Erismodegib

Erismodegib (LDE225) is a potent and selective Smoothened (Smo) antagonist with IC50s of 1.3 nM and 2.5 nM for mouse and human Smo, respectively.
Sonidegib is a member of the classo of biphenyls that is the amide obtained by formal condensation of the carboxy group of 2-methyl-4'-(trifluoromethoxy)[1,1'-biphenyl]-3-carboxylic acid with the amino group of 6-(2,6-dimethylmorpholin-4-yl)pyridin-3-amine. Used (as its phosphate salt) for treatment of locally advanced basal cell carcinoma. It has a role as an antineoplastic agent, a SMO receptor antagonist and a Hedgehog signaling pathway inhibitor. It is a member of morpholines, an aminopyridine, a member of biphenyls, a member of benzamides, an aromatic ether, an organofluorine compound and a tertiary amino compound.|Sonidegib is a Hedgehog signaling pathway inhibitor (via smoothened antagonism) developed as an anticancer agent by Novartis. It was FDA approved in 2015 for the treatment of basal cell carcinoma.|Sonidegib is a Hedgehog Pathway Inhibitor. The mechanism of action of sonidegib is as a Smoothened Receptor Antagonist.|Sonidegib is a small molecule kinase inhibitor that blocks signaling in the hedgehog pathway and is used in the therapy of unresectable or metastatic basal cell carcinoma. Sonidegib therapy is associated with a low rate or transient serum aminotransferase elevations during therapy, but has not been linked to instances of clinically apparent acute liver injury.|Sonidegib is an orally bioavailable small-molecule smoothened (Smo) antagonist with potential antineoplastic activity. Sonidegib selectively binds to the hedgehog (Hh)-ligand cell surface receptor Smo, which may result in the suppression of the Hh signaling pathway and, so, the inhibition of tumor cells in which this pathway is abnormally activated. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair. Inappropriate activation of Hh pathway signaling and uncontrolled cellular proliferation, as is observed in a variety of cancers, may be associated with mutations in the Hh-ligand cell surface receptor Smo.