| Name | EHT 1864 |
| Description | EHT 1864 (EHT 1864 2HCl) is a Rac family GTPase inhibitor that blocks activation by direct binding to Rac1, Rac1b, Rac2, and Rac3 (Kd=40/50/60/250 nM). EHT 1864 inhibits Rac, Ras, and Tiam-induced growth transformation of NIH-3T3 fibroblasts. |
| Cell Research | NIH 3T3 cells stably expressing oncogenic Ras are plated in 96-well plates. The cells are cultured for up to 4 days in complete growth medium, either alone, or supplemented with 5 μM EHT 1864. Cell growth is then assessed using the conversion of MTT to a formazan product. Briefly, the MTT reagent (from a 5 mg/ml solution diluted in PBS) is added to the wells at a final concentration of 0.5 mg/ml, and the cells are further incubated for 4 h at 37°C. The medium is then removed, and the reaction is terminated by adding 100 μl/well Me2SO. The absorbance is read at 570 nm using a microplate reader.(Only for Reference) |
| Kinase Assay | Inhibitor:GTPase binding analyses: For inhibitor:GTPase binding analyses, aliquots of small GTPase solution (containing 1 μM inhibitor) are titrated into a solution of 1 μM inhibitor in the cuvette. Changes in fluorescence anisotropy are monitored at λex = 360 nm, λem = 440 nm, 30 s after each addition. All data analysis and curve fitting were performed using Microsoft Excel and QuantumSoft's ProFit for Mac OS X. |
| In vitro | METHODS: U87-MG cells were treated with EHT 1864 (10-25 µM) for 5 min and the levels of activated Rac1 or RhoA were measured by pull-down.
RESULTS: EHT 1864 strongly inhibited the ability of Rac1 to interact with its effector Pak1 in a dose-dependent manner. In contrast, EHT 1864 did not affect the activation state of RhoA even at the highest dose tested (25 µM). [1]
METHODS: Mouse fibroblasts NIH 3T3 were treated with EHT 1864 (5 µM) for 4 h. Cultures were then stimulated with PDGF, LPA, or bradykinin for 15 min, fixed, and visualized for the actin filaments using Alexa phalloidin.
RESULTS: PDGF, LPA and bradykinin were effective in inducing membrane wrinkling and lamellipodia formation, actin stress fibers and filamentous pseudopods, respectively. However, in the presence of EHT 1864, PDGF-induced lamellipodia formation was completely blocked, although LPA and bradykinin still induced their respective changes in actin cytoskeletal organization. EHT 1864-treated cells showed an approximately 80% reduction in lamellipodia stimulation by PDGF. [2] |
| In vivo | METHODS: To test the antitumor activity in vivo, EHT 1864 (100 mg/kg) was injected intraperitoneally twice daily for two weeks into NSG mice bearing BT-474 xenografts.
RESULTS: EHT 1864 significantly slowed down tumor growth, with an average weekly growth rate of 50% vs. 27%. EHT 1864 greatly reduced the levels of P-ERK1/2, P-AKT, P-p70S6K, and P-Histone H3S10 (mitotic markers). [3] |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | DMSO : 50 mg/mL (85.99 mM)
H2O : 58.2 mg/mL (100 mM)
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| Keywords | precursor | β-amyloid | EHT 1864 | protein | disease | Alzheimer | amyloid | Ras | EHT1864 | inhibit | transformation | Inhibitor | EHT-1864 |
| Inhibitors Related | Adagrasib | (S)-AMG-510 | BI-2493 | CCG-257081 | Ketoconazole | SKLB-163 | MRTX1133 | Salirasib | RMC-6236 | (S)-(-)-Perillyl alcohol | CASIN | Sotorasib |
| Related Compound Libraries | 抗结直肠癌化合物库 | 疼痛相关化合物库 | 经典已知活性库 | 神经退行性疾病化合物库 | 膜蛋白靶向化合物库 | 激酶抑制剂库 | 抑制剂库 | 已知活性化合物库 | GPCR靶点分子库 | 抗癌活性化合物库 |
United States
