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≥99% for sensitive chromatographic and analytical workflows requiring minimal baseline interference.
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Cited in 0 peer-reviewed publications across chromatography, organic synthesis, and cross-coupling reactions.
RP-6306\t((S)-RP-6306) is a potent, selective and orally active PKMYT1 inhibitor with an IC 50 of 14 nM. RP-6306 shows a high degree of selectivity over other kinases in cellular binding assays. RP-6306 shows anticancer effects
In Vitro
RP-6306 (500 nM; for 24 h) treatment induces pan-γH2AX in an HCC1569 breast cancer cell line, indicating that tumour-derived CCNE1 amplification also renders cells vulnerable to DNA damage induction following PKMYT1 inhibition. RP-6306 treatment causes unscheduled activation of CDK1 selectively in CCNE1-overexpressing cells, promoting early mitosis in cells undergoing DNA synthesis. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
RP-6306 (15, 50, and 300 ppm; oral; daily; for 21 days) results in a statistically significant and dose-dependent reduction in OVCAR3 tumor growth in CCNE1-amplified ovarian xenograft model (OVCAR3) . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: OVCAR3-bearing mice Dosage: 15, 50, and 300 ppm (equivalent to approximately 3, 10, and 60 mg/kg/day) Administration: Oral; daily; for 21 days Result: Resulted in a statistically significant and dose-dependent reduction in OVCAR3 tumor growth.
Form:Solid
IC50& Target:IC50: 14 nM (PKMYT1)
| Molecular Weight | 324.38 |
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View spec sheet →| Solubility | DMSO : 50 mg/mL (154.14 mM; Need ultrasonic) |
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