Sonidegib (Erismodegib, NVP-LDE225)

Catalog No.S2151

Sonidegib (Erismodegib, NVP-LDE225) Chemical Structure

Molecular Weight(MW): 485.5

Sonidegib (Erismodegib, NVP-LDE225) is a Smoothened (Smo) antagonist, inhibiting Hedgehog (Hh) signaling with IC50 of 1.3 nM (mouse) and 2.5 nM (human) in cell-free assays, respectively. Phase 3.

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In DMSO USD 210 In stock
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3 Customer Reviews

  • RU-SKI 43 blocks Shh signaling. (a) RU-SKI 43 blocks Gli activation. NIH 3T3 cells were cotransfected with vectors encoding 8× Gli-binding site (GliBS)-Firefly luciferase (unless indicated otherwise), Renilla luciferase reporter (pRL-TK) and Shh. Confluent cells were treated with DMSO, 10 μM LDE225, 10 μM RU-SKI 43 or 10 μM C-2. The firefly luciferase (FL)/Renilla luciferase (RL) ratio in cell lysates was calculated and normalized to that measured in DMSO-treated samples; error bars represent mean ± s.d. (n = 2–3). 

    Nat Chem Biol 2013 9, 247-9. Sonidegib (Erismodegib, NVP-LDE225) purchased from Selleck.

    Western blot analysis on total cell lysates from renal cancer cell lines treated with NVP-LDE225 at different concentrations. Densitometric measurements were normalised to b-actin and reported under western blot images.

    Br J Cancer 2014 111(6), 1168-79. Sonidegib (Erismodegib, NVP-LDE225) purchased from Selleck.

  • NVP-LDE225, everolimus, sunitinib, and their combination interfere with actin and with intracellular organisation of focal adhesion points. Cytoskeleton organisation of 786-O SuR treated with NVP-LDE225 ( 2.5 uM ), everolimus (1 uM ), sunitinib (1 uM ), and their combination for 24 h was analysed by confocal microscopy. Actin-based structures were revealed by rhodaminated phalloidin staining (red fluorescence). Localisation of focal adhesion points was obtained by immunofluorescent staining of p-paxillin (green fluorescence). Merged row images show overlapping of p-paxillin and actin signals. Moreover, all captures were shown in transmitted light. Scale bars, 10 um.

    Br J Cancer 2014 111(6), 1168-79. Sonidegib (Erismodegib, NVP-LDE225) purchased from Selleck.

Purity & Quality Control

Choose Selective Hedgehog/Smoothened Inhibitors

Biological Activity

Description Sonidegib (Erismodegib, NVP-LDE225) is a Smoothened (Smo) antagonist, inhibiting Hedgehog (Hh) signaling with IC50 of 1.3 nM (mouse) and 2.5 nM (human) in cell-free assays, respectively. Phase 3.
Smo (mouse) [1]
(Cell-free assay)
Smo (human) [1]
(Cell-free assay)
1.3 nM 2.5 nM
In vitro

Sonidegib (Erismodegib, NVP-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. [1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
A2780ip2 NIexN2hEgXSxeHnjbZR6KGG|c3H5 NIDCZlN,OTBizszN NWTpUodLUUN3ME2xNkDPxE1? M1vvXVIzPTV|M{W1
A2780cp20 M1jDdWN6fG:6aXPpeJkh[XO|YYm= NWf5bHpQhjFyIN88US=> MWXJR|UxRTdwNTFOwG0> MYiyNlU2OzN3NR?=
SKOV3ip1 M2DtO2N6fG:6aXPpeJkh[XO|YYm= MWj+NVAh|ryP Mlr6TWM2OD1{NDFOwG0> NIXUd44zOjV3M{O1OS=>
HeyA8MDR NVv6R3cxS3m2b4jpZ4l1gSCjc4PhfS=> NVf0NFVOhjFyIN88US=> NUPGUXJrUUN3ME24JO69VQ>? NEjqTlczOjV3M{O1OS=>
OS5 NVL3RZVET3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MkDSglUh|ryP Mln1doVlfWOnczD0bIUheHKxbHnm[ZJifGmxbh?= M{T5blI{OjR|NUm1
OS18 M1LCOGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NVXiVHBIhjVizszN MYLy[YR2[2W|IITo[UBxem:uaX\ldoF1cW:w M4i2UFI{OjR|NUm1
Glioblastoma initiating cells M4HVTGN6fG:6aXPpeJkh[XO|YYm= M3Hjc54yOCEQvF2= MmTXTY5pcWKrdIOgR4VtdCCYaXHibYxqfHl? NU\L[XJ[OjN2OEK2O|E>
Glioblastoma initiating cells NGi3bFNHfW6ldHnvckBie3OjeR?= MYr+NVAh|ryP NWDOcGFKcW6qaXLpeJMhdmW3cn;zdIhmemViZn;ycYF1cW:w NELpR5czOzR6Mk[3NS=>
Glioblastoma initiating cells Mm\oR5l1d3irY3n0fUBie3OjeR?= NFHtToJ,OTBizszN M2Lqbolv\HWlZYOgZZBweHSxc3nz NYfqUXNoOjN2OEK2O|E>
Glioblastoma initiating cells NHe1Z2VHfW6ldHnvckBie3OjeR?= NITQTGx,OTBizszN MYnkc5dvemWpdXzheIV{KHSqZTDTTGghe2mpbnHsbY5oKHCjdHj3ZZk> M4HE[lI{PDh{Nkex
Glioblastoma initiating cells MkDvSpVv[3Srb36gZZN{[Xl? MYj+NVAh|ryP Mlv0TY5pcWKrdIOgeIhmKEW6cILld5Nqd25ib3[gS4Vv\XNiSX72c4x3\WRiaX6gUYFqdnSjaX7pcochWGy3cnnwc5RmdmO7 MX:yN|Q5OjZ5MR?=
Glioblastoma initiating cells MofwSpVv[3Srb36gZZN{[Xl? MUf+NVAh|ryP M2PJS2lvcGmkaYTzJG1wfGmuaYT5MEBKdn[jc3nvckwh[W6mIF3p[5JifGmxbh?= NH7OSHQzOzR6Mk[3NS=>
LOX IMVI M1rMWGZ2dmO2aX;uJIF{e2G7 MlzINVAh|ryP NWrhRYJ7TE2VTx?= M1\CO4lvcGmkaYTzJGhm\GenaH;nMWdNUSCyYYToe4F6 M{\0[VI{QTN3OUK1
UACC 257 M3P3fmZ2dmO2aX;uJIF{e2G7 Ml\MNVAh|ryP MmD5SG1UVw>? MYDpcohq[mm2czDI[YRo\WixZz3HUGkheGG2aIfhfS=> NWLLV3BMOjN7M{W5NlU>
UACC 257 NVm0VIN4TnWwY4Tpc44h[XO|YYm= MUmxNEDPxE1? NFGzXZFFVVOR Mn20bY5lfWOnczDHNUBk\WyuIHP5Z4xmKGG{cnXzeC=> Mli0NlM6OzV7MkW=
UACC 257 NEGycYJEgXSxeHnjbZR6KGG|c3H5 NXPjcVByOTBizszN MUXEUXNQ NX\JXG5b\GWlcnXhd4V{KHS3bX;yJINmdGxidnnhZoltcXS7 NEnlXFkzOzl|NUmyOS=>
UACC 257 NXTreXNLSXCxcITvd4l{KGG|c3H5 MYWxNEDPxE1? NX;WZmM5TE2VTx?= NWq4e3UzcW6mdXPld{BieG:ydH;zbZM> M4HsTlI{QTN3OUK1
769-P M1Xqe2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M3fRTp42KM7:TR?= MnvHSG1UVw>? M3\uTmlEPTB;Mj2z5qCK|ryP Mnu2NlUxQTN2OUG=
786-O SuR NXS3d|lXT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NET4blZ,PSEQvF2= M{PhSmROW09? NUfzWHBJUUN3ME2yMVPjiIoQvF2= M4jJeFI2ODl|NEmx
SP53 M2PlWGZ2dmO2aX;uJIF{e2G7 Ml;3N|Ah|ryP M3r2O2ROW09? NF;sUnpqdmirYnn0d{Bk\WyuIHHkbIV{cW:wIHHu[EBucWe{YYTpc44> NETDPYYzPjh6NU[wPC=>
SP53 MYLGeY5kfGmxbjDhd5NigQ>? NGHiZ4M{OCEQvF2= MmDsSG1UVw>? NYPaNmJGcW6qaXLpeJMhfGinIG\MRVQudWWmaXH0[YQhTkGNIIPp[45idGmwZzDwZZRpf2G7 M3jMNFI3QDh3NkC4
HS5 MVjGeY5kfGmxbjDhd5NigQ>? Ml\WN|Ah|ryP MXjEUXNQ NUjKVlVpcW6qaXLpeJMh[2WubDDh[Ihme2mxbjDhcoQhdWmpcnH0bY9v Mn\4NlY5QDV4MEi=
HS27a NGCze29HfW6ldHnvckBie3OjeR?= MlLFN|Ah|ryP MnL6SG1UVw>? M4PzVIlvcGmkaYTzJINmdGxiYXTo[ZNqd25iYX7kJI1q\3KjdHnvci=> NYD0fG1zOjZ6OEW2NFg>
SP53 MXjDfZRwgGmlaYT5JIF{e2G7 MWizNEDPxE1? MYHEUXNQ Ml\obY5lfWOnczDheZRweGijZ4m= NGTLTnozPjh6NU[wPC=>
Jeko M1vPOGN6fG:6aXPpeJkh[XO|YYm= NF3tUHY{OCEQvF2= MWnEUXNQ NWPtS4JkcW6mdXPld{BifXSxcHjh[5k> NGnyO4EzPjh6NU[wPC=>

... Click to View More Cell Line Experimental Data

In vivo Sonidegib (Erismodegib, NVP-LDE225) is highly bound to mouse, rat, and human plasma proteins (>99%) and moderately bound to dog and monkey plasma proteins (77 and 85%, respectively). LDE225 has high permeability (90.8% in man) in the PAMPA assay. LDE225 shows good oral bioavailability ranging from 69 to 102% in preclinical species when dosed in solution. LDE225 is a weak base with a measured pKa of 4.20 and exhibits relatively poor aqueous solubility. LDE225 demonstrates dose-related antitumor activity. At a dose of 5 mg/kg/day qd, LDE225 significantly inhibits tumor growth, corresponding to a T/C value of 33%. When dosed at 10 and 20 mg/kg/day qd, LDE225 gives rise to 51 and 83% regression, respectively. Gli1 mRNA inhibition correlates with tumor and plasma exposure of LDE225. LDE225 successfully penetrates the blood−brain barrier in tumor-bearing animals and results in tumor growth inhibition after 4 days of treatment. [1] LDE225 significantly reduces the tumor volume by 95.7% in Rip1-Tag2 mice. LDE225 prolongs survival in Rip1Tag2 mice. LDE225 decreases expression of stromal markers in the LDE225-treated mice. [2]


Cell Research:


+ Expand
  • Cell lines: TM3Hh12 cells
  • Concentrations: ~10 μM
  • Incubation Time: 30 minutes
  • Method:

    LDE225 is prepared for assay by serial dilution in DMSO and then added to empty assay plates. TM3Hh12 cells (TM3 cells containing Hh-responsive reporter gene construct pTA-8xGli-Luc) are cultured in F12 Ham's/DMEM (1:1) containing 5% horse serum, 2.5% fetal bovine serum (FBS), and 15 mM HEPES, pH 7.3. Cells are harvested by trypsin treatment, resuspended in F12 Ham's/DMEM (1:1) containing 5% horse serum and 15 mM HEPES, pH 7.3, added to assay plates, and incubated with LDE225 for approximately 30 min at 37 °C in 5% CO2. Then 1 nM or 25 nM Ag1.5 is added to assay plates and incubated at 37 °C in the presence of 5% CO2. After 48 hours, either Bright-Glo or MTS reagent is added to the assay plates and luminescence or absorbance at 492 nm is determined. IC50 values, defined as the inflection point of the logistic curve, are determined by nonlinear regression of the Gli-driven luciferase luminescence or absorbance signal from MTS assay vs log10 (concentration) of LDE225 using the R statistical software pack

    (Only for Reference)
Animal Research:


+ Expand
  • Animal Models: Orthotopic Ptch+/-p53-/- medulloblastoma allograft model in athymic nude mice
  • Formulation: 0.5% sodium carboxymethyl cellulose
  • Dosages: 40 mg/kg/day
  • Administration: Administered via p.o. or b.i.d
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 97 mg/mL (199.79 mM)
Ethanol 97 mg/mL warmed (199.79 mM)
Water Insoluble
In vivo Add solvents individually and in order:
2% DMSO+corn oil

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 485.5


CAS No. 956697-53-3
Storage powder

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01787552 Active, not recruiting Primary Myelofibrosis|Thrombocythemia, Essential|Thrombocytosis|Myeloproliferative Disorders|Bone Marrow Diseases|Hematologic Diseases|Blood Coagulation Disorders|Blood Platelet Disorders|Hemorrhagic Disorders Novartis Pharmaceuticals|Novartis May 8, 2013 Phase 1|Phase 2
NCT02254551 Terminated Multiple Myeloma SCRI Development Innovations, LLC|Novartis January 2015 Phase 2
NCT02138929 Recruiting Esophageal Cancer M.D. Anderson Cancer Center|Novartis|National Cancer Institute (NCI) November 2014 Phase 1
NCT02195973 Active, not recruiting Recurrent Ovarian Cancer University of Alabama at Birmingham|Novartis Pharmaceuticals September 2014 Phase 1
NCT02151864 Recruiting Hepatocellular Carcinoma|Cirrhosis Jason K. Sicklick, M.D.|Novartis Pharmaceuticals|University of California, San Diego July 2014 Phase 1
NCT02182622 Unknown status Prostate Cancer Martin Gutierrez|Novartis|Hackensack University Medical Center July 2014 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID