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22966-15-0

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22966-15-0 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 22966-15-0 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 2,2,9,6 and 6 respectively; the second part has 2 digits, 1 and 5 respectively.
Calculate Digit Verification of CAS Registry Number 22966-15:
(7*2)+(6*2)+(5*9)+(4*6)+(3*6)+(2*1)+(1*5)=120
120 % 10 = 0
So 22966-15-0 is a valid CAS Registry Number.
InChI:InChI=1/C15H10Cl2O/c16-13-8-6-11(14(17)10-13)7-9-15(18)12-4-2-1-3-5-12/h1-10H/b9-7+

22966-15-0Relevant articles and documents

Synthesis, characterization and biological evaluation of new 3,5-disubstituted-pyrazoline derivatives as potential anti-Mycobacterium tuberculosis H37Ra compounds

Azmi, Mohamad Nurul,Che Omar, Mohammad Tasyriq,Osman, Hasnah,Parumasivam, Thaigarajan,Supratman, Unang,Wong, Kok Tong

, (2021/05/29)

A total of fourteen pyrazoline derivatives were synthesized through cyclo-condensation reactions by chalcone derivatives with different types of semicarbazide. These compounds were characterized by IR, 1D-NMR (1H, 13C and Distortionless Enhancement by Polarization Transfer-DEPT-135) and 2D-NMR (COSY, HSQC and HMBC) as well as mass spectroscopy analysis (HRMS). The synthesized compounds were tested for their antituberculosis activity against Mycobacterium tuberculosis H37Ra in vitro. Based on this activity, compound 4a showed the most potent inhibitory activity, with a minimum inhibitory concentration (MIC) value of 17 μM. In addition, six other synthesized compounds, 5a and 5c–5g, exhibited moderate activity, with MIC ranges between 60 μM to 140 μM. Compound 4a showed good bactericidal activity with a minimum bactericidal concentration (MBC) value of 34 μM against Mycobacterium tuberculosis H37Ra. Molecular docking studies for compound 4a on alpha-sterol demethylase was done to understand and explore ligand– receptor interactions, and to hypothesize potential refinements for the compound.

Environmentally benign synthesis of substituted pyrazoles as potent antioxidant agents, characterization and docking studies

Vagish, Channa Basappa,Dileep Kumar, Achutha,Kumara, Karthik,Vivek, Hamse Kameshwar,Renuka, Nagamallu,Lokanath, Neratur Krishnappagowda,Ajay Kumar, Kariyappa

, p. 479 - 493 (2020/09/01)

Oxidative stress is an important cause of neurogenerative diseases; treatment with a reliable antioxidant with no side effects is a potential tool?to overcome with such diseases. The aim of this study is to explore new and effective antioxidants and their

Antiproliferative effects of chalcones on T cell acute lymphoblastic leukemia-derived cells: Role of PKCβ

Corsini, Emanuela,Facchetti, Giorgio,Esposito, Sara,Maddalon, Ambra,Rimoldi, Isabella,Christodoulou, Michael S.

, (2020/05/16)

In this study, a series of 20 chalcone derivatives was synthesized, and their antiproliferative activity was tested against the human T cell acute lymphoblastic leukemia-derived cell line, CCRF-CEM. On the basis of the structural features of the most active compounds, a new library of chalcone derivatives, according to the structure–activity relationship design, was synthesized, and their antiproliferative activity was tested against the same cancer cell line. Furthermore, four of these derivatives (compounds 3, 4, 8, 28), based on lower IC50 values (between 6.1 and 8.9 μM), were selected for further investigation regarding the modulation of the protein expression of RACK1 (receptor for activated C kinase), protein kinase C (PKC)α and PKCβ, and their action on the cell cycle level. The cell cycle analysis indicated a block in the G0/G1 phase for all four compounds, with a statistically significant decrease in the percentage of cells in the S phase, with no indication of apoptosis (sub-G0/G1 phase). Compounds 4 and 8 showed a statistically significant reduction in the expression of PKCα and an increase in PKCβ, which together with the demonstration of an antiproliferative role of PKCβ, as assessed by treating cells with a selective PKCβ activator, indicated that the observed antiproliferative effect is likely to be mediated through PKCβ induction.

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