Ras farnesyltransferase inhibitor. Induces tumor regression in transgenic mice with multiple oncogenic mutations by mediating alterations in both cell cycle control and apoptosis. Induces p21 expression and arrests cells at G1. Causes enhanced mitotic sensitivity to taxol.
Product Details
| Formula: | C26H47Cl2N3O6S2 |
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| MW: | 632.7 |
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| CAS: | 1177806-11-9 |
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| Purity: | ≥98% (TLC) |
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| Appearance: | White solid. |
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| Solubility: | Soluble in DMSO, water, or acetonitrile. |
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| Shipping: | Ambient Temperature |
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| Long Term Storage: | -20°C |
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| Use/Stability: | Store solutions at -20°C for up to 3 months. |
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| Regulatory Status: | RUO - Research Use Only |
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Product Literature References
Farnesyltransferase inhibitors interact synergistically with the Chk1 inhibitor UCN-01 to induce apoptosis in human leukemia cells through interruption of both Akt and MEK/ERK pathways and activation of SEK1/JNK: Y. Dai, et al.; Blood
105, 1706 (2005),
Abstract;
Normoxic and hypoxic regulation of vascular endothelial growth factor (VEGF) by astrocytoma cells is mediated by Ras: M.M. Feldkamp, et al.; Int. J. Cancer
81, 118 (1999),
Abstract;
A farnesyl-protein transferase inhibitor induces p21 expression and G1 block in p53 wild type tumor cells: L. Sepp-Lorenzino & N. Rosen; J. Biol. Chem.
273, 20243 (1998),
Abstract;
A farnesyltransferase inhibitor induces tumor regression in transgenic mice harboring multiple oncogenic mutations by mediating alterations in both cell cycle control and apoptosis: R.E. Barrington, et al.; Mol. Cell Biol.
18, 85 (1998),
Abstract;
Farnesyl transferase inhibitors cause enhanced mitotic sensitivity to taxol and epothilones: M.M. Moasser, et al.; PNAS U.S.A.
95, 1369 (1998),
Abstract;
