1006378-90-0 Usage
Description
p38 MAPK-IN-1 is a chemical compound that serves as a selective inhibitor of p38α MAP kinase, a protein that plays a crucial role in various cellular processes such as inflammation, apoptosis, and stress response. Its ability to effectively inhibit the phosphorylation and activation of p38α MAP kinase makes it a valuable tool in research and a potential candidate for therapeutic treatments.
Uses
Used in Pharmaceutical Research and Development:
p38 MAPK-IN-1 is used as a research tool for studying the role of p38α MAP kinase in cellular signaling pathways. Its potential in the development of therapeutic treatments makes it a promising candidate for diseases such as rheumatoid arthritis, inflammatory bowel disease, and cancer.
Used in Preclinical Research:
p38 MAPK-IN-1 is used as a selective inhibitor in preclinical research to investigate its effects on cell proliferation, survival, and differentiation. The promising results obtained from these studies could lead to the development of novel drugs for various medical conditions.
Check Digit Verification of cas no
The CAS Registry Mumber 1006378-90-0 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,0,0,6,3,7 and 8 respectively; the second part has 2 digits, 9 and 0 respectively.
Calculate Digit Verification of CAS Registry Number 1006378-90:
(9*1)+(8*0)+(7*0)+(6*6)+(5*3)+(4*7)+(3*8)+(2*9)+(1*0)=130
130 % 10 = 0
So 1006378-90-0 is a valid CAS Registry Number.
1006378-90-0Relevant articles and documents
1,7-naphthyridine 1-oxides as novel potent and selective inhibitors of p38 mitogen activated protein kinase
Lumeras, Wenceslao,Vidal, Laura,Vidal, Bernat,Balagué, Cristina,Orellana, Adelina,Maldonado, M?nica,Dom?nguez, Mar?a,Segarra, V?ctor,Caturla, Francisco
experimental part, p. 7899 - 7910 (2012/01/05)
The design, synthesis, and ability to inhibit p38 MAP kinase by a novel series of naphthyridine N-oxides will be described. Some of these compounds showed a significant reduction in the LPS-induced TNF production in human whole blood. Structure-activity relationship studies revealed that N-oxide oxygen was essential for activity and was probably a determinant factor for its marked selectivity against other related kinases. After an extensive SAR exercise, several compounds from this series were identified as very potent p38 inhibitors. In vivo efficacy of some derivatives was demonstrated to reduce TNF levels in an acute murine model of inflammation (ED50 = 0.5 mg/kg in LPS-induced TNF production when dosed orally 1.5 h prior to LPS administration). The oral efficacy was further demonstrated in a chronic model of adjuvant arthritis in rats with established disease when administered orally (ED 50 1 mg/kg).
