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Results for "

fak-in-10

" in TargetMol Product Catalog
  • Inhibitors & Agonists
    6
    TargetMol | Inhibitors_Agonists
  • Peptide Products
    1
    TargetMol | Peptide_Products
FAK-IN-10
T77718491839-65-7
FAK-IN-10 is an inhibitor of FAK (IC50: 76.3 μM) and demonstrates antitumor activity in MCF-7 and A431 cell lines with IC50 values of 4.23 μM and 0.78 μM, respectively.
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TargetMol | Inhibitor Sale
PF-562271 hydrochloride
PF-562271 HCl
T21768939791-41-0
PF-562271 hydrochloride (PF-562271 HCl) is a potent, ATP-competitive, reversible inhibitor of FAK with IC50 of 1.5 nM in cell-free assays, ~10-fold less potent for Pyk2 than FAK and >100-fold selectivity against other protein kinases, except for some CDKs.
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TargetMol | Inhibitor Sale
CDK12/13 ligand 1
T2011592244986-40-9
ALK-IN-29 (compound 4c) exhibits notable inhibitory activity against tyrosine kinases such as ALK, CDK2 CyclinE1, and FAK, with the strongest inhibition observed against ALK kinase, showing a 40.63% inhibition rate at a concentration of 10 μM. ALK-IN-29 is useful for cancer research.
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6-8 weeks
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ALK-IN-29
T201303
ALK-IN-29 (compound 4c) exhibits inhibitory effects on tyrosine protein kinases such as ALK, CDK2 CyclinE1, and FAK, with the strongest inhibition observed against ALK kinase, displaying a 40.63% inhibition rate at a concentration of 10 μM. ALK-IN-29 is applicable in cancer research.
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Protein kinase inhibitor 10
T205111871317-00-9
Protein kinase inhibitor 10 is a protein kinase inhibitor with IC50 values of 28.9 μM, 13.6 μM, and 2.41 μM for TAM receptors, FAK, and KIT, respectively. It can inhibit abnormal and excessive cell proliferation, showing potential for research in the field of cancer treatment.
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10-14 weeks
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Azurin (50-77) (P. aeruginosa) TFA
p28, Azurin p28
T83680
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.
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