2107327-36-4
Chemical Structure
PaPE-1
- CAS No.: 2107327-36-4
- Formula:C17H18O2
- Molecular Weight:254.33
IUPAC Name: (S)-5-(4-hydroxy-3,5-dimethylphenyl)-2,3-dihydro-1H-inden-1-ol
InChIKey: UCXWFKNKSWDWCD-INIZCTEOSA-N
SMILES: O[C@@H]1C=2C(=CC(=CC2)C3=CC(C)=C(O)C(C)=C3)CC1
Biological Activity: PaPE-1 is a pathway-preferential estrogen receptor (ER) agonist that preferentially activates ER non-nuclear-initiated signaling while minimally activating nuclear-initiated signaling. PaPE-1 exhibits Ki values of 10 μM and 25 μM for human ERα and ERβ, respectively. The relatively low ER affinity and rapid receptor dissociation of PaPE-1 facilitate the triggering of non-nuclear mTOR/MAPK/AKT signaling, while reducing the recruitment of ERα to chromatin and sustained nuclear ER-dependent transcription. PaPE-1 is suitable for research related to non-nuclear ER signaling, metabolic disorders, ischemic brain injury, Alzheimer's disease, and ER-positive breast cancer[1][2][3][4][5][6][7].
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PaPE-1 | PaPE-1 is a pathway-preferential estrogen receptor (ER) agonist that preferentially activates ER non-nuclear-initiated signaling while minimally activating nuclear-initiated signaling. PaPE-1 exhibits Ki values of 10 μM and 25 μM for human ERα and ERβ, respectively. The relatively low ER affinity and rapid receptor dissociation of PaPE-1 facilitate the triggering of non-nuclear mTOR/MAPK/AKT signaling, while reducing the recruitment of ERα to chromatin and sustained nuclear ER-dependent transcription. PaPE-1 is suitable for research related to non-nuclear ER signaling, metabolic disorders, ischemic brain injury, Alzheimer's disease, and ER-positive breast cancer. | |||||||||||||||||||||
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References
- [1]. Madak-Erdogan Z, et al. Design of pathway preferential estrogens that provide beneficial metabolic and vascular effects without stimulating reproductive tissues. Science signaling. 2016 May 24;9(429):ra53.
- [2]. Madak-Erdogan Z, et al. Free Fatty Acids Rewire Cancer Metabolism in Obesity-Associated Breast Cancer via Estrogen Receptor and mTOR Signaling. Cancer research. 2019 May 15;79(10):2494-2510.
- [3]. Pietrzak-Wawrzyńska BA, et al. Non-nuclear Estrogen Receptor Signaling as a Promising Therapeutic Target to Reverse Alzheimer's Disease-related Autophagy Deficits and Upregulate the Membrane ESR1 and ESR2 Which Involves DNA Methylation-dependent Mechanisms. Journal of molecular biology. 2025 Apr 01;437(7):168982.
- [4]. Zuo Q, et al. Pathway Preferential Estrogens Prevent Hepatosteatosis Due to Ovariectomy and High-Fat Diets. Nutrients. 2021 Sep 23;13(10):3334.
- [5]. Selvaraj UM, et al. Selective Nonnuclear Estrogen Receptor Activation Decreases Stroke Severity and Promotes Functional Recovery in Female Mice. Endocrinology. 2018 Nov 01;159(11):3848-3859.
- [6]. Wnuk A, et al. Posttreatment Strategy Against Hypoxia and Ischemia Based on Selective Targeting of Nonnuclear Estrogen Receptors with PaPE-1. Neurotoxicity research. 2021 Dec;39(6):2029-2041.
- [7]. Marroqui L, et al. Bisphenol-S and Bisphenol-F alter mouse pancreatic β-cell ion channel expression and activity and insulin release through an estrogen receptor ERβ mediated pathway. Chemosphere. 2021 Feb;265:129051.
