BG47
BG47 is a prototypical histone deacetylases HDAC1 and HDAC2 selective, optoepigenetic probe. BG47 can bind to and competitively inhibits the deacetylase activity of HDAC targets upon a light-induced trans-to-cis isomerization, and increases Histone Methyltransferase H3K9 acetylation. BG47 can be used for neurological disease research.
For research use only. We do not sell to patients.
- CAS No.: 1628784-54-2
- Formula: C25H22N4O2S
- Molecular Weight:442.53
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Histone Methyltransferase Isoforms
More
Biological Activity
Description
IC50 & Target
[1]|
HDAC1 |
HDAC2 |
In Vitro
BG47 (10 μM, 16 hours) elevates H3K9 acetylation only in the presence of light and also significantly upregulates the expression of haploinsufficiency of progranulin (PGRN) only in the presence of light (25 ms on/75 ms off) in human neural progenitor cells (NPCs)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:Human neural progenitor cells (NPCs)
-
Concentration:10 μM
-
Incubation Time:16 hours
-
Result:Elevated H3K9 acetylation and significantly upregulated PGRN expression only in the presence of light (25 ms on/75 ms off).
Chemical Information
-
CAS No. 1628784-54-2
-
Molecular Weight 442.53
-
Formula C25H22N4O2S
-
SMILES
O=C(C1=CC=C(C=C1)/N=N/C2=CC=C(N(C)C)C=C2)NC3=C(O)C=CC(C4=CC=CS4)=C3
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)