Epigenetic modifier; Inhibits lysine-specific demethylase 1 (LSD1)

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Epigenetic modifier; Inhibits lysine-specific demethylase 1 (LSD1)
From: 44 USD


Tranylcypromine is an epigenetic modifier that is an irreversible inhibitor of lysine-specific demethylase 1 (LSD1; IC₅₀ = 20.7 µM). The catalytic site of LSD1 shares similarity with monoamine oxidase (MAO) enzymes; Tranylcypromine also inhibits MAO A (IC₅₀ = 2.3 µM) and MAO B (IC₅₀ = 0.95 µM; Lee et al.; Schmidt and McCafferty). This product is supplied as the hydrochloride salt of the molecule, and is a racemic mixture of the (1R,2S) and the (2R,1S) enantiomers.

· Enables chemical reprogramming (without genetic factors) of mouse embryonic fibroblasts to induced pluripotent stem (iPS) cells, in combination with CHIR99021, Forskolin, Valproic Acid, 3-Deazaneplanocin A, and E-616452 (Hou et al.).
· Promotes reprogramming of human keratinocytes to iPS cells using only 2 factors (OCT4 and KLF4), in combination with CHIR99021 (Li et al.).
· Converts mouse epiblast-like stem cells to a more primitive embryonic stem (ES)-like state, in combination with several other small molecules (Zhou et al.).

· Inhibits proliferation of mouse neural stem cells (Sun et al.).
·Blocks differentiation of mouse ES cells as well as the differentiation-induced demethylation of ES-specific enhancers (Whyte et al.).
Alternative Names:
2-PCPA hydrochloride; Parnate; Trans-2-phenylcyclopropylamine hydrochloride
CAS Number:
Chemical Formula:
C₉H₁₁N · HCl
Molecular Weight:
169.7 g/mol
≥ 98%
Histone Demethylase

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Data and Publications


Science (New York, N.Y.) 2013 AUG

Pluripotent stem cells induced from mouse somatic cells by small-molecule compounds.

Hou P et al.


Pluripotent stem cells can be induced from somatic cells, providing an unlimited cell resource, with potential for studying disease and use in regenerative medicine. However, genetic manipulation and technically challenging strategies such as nuclear transfer used in reprogramming limit their clinical applications. Here, we show that pluripotent stem cells can be generated from mouse somatic cells at a frequency up to 0.2% using a combination of seven small-molecule compounds. The chemically induced pluripotent stem cells resemble embryonic stem cells in terms of their gene expression profiles, epigenetic status, and potential for differentiation and germline transmission. By using small molecules, exogenous master genes" are dispensable for cell fate reprogramming. This chemical reprogramming strategy has potential use in generating functional desirable cell types for clinical applications."
Nature 2012 FEB

Enhancer decommissioning by LSD1 during embryonic stem cell differentiation.

Whyte WA et al.


Transcription factors and chromatin modifiers are important in the programming and reprogramming of cellular states during development. Transcription factors bind to enhancer elements and recruit coactivators and chromatin-modifying enzymes to facilitate transcription initiation. During differentiation a subset of these enhancers must be silenced, but the mechanisms underlying enhancer silencing are poorly understood. Here we show that the histone demethylase lysine-specific demethylase 1 (LSD1; ref. 5), which demethylates histone H3 on Lys 4 or Lys 9 (H3K4/K9), is essential in decommissioning enhancers during the differentiation of mouse embryonic stem cells (ESCs). LSD1 occupies enhancers of active genes that are critical for control of the state of ESCs. However, LSD1 is not essential for the maintenance of ESC identity. Instead, ESCs lacking LSD1 activity fail to differentiate fully, and ESC-specific enhancers fail to undergo the histone demethylation events associated with differentiation. At active enhancers, LSD1 is a component of the NuRD (nucleosome remodelling and histone deacetylase) complex, which contains additional subunits that are necessary for ESC differentiation. We propose that the LSD1-NuRD complex decommissions enhancers of the pluripotency program during differentiation, which is essential for the complete shutdown of the ESC gene expression program and the transition to new cell states.
The Journal of biological chemistry 2010 SEP

Conversion of mouse epiblast stem cells to an earlier pluripotency state by small molecules.

Zhou H et al.


Epiblast stem cells (EpiSCs) are pluripotent cells derived from post-implantation late epiblasts in vitro. EpiSCs are incapable of contributing to chimerism, indicating that EpiSCs are less pluripotent and represent a later developmental pluripotency state compared with inner cell mass stage murine embryonic stem cells (mESCs). Using a chemical approach, we found that blockage of the TGFβ pathway or inhibition of histone demethylase LSD1 with small molecule inhibitors induced dramatic morphological changes in EpiSCs toward mESC phenotypes with simultaneous activation of inner cell mass-specific gene expression. However, full conversion of EpiSCs to the mESC-like state with chimerism competence could be readily generated only with the combination of LSD1, ALK5, MEK, FGFR, and GSK3 inhibitors. Our results demonstrate that appropriate synergy of epigenetic and signaling modulations could convert cells at the later developmental pluripotency state to the earlier mESC-like pluripotency state, providing new insights into pluripotency regulation.
Molecular and cellular biology 2010 APR

Histone demethylase LSD1 regulates neural stem cell proliferation.

Sun G et al.


Lysine-specific demethylase 1 (LSD1) functions as a transcriptional coregulator by modulating histone methylation. Its role in neural stem cells has not been studied. We show here for the first time that LSD1 serves as a key regulator of neural stem cell proliferation. Inhibition of LSD1 activity or knockdown of LSD1 expression led to dramatically reduced neural stem cell proliferation. LSD1 is recruited by nuclear receptor TLX, an essential neural stem cell regulator, to the promoters of TLX target genes to repress the expression of these genes, which are known regulators of cell proliferation. The importance of LSD1 function in neural stem cells was further supported by the observation that intracranial viral transduction of the LSD1 small interfering RNA (siRNA) or intraperitoneal injection of the LSD1 inhibitors pargyline and tranylcypromine led to dramatically reduced neural progenitor proliferation in the hippocampal dentate gyri of wild-type adult mouse brains. However, knockout of TLX expression abolished the inhibitory effect of pargyline and tranylcypromine on neural progenitor proliferation, suggesting that TLX is critical for the LSD1 inhibitor effect. These findings revealed a novel role for LSD1 in neural stem cell proliferation and uncovered a mechanism for neural stem cell proliferation through recruitment of LSD1 to modulate TLX activity.
Stem cells (Dayton, Ohio) 2009 DEC

Generation of human-induced pluripotent stem cells in the absence of exogenous Sox2.

Li W et al.


Induced pluripotent stem cell technology has attracted enormous interest for potential application in regenerative medicine. Here, we report that a specific glycogen synthase kinase 3 (GSK-3) inhibitor, CHIR99021, can induce the reprogramming of mouse embryonic fibroblasts transduced by only two factors, Oct4 and Klf4. When combined with Parnate (also named tranylcypromine), an inhibitor of lysine-specific demethylase 1, CHIR99021 can cause the reprogramming of human primary keratinocyte transduced with the two factors, Oct4 and Klf4. To our knowledge, this is the first time that human iPS cells have been generated from somatic cells without exogenous Sox2 expression. Our studies suggest that the GSK-3 inhibitor might have a general application to replace transcription factors in both mouse and human reprogramming.