SAG dihydrochloride is a potent Smoothened (Smo) receptor agonist ( EC 50 =3 nM; K d =59 nM). SAG dihydrochloride activates the Hedgehog signaling pathway and counteracts Cyclopamine (HY-17024) inhibition of Smo.

SAG (0.1 nM-100 μM; 30 h) induces firefly luciferase expression in Shh-LIGHT2 cells with an EC 50 of 3 nM and then inhibits expression at higher concentrations[1]. SAG (1-1000 nM; 1 h) competes for the binding of BODIPY-cyclopamine to Smo-expressing Cos-1 cells, yielding an apparent dissociation constant (K d ) of 59 nM for the SAG/Smo complex[1]. SAG (100 nM) inhibits the inhibitory effect of ShhN-induced pathway activation by Robotnikinin[2]. SAG (250 nM; 48 h) significantly increases SMO mRNA and protein expression in MDAMB231 cells[3]. SAG (250 nM; 24 and 48 h) increases CAXII mRNA expression in MDAMB231 cells at 24h in normoxic and hypoxic conditions in MDAMB231 cells[3]. SAG (250 nM; 24 h) increases MDAMB231 cells migration[3].

SAG (1.0 mM) induces more osteogenesis mainly at the defect borders and a significant increase in BV/TV at the eight week timepoint in CD-1 mice[4]. SAG (15-20 mg/kg; i.p.) induces pre-axial polydactyly prevalently in a dose-dependent manner in mice[5]. Animal Model: Pregnant C57BL/6J mice[5]Dosage: 15, 17, 20 mg/kg Administration: A single i.p. Result: Effective in ca. 80% of the embryos and increased Gli1 and Gli2 mRNA expression in the limb bud, with Gli1 mRNA being the most upregulated at the dose of 20 mg/kg.

SAG dihydrochloride

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years