(E)-4-[2-(2-Amino-4-hydroxy-5-methylphenyl)diazenyl]-N-2-pyridinylbenzenesulfonamide, 4-[(1E)-2-(2-Amino-4-hydroxy-5-methylphenyl)diazenyl]-N-2-pyridinylbenzenesulfonamide, MS 436, MS-436
BRD4 inhibitor with selective affinity toward the first bromodomain (BrD1) over BRD4 BrD2, CBP BrD, PCAF BrD.
MS436 is a diazobenzene-based potent BRD4 inhibitor with selective affinity toward the first bromodomain (BrD) of BRD4 (BRD4 BrD1 Ki <85 nM vs. BRD4 BrD2 Ki = 340 nM; IC50 = 460 nM/BRD4 BrD1 vs. 1.29 μM/BRD4 BrD2, 4.95 μM/CBP BrD, 20.29 μM/PCAF BrD). MS436 is a useful tool for probing BRD4-dependent cellular functions, including NF-κB-mediated proinflammatory response in RAW264.7 murine macrophages (IC50 in μM = 4.9/3.8 against LPS-induced IL-6/NO production), human and murine embryonic stem cell (ESC) pluripotency maintenance (10 μM), telomere elongation in mTERT/mTR-overexpressing murine fibroblasts (5 μM), and bioenergetic deficiency caused by mitochondrial complex I (CI)-mutation in human cybrid cells (0.9 μM).
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Loss of the tumor suppressors RB1 and TP53 and MYC amplification are frequent oncogenic events in small cell lung cancer (SCLC). We show that Myc expression cooperates with Rb1 and Trp53 loss in the mouse lung to promote aggressive, highly
Pluripotent stem cells (PSCs) hold great clinical potential, as they possess the capacity to differentiate into fully specialised tissues such as pancreas, liver, neurons and cardiac muscle. However, the molecular mechanisms that coordinate pluripotent exit with lineage specification remain poorly
Cancer cells maintain telomere length equilibrium to avoid senescence and apoptosis induced by short telomeres, which trigger the DNA damage response. Limiting the potential for telomere maintenance in cancer cells has been long been proposed as a therapeutic target. Using
Transcription factors and chromatin-remodeling complexes are key determinants of embryonic stem cell (ESC) identity. Here, we demonstrate that BRD4, a member of the bromodomain and extraterminal domain (BET) family of epigenetic readers, regulates the self-renewal ability and pluripotency of ESCs.
Mitochondrial diseases comprise a heterogeneous group of genetically inherited disorders that cause failures in energetic and metabolic function. Boosting residual oxidative phosphorylation (OXPHOS) activity can partially correct these failures. Herein, using a high-throughput chemical screen, we identified the bromodomain inhibitor
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