. Tranylcypromine (500 mM) injection exerts neuroprotective effects within intracellular apoptotic signaling pathways and suppresses morphologic changes in the retina of the rat, suppresses caspase 3 activity and recovers p38 MAPKγ expression in the retina after NMDA-induced injury, and enhances RGC survival after retinal injury via the attenuation of NMDA neurotoxicity[5].
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