SB 202474

The Uses of SB 202474

SB 202474 is structurally similar to SB 202190 (S154495) and SB 203580 (S154600), which are p38 MAP kinase inhibitors. SB 202747 can be employed in p38 inhibition research.

What are the applications of Application

SB 202474 is a negative control for SB202190 and SB203580 in p38 MAP kinase inhibition studies

Biological Activity

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.