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61881-50-3

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61881-50-3 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 61881-50-3 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 6,1,8,8 and 1 respectively; the second part has 2 digits, 5 and 0 respectively.
Calculate Digit Verification of CAS Registry Number 61881-50:
(7*6)+(6*1)+(5*8)+(4*8)+(3*1)+(2*5)+(1*0)=133
133 % 10 = 3
So 61881-50-3 is a valid CAS Registry Number.

61881-50-3Relevant articles and documents

TRICYCLIC PYRIDINE DERIVATIVES, MEDICAMENTS CONTAINING SUCH COMPOUNDS, THEIR USE AND PROCESS FOR THEIR PREPARATION

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Page/Page column 177, (2012/03/10)

The present invention relates to compounds defined by formula I wherein the variables R1-R8 are defined as in the description, possessing valuable pharmacological activity. Particularly, the compounds are inhibitors of cholesterol ester transfer protein (CETP) and thus are suitable for treatment and prevention of diseases which can be influenced by inhibition of this enzyme.

Synthesis and biological activity of flurbiprofen analogues as selective inhibitors of β-amyloid1-42 secretion

Peretto, Ilaria,Radaelli, Stefano,Parini, Carlo,Zandi, Michele,Raveglia, Luca F.,Dondio, Giulio,Fontanella, Laura,Misiano, Paola,Bigogno, Chiara,Rizzi, Andrea,Riccardi, Benedetta,Biscaioli, Marcello,Marchetti, Silvia,Puccini, Paola,Catinella, Silvia,Rondelli, Ivano,Cenacchi, Valentina,Bolzoni, Pier Tonino,Caruso, Paola,Villetti, Gino,Facchinetti, Fabrizio,Del Giudice, Elda,Moretto, Nadia,Imbimbo, Bruno P.

, p. 5705 - 5720 (2007/10/03)

Flurbiprofen, a nonsteroidal antiinflammatory drug (NSAID), has been recently described to selectively inhibit β-amyloid1-42 (Aβ42) secretion, the most toxic component of the senile plaques present in the brain of Alzheimer patients. The use of this NSAID in Alzheimer's disease (AD) is hampered by a significant gastrointestinal toxicity associated with cyclooxygenase (COX) inhibition. New flurbiprofen analogues were synthesized, with the aim of increasing Aβ42 inhibitory potency while removing anti-COX activity. In vitro ADME developability parameters were taken into account in order to identify optimized compounds at an early stage of the project. Appropriate substitution patterns at the alpha position of flurbiprofen allowed for the complete removal of anti-COX activity, while modifications at the terminal phenyl ring resulted in increased inhibitory potency on Aβ42 secretion. In rats, some of the compounds appeared to be well absorbed after oral administration and to penetrate into the central nervous system. Studies in a transgenic mice model of AD showed that selected compounds significantly decreased plasma Aβ42 concentrations. These new flurbiprofen analogues represent potential drug candidates to be developed for the treatment of AD.

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