10mM in DMSO for sensitive chromatographic and analytical workflows requiring minimal baseline interference.
Store at -80°C Ships Dry ice packs + Cold packs Check lot-specific COA for exact specifications.
SDS, COA, datasheet, and spec sheet available for download. Lot-specific COA accessible via lot number lookup.
Cited in 0 peer-reviewed publications across chromatography, organic synthesis, and cross-coupling reactions.
MPT0G211 is a potent, orally active and selective HDAC6 inhibitor ( IC 50 =0.291 nM). MPT0G211 displays >1000-fold selective for HDAC6 over other HDAC isoforms. MPT0G211 can penetrate the blood-brain barrier. MPT0G211 ameliorates tau phosphorylation and cognitive deficits in an Alzheimer’s disease model. MPT0G211 has anti-metastatic and neuroprotective effects. Anticancer activities
In Vitro
MPT0G211 (0.1 μM; cells were transfected with pCAX APP 695 and pRK5-EGFP-Tau P301L for 24 h) significantly inhibits the phosphorylation of tau Ser396. MPT0G211 inhibits HDAC6/Hsp90 binding and causes subsequent proteasomal degradation of polyubiquitinated proteins. MPT0G211 significantly decreases the phosphorylation of tau by GSK3β inactivation. MPT0G211 (0.1 μM; 24 hours) significantly attenuates the phosphorylation of tau Ser396 and Ser404 in both cell lines (SH-SY5Y and Neuro-2a cells were transfected for 24 h with pCAX APP 695 and pRK5-EGFP-Tau P301L). MPT0G211 inhibits MDA-MB-231 and MCF-7 cells growth (GI 50 =16.19 and 5.6 μM, respectively). In AML cells, MPT0G211 potentiated the cytotoxic effects of DOXO by impairing DNA repair machinery and activating Bcl-2-associated X protein (BCL-XL)-dependent cell apoptosis. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
MPT0G211 (50 mg/kg; p.o.; daily for 3 months) significantly ameliorates the spatial memory impairment . MPT0G211 (25 mg/kg; i.p. ; qd; day 73 post-tumor injection) reduces numbers of nodules and lung weights. MPT0G211 treatment not only diminishes tau phosphorylation by inhibition GSK3β activity but also enhances the acetylation of Hsp90, which causes the downregulation of HDAC6/Hsp90 binding and facilitates proteasomal degradation of polyubiquitinated p-tau . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Triple transgenic (3×Tg-AD) mice (harboring APP Swe and tau P301L mutant transgenes Dosage: 50 mg/kg Administration: P.o.; daily for 3 months Result: Significantly ameliorated the spatial memory impairment. Animal Model: Female SCID mice (bearing MDA-MB-231 cells)Dosage: 25 mg/kg Administration: I.p.; qd; day 73 post-tumor injection Result: Significantly reduced numbers of nodules and lung weights.
IC50& Target:HDAC6 0.291 μM (IC 50 )
| Isomeric SMILES | C1=CC2=C(C(=C1)NCC3=CC=C(C=C3)C(=O)NO)N=CC=C2 |
|---|---|
| PubChem CID | 132157820 |
| MeSH Entry Terms | MPT0G211;N-hydroxy-4-((quinolin-8-ylamino)methyl)benzamide |
| Molecular Weight | 293.32 |
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