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SB 202474
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
SB 202474图片
CAS NO:172747-50-1
包装:1mg
市场价:1750元

产品介绍
SB 202474,SB203580 的负模拟物。 SB 202474 没有抑制 p38 MAPK 活性的能力,在 p38 MAPK 研究中被广泛用作阴性对照化合物,它也抑制黑色素合成诱导。
Cas No.172747-50-1
化学名4-[4-ethyl-2-(4-methoxyphenyl)-1H-imidazol-5-yl]-pyridine
Canonical SMILESCCC1=C(C2=CC=NC=C2)N=C(C3=CC=C(OC)C=C3)N1
分子式C17H17N3O
分子量279.3
溶解度Soluble in methanol;Soluble in DMSO
储存条件Store at -20℃
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

SB 202474 is a structural analog of SB 202190 and SB 203580 that is used as a negative control in researches of p38 inhibition. SB 202190 and SB 203580 are potent and selective inhibitors of the MAP kinases p38α and p38β [1][2][3].

Mitogen-activated protein kinases (MAPKs) are ser/thr-specific protein kinases that regulate gene expression, proliferation, differentiation, cell survival and apoptosis. Three most widely characterized MAPK subfamilies are ERK1/2, JNK and p38MAPK, of which JNK and p38MAPK are identified as a stress-activated protein kinase (SAPK) that primarily mediates inflammatory response and promotes cell death [3].

SB 202474 is a structural analog of SB 202190 and SB 203580 that is used as a negative control in researches of p38 inhibition. In 3T3-L1 adipocytes and L6 myotubes, SB203580 but not SB202474 prevented insulin-stimulated glucose transport [2].

Pretreatment with microinjection into the bilateral rostral ventrolateral medulla (RVLM) of SB203580 (2 nmol) significantly exacerbated the depressor effect and blunted the augmented power density of the LF component of SAP signals during the pro-life phase. SB203580 also significantly shortened the pro-life phase to 60 min. SB202474 (2 nmol) was ineffective against the phasic cardiovascular responses in the aCSF-control group or Mev-experimental group [3].

References:
[1].  Davies SP, Reddy H, Caivano M, et al. Specificity and mechanism of action of some commonly used protein kinase inhibitors. Biochem J. 2000 Oct 1;351(Pt 1):95-105.
[2].  Sweeney G, Somwar R, Ramlal T, et al. An inhibitor of p38 mitogen-activated protein kinase prevents insulin-stimulated glucose transport but not glucose transporter translocation in 3T3-L1 adipocytes and L6 myotubes. J Biol Chem. 1999 Apr 9;274(15):10071-8.
[3].  Chang AY. Pro-life role for c-Jun N-terminal kinase and p38 mitogen-activated protein kinase at rostral ventrolateral medulla in experimental brain stem death. J Biomed Sci. 2012 Nov 17;19:96.