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202592-24-3

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202592-24-3 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 202592-24-3 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 2,0,2,5,9 and 2 respectively; the second part has 2 digits, 2 and 4 respectively.
Calculate Digit Verification of CAS Registry Number 202592-24:
(8*2)+(7*0)+(6*2)+(5*5)+(4*9)+(3*2)+(2*2)+(1*4)=103
103 % 10 = 3
So 202592-24-3 is a valid CAS Registry Number.

202592-24-3Relevant articles and documents

METHODS AND COMPOUNDS FOR THE TREATMENT OF GENETIC DISEASE

-

, (2021/08/13)

The present disclosure relates to compounds and methods for modulating the expression of dmpk, and treating diseases and conditions in which dmpk plays an active role. The compound can be a transcription modulator molecule having a first terminus, a second terminus, and oligomeric backbone, wherein: a) the first terminus comprises a DNA-binding moiety capable of noncovalently binding to a nucleotide repeat sequence CAG or CTG; b) the second terminus comprises a protein-binding moiety binding to a regulatory molecule that modulates an expression of a gene comprising the nucleotide repeat sequence CAG or CTG; and c) the oligomeric backbone comprising a linker between the first terminus and the second terminus.

Potent Dual BET/HDAC Inhibitors for Efficient Treatment of Pancreatic Cancer

Dong, Guoqiang,He, Shipeng,Li, Yu,Sheng, Chunquan,Wang, Wei,Wu, Shanchao

supporting information, p. 3028 - 3032 (2020/02/11)

As one of the most aggressive and lethal human malignancies with extremely poor prognosis, there is an urgent demand of more effective therapy for the treatment of pancreatic cancer. Reported here is a new, effective therapeutic strategy and the design of small-molecule inhibitors that simultaneously target bromodomain and extra-terminal (BET) and histone deacetylase (HDAC), potentially serving as promising therapeutic agents for pancreatic cancer. A highly potent dual inhibitor (13 a) is identified to possess excellent and balanced activities against BRD4 BD1 (IC50=11 nm) and HDAC1 (IC50=21 nm). Notably, this compound shows higher in vitro and in vivo antitumor potency than the BET inhibitor (+)-JQ1 and the HDAC inhibitor vorinostat, either alone or and in combination, highlighting the advantages of BET/HDAC dual inhibitors for more effective treatment of pancreatic cancer.

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