Molecular Weight(MW): 350.45
IPA-3 is a selective non-ATP competitive Pak1 inhibitor with IC50 of 2.5 μM in a cell-free assay, no inhibition to group II PAKs (PAKs 4-6).
Cited by 12 Publications
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(e) Immunoblot analysis of p-ERM, p-Pak1 and Pak1 in Ishikawa cells treated with various doses of Pak1 inhibitor IPA-3 for 24 h. Actin serves as a loading control
Cell Death Differ, 2016, 23(1):169-81. IPA-3 purchased from Selleck.
Effect of endocytic pathway inhibitors on the uptake of 0.5 μm and 1 μm beads by IgM+ and IgM− cells in peripheral blood leukocytes (PBL). A. Endocytic rate of IgM+ cells and IgM− cells for 0.5 μm beads in the presence of inhibitors (CPZ, dynasore, M-β-CD, nystatin, IPA-3, and NSC23766). B. Endocytic rate of IgM+ cells and IgM− cells for 1 μm beads in the presence of inhibitors. Data are obtained from three independent experiments. *, P < 0.05; **, P < 0.01.
Fish Shellfish Immunol, 2019, 84:138-147. IPA-3 purchased from Selleck.
The cells were treated with 5 μM of the PAK1-specific inhibitor IPA-3 or 1 μM of the ROCK1/2-specific inhibitor RKI-1447 for 24 h. Total cell lysates were immunoblotted with antibodies against p110β, p110δ, p-PAK1, PAK1, ROCK1, ROCK2, p-LIMK1, LIMK1 or β-actin, which served as an internal control. The results are representative of three independent experiments.
Anticancer Res, 2017, 37(4):1805-1818. IPA-3 purchased from Selleck.
Purity & Quality Control
Choose Selective PAK Inhibitors
|Description||IPA-3 is a selective non-ATP competitive Pak1 inhibitor with IC50 of 2.5 μM in a cell-free assay, no inhibition to group II PAKs (PAKs 4-6).|
|Features||IPA-3 binds covalently to the Pak1 regulatory domain and prevents binding to the upstream activator Cdc42.|
IPA-3 is a non ATP-competitive, allosteric inhibitor of p21-activated kinase 1 (Pak1). PIR3.5 is the control compound of IPA-3. IPA-3 prevents Cdc42-stimulated Pak1 autophosphorylation on Thr423. IPA-3 also prevents sphingosine-dependent Pak1 autophosphorylation. IPA-3 does not target exposed cysteine residues on Pak1. The disulfide bond of IPA-3 is critical for inhibition of Pak1 and in vitro reduction by the reducing agent dithiothreitol (DTT) abolishes Pak1 inhibition by IPA-3. IPA-3 inhibits activation of Pak1 by diverse activators, but does not inhibit preactivated Pak1. IPA-3 inhibits PDGF-stimulated Pak activation in mouse embryonic fibroblasts.  IPA-3 inhibits Pak1 activation in part by binding covalently to the regulatory domain of Pak1. IPA-3 binds Pak1 covalently in a time- and temperature-dependent manner. IPA-3 prevents binding of the Pak1 activator Cdc42. IPA-3 binds directly to the Pak1 autoregulatory domain. IPA-3 reversibly inhibits PMA-induced membrane ruffling in cells. 
|In vitro||DMSO||70 mg/mL (199.74 mM)|
|Ethanol||7 mg/mL (19.97 mM)|
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Frequently Asked Questions
If this product is cell membrane permeable and would it be suitable for PAK1 inhibition on a pancreatic beta cell line?
Based on the reference, I think IPA-3 is able to penetrate the cell membrane, it's likely to inhibit PAK1 on a pancreatic beta cell line although there is no reference confirming it: Figure 3: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963893/; http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4353635/