S-4680 Sonidegib, Free Base, >99%

Synonyms : [Erismodegib] [LDE225] [NPV-LDE225]

  • Size
  • US $
  • £
  • ¥
  • 5 mg
  • 59
  • 52
  • 46
  • 6,600
  • Add to Cart Qty:
  • In stock
  • 10 mg
  • 86
  • 76
  • 67
  • 9,600
  • Add to Cart Qty:
  • In stock
  • 25 mg
  • 158
  • 140
  • 124
  • 17,600
  • Add to Cart Qty:
  • In stock
  • 50 mg
  • 264
  • 234
  • 207
  • 29,500
  • Add to Cart Qty:
  • In stock
  • 100 mg
  • 442
  • 392
  • 346
  • 49,300
  • Add to Cart Qty:
  • In stock
  • 200 mg
  • 698
  • 620
  • 547
  • 77,900
  • Add to Cart Qty:
  • In stock
  • 500 mg
  • 1,485
  • 1,320
  • 1,165
  • 165,700
  • Add to Cart Qty:
  • In stock

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  • M.W. 485.50
  • C26H26F3N3O3
  • [956697-53-3]

Certificate of Analysis

  • Sonidegib, also known as NPV-LDE-225 and LDE-225, is a potent and selective smoothened (Smo) antagonist. It inhibited the activation of hedgehog signaling, stimulated with 1 nM and 25 nM Ag1.5, with IC50 values of 0.6 and 8 nM, respectively. It inhibited Smo binding with IC50 values of 1.3 nM for mouse Smo and 2.5 nM for human Smo. Sonidegib demonstrated in vivo antitumor activity in subcutaneous and orthotopic Ptch+/-p53-/- medulloblastoma allograft models. Pan S., et al. "Discovery of NVP-LDE225, a Potent and Selective Smoothened Antagonist." ACS Med. Chem. Lett. 1: 130–134 (2010).
  • This research compound is the free base form of sonidegib. We also offer the diphosphate salt form; please see Sonidegib, Diphosphate Salt, Cat. No. [S-4699]
  • Treatment with sonidegib inhibited the Hedgehog-GLI pathway, induced G1 cell cycle arrest, and resulted in decreased viability and induction of apoptosis in human melanoma cell lines in vitro. It demonstrated antitumor activity against human melanoma and reduced GLI1 expression in vivo. Jalili A., et al. "NVP-LDE225, a potent and selective SMOOTHENED antagonist reduces melanoma growth in vitro and in vivo." PLoS One 8: e69064 (2013).
  • Addition of the PI3K inhibitor NVP-BKM120 or the dual PI3K-mTOR (mammalian target of rapamycin) inhibitor NVP-BEZ235 to the initial treatment of medulloblastoma with sonidegib markedly delayed the development of resistance to sonidegib in mice. Buonamici S., et al. "Interfering with resistance to smoothened antagonists by inhibition of the PI3K pathway in medulloblastoma." Sci. Transl. Med. 2: 51ra70 (2010).
  • Sonidegib inhibited epithelial-mesenchymal transition and human prostate cancer stem cell growth. Nanta R., et al. "NVP-LDE-225 (Erismodegib) inhibits epithelial-mesenchymal transition and human prostate cancer stem cell growth in NOD/SCID IL2Rγ null mice by regulating Bmi-1 and microRNA-128." Oncogenesis 2: e42 (2013).
  • Sonidegib inhibited melanoma cell growth in vitro and in vivo. O'Reilly K.E., et al. "Hedgehog pathway blockade inhibits melanoma cell growth in vitro and in vivo." Pharmaceuticals (Basel) 6: 1429-1450 (2013).
  • This sonidegib product is the free base form, whose CAS number is given above. The CAS number of the diphosphate salt form is 1218778-77-8.
  • Another CAS number previously assigned to Sonidegib, Free Base , namely 1270169-93-1, has been deleted by CAS and is no longer in use.
  • Sold for laboratory or manufacturing purposes only; not for human, veterinary, food, or household use
  • This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries.
  • Not available in some countries; not available to some institutions; not available for some uses.
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