≥96% for sensitive chromatographic and analytical workflows requiring minimal baseline interference.
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Storage & shipping
Store at 2-8°C,Desiccated Ships Wet ice Check lot-specific COA for exact specifications.
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Quality documents
SDS, COA, datasheet, and spec sheet available for download. Lot-specific COA accessible via lot number lookup.
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Literature proof
Cited in 0 peer-reviewed publications across chromatography, organic synthesis, and cross-coupling reactions.
Panoramica
CYH33 methanesulfonate is an orally active, highly selective PI3Kα inhibitor with IC 50 s of 5.9 nM/598 nM/78.7 nM/225 nM against α/β/δ/γ isoform, respectively. CYH33 methanesulfonate inhibits phosphorylation of Akt , ERK and induces significant G1 phase arrest in breast cancer cells and non-small cell lung cancer (NSCLC) cells. CYH33 methanesulfonate has potent activity against solid tumors
In Vitro
CYH33 methanesulfonate inhibits cell proliferation with IC 50 s below 1 μM in 56% (18/32) of the breast cancer cell lines. CYH33 (0.012-1 μM; for 24 hours) methanesulfonate significantly arrests T47D and MCF7 cells in G1 phase in a concentration-dependent manner. CYH33 (4-1000 nM; 1 hour) methanesulfonate concurrently inhibits phosphorylation of ERK and Akt in both T47D and MCF7 cells. CYH33 (0.11-1 μM; 24 hours) methanesulfonate fails to induce apoptosis in MCF7 and MDA-MB-231 cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Cycle AnalysisCell Line: Sensitive T47D, MCF7 and resistant MDA-MB-231 cells Concentration: 0.012, 0.037, 0.11, 0.33, 1 μM Incubation Time: For 24 hours Result: Arrested T47D and MCF7 cells in G1 phase in a concentration-dependent manner, accompanied with concomitant reduced cell population in S phase. Had little effect on cell cycle distribution in resistant MDA-MB-231 cells. Western Blot AnalysisCell Line: Sensitive T47D, MCF7 and resistant MDA-MB-231 cells Concentration: 4, 12, 37, 111, 333, 1000 nM Incubation Time: 1 hour Result: Concurrently inhibited phosphorylation of ERK and Akt in both T47D and MCF7 cells, whereas it had little effect on phosphorylated ERK (pERK) in MDA-MB-231 cells up to 1 μM.
In Vivo
CYH33 (2-20 mg/kg; oral; once a day for 21 days) methanesulfonate potently restrains tumor growth in mice bearing human breast cancer cell xenografts. Single administration of CYH33 (20 mg/kg; oral) methanesulfonate significantly down-regulates the level of phosphorylated Akt in tumor tissues, demonstrating the suppression of PI3K signaling in nude mice. CYH33 (10 mg/kg; oral; once a day for 18-d or 20-d respectively) methanesulfonate delays the restoration of blood glucose and area under the curve (AUC) of blood glucose increased upon CYH33 treatment in T47D xenografts and R26-Pik3ca H1047R ;MMTV-Cre mice. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: SCID mice aged 4-6 weeks bearing human breast cancer T47D xenograftsDosage: 2, 5, 10, 20 mg/kg Administration: Oral; once a day for 21 days Result: Displayed marginal inhibitory effect on the tumor growth at lower doses (2 and 5 mg/kg) and significantly attenuated tumor growth at the dose of 10 or 20 mg/kg, yielding T/C values of 58.36% and 49.42% respectively.
CYH33 methanesulfonate is an orally active, highly selective PI3Kα inhibitor with IC 50 s of 5.9 nM/598 nM/78.7 nM/225 nM against α/β/δ/γ isoform, respectively. CYH33 methanesulfonate inhibits phosphorylation of Akt , ERK and induces significant G1 phase
Condizioni di conservazione di stoccaggio
Store at 2-8°C,Desiccated
Spedito in
Wet ice
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