(1,3-Benzothiazol-2-yl)[2-[[4-[(morpholin-4-yl)methyl]benzyl]oxy]pyrimidin-4-yl]acetonitrile Property

Boiling point:

666.5±65.0 °C(Predicted)

Density 

1.326

storage temp. 

2-8°C

solubility 

insoluble in H2O; insoluble in EtOH; ≥11.45 mg/mL in DMSO

form 

solid

pka

6.47±0.10(Predicted)

Safety

HS Code 

2934999090

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Warning

Hazard statements

H315Causes skin irritation

H319Causes serious eye irritation

H335May cause respiratory irritation

Precautionary statements

P301+P312IF SWALLOWED: call a POISON CENTER or doctor/physician IF you feel unwell.

P302+P352IF ON SKIN: wash with plenty of soap and water.

P305+P351+P338IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continuerinsing.

(1,3-Benzothiazol-2-yl)[2-[[4-[(morpholin-4-yl)methyl]benzyl]oxy]pyrimidin-4-yl]acetonitrile Chemical Properties,Usage,Production

Description

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.

Uses

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.

in vitro

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].

in vivo

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].

References

[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.