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Purity: ≥98%
Tranylcypromine hemisulfate, also known as 2-PCPA, is a nonselective and irreversible monoamine oxidase inhibitor, which inhibits CYP2A6 with Ki of 0.08 μM and 0.2 μM in cDNA-expressing microsomes and Human Liver Microsomes, respectively. Tranylcypromine is used as an antidepressant and anxiolytic agent in the clinical treatment of mood and anxiety disorders, respectively.
| Targets |
monoamine oxidase (MAO); KDM1/lysine-specific demethylase 1 (LSD1)
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| ln Vitro |
Independent of glial cells, tranylcypromine (10 nM to 10 μM) has neuroprotective benefits against toxicity generated by human Aβ (1-42) oligomers. RGCs are considerably shielded from both oxidative stress- and glutamate neurotoxicity-induced apoptosis by tranylcypromine (100 μM). Under glutamate (Glu)-induced stress circumstances, tranylcypromine increases the expression of mitogen-activated protein kinase 12 (p38 MAPKγ). Furthermore, tranylcypromine alters p38 MAPKγ activity to increase RGC survival [3].
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| ln Vivo |
Tranylcypromine treatment improved dose-dependent generalized hyperalgesia and significantly and significantly decreased lesion size in mice with induced endometriosis. Additionally, treatment with tranylcypromine decreases immune reactivity to biomarkers like angiogenesis, proliferation, and H3K4 methylation, which causes EMT and inhibits the growth of lesions [2]. After NMDA-induced retinal injury, tranylcypromine hemisulfate (500 mM) injection inhibits morphological changes in the rat retina, inhibits caspase 3 activity, and restores p38 MAPKγ in the retina. These neuroprotective effects are observed on intracellular apoptosis signaling pathways. expression, and reduces the neurotoxicity of NMDA to increase the survival rate of RGCs following retinal damage [3]. BrdU immunohistochemistry revealed that tranylcypromine hemisulfate (10 μg/g) caused an approximate and significant doubling of labeled cells in the combined brain regions examined. The most significant increase in cerebellar cell proliferation is caused by tranylcypromine [4].
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| Enzyme Assay |
Monoamine oxidase (MAO) enzymes play a central role in the pathogenesis of Alzheimer's disease (AD) and MAO inhibitors (MAOIs) are antidepressant drugs currently studied for their neuroprotective properties in neurodegenerative disorders. In the present work MAOIs such as tranylcypromine [trans-(+)-2-phenylcyclopropanamine, TCP] and its amide derivatives, TCP butyramide (TCP-But) and TCP acetamide (TCP-Ac), were tested for their ability to protect cortical neurons challenged with synthetic amyloid-β (Aβ)-(1-42) oligomers (100 nM) for 48 h. TCP 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, was more efficacious than TCP and TCP-But and significantly protected cortical neurons against Aβ toxicity at nanomolar concentrations (100 nM). Experiments carried out with the Thioflavin-T (Th-T) fluorescence assay for fibril formation showed that TCP and its amide derivatives influenced the early events of the Aβ aggregation process in a concentration-dependent manner. TCP-Ac was more effective than TCP-But and TCP in slowing down the Aβ(1-42) aggregates formation through a lengthening at the lag phase. In our experimental model co-incubation of Aβ(1-42) oligomers with TCP-Ac was able to almost completely prevent Aβ-induced neurodegeneration. These results suggest that inhibition of Aβ oligomer-mediated aggregation significantly contributes to the overall neuroprotective activity of TCP-Ac and also raise the possibility that TCP, and in particular the new compound TCP-Ac, might represent new pharmacological tools to yield neuroprotection in AD[1].
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| Cell Assay |
Apoptosis of RGCs (retinal ganglion cells)[3]
The evaluation of RGC apoptosis was performed as previously described. Briefly, the primary cultured RGCs were washed twice (15-minute incubation at 37°C) with Hanks' balanced salt solution containing 2.4 mM CaCl2 and 20 mM HEPES without magnesium; the magnesium was omitted from the washing solution to avoid blocking the NMDA receptor.32 Subsequently, the RGCs were incubated in 300 μM glutamate and 10 μM glycine, which is a coactivator of the NMDA receptor, in HBSS containing 2.4 mM CaCl2 and 20 mM HEPES without magnesium for 2 hours at 37°C. After treatment with glutamate, the RGCs were cultured in the same medium without any neurotrophic factors such as forskolin, BDNF, CNTF, or bFGF for 22 hours at 37°C. Oxidative stress–induced cell death was achieved by the addition of 50 μM hydrogen peroxide (H2O2) with trophic additives containing B27 supplement AO depleted of antioxidants for 30 minutes and then incubating the cells for 24 hours. Tranylcypromine (100 μM) and wortmannin (100 nM) were simultaneously administered with the glutamate or H2O2, while S2101, BIRB796 (10 μM, no. S1574), and SB203580 (10 μM) were added 24 hours before the induction of apoptosis. Subsequently, the treated RGCs were incubated for 24 hours prior to the detection of apoptosis. Apoptosis was detected by incubating the RGCs with 1.0 μg/mL Hoechst 33342 for 15 minutes. The fluorescent images were observed using an IX71 fluorescence microscope, and at least six images/well were obtained from the 96-well plates. As previously described,30,31 the fragmented or shrunken nuclei stained with Hoechst dye were counted as apoptotic neurons and the round/smooth nuclei were considered to be healthy neurons. For each condition, more than 200 neurons were counted using MetaMorph imaging software to minimize measurement biases. |
| Animal Protocol |
Methods: [2]
Forty-seven female C57BL/6 mice were used in this experimentation. All mice, except those randomly selected to form Sham surgery (M) and specificity control (S) groups, received an endometriosis-inducing surgery. Group S was set up mainly to ensure that the reduced generalized hyperalgesia in mice treated with TC is not due to any possible analgesic effect of TC, but rather resulting from the treatment effect specific to endometriosis. Two weeks after the surgery, mice that received surgery were further divided randomly into 3 groups: 1) untreated group (U); 2) low-dose TC group (L); 3) high-dose TC group (H). Group S received the same treatment as in group H. Two weeks after treatment, all mice were sacrificed and their ectopic endometrial tissues were harvested and analyzed by immunohistochemistry analysis. Hotplate test was administrated to all mice before the induction, treatment and sacrifice. Lesion size, hotplate latency, immunoreactivity against markers of proliferation, angiogenesis, H3K4 methylation, and of epithelial-mesenchymal transition (EMT). Results: [2] TC 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 and lesion growth. |
| References |
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| Additional Infomation |
Tranylcypromine Sulfate is the sulfate salt form of tranylcypromine, an orally bioavailable, nonselective, irreversible, non-hydrazine inhibitor of both monoamine oxidase (MAO) and lysine-specific demethylase 1 (LSD1/BHC110), with antidepressant and anxiolytic activities, and potential antineoplastic activities. Upon oral administration, tranylcypromine exerts its antidepressant and anxiolytic effects through the inhibition of MAO, an enzyme that catalyzes the breakdown of the monoamine neurotransmitters serotonin, norepinephrine, epinephrine and dopamine. This increases the concentrations and activity of these neurotransmitters. Tranylcypromine exerts its antineoplastic effect through the inhibition of LSD1. Inhibition of LSD1 prevents the transcription of LSD1 target genes. LSD1, a flavin-dependent monoamine oxidoreductase and a histone demethylase, is upregulated in a variety of cancers and plays a key role in tumor cell proliferation, migration, and invasion.
A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders. (From AMA Drug Evaluations Annual, 1994, p311) See also: Tranylcypromine Sulfate (annotation moved to). |
| Molecular Formula |
C9H12NO₂S₀.₅
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| Molecular Weight |
182.23
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| Exact Mass |
133.09
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| Elemental Analysis |
C, 59.32; H, 6.64; N, 7.69; O, 17.56; S, 8.80
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| CAS # |
13492-01-8
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| Related CAS # |
Tranylcypromine hydrochloride;1986-47-6;Tranylcypromine;155-09-9; 13492-01-8 (sulfate); 54779-58-7 (Cis_HCl); 4548-34-9 (HCl)
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| PubChem CID |
25267092
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| Appearance |
White to off-white solid powder
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| Density |
1.065g/cm3
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| Boiling Point |
218.3ºC at 760mmHg
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| Flash Point |
90.8ºC
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| Vapour Pressure |
0.127mmHg at 25°C
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| LogP |
4.831
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
25
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| Complexity |
197
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| Defined Atom Stereocenter Count |
4
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| SMILES |
C1[C@@H]([C@H]1N)C2=CC=CC=C2.C1[C@@H]([C@H]1N)C2=CC=CC=C2.OS(=O)(=O)O
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| InChi Key |
BKPRVQDIOGQWTG-FKXFVUDVSA-N
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| InChi Code |
InChI=1S/2C9H11N.H2O4S/c2*10-9-6-8(9)7-4-2-1-3-5-7;1-5(2,3)4/h2*1-5,8-9H,6,10H2;(H2,1,2,3,4)/t2*8-,9+;/m00./s1
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| Chemical Name |
(1R,2S)-2-phenylcyclopropan-1-amine; sulfuric acid (2:1)
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: 20 mg/mL (109.75 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication (<60°C).
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 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 |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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