1. Neuronal Signaling
  2. Monoamine Oxidase
    Histone Demethylase
  3. Tranylcypromine hemisulfate

Tranylcypromine hemisulfate (Synonyms: dl-Tranylcypromine hemisulfate; trans-2-Phenylcyclopropylamine hemisulfate salt)

Cat. No.: HY-B1496 Purity: 99.05%
Handling Instructions

Tranylcypromine hemisulfate is an irreversible, nonselective MAO inhibitor used in the treatment of depression.

For research use only. We do not sell to patients.

Tranylcypromine hemisulfate Chemical Structure

Tranylcypromine hemisulfate Chemical Structure

CAS No. : 13492-01-8

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10 mM * 1 mL in DMSO USD 66 In-stock
Estimated Time of Arrival: December 31
100 mg USD 60 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 3 publication(s) in Google Scholar

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Tranylcypromine hemisulfate is an irreversible, nonselective MAO inhibitor used in the treatment of depression.

In Vitro

Tranylcypromine (10 nM to 10 µM) exerts neuroprotective effects against toxicity induced by human Aβ(1-42) oligomers independently from the presence of glial cells[1]. Tranylcypromine (100 μM) significantly protects RGCs 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[3].

In Vivo

Tranylcypromine treatment significantly and substantially reduces the lesion size and improves generalized hyperalgesia in a dose-dependent fashion in mice with induced endometriosis. In addition, tranylcypromine treatment results in reduced immunoreactivity to biomarkers of proliferation, angiogenesis, and H3K4 methylation, leading to arrested EMT and lesion growth[2]. 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[3]. Tranylcypromine (10 µg/g) causes an approximate and significant doubling of labeled cells in the combined brain regions examined, as detected by BrdU immunohistochemistry. Tranylcypromine causes the greatest increase in cell proliferation in the cerebellum[4].

Molecular Weight







N[[email protected]]1[[email protected]](C2=CC=CC=C2)C1.[0.5H2SO4]


Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

H2O : 25 mg/mL (137.19 mM; Need ultrasonic)

DMSO : 5 mg/mL (27.44 mM; ultrasonic and warming and heat to 60°C)

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 5.4876 mL 27.4379 mL 54.8757 mL
5 mM 1.0975 mL 5.4876 mL 10.9751 mL
10 mM 0.5488 mL 2.7438 mL 5.4876 mL
*Please refer to the solubility information to select the appropriate solvent.
Animal Administration

Briefly, the rats are anesthetized with an intraperitoneal injection of a 1:1 mixture of xylazine hydrochloride (4 mg/kg) and ketamine hydrochloride (10 mg/kg). Then, the pupil is dilated with phenylephrine hydrochloride and tropicamide eye drops, and 20 nmol NMDA with or without tranylcypromine is injected into the vitreous cavity. To assess the inhibitory effect of mitogen-activated protein kinase (MAPK), 100 nmol BIRB796 is intravitreally injected at the same time of NMDA injection. The injections are performed under a microscope using a 33-gauge needle connected to a microsyringe; the needle is inserted approximately 1.0 mm behind the corneal limbus. Next, either PBS (vehicle control) or 500 mM tranylcypromine (1000 nmol) mixed with 10 mM NMDA (20 nmol) in a total volume of 2.0 μL is injected into the vitreous cavity.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.


Purity: 99.05%

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