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Description: Sonidegib phosphate or Sonidegib diphosphate, the diphosphate salt of sonidegib (also known as NVP-LDE225, Erismodegib, Sonidegib; trade name of Odomzo) is a potent and orally bioavailable small-molecule antagonist of the Smoothened (Smo) with potential anticancer activity. It inhibits the Hedgehog (Hh) signaling with IC50 of 1.3 nM (mouse) and 2.5 nM (human) in cell-free assays, respectively. LDE225 (NVP-LDE225, Erismodegib, Sonidegib) specifically binds to the Hedgehog (Hh)-ligand cell surface receptor Smo, resulting in the suppression of the Hedgehog signaling pathway and thus the inhibition of tumor cell growth in which the Hedgehog pathway is abnormally activated. It is an anticancer drug that received FDA approval in 2015 for the treatment of basal cell carcinoma.
References: Ann Surg. 2011 Nov;254(5):818-23; ACS Med. Chem. Lett., 2010, 1 (3), 130–134.
Related CAS: 956697-53-3 (free base)
Product Catalog 2023
Guide to Product Handling
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
In vitro activity: LDE225 (also known as NVP-LDE225, Erismodegib, Sonidegib; trade name of Odomzo) is an orally bioavailable small-molecule antagonist of the Smoothened (Smo) which inhibits the Hedgehog (Hh) signaling with IC50 of 1.3 nM (mouse) and 2.5 nM (human) in cell-free assays, respectively. LDE225 (NVP-LDE225, Erismodegib, Sonidegib) specifically binds to the Hedgehog (Hh)-ligand cell surface receptor Smo, resulting in the suppression of the Hedgehog signaling pathway and thus the inhibition of tumor cell growth in which the Hedgehog pathway is abnormally activated. It is an anticancer drug that received FDA approval in 2015 for the treatment of basal cell carcinoma.
Kinase Assay: LDE225 inhibits TM3 luciferized cell line with 0.6 nM and 8 nM, at the presence of 1 nM and 25 nM Hh agonist Ag1.5, respectively.
Cell Assay: LDE225 induced apoptosis in a dose-dependent manner. Treatment of prostate CSCs resulted in an increase in the expression of cleaved caspase-3 and PARP. LDE225 inhibited cell viability in primary and secondary spheroids in a dose-dependent manner.
Purity ≥98%
COA
MSDS
NMR
Antitumor activity in an orthotopic Ptch+/−p53−/− medulloblastoma allograft model in nude mice upon treatment with 5mdiphosphate salt dosed at 40 mg/kg/day po bid or vehicle at equal dose volume. ACS Med Chem Lett. 2010 Jun 10; 1(3): 130–134.
Antitumor activity upon treatment with 5m diphosphate salt or vehicle in a Ptch+/−p53−/− medulloblastoma subcutaneous allograft model in nude mice. ACS Med Chem Lett. 2010 Jun 10; 1(3): 130–134.
Gli1 mRNA inhibition (open circle), tumor PK (filled squares), and plasma PK (filled triangles) in Ptch+/−p53−/− medulloblastoma model after treatment with 5m (Sonidegib, or erismodegib, LDE225, NVP-LDE225). ACS Med Chem Lett. 2010 Jun 10; 1(3): 130–134.