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3-[4-[2-(N-tert-butoxycarbonyl)amino]ethoxybenzyl]amino-β-carboline is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

1269418-53-2

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1269418-53-2 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 1269418-53-2 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,2,6,9,4,1 and 8 respectively; the second part has 2 digits, 5 and 3 respectively.
Calculate Digit Verification of CAS Registry Number 1269418-53:
(9*1)+(8*2)+(7*6)+(6*9)+(5*4)+(4*1)+(3*8)+(2*5)+(1*3)=182
182 % 10 = 2
So 1269418-53-2 is a valid CAS Registry Number.

1269418-53-2Downstream Products

1269418-53-2Relevant academic research and scientific papers

3-Benzylamino-β-carboline derivatives induce apoptosis through G 2/M arrest in human carcinoma cells HeLa S-3

Ikeda, Reiko,Iwaki, Toshie,Iida, Tomoko,Okabayashi, Takasumi,Nishi, Eishiro,Kurosawa, Masaki,Sakai, Norio,Konakahara, Takeo

, p. 636 - 646 (2011)

β-Carboline derivatives are known as the lead compounds for anti-tumor agents. To examine an optimal structure for anti-tumor activity, we synthesized a variety of β-carboline derivatives, possessing a variety of substituents on the nitrogen atom of the amino group of 3-amino-β-carboline, and evaluated their anti-tumor activity for HeLa S-3 cell line. 3-(4,5- Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that an optimal structure for anti-tumor activity was 3-cyclohexylmethylamino (1e) or 3-benzylamino-β-carboline (1f). An optimal counter anion of 2-methyl-3-benzylamino- β-carbolinium salts was a triflate anion 2c. In addition, the introduction of a hydroxyl group on the meta-position of the benzyl group of 3-benzylamino-β-carboline (3e) enhanced its anti-tumor activity. Hoechst 33342 staining and DNA fragmentation assay suggested that 1f, 2c and 3e induced cell death by apoptosis unlike 1e. Flow cytometry analysis showed that 1f, 2c and 3e induced cell apoptosis through arrest of the cell cycle in the G2/M phase.

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