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Cited in 0 peer-reviewed publications across chromatography, organic synthesis, and cross-coupling reactions.
Rohinitib is a potent and specific eIF4A inhibitor. Rohinitib induces cell apoptosis of acute myeloid leukemia (AML) cell lines and reduces the leukemia burden of AML xenograft model. Rohinitib can be used for the research of AML.
In Vitro
Rohinitib (6.25-50 nM; 72 h) induces cell apoptosis of AML cell lines and FLT3 -ITD-positive AML cell lines. Primary AML cells is more sensitive to Rohinitib (25 nM; 72 h) than normal bone marrow (BM) and FLT3 -ITD-positive cells is more sensitive to Rohinitib than FLT3 wild-type AML cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Apoptosis AnalysisCell Line: AML cell lines Concentration: 6.25, 12.5, 25 and 50 nM Incubation Time: 72 h Result: Dose-dependently induced apoptosis of MOLM-13, MOLM-14, MV4;11, OCI-AML3, THP-1, HL-60, Kasumi-1 and NB4 cell lines. And significantly induced cell apoptosis of FLT3 -ITD, FLT3 -ITD-expressing murine Ba/F3 and human OCI-AML3 cells.
In Vivo
Rohinitib (0.75 and 1.0 mg/kg; s.c. once daily for 5 consecutive days until mice get moribund) shows anti-AML effects in vivo . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Female NSG mice with AML xenografts generated by intravenous injections of MOLM-13 cells Dosage: 0.75 and 1.0 mg/kg Administration: Subcutaneous injection; 0.75 and 1.0 mg/kg once daily 5 days a week until mice get moribund Result: Significantly reduced the leukemia burden, circulating and BM leukemic human CD45 + cells. Dose-dependently prolonged the survival rate of mice.
Form:Solid
| Canonical Smiles | COC1=CC=C([C@@]23OC4=CC(OC)=CC(OC)=C4[C@]2(O)[C@@H]([C@@H]([C@H]3C5=CC=CC=C5)C(N(OC)C)=O)O)C=C1 |
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| Molecular Weight | 521.56 |
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View spec sheet →| Solubility | DMSO : 200 mg/mL (383.46 mM; Need ultrasonic) |
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