Tipifarnib

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.

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.

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.

Effects of FTIs on body weight and food intake in mice treated with LPV/RTV. (A) Treatment with LPV/RTV for 2 weeks significantly decreased body weight compared with vehicle alone. The effect of LPV/RTV on body weight was attenuated by FTIs: When the mice were co-treated with tipifarnib or lonafarnib, LPV/RTV failed to significantly decrease body weight. (B) LPV/RTV significantly increased food intake in the second week of the treatment compared with vehicle alone. FTIs prevented LPV/RTV-induced increased food intake. In the first week of the treatments, no significant difference in food intake between the groups was observed, although LPV/RTV tended to increase it. *P<0.05, **P<0.01 vs. LPV/RTV treatment, n=8 mice per group. FTI, farnesyltransferase inhibitor; LPV, lopinavir; RTV, ritonavir; NS, not significant.

Exp Ther Med, 2018, 15(2):1314-1320. Tipifarnib purchased from Selleck.