CEP33779|cas 1257704-57-6| DC Chem|Supplier|Price|Buy  

CEP33779|cas 1257704-57-6| DC Chem|Supplier|Price|Buy

DC Chemicals Supply: CEP33779|cas 1257704-57-6,Purity: >98% ,Cat No. DC7099, In stock.

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CEP33779|cas 1257704-57-6 ,Synonym: CEP33779; CEP-33779; CEP 33779. ,Chemical name: [1,2,4]Triazolo[1,5-a]pyridin-2-amine,N-[3-(4-methyl-1-piperazinyl)phenyl]-8-[4-(methylsulfonyl)phenyl]- ,Molecular Formula: C24H26N6O2S ,MW:462.57

CEP33779, cas 1257704-57-6,Purity: >98%, Best Price and quality from DC Chemicals. 

CEP33779(< 3 μM) inhibits phosphorylation of downstream target signal transducer and activator of transcription 5(pSTAT5) of JAK2 in a concentration dependent manner in HEL92 cells. CEP33779 orally administrated with 55 mg/kg inhibits phosphorylation of STAT5 in HEL92 tumor extracts from HEL92 xenograft mice. CEP33779 orally administered twice daily at dose of 55 mg/kg reduces mean paw edema and clinical scores in mice with collagen-antibody induced arthritis (CAIA) or collagen-induced arthritis (CIA). CEP33779 orally administered twice daily at dose of 55 mg/kg totally inhibits paw phospho-STAT3 expression in CAIA or CIA mice, associated with decreased cytokines including IL-12, IFNγ, IL-2, IL-1β, TNFα and GM-CSF. CEP33779 results in reduced bone degradation, reduced tissue destruction, and reduced osteoarthritis in dose-dependent manner in CAIA or CIA mice. [1] CEP33779 orally administrated at 100 mg/kg extends survival and reduces splenomegaly/lymphomegaly in MRL/lpr systemic lupus erythematosus mice, thus protect mice from developing glomerulonephritis. CEP33779 orally administrated at 100 mg/kg decreases several SLE-associated proinflammatory cytokines and reduces levels of a bone resorption biomarker associated with increased osteoclast activity in MRL/lpr systemic lupus erythematosus mice. [2] CEP33779 orally administered twice daily at dose of 55 mg/kg induces regression of established colorectal tumors, reduces angiogenesis, and reduces proliferation of tumor cells in a mouse model of colitis-induced colorectal cancer. Tumor regression correlated with inhibition of STAT3 and NF-κB (RelA/p65) activation, and decreased the expression of proinflammatory, tumor-promoting cytokines interleukin (IL)-6 and IL-1β.