694438-95-4

Basic information

• Product Name: 17-PA
• Synonyms: 17-PA;17-PHENYL-(3A,5A)-ANDROST-16-EN-3-OL;17-Phenyl-(3α,5α)-androst-16-en-3-ol
• CAS NO: 694438-95-4
• Molecular Formula: C25H34O
• Molecular Weight: 350.54
• Mol File: 694438-95-4.mol
• Article Data: 3

Chemical Properties

• Boiling Point: 472.9°C at 760 mmHg
• Flash Point: 197.4°C
• Appearance: /
• Density: 1.073g/cm³
• Vapor Pressure: 9.47E-10mmHg at 25°C
• Refractive Index: 1.571
• Storage Temp.: Store at RT
• CAS DataBase Reference: 17-PA(CAS DataBase Reference)
• NIST Chemistry Reference: 17-PA(694438-95-4)
• EPA Substance Registry System: 17-PA(694438-95-4)

Safety Data

• Hazardous Substances Data: 694438-95-4(Hazardous Substances Data)

Usage

Uses

17-PA is an antagonist of neurosteroid GABA potentiation.

Biological Activity

Selective antagonist of neurosteroid potentiation and direct gating of GABA A receptors. Selectively reduces the effects of 5 α -reduced steroids compared to 5 β -reduced steroids and displays no effect on potentiation evoked by barbiturates and benzodiazepines. Attenuates 3 α ,5 α -THP-induced loss of righting reflex and total sleep time following i.c.v administration in rats.

Enzyme inhibitor

This selective neurosteroid antagonist (FW = 350.54 g/mol; CAS 694438- 95-4; Soluble to 25 mM in DMSO and to 50 mM in ethanol), also known as 17-PA, targets neurosteroid potentiation and directly gates GABAA receptors. 17-PA inhibition was also useful in demonstrating that ethanol modulates the interaction of the endogenous neurosteroid allopregnanolone with the α1β2γ2L GABAA receptor. 17-PA selectively reduces the effects of 5α-reduced steroids compared to 5β-reduced steroids and displays no effect on potentiation evoked by barbiturates and benzodiazepines. It also attenuates 3α,5α-THP-induced loss of righting reflex and total sleep time, following intracerebroventricular administration in rats.

InChI:InChI=1/C25H34O/c1-24-14-12-19(26)16-18(24)8-9-20-22-11-10-21(17-6-4-3-5-7-17)25(22,2)15-13-23(20)24/h3-7,10,18-20,22-23,26H,8-9,11-16H2,1-2H3/t18-,19+,20-,22-,23-,24-,25+/m0/s1

Upstream product

• 1135993-41-7 3α-methoxymethoxy-17-phenyl-5α-androst-16-ene 
• 10481-80-8 3β-hydroxy-17-hydrozone-5α-androstane 
• 481-29-8 Epiandrosterone 
• 95043-81-5 17-iodo-3β-hydroxy-5α-androstan-16-ene 
• 98-80-6 phenylboronic acid 
• 591-51-5 phenyllithium 
• 53-41-8 cis-androsterone 
• 694438-97-6 (3α,5α,17β)-17-phenylandrostane-3,17-diol-3-acetate 
• 694438-96-5 (3α,5α,17β)-17-phenylandrostane-3,17-diol 
• 694438-98-7 (3α,5α)-17-phenylandrost-16-en-3-ol acetate 

Relevant articles and documents

Stille and Suzuki Cross-Coupling Reactions as Versatile Tools for Modifications at C-17 of Steroidal Skeletons – A Comprehensive Study

Herein, we report on a comparative Stille and Suzuki cross-coupling study of steroidal vinyl (pseudo)halides with different boronic acids and tributyltin organyls. Furthermore, we have investigated the “inverse” case of those cross-coupling reactions, i.e., the reaction of a steroidal vinylpinacolatoborane or a tributyltin steroid with various bromides. The development of both methods allows the introduction of different residues at C-17 of steroid skeletons providing access to a broad variety of steroid analogues which are of high interest for biological screenings or natural product synthesis. (Figure presented.).

Selective antagonism of 5α-reduced neurosteroid effects at GABA A receptors

Although neurosteroids have rapid effects on GABAA receptors, study of steroid actions at GABA receptors has been hampered by a lack of pharmacological antagonists. In this study, we report the synthesis and characterization of a steroid analog, (3α,5α)-17-phenylandrost-16- en-3-ol (17PA), that selectively antagonized neurosteroid potentiation of GABA responses. We examined 17PA using the α1β2γ2 subunit combination expressed in Xenopus laevis oocytes. 17PA had little or no effect on baseline GABA responses but antagonized both the response augmentation and the direct gating of GABA receptors by 5α-reduced potentiating steroids. The effect was selective for 5α-reduced potentiating steroids; 5β-reduced potentiators were only weakly affected. Likewise, 17PA did not affect barbiturate and benzodiazepine potentiation. 17PA acted primarily by shifting the concentration response for steroid potentiation to the right, suggesting the possibility of a competitive component to the antagonism. 17PA also antagonized 5α-reduced steroid potentiation and gating in hippocampal neurons and inhibited anesthetic actions in X. laevis tadpoles. Analogous to benzodiazepine site antagonists, the development of neurosteroid antagonists may help clarify the role of GABA-potentiating neurosteroids in health and disease.