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TG100-115 677297-51-7

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Synonyms ：
Appearance ：
Chemical Formula ：
C18H14N6O2
Solubility ：
Molecular Weight ：
346.34
Storage and Stability ：
in stock
CAS No. ：
677297-51-7
Purity ：
98%+
Introduction
TG100-115 inhibits PI3Kγ and -δ, with IC50 of 83 and 235 nM, respectively. TG100-115 is not active for PI3Kα and -β, with IC50 of 1.2 and 1.3 mM. In human umbilical vein endothelial cells (HUVECs), TG100-115 (up to 10 μM) has no effects on cell proliferation and VEGF-stimulated ERK phosphorylation. However, TG100-115 (10 μM) interrupts other VEGF signaling pathways, such as those that culminate in VE-cadherin phosphorylation.  In HUVECs, TG100-115 (10 μM) inhibits the VEGF-induced increase of total level of VE-cadherin. TG100-115 inhibits VEGF mediated phosphorylation of mTOR and p70S6 kinase, both of which are downstream of PI3K. TG100-115 (125 nM to 10 μM) also inhibits FGF-stimulated phosphorylation of Akt.

In Miles assay models, TG100-115 (1-5 mg/kg) reduces edema formation and inflammation in rats. In rigorous rodent and porcine models of myocardial ischemia (MI), TG100-115 (0.5-5 mg/kg) provides potent cardioprotection, limits infarct development, and preserves myocardial function. In mice, TG100-115 (5 mg/kg) markedly diminishes vascular permeability (VP) in response to either Sema3A or VEGF, indicating that both factors may depend on PI3Kγ/δ to induce VP.  In a mouse asthma model, aerosolized TG100-115 markedly reduces the pulmonary eosinophilia, inhibits interleukin-13 and mucin accumulation. 

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