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2-chloro-N6-phenethyl-adenosine is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

23558-63-6

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23558-63-6 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 23558-63-6 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 2,3,5,5 and 8 respectively; the second part has 2 digits, 6 and 3 respectively.
Calculate Digit Verification of CAS Registry Number 23558-63:
(7*2)+(6*3)+(5*5)+(4*5)+(3*8)+(2*6)+(1*3)=116
116 % 10 = 6
So 23558-63-6 is a valid CAS Registry Number.

23558-63-6Downstream Products

23558-63-6Relevant academic research and scientific papers

Discovery of Potent and Selective Methylenephosphonic Acid CD73 Inhibitors

Sharif, Ehesan U.,Kalisiak, Jaroslaw,Lawson, Kenneth V.,Miles, Dillon H.,Newcomb, Eric,Lindsey, Erick A.,Rosen, Brandon R.,Debien, Laurent P. P.,Chen, Ada,Zhao, Xiaoning,Young, Stephen W.,Walker, Nigel P.,Str?ter, Norbert,Scaletti, Emma R.,Jin, Lixia,Xu, Guifen,Leleti, Manmohan R.,Powers, Jay P.

, p. 845 - 860 (2021)

Solid tumors are often associated with high levels of extracellular ATP. Ectonucleotidases catalyze the sequential hydrolysis of ATP to adenosine, which potently suppresses T-cell and NK-cell functions via the adenosine receptors (A2a and A2b). The ectonucleotidase CD73 catalyzes the conversion of AMP to adenosine. Thus, increased CD73 enzymatic activity in the tumor microenvironment is a potential mechanism for tumor immune evasion and has been associated with poor prognosis in the clinic. CD73 inhibition is anticipated to restore immune function by skirting this major mechanism of adenosine generation. We have developed a series of potent and selective methylenephosphonic acid CD73 inhibitors via a structure-based design. Key binding interactions of the known inhibitor adenosine-5′-(α,β-methylene)diphosphate (AMPCP) with hCD73 provided the foundation for our early designs. The structure-activity relationship study guided by this structure-based design led to the discovery of 4a, which exhibits excellent potency against CD73, exquisite selectivity against related ectonucleotidases, and a favorable pharmacokinetic profile.

A3 Adenosine Receptor Antagonists with Nucleoside Structures and Their Anticancer Activity

Buccioni, Michela,Dal Ben, Diego,Francucci, Beatrice,Lambertucci, Catia,Maggi, Federica,Marucci, Gabriella,Santoni, Giorgio,Spinaci, Andrea,Volpini, Rosaria

, (2022/02/10)

The overexpression of the A3 adenosine receptor (AR) in a number of cancer cell types makes it an attractive target for tumor diagnosis and therapy. Hence, in the search for new A3AR ligands, a series of novel 2,N6-disubstituted adenosines (Ados) was synthesized and tested in radioligand binding and functional assays at ARs. Derivatives bearing a 2-phenethylamino group in the N6-position were found to exert higher A3AR affinity and selectivity than the corresponding N6-(2,2-diphenylethyl) analogues. 2-Chloro-N6-phenylethylAdo (15) was found to be a potent full A3AR agonist with a Ki of 0.024 nM and an EC50 of 14 nM, in a cAMP accumulation assay. Unlike 15, the other ligands behaved as A3AR antagonists, which concentration-dependently reduced cell growth and exerted cytostatic activity on the prostate cancer cell line PC3, showing comparable and even more pronounced effects with respect to the ones elicited by the reference full agonist Cl-IB-MECA. In particular, the N6-(2,2-diphenylethyl)-2-phenylethynylAdo (12: GI50 = 14 μM, TGI = 29 μM, and LC50 = 59 μM) showed the highest activity proving to be a potential antitumor agent. The cytostatic effect of both A3AR agonist (Cl-IB-MECA) and antagonists (12 and other newly synthesized com-pounds) confirm previous observations according to which, in addition to the involvement of A3ARs, other cellular mechanisms are responsible for the anticancer effects of these ligands.

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