Catalog No.S1453 Synonyms: R115777
Molecular Weight(MW): 489.4
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.
Cited by 12 Publications
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Effect of the inhibition of mutated RAS on thyroid cancer cell response to gefitinib . C-643 (RAS mutated thyroid cancer cells) and BC-PAP (wild type RAS thyroid cancer cells) were seeded in 96-well plates and incubated with increasing doses of gefitinib (Gef.; 0.5, 1.0 , and 5.0 uM), the RAS inhibitor tipifarnib (0.1, 1.0 and 10 uM) or both for 48 hours. Cell viability was then measured by the MTT assay.
J Clin Endocrinol Metab 2013 98(6), 2502-12. Tipifarnib purchased from Selleck.
Simvastatin/tipifarnib alters subcellular localization of RAS in human leukemia cells. Leukemia cells were treated with simvastatin (4 uM) and tipifarnib (1 uM), alone and in combination for 72hrs. Cytosolic and membrane fractions were prepared and western blot analysis was performed as described in the method section using the indicated antibodies. Calnexin was used as a membrane marker, whereas GAPDH is a marker of the cytosolic fraction. SIM, simvastatin. TIP, tipifarnib.
Leuk Res 2014 10.1016/j.leukres.2014.09.002. Tipifarnib purchased from Selleck.
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).
Dr. Milica Pesic from Institute for Biological Research. Tipifarnib purchased from Selleck.
WZ 811 and Tipifarnib inhibit the cell growth of anaplastic thyroid carcinoma cell lines (FRO and SW1736). 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. Both cell lines are p53 null. FRO cells possess mutated HRas and SW1736 cells possess mutated BRaf.
Tipifarnib purchased from Selleck.
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|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.|
|Features||A potent and selective farnesyl protein transferase inhibitor with significant antitumor effects.|
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.  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.  Combining Tipifarnib with 10 nM 4-OH-tamoxifen in the presence of E2 reduces the IC50 8-fold from 400 to 50 nM.  Tipifarnib induces apoptosis in U937 cells.  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. 
|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).  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. |
-  Margolin KA, et al. Clin Cancer Res. 2012, 18(4), 1129-1137.
-  Bai F, et al. Cancer Immunol Immunother. 2012, 61(4), 523-533.
-  Kotsianidis I, et al. Acta Haematol. 2008, 120(1), 51-56.
|In vitro||DMSO||14 mg/mL (28.6 mM)|
|In vivo||15% Captisol+citrate vehicle||5 mg/mL|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02807272||Recruiting||Leukemia, Myelomonocytic, Chronic||Kura Oncology, Inc.||October 2016||Phase 2|
|NCT02779777||Recruiting||Myelodysplastic Syndromes||Kura Oncology, Inc.||May 2016||Phase 2|
|NCT02535650||Not yet recruiting||Urothelial Carcinoma||Samsung Medical Center||September 2015||Phase 2|
|NCT02464228||Recruiting||Relapsed Peripheral T-Cell Lymphoma|Refractory Peripheral T-Cell Lymphoma||Kura Oncology, Inc.||September 2015||Phase 2|
|NCT02383927||Recruiting||Thyroid Cancer|Squamous Head and Neck Cancer|HRAS Mutant Tumor||Kura Oncology, Inc.||March 2015||Phase 2|
|NCT01361464||Completed||Adult Acute Megakaryoblastic Leukemia|Adult Acute Monoblastic Leukemia|Adult Acute Monocytic Leukemia|Adult Acute Myeloid Leukemia With Inv(16)(p13.1q22); CBFB-MYH11|Adult Acute Myeloid Leukemia With Maturation|Adult Acute Myeloid Leukemia With Minimal Differentiation|Adult Acute Myeloid Leukemia With t(16;16)(p13.1;q22); CBFB-MYH11|Adult Acute Myeloid Leukemia With t(8;21)(q22;q22); RUNX1-RUNX1T1|Adult Acute Myeloid Leukemia With t(9;11)(p22;q23); MLLT3-MLL|Adult Acute Myeloid Leukemia Without Maturation|Adult Acute Myelomonocytic Leukemia|Adult Erythroleukemia|Adult Pure Erythroid Leukemia|Alkylating Agent-Related Acute Myeloid Leukemia|Secondary Acute Myeloid Leukemia|Untreated Adult Acute Myeloid Leukemia||National Cancer Institute (NCI)||May 2011||Phase 2|
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