1-benzyl-3-(4-chlorophenyl)-5-MethyliMidazolidine-2,4-dione Property

Boiling point:

452.0±55.0 °C(Predicted)

Density 

1.321±0.06 g/cm3(Predicted)

storage temp. 

2-8°C

solubility 

DMSO: >10mg/mL

pka

-1.30±0.40(Predicted)

form 

powder

color 

white to beige

Safety

Hazard Codes 

Xn,N

Risk Statements 

22-50

Safety Statements 

61

RIDADR 

UN 3077 9 / PGIII

WGK Germany 

3

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Warning

Hazard statements

H302Harmful if swallowed

H317May cause an allergic skin reaction

H319Causes serious eye irritation

H400Very toxic to aquatic life

Precautionary statements

P273Avoid release to the environment.

P280Wear protective gloves/protective clothing/eye protection/face protection.

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

1-benzyl-3-(4-chlorophenyl)-5-MethyliMidazolidine-2,4-dione Chemical Properties,Usage,Production

Uses

ALLO-1 is a small molecule antagonist that inhibits drug-resistant mutant of Smoothened (Smo), related to cancers.

Biological Activity

allo-1 is a smo antagonist.hedgehog (hh) proteins are important development regulators that bind the cell-surface protein, which allows the activation of a gpcr-like receptor, smoothened (smo). in vertebrates, the smo activation finally results in the activation of the zinc-finger transcription factors of the gli family. in addition, the overactivation of smo may lead to certain cancers.

Biochem/physiol Actions

ALLO-1 is a Smoothened (Smo) antagonist that inhibits both wild-type and mutant Smo, including D473H SMO mutant. ALLO-1 binds to a different domain of Smo than other known Smo ligands.

in vitro

previous study found that allo-1 and its close analog allo-2 could inhibit smo agonist hh-ag 1.5-induced luciferase expression in tm3-gli-luc cells. the potency of allo-1 did not change when either low dose or high dose of hh-ag 1.5 was used, in contrast to other known smo antagonists that are strong sag or hh-ag 1.5 competitors. moreover, it was found that in contrast to gdc-0449, both allo-1 and allo-2 inhibited wild-type and the d477g mutant with only around2-fold shift in ic50, indicating that the d477g mutation did not significantly interfere with the binding of allo-1 and allo-2 to smo. in addition, allo-1 as well as allo-2 were able to inhibit both wild-type and d473h mutant human smo with similar potencies [1].

IC 50

50 nm for wile type smo

References

[1] tao, h. ,jin, q.,koo, d.i., et al. small molecule antagonists in distinct binding modes inhibit drug-resistant mutant of smoothened. chemistry & biology 18, 432-437 (2011).