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BI 78D3

Catalog #: 3314
4 Citations Datasheet
Catalog # Availability Size / Price Qty
3314/10
3314/50
BI 78D3 | CAS No. 883065-90-5 | JNK/c-jun Inhibitors
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Description: Selective, competitive JNK inhibitor

Chemical Name: 4-(2,3-Dihydro-1,4-benzodioxin-6-yl)-2,4-dihydro-5-[(5-nitro-2-thiazolyl)thio]-3H-1,2,4-triazol-3-one

Purity: ≥99%

Product Details
Citations (4)
Reviews
Biological Activity Technical Data Background Product Datasheets Calculators

Biological Activity

BI 78D3 is a competitive c-Jun N-terminal kinase (JNK) inhibitor (IC50 = 280 nM) that displays > 100 fold selectivity over p38α and no activity at mTOR and PI-3K. Inhibits JNK interacting protein 1 (JIP1)-JNK binding (IC50 = 500 nM) and prevents JNK substrate phosphorylation. Blocks JNK-dependent Con A-induced liver damage and restores insulin sensitivity in a mouse model of type II diabetes.

Technical Data

M.Wt:
379.37
Formula:
C13H9N5O5S2
Solubility:
Soluble to 100 mM in DMSO and to 5 mM in ethanol
Purity:
≥99%
Storage:
Store at +4°C
CAS No:
883065-90-5

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.

Background References

  1. Getting rid of JNK.
    Flight
    Nat.Rev.Drug Disc., 2008;7:975
  2. Block JNK at the dock.
    Haas and Writer
    SCiBX, 2008;1:1

Product Datasheets

Citations for BI 78D3

The citations listed below are publications that use Tocris products. Selected citations for BI 78D3 include:

4 Citations: Showing 1 - 4

  1. ERK2 phosphorylates Krüppel-like factor 8 protein at serine 48 to maintain its stability.
    Authors: Lahiri Et al.
    Am J Cancer Res  2016;6:910
  2. Critical role of c-jun N-terminal protein kinase in promoting mitochondrial dysfunction and acute liver injury.
    Authors: Jang Et al.
    PLoS Biol  2015;6:552
  3. Effects of Y27632 on keratinocyte procurement and wound healing.
    Authors: Gandham Et al.
    Redox Biol  2013;38:782
  4. HIF1A reduces acute lung injury by optimizing carbohydrate metabolism in the alveolar epithelium.
    Authors: Eckle Et al.
    Br J Pharmacol  2013;11:e1001665

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