Tipifarnib (R115777) is a potent and specific farnesyltransferase (FTase) inhibitor with IC50 of 0.6 nM, its anti-proliferative effects are most prominent in H-ras or N-ras mutant cells. Phase 3.

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Tipifarnib  Chemical Structure

Tipifarnib Chemical Structure
Molecular Weight: 489.4

Validation & Quality Control

Customer Product Validation(5)

Quality Control & MSDS

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  • Tipifarnib Mechanism

Product Description

Biological Activity

Description Tipifarnib (R115777) is a potent and specific farnesyltransferase (FTase) inhibitor with IC50 of 0.6 nM, its anti-proliferative effects are most prominent in H-ras or N-ras mutant cells. Phase 3.
Targets FTase [1]
IC50 0.6 nM
In vitro Using Tipifarnib 5 μM for 72 hours, the percentage of apoptotic cells is significantly higher in drug-treated compared to DMSO-treated LGL T-cells. Using T-cells from healthy donors, Tipifarnib reduces the percentage of IFNγ-positive cells in a time-dependent manner. Tipifarnib reduces the amount of activated Ras in precipitates compared to DMSO. [2] Tipifarnib exerts selective in vitro toxicity against clonal MDS hematopoiesis at concentrations less than 10 nM the effect being more prominent in white cell progenitors. This action is not due to apoptosis induction as both normal and MDS progenitors displays equivalent DiOC3 and annexin V expression up to 72 hours after exposure to Tipifarnib. [3] Combining Tipifarnib with 10 nM 4-OH-tamoxifen in the presence of E2 reduces the IC50 8-fold from 400 to 50 nM. [4] Tipifarnib induces apoptosis in U937 cells. [5] In addition, Tipifarnib inhibits isolated human farnesyltransferase for a lamin B peptide and for the K-RasB peptide with IC50 of 0.86 nM and 7.9 nM, respectively. [6]
In vivo Ki-67 is lower in the tumors treated with E2 withdrawal plus R115777 compared with E2 withdrawal alone. The combination of tamoxifen and R115777 results in significantly lower Ki-67 compared with either tamoxifen or R115777 alone (mean of 5% versus 16.9% and 67.3%, respectively). [4] In contrast, no significant difference in apoptotic scores is seen between the treatment groups. R115777 alone also reduces the CTI compared with control. The combination of tamoxifen and R115777 or R115777 coupled with E2 withdrawal is most effective at lowering the CTI (0.8 and 0.7, respectively), which may account for the decrease in tumor volume. [4]
Features A potent and selective farnesyl protein transferase inhibitor with significant antitumor effects.

Protocol(Only for Reference)

Cell Assay: [4]

Cell lines MACS-selected CD34+ cells
Concentrations 2.5 nM, 10 nM, 25 nM and 50 nM
Incubation Time 48 hours
Method MACS-selected CD34+ cells are seeded in Methocult 4435 'complete' 1% bovine serum albumin, 3 U/mL recombinant human (rh) erythropoietin, 0.1 mM 2-mercaptoethanol, 2 mM L-glutamine and the following cytokines: 50 ng/mL rh stem cell factor, 20 ng/mL rh GM-CSF, 20 ng/mL rh IL-3, 20 ng/mL rh IL-6 and 20 ng/mL h G-CSF. DMSO or Tipifarnib is added at the concentrations of 2.5, 10, 25 and 50 nM at day 1. All cultures are performed in duplicates and the numbers of colonies are scored after 14 days of incubation at 37 °C in a humidified incubator containing 5% CO2

Animal Study: [4]

Animal Models Female ovariectomized Ncr foxhead nude mice
Formulation 20% w/v β-cyclodextrin (pH 2.5)
Dosages 50 mg/kg
Administration Oral gavage

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDog
Weight (kg)
Body Surface Area (m2)0.0070.0250.
Km factor36128520
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)


[1] Margolin KA, et al. Clin Cancer Res. 2012, 18(4), 1129-1137.

[2] Bai F, et al. Cancer Immunol Immunother. 2012, 61(4), 523-533.

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Clinical Trial Information( data from http://clinicaltrials.gov, updated on 2015-09-19)

NCT Number Recruitment Conditions Sponsor
Start Date Phases
NCT02535650 Not yet recruiting Urothelial Carcinoma Samsung Medical Center September 2015 Phase 2
NCT02535650 Not yet recruiting Urothelial Carcinoma Samsung Medical Center September 2015 Phase 2
NCT02464228 Not yet recruiting Relapsed Peripheral T-Cell Lymphoma|Refractory Peripheral T-Cell Lymphoma Kura Oncology, Inc. June 2015 Phase 2
NCT02464228 Not yet recruiting Relapsed Peripheral T-Cell Lymphoma|Refractory Peripheral T-Cell Lymphoma Kura Oncology, Inc. June 2015 Phase 2
NCT02383927 Recruiting Thyroid Cancer|Advanced Non-hematological Malignancies|HRAS Mutant Tumor Kura Oncology, Inc. March 2015 Phase 2

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Chemical Information

Download Tipifarnib SDF
Molecular Weight (MW) 489.4


CAS No. 192185-72-1
Storage 3 years -20℃powder
6 months-80℃in solvent
Synonyms R115777
Solubility (25°C) * In vitro DMSO 14 mg/mL (28.6 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 15% Captisol/citrate vehicle 5 mg/mL
* <1 mg/ml means slightly soluble or 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 Name (R)-6-(amino(4-chlorophenyl)(1-methyl-1H-imidazol-5-yl)methyl)-4-(3-chlorophenyl)-1-methylquinolin-2(1H)-one

Customer Product Validation (5)

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Source J Clin Endocrinol Metab 2013 98(6), 2502-12. Tipifarnib purchased from Selleck
Method MTT assay, Western blot
Cell Lines C-643, BC-PAP cells
Concentrations 0.1, 1.0, 10 uM
Incubation Time 3 weeks
Results Tipifarnib significantly enhanced the effect of increasing doses of gefitinib on cell viability in C-643 cells harboring the HRASG12A/Q61R mutation but did not change the effect of gefitinib in BC-PAP cells harboring wild-type RAS. In C-643 cells, anti-pERK Western blotting indicated that combined treatment with tipifarnib and gefitinib almost completely inhibited the phosphorylation of ERK.

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Source Shock 2014 42(6), 570-7. Tipifarnib purchased from Selleck
Method H/E staining
Cell Lines GalN/LPS-induced mice
Concentrations 10 mg/kg
Incubation Time 60 min
Results Hepatic architecture in vehicle-treated mice was disrupted with hemorrhage, necrosis and neutrophil infiltratioin at 5 h after GalN/LPS challenge. In contrast, tipifarnib treatment markedly ameliorated liver injury as reflected by histological alterations after Gal/LPS challenge.

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Source Leuk Res 2014 10.1016/j.leukres.2014.09.002. Tipifarnib purchased from Selleck
Method Western blot
Cell Lines Leukemia cells
Concentrations 1 uM
Incubation Time 72 h
Results To evaluate whether coadministration of simvastation and tipifarnib could disrupt the RAS prenylation process and its membrane association, leukemia cells were treated with simvastatin (4 uM) and tipifarnib (1 uM) alone or in combination for 72 hr and cells subjected to a fractionation procedure to isolate the membrane and the cytosolic protein fractions. Western blot analysis was performed to determine RAS location in both fractions. Interestingly, simwastatin/tipifarnib was found to inhibit the membrane association of RAS with its subsequent sequestration into the cytosol. This effect was not observed in the control cells or those exposed to a single drug treatment.

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Source Dr. Milica Pesic from Institute for Biological Research. Tipifarnib purchased from Selleck
Cell Lines Sea urchin embryo
Incubation Time 24 h
Results The effects of SelleckChem inhibitors on sea urchin embryo development evaluated 24 h after fertilization. All compounds were added to embryos suspension 20 min after fertilization. The relative presence of late gastrula, swimming blastula, undeveloped embryos and dead embryos was compared next to untreated control embryos (A). Fertilized egg, swimming blastula and late gastrula are illustrated (B). The embryonic development was relatively synchronized in untreated control samples after 24 h (A, E). GSK690693 treatment sustained the development of embryos. Swimming blastulas kept normal motility regardless the deformities in their shape. Tipifarnib treatment induced significant toxicity due to occurrence of dead fragmented embryos. Some abnormal blastulas kept the motility. AZD2014 treatment sustained the development of embryos. Some developed gastrulas and blastulas were less motile in comparison with control (A, C). WZ811 was the least toxic compound. Significant number of gastrulas and blastulas was developed. However, their motility was considerably suppressed (A, D). In contrast to SelleckChem inhibitors, classic anticancer agent – cisplatin was extremely toxic to sea urchin embryos (A). Cisplatin killed many embryos, while a small amount of survived embryos was stopped at early phases of development: immediately after fertilization or after first and second division (A, F).

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Source Tipifarnib purchased from Selleck
Cell Lines FRO cells/SW1736 cells
Concentrations 0-10 mM
Incubation Time
Results There is no difference in sensitivity of tested cell lines to WZ 811, while FRO cells are more sensitive to Tipifarnib in comparison with SW1736 cells.

Product Use Citation (12)

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