RWJ 67657

RWJ 67657 is an orally active inhibitor of the MAP kinases p38α and p38β (IC₅₀s = 1 and 11 µM, respectively, in vitro) that is inactive against p38γ and p38δ, as well as several other kinases.¹ It blocks the release of TNF-α and IL-1β from peripheral blood mononuclear cells stimulated with LPS (IC₅₀s = 3 and 11 nM, respectively) and inhibits TNF-α production in LPS-treated mice and rats.¹ RWJ 67657 potently blocks the proliferation of CD4⁺ peripheral blood T cells induced by CD28 stimulation alone (IC₅₀ = 0.5-4 nM).² It is commonly used to study the roles of p38α and p38β in cellular and whole animal systems.^3,4,5

WARNING This product is not for human or veterinary use.

1. Wadsworth, S.A., Cavender, D.E., Beers, S.A., et al. RWJ 67657, a potent, orally active inhibitor of p38 mitogen-activated protein kinase. J. Pharmacol. Exp. Ther. 291(2), 680-687 (1999).

2. Schafer, P.H., Wadsworth, S.A., Wang, L., et al. p38 α mitogen-activated protein kinase is activated by CD28-mediated signaling and is required for IL-4 production by human CD4⁺ CD45RO+ T cells and Th2 effector cells. J. Immunol. 162(12), 7110-7119 (2016).

3. Kompa, A.R., See, F., Lewis, D.A., et al. Long-term but not short-term p38 mitogen-activated protein kinase inhibition improves cardiac function and reduces cardiac remodeling post-myocardial infarction. J. Pharmacol. Exp. Ther. 325(3), 741-750 (2008).

4. Antoon, J.W., Nitzchke, A.M., Martin, E.C., et al. Inhibition of p38 mitogen-activated protein kinase alters microRNA expression and reverses epithelial-to-mesenchymal transition. Int. J. Oncol. 42(4), 1139-1150 (2013).

5. Bai, Y.Y., Wang, L., Chang, D., et al. Synergistic effects of transplanted endothelial progenitor cells and RWJ 67657 in diabetic ischemic stroke models. Stroke 46(7), 1938-1946 (2015).