2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Biological activity
Description
Target:
In Vivo
Compound 3PO treatment significantly reduced Fru-2,6-BP in tumor xenografts compared with vehicle control (vehicle: 13.1 ± 1.9 pmol/mg, 3PO: 8.5 ± 1.7 pmol/mg). [1] 3PO also impairs (pathological) angiogenesis. [2]
In Vitro
3PO inhibits recombinant PFKFB3 activity, suppresses glucose uptake, and decreases the intracellular concentration of Fru-2,6-BP, lactate, ATP, NAD+, and NADH. 3PO markedly attenuates the proliferation of several human malignant hematopoietic and adenocarcinoma cell lines (IC50, 1.4-24 μM) and is selectively cytostatic to ras-transformed human bronchial epithelial cells relative to normal human bronchial epithelial cells. The PFKFB3+/- fibroblasts were more sensitive to compound 3PO treatment (IC50, 26 μM) compared with the wild-type PFKFB3+/+transformed cells (IC50, 49 μM).3PO Causes G2-M Phase Arrest, Which Is Preceded by Decreased Fru-2,6-BP and Glucose Uptake. 3PO slows growth through inhibition of PFK-2 activity, then ectopic expression of the PFKFB3 isozyme may thwart the cytostatic activity of 3PO. [1] 3PO inhibits the glycolytic regulator PFKFB3 in endothelial cells (ECs). 3PO decreases glycolysis in ECs and impairs vessel sprouting. 3PO also suppresses vascular hyperbranching induced by inhibition of Notch or VEGF receptor 1 (VEGFR1) and amplified the antiangiogenic effect of VEGF blockade. [2]
Kinase Assay
Cell Assay
Animal Administration
References
Return Policy
If you are in any way unsatisfied with your purchase, you may return any item(s) within 365 days of its original purchase date.
Please provide your Order Number in the email. We strive to reply to all email inquiries within one business day.
