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≥98% 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.
CC214-2 is an oral active and selective mTOR kinase inhibitor. CC214-2 targets to both of mTORC1 (pS6) and mTORC2 (pAktS473). CC214-2 induces autophagy , which is a potential target for host-directed therapy (HDT) in tuberculosis. CC214-2 exhibits synergistic bactericidal and sterilizing activity agasinst tuberculosis (TB), and shortens the treatment duration. CC214-2 also inhibits Rapamycin -resistant signaling and the growth of glioblastomas in vitro and in vivo
In Vivo
CC214-2 (25 mg/kg, 50 mg/kg; po; once daily for 21 days) results tumor volume reductions in PC3 tumor xenograft model . CC214-2 (30 mg/kg, 100 mg/kg; po; single dose) inhibits both mTORC1 (pS6) and mTORC2 (pAktS473) in vivo for at least 8 and 24 h, respectively . CC214-2 (30 mg/kg; po) reduces M. tuberculosis CFU numbers and prevents mortality in mice with Chronic M. tuberculosis infection . CC214-2 (50 mg/kg; po; once daily for 6 days) significantly reduces the growth of mouse U87EGFRvIII flank xenografts. CC214-2 (100 mg/kg; po; once every 2 days for 6 days) inhibits mTORC1 and mTORC2 signaling in an intracranial glioblastoma model. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: U87EGFRvIII flank xenografts in miceDosage: 50 mg/kg Administration: PO; once daily for 6 days Result: Inhibited tumor growth. Similarly activated autophagy in U87EGFRvIII xenografts.
Form:Solid
IC50& Target:mTORC1|mTORC2
| Molecular Weight | 383.44 |
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Comprehensive hazard, handling, storage, and regulatory compliance document.
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View spec sheet →| Solubility | DMSO : 12.5 mg/mL (32.60 mM; ultrasonic and warming and heat to 80°C) |
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