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DRUG:

PF-573228

i
Other names: PF-573228
Associations
Trials
Company:
Pfizer
Drug class:
FAK inhibitor
Associations
Trials
1year
Loss of MTA2-mediated downregulation of PTK7 inhibits hepatocellular carcinoma metastasis progression by modulating the FAK-MMP7 axis. (PubMed, Environ Toxicol)
Furthermore, deactivation of FAK using siFAK or FAK inhibitor (PF-573228, PF) synergistically contributed to PTK7 knockdown-inhibited FAK activity, MMP7 expression, and the migration and invasion abilities of HCC cells. Collectively, our findings show that PTK7 mediates HCC progression by regulating the MTA2-FAK-MMP7 axis and may be a diagnostic value for HCC patients.
Journal
|
PTK7 (Protein Tyrosine Kinase 7) • MTA2 (Metastasis Associated 1 Family Member 2) • MMP7 (Matrix metallopeptidase 7)
|
PTK7 expression • MTA2 expression
|
PF-573228
almost2years
Role of synaptotagmin 13 (SYT13) in promoting breast cancer and signaling pathways. (PubMed, Clin Transl Oncol)
The results indicated that SYT13 promoted the malignant phenotypes of breast cancer cells by the activation of FAK/AKT signaling pathway.
Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • CCND1 (Cyclin D1) • CDK4 (Cyclin-dependent kinase 4) • CDH1 (Cadherin 1) • BAX (BCL2-associated X protein) • VIM (Vimentin) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • ANXA5 (Annexin A5)
|
VIM expression
|
MK-2206 • PF-573228
almost4years
Long noncoding RNA TPT1-AS1 promotes the progression and metastasis of colorectal cancer by upregulating the TPT1-mediated FAK and JAK-STAT3 signalling pathways. (PubMed, Aging (Albany NY))
The inhibition of FAK activation by PF573228 significantly attenuated the oncogenic effect of TPT1-AS1. These findings indicated that TPT1-AS1 promoted tumour progression and metastasis in CRC by upregulating TPT1 levels and activating the FAK and JAK-STAT3 signalling pathways. Thus, TPT1-AS1 may be considered as a potential therapeutic target for CRC.
Journal
|
PF-573228
over4years
FAK Inhibition Induces Glioblastoma Cell Senescence-Like State through p62 and p27. (PubMed, Cancers (Basel))
Our results indicate that FAK inhibition arrests GBM cell proliferation, resulting in cell senescence, and pinpoint p62 as being key to this process. These findings highlight the possible therapeutic value of targeting FAK in GBM.
Journal
|
SQSTM1 (Sequestosome 1) • CDKN1B (Cyclin dependent kinase inhibitor 1B)
|
PF-573228