BRD-6929 is a?potent, selective brain-penetrant inhibitor of class I histone deacetylase HDAC1 and HDAC2 inhibitor with IC₅₀ of 1 nM and 8 nM, respectively. BRD-6929 shows high-affinity to HDAC1 and HDAC2 with?K_i?of 0.2 and 1.5 nM, respectively. BRD-6929 can be used for mood-related behavioral model research^[3].

In vitro?IC₅₀ for HDAC1-9 by BRD-6929 using recombinant human HDAC enzymes and HDAC class-specific substrates. BRD-6929 and substrate are incubated for 180 min (HDAC1-3)?to control for HDAC1-3 inhibition, BRD-6929 is against HDAC1, HDAC2, HDAC3 and HDAC4-9 with IC₅₀s of 0.001 μM, 0.008 μM, 0.458 μM and >30 μM, respectively^[1].
In vitro?binding affinity (K_i) and kinetics (half-life ‘T_1/2′?in minutes) for HDAC 1, 2 and 3 incubated with BRD-6929 (10 μM), the K_i values are <0.2 nM, 1.5nM, and 270 nM for HDAC 1, 2 and 3, respectively. The T_1/2 values are >2400 mins, >4800 mins, and 1200 mins for HDAC 1, 2 and 3, respectively^[1].
BRD-6929 (1 and 10 uM) does not cause an increase or decrease in overall cell number in brain region specific primary cultures. Additionally, BRD-6929 (10 uM) causes an increase in H4K12 acetylation in brain region specific primary cultures (striatum)^[1].
BRD-6929 (1-10 uM; 6 hours) causes a significant increase in H2B acetylation in primary neuronal cell cultures. BRD-6929 (1-20 uM; 24 hours) induces a dose-dependent acetylation of H4K12ac with an EC₅₀ of 7.2 μM in cultured neurons^[1].
BRD-6929 potentiates the efficacy of gnidimacrin (a PKC Agonist) against latent HIV-1^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

BRD-6929 (intraperitoneal?injection; 45 mg/kg; single dose) exhibits a C_max, T_1/2 and AUC values of 17.7 μM, 7.2 hours, and 25.6 μM/L*hr, respectively in plasma. It shows a C_max, T_1/2 and AUC values of 0.83 μM, 6.4 hours, and 3.9 μM/L*hr, respectively in brain^[1].
BRD-6929 (intraperitoneal?injection; 45 mg/kg; 10 days) acts as a deacetylase inhibitor in mouse brain. It significantly increases acetylation in each brain region by 1.5- to 2.0-fold compared to vehicle. The western blotting reveals that BRD-6929 significantly increases acetylation of histone H2B (tetra-acetylated), H3K9 and H4K12 in cortex, ventral striatum and hippocampus after the 10th daily treatment in adult male C57BL/6J mice^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

351.42

C₁₉H₁₇N₃O₂S

849234-64-6

固體

Off-white to gray

Room temperature in continental US; may vary elsewhere.

• [1]. Li-Huei Tsai, et al. Inhibition of hdac2 to promote memory. patent/US20120101147

  [2]. Schroeder FA, et al. A selective HDAC 1/2 inhibitor modulates chromatin and gene expression in brain and altersmouse behavior in two mood-related tests. PLoS One. 2013 Aug 14;8(8):e71323.  [Content Brief]

  [3]. Huang L, et al. Elimination of HIV-1 Latently Infected Cells by Gnidimacrin and a Selective HDAC Inhibitor. ACS Med Chem Lett. 2018 Feb 6;9(3):268-273.  [Content Brief]