Catalog No.S2797 Synonyms: SCH66336

Lonafarnib Chemical Structure

Molecular Weight(MW): 638.82

Lonafarnib is an orally bioavailable FPTase inhibitor for H-ras, K-ras-4B and N-ras with IC50 of 1.9 nM, 5.2 nM and 2.8 nM in cell-free assays, respectively. Phase 3.

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In DMSO USD 430 In stock
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2 Customer Reviews

  • Huh-7/hNTCP cells were infected with in vitro generated HDV in the presence or absence of MyrB (50 nM) or lonafarnib (200 nM). After 5 days cells were labeled with HDAg#280, secondary AF488 and stained with DAPI. A representative of four independent experiments is shown.

    Antiviral Res, 2017, 141:116-123. Lonafarnib purchased from Selleck.

    Low-dose lonafarnib decreased HIF-1α expression without inhibiting cell growth in MDA-MB-231 cells. (A, B) Lonafarnib (1 μM) treatment for 24 h significantly decreased HIF-1α expression, which was normalized to that of GAPDH. In contrast, lonafarnib (1 μM) did not decrease HIF-2α expression.

    J Cell Physiol, 2017, 232(1):192-201. Lonafarnib purchased from Selleck.

Purity & Quality Control

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Biological Activity

Description Lonafarnib is an orally bioavailable FPTase inhibitor for H-ras, K-ras-4B and N-ras with IC50 of 1.9 nM, 5.2 nM and 2.8 nM in cell-free assays, respectively. Phase 3.
H-ras [1]
(Cell-free assay)
N-ras [1]
(Cell-free assay)
K-ras-4B [1]
(Cell-free assay)
1.9 nM 2.8 nM 5.2 nM
In vitro

SCH66336 at concentration ranging from 0.1 μM to 8 μM suppress growth and induce apoptosis of human head and neck squamous carcinoma cells (HNSCC) in a dose and time dependent manner. SCH66336 (8 μM) suppresses protein kinase B/Akt activity as well as the phosphorylation of the Akt substrates glycogen synthase kinase (GSK)-3β, forkhead transcription factor, and BAD in SqCC/Y1 cells. [2] SCH66336 demonstrate variable antiproliferative effects against the cell lines, with IC50 ranging from 0.6 μM to 32.3 μM. [3] Lonafarnib induces a CCAAT/enhancer-binding protein homologous protein (CHOP)-dependent transactivation of the DR5 promoter, thus induces CHOP-dependent DR5 up-regulation. Lonafarnib (< 10 μM) activates caspase-8 and its downstream caspases, thus induces caspase-8-dependent apoptosis in H1792 cells. Lonafarnib (5 μM) up-regulate DR5 expression, increase cell-surface DR5 distribution, and enhance tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in H1792 cells.[4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Cos-1 monkey kidney cells NFy5fnlHfW6ldHnvckBie3OjeR?= MnLTTY5pcWKrdHnvckBw\iCScn;0[YlvKG[jcn7ld5ltfHKjboPm[ZJie2ViaX6gR49{NTFibX;ub4V6KGurZH7lfUBk\WyuczDlfJBz\XO|aX7nJGguWmG|LY\hcEwhUUN3ME2wMlAxOTlizszN M{nIe|EzOTlyM{C5
COS-7 monkey cells MX;GeY5kfGmxbjDhd5NigQ>? NUf5dJI5UW6qaXLpeIlv\yC2aHWg[oFzdmW|eXzheIlwdiCxZjDIMZJieyCycn;0[YlveyCrbjDDU3MuPyCvb37r[Zkh[2WubIOgeJJidnOrZX70cJkh\XiycnXzd4lv\yCKLYLhd3tX[WxzMm2tR3ZNWyCrbjD0bIUhf2ixbHWgZ4VtdCCjc4PhfUwhUUN3ME2wMlAyKM7:TR?= M2XUOVk5OjJ3NUi=
MCF-7 tumor cell line NGXyUYZIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NEXUSGVEd22yb4Xu[EB4[XNibXXhd5Vz\WRiZn;yJIlvcGmkaYTpc44hd2ZiTVPGMVchfHWvb4KgZ4VtdCCuaX7lJIlvKGK{ZXHzeEB2dmSncjDzc4Z1KGGpYYKgZZN{[XluIFnDOVA:OC5yNTFOwG0> NW\wdlZ7QTh{MkW1PC=>
HCT116 M{j6[Gdzd3e2aDDpcohq[mm2aX;uJIF{e2G7 Ml7NR49ueG:3bnSge4F{KG2nYYP1doVlKG[xcjDpcohq[mm2aX;uJI9nKEiFVEGxOkB1fW2xcjDj[YxtKGyrbnWgbY4h[2:ub36geY5l\XJic3;meEBi\2G{IHHzd4F6NCCLQ{WwQVAvODdizszN MkTkPVgzOjV3OB?=
NIH-H tumor cell lines MlnPS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NYL5OGM1S2:vcH;1coQh[WKrbHn0fUB1dyCrbnjpZol1KGGwY3jvdoFo\S2rbnTldIVv\GWwdDDndo94fGhib3[gUmlJNUhidIXtc5Ih[2WubDDsbY5meyCrbjDzc4Z1KGGpYYKsJGlEPTB;MD6wO|Ih|ryP MWi5PFIzPTV6
NIH3T3 cells MXXGeY5kfGmxbjDhd5NigQ>? NF3TdoxKdmirYnn0bY9vKG:oIGLhd{Bn[XKwZYP5cIF1cW:wIHnuJGguWmG|IITyZY5{\m:{bXXkJG5KUDOWMzDj[YxteyxiRVO1NF0xNjFizszN NYHLfWR{OTV2NUSyNlg>
NIH-K tumor cell lines M3\PT2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 NEDFfpdEd22yb4Xu[EBi[mmuaYT5JJRwKGmwaHnibZQh[W6laH;yZYdmNWmwZHXw[Y5l\W62IHfyc5d1cCCxZjDOTWguUyC2dX3vdkBk\WyuIHzpcoV{KGmwIIPv[pQh[WejcjygTWM2OD1yLkWg{txO M2ftXlk5OjJ3NUi=

... Click to View More Cell Line Experimental Data

In vivo SCH66336 inhibits HTBI77 human lung carcinoma xenograft growth in nude mice in a dose-dependent fashion. [1] SCH66336 dosed at 50 mg/kg p.o. bid by oral gavage inhibits tumor growth with up to 69% growth inhibition after 21 days of treatment in NOD/SCID mice bearing s.c. flank XEN01, XEN05 or XEN08 GBM xenografts. [3]


Cell Research:[2]
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  • Cell lines: UMSCC10B, UMSCC14B, UMSCC17B, UMSCC22B, and UMSCC35, UMSCC38 cell lines
  • Concentrations: 0.1 μM - 8 μM
  • Incubation Time: 24 hours
  • Method: The cells are seeded in 96-well cell-culture cluster plates at a density that allowed control cultures to grow exponentially for 5 days. After 24 hours, the cells are treated with different concentrations of SCH66336. SCH66336 is dissolved in DMSO. Control cultures received the same amount of DMSO as the treated cultures do. Cell numbers are estimated after 5 days of treatment by SRB assay. The percentage of growth inhibition is calculated by using the equation: percentage growth inhibition = (1 − At/Ac) × 100, where At and Ac represent the absorbance in treated and control cultures, respectively. The drug concentration causing a 50% cell growth inhibition (IC50), is determined by interpolation from dose-response curves.
    (Only for Reference)
Animal Research:[3]
+ Expand
  • Animal Models: NOD/SCID mice between 6–12 weeks of age
  • Formulation: 20% (w/v) HPβCD
  • Dosages: 50 mg/kg
  • Administration: p.o. bid by oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 127 mg/mL (198.8 mM)
Ethanol 127 mg/mL (198.8 mM)
Water Insoluble

* 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 638.82


CAS No. 193275-84-2
Storage powder
Synonyms SCH66336

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02511431 Recruiting Hepatitis D National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)|National Institutes of Health Clinical Center (CC) July 21, 2015 Phase 2
NCT02968641 Not yet recruiting Chronic Delta Hepatitis Eiger BioPharmaceuticals March 2017 Phase 2
NCT02579044 Recruiting Progeria Boston Children’s Hospital December 2015 Phase 1|Phase 2
NCT02527707 Completed Chronic Delta Hepatitis Eiger BioPharmaceuticals|Hannover Medical School September 2015 Phase 2
NCT02430194 Recruiting Chronic Hepatitis D Infection Eiger BioPharmaceuticals|Ankara University December 2014 Phase 2
NCT02430181 Completed Chronic Hepatitis D Infection Eiger BioPharmaceuticals November 2014 Phase 2

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Transferase Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID