paxillin

Tyrphostin AG957, a tyrosine kinase inhibitor with anti-BCR/ABL tyrosine kinase activity restores beta1 integrin-mediated adhesion and inhibitory signaling in chronic myelogenous leukemia hematopoietic progenitors[1].

Paxilline is an indole alkaloid mycotoxin from *Penicillium paxilli*, acting as a potent BK channel inhibitor via an almost exclusively closed-channel block mechanism. Paxilline possesses significant anticonvulsant activity.

I194496 is an effective inhibitor of cystathionine γ-lyase (CSE) with an IC50 value of 0.79 mM. It inhibits the growth of human TNBC cells by dual targeting the PI3K Akt and Ras Raf ERK pathways. Additionally, I194496 suppresses the metastasis of human TNBC cells by downregulating the Anxa2 STAT3 and VEGF FAK Paxillin signaling pathways.

JP-153 is an inhibitor of Src-FAK-Paxillin signaling. It suppresses Src-dependent phosphorylation of paxillin (Y118) and subsequent activation of Akt (S473). JP-153 reduces VEGF-induced migration and proliferation of retinal endothelial cells and is applicable in the study of neovascular eye diseases.

SPP-037 is an orally active selective inhibitor of ST6GAL1, with an IC50 of 3.59 μM. It exhibits anti-migration activity against MDA-MB-231 cells by inhibiting integrin α2,6-sialylation and the integrin-FAK-paxillin pathway. In MDA-MB-231 xenograft mouse models, SPP-037 demonstrates antitumor properties. This compound is applicable in breast cancer research.

RNF5 inhibitor inh-02 is a selective inhibitor of the ubiquitin ligase RNF5/RMA1, which can significantly rescue F508del-CFTR (cystic fibrosis transmembrane conductance regulator with a deletion at position 508 of phenylalanine) and regulate ATG4B and paxillin, making it useful for studying cystic fibrosis (CF).

Azurin (50-77) is a peptide fragment derived from the copper-containing bacterial protein azurin, present in P. aeruginosa. It exhibits properties that regulate the cell cycle, inhibit cancer proliferation, and manage angiogenesis, proving its potential as an anticancer agent. Specifically, this compound acts as a VEGFR2 inhibitor with an IC20 of approximately 10.7 µM. At a concentration of 20 µM, it effectively induces cell cycle arrest at the G2 M phase in MCF-7 breast cancer cells, while a higher concentration of 50 µM significantly reduces the proliferation of both MCF-7 and ZR-75-1 breast cancer cell lines. Furthermore, Azurin (50-77) impedes VEGF-A-induced capillary tube formation with an IC50 of 12 µM, and alters the cellular and extracellular levels of critical signaling and structural proteins such as F-actin, focal adhesion kinase (FAK), paxillin, and platelet endothelial cell adhesion molecule-1 (PECAM-1) in human umbilical vein endothelial cells (HUVECs) at a concentration of 25 µM. Demonstrating its efficacy in vivo, Azurin (50-77) administered at 10 mg kg per day notably reduces tumor volume in an MCF-7 mouse xenograft model, highlighting its therapeutic potential.