product name GSK2801
Description: GSK2801 is a selective bromodomains BAZ2A/B inhibitor with Kd of 257 nM and 136 nM, respectively. Proteins of the BAZ family are characterized by a carboxy-terminal bromodomain adjacent to a PHD finger and a WACZ motif. In addition four other conserved motifs are typically found in the N-terminus of BAZ family members, namely the LH motif (a leucine-rich helical domain), the ZB2 motif and the BAZ 1 and BAZ 2 motifs.
References: J Med Chem. 2016 Feb 25;59(4):1410-24.
371.45
Formula
C20H21NO4S
CAS No.
1619994-68-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 74 mg/mL (199.2 mM)
Water: <1 mg/mL
Ethanol: 7 mg/mL (18.8 mM)
Solubility (In vivo)
0.5% CMC+1% Tween 80: 30mg/mL
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19419662
| In Vitro |
In vitro activity: In U2OS cells transfected with mutant BAZ2A (N1873F), GSK2801 (1 μM) accelerates FRAP half-recovery time by displacing BAZ2A from chromatin. Kinase Assay: GSK2801 is a potent, selective and cell active acetyl-lysine competitive inhibitor of BAZ2A(Kd=136 nM) and BAZ2B(Kd=257 nM) bromodomains. Cell Assay: In U2OS cells, treatment with the SAHA induced hyperacetylated chromatin. In a GFP-BAZ2A fusion construct, the conserved asparagines that are essential for recognizing the acetylated lysine has been mutated. When a GFP-BAZ2A fusion construct was transfected into SAHA-treated U2OS cells, the mutant construct accelerated FRAP half-recovery time. Treatment with GSK2801 alone in U2OS cells also accelerated FRAP half-recovery time. Both acceleration extents are the same. This meant that GSK2801 can displace BAZ2A from chromatin. |
|---|---|
| In Vivo | In male CD1 mice, GSK2801 (30 mg/kg, p.o. and i.p.) has reasonable in vivo exposure after oral dosing, modest clearance, and reasonable plasma stability. |
| Animal model | Male CD1 mice |
| Formulation & Dosage | Formulated in 0.5% CMC+1% Tween 80; 30 mg/kg; i.p. or p.o. |
| References | J Med Chem. 2016 Feb 25;59(4):1410-24. |
