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Bentamapimod is an orally bioavailable inhibitor of Jun kinases (JNKs), with IC₅₀ values for JNK1, JNK2, and JNK3 of 80, 90, and 230 nM, respectively. It is selective for JNKs over a panel of 25 related kinases. Bentamapimod induces regression of endometriotic lesions without suppressing estrogen action in animal models of endometriosis. It blocks proliferation and induces apoptosis of T cells in vitro and inhibits cancer stem cell survival, self-renewal, and tumor-initiating capacity in vitro and in mice.

Bentamapimod is a potent and selective JNK inhibitor with therapeutic potential in MS (multiple sclerosis) and fibrosis. Studies show that Bentamapimod also reduced induced endometriosis in baboons.

as602801 blocked t-lymphocyte proliferation and induced apoptosis. in rrms cd4t and cd8t cells, as602801 induced apoptosis genes and expression of surface markers, while in rrms cd11bt cells it induced expression of innate immunity receptors and co-stimulatory molecules [1].

as602801, the best jnk inhibitors identified so far, were currently evaluated in preclinical studies, based on preliminary promising results in animal model of auto-immune diseases and neuronal apoptosis [1].

[1] ferrandi c, richard f, tavano p, hauben e, barbié v, gotteland jp, greco b, fortunato m, mariani mf, furlan r, comi g, martino g, zaratin pf. characterization of immune cell subsets during the active phase of multiple sclerosis reveals disease and c-jun n-terminal kinase pathway biomarkers. mult scler. 2011;17(1):43-56.