| Identification | Back Directory | [Name]
BRD3308
(BRD 3308) | [CAS]
1550053-02-5 | [Synonyms]
BRD3308
BRD3308
(BRD 3308)
BRD3308 >=98% (HPLC)
4-(Acetylamino)-N-(2-amino-4-fluorophenyl)benzamide
Benzamide, 4-(acetylamino)-N-(2-amino-4-fluorophenyl)- | [Molecular Formula]
C15H14FN3O2 | [MDL Number]
MFCD30187588 | [MOL File]
1550053-02-5.mol | [Molecular Weight]
287.29 |
| Chemical Properties | Back Directory | [Boiling point ]
449.9±45.0 °C(Predicted) | [density ]
1.382±0.06 g/cm3(Predicted) | [storage temp. ]
2-8°C | [solubility ]
DMSO:57.0(Max Conc. mg/mL);198.41(Max Conc. mM) | [form ]
A solid | [pka]
12.13±0.70(Predicted) | [color ]
Off-white to light yellow |
| Hazard Information | Back Directory | [Uses]
BRD3308 is a highly selective HDAC3 inhibitor with an IC50 of 54 nM. BRD3308 is 23-fold selectivity for HDAC3 over HDAC1 (IC50 of 1.26 μM) or HDAC2 (IC50 of 1.34 μM). BRD3308 suppresses pancreatic β-cell apoptosis induced by inflammatory cytokines or glucolipotoxic stress, and increases functional insulin release. BRD3308 activates HIV-1 transcription and disrupts HIV-1 latency[1][2][3]. | [Biological Activity]
BRD3308 is a highly selective inhibitor of histone deacetylase 3 (HDAC3) with an IC50 value of 65 nM for HDAC3 vs. IC50 values of 1.08 μM and 1.15 μM for HDAC1 and HDAC2respectively. BRD3308 protected pancreatic β cellssuppressing inflammatory cytokine-induced apoptosis and increasing insulin release without the toxicity associated with HDAC1 and HDAC2 inhibitors. In a r at model of type 2 diabetesBRD3308 reduced hyperglycemia and increased insulin secretion without affecting weight gain. In another studyBRD3308 was found to activate HIV-1 transcriptiondisrupting HIV-1 latency.''BRD3308 promotes outgrowth of HIV-1 (human immunodeficiency virus 1) from inactive infected patient cells. It helps to increase β-cell proliferation. | [in vivo]
BRD3308 (5 mg/kg; intraperitoneal injection; every second day; male Zucker Diabetic Fatty rats) treatment reduces hyperglycaemia and increases insulin secretion in a rat model of type 2 diabetes. At the end of the hyperglycaemic clamp, circulating insulin levels are significantly higher in BRD3308-treated rats. Pancreatic insulin staining and contents are also significantly higher. BRD3308 preserves the functional β-cell mass against glucolipotoxicity in vivo[2]. | Animal Model: | Male Zucker Diabetic Fatty (Obese) rats (6-week-old)[2] | | Dosage: | 5 mg/kg | | Administration: | Intraperitoneal injection; every second day | | Result: | Reduced hyperglycaemia and increased insulin secretion in a rat model of type 2 diabetes.
|
| [IC 50]
HDAC3: 54 nM (IC50); HDAC3: 29 nM (Ki); HDAC1: 1260 nM (IC50); HDAC1: 5100 nM (Ki); HDAC2: 1340 nM (IC50); HDAC2: 6300 nM (Ki); HIV-1 | [References]
[1] Barton KM, et al. Selective HDAC inhibition for the disruption of latent HIV-1 infection. PLoS One. 2014 Aug 19;9(8):e102684. DOI:10.1371/journal.pone.0102684
[2] Lundh M, et al. Histone deacetylase 3 inhibition improves glycaemia and insulin secretion in obese diabetic rats. Diabetes Obes Metab. 2015 Jul;17(7):703-7. DOI:10.1111/dom.12470
[3] Wagner FF, et al. An Isochemogenic Set of Inhibitors To Define the Therapeutic Potential of Histone Deacetylases in β-Cell Protection. ACS Chem Biol. 2016 Feb 19;11(2):363-74. DOI:10.1021/acschembio.5b00640 |
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BOC Sciences
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DC Chemicals
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Energy Chemical
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http://www.energy-chemical.com |
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