fak

FAK-IN-7 has potential antiproliferative activity and is a FAK inhibitor.

FAK ligand-Linker Conjugate 1 is a chemical compound designed to facilitate PROTAC-mediated protein degradation. This compound consists of a ligand specifically targeting FAK and a PROTAC linker module, which acts as a recruitment agent for E3 ligases including VHL, CRBN, MDM2, and IAP[1].

FAK-IN-12 (Compound 12S) is a selective FAK inhibitor with an IC50 of 47 nM. It effectively suppresses proliferation of MGC-803, HCT-116, and KYSE30 cells with IC50 values of 0.24, 0.45, and 0.44 μM, respectively. Additionally, FAK-IN-12 promotes apoptosis and cellular senescence [1].

FAK-IN-10 is an inhibitor of FAK (IC50:76.3 μM).FAK-IN-10 z MCF-7 and A431 cell lines showed antitumor activity with IC50 of 4.23 and 0.78 μM, respectively.

FAK-IN-11 (Compound 4l), a FAK inhibitor, specifically targets the ATP binding pocket of FAK to prevent its phosphorylation. It exhibits cytotoxic effects on MDA-MB-231 cells, achieving an IC50 value of 13.73 μM, and induces non-apoptotic cell death in these cells [1].

PROTAC FAK degrader 1 is a selective and potent degrader of focal adhesion kinase (Fak) (IC50 of 6.5 nM).

FAK-IN-3 is a potent inhibitor of adherens spot kinase (FAK). FAK-IN-3 reduces migration and invasion of PA-1 cells and inhibits the expression of MMP-2 and MMP-9. FAK-IN-3 inhibits tumor growth and metastasis with no significant adverse effects. FAK-IN-3 has shown investigational potential in ovarian cancer.

FAK inhibitor 5 is a novel allosteric FAK inhibitor, with IC50 values in the low micromolar range.

FAK-IN-1 is a FAK inhibitor with anticancer activities (WO2020231726 (Example 27)).

FAK-IN-8 (compound 5h), a FAK inhibitor with an IC50 of 5.32 μM, exhibits potent anti-proliferative activity, making it suitable for use in cancer research [1].

FAK-IN-9 (Compound 8f) is a potent, orally active inhibitor of FAK, demonstrating an IC50 value of 27.44 nM. This compound effectively induces apoptosis in triple-negative breast cancer (TNBC) cells [1].

FAK-IN-5 is a FAK signaling inhibitor that induces apoptosis and autophagy.

FAK-IN-4 (Compound 7d) has anticancer activities that can induce cell apoptosis. FAK-IN-4 is potential inhibitor of FAK [1].

Compound B5 (FAK PROTAC B5) is a FAK PROTAC degrader exhibiting potent FAK degradation and antiproliferative activities, with an IC50 of 14.9 nM. It also shows excellent plasma stability, moderate membrane permeability, and inhibits cell migration and invasion [1].

FAK inhibitor 2, antitumor and anti-angiogenesis activitiesis ,is a potent focal adhesion kinase (FAK) inhibitor with an IC50 of 0.07 nM .

FAK-IN-6 is a potent inhibitor of FAK (IC50: 1.415 nM). FAK-IN-6 exhibits anti-proliferative effects on certain cancer cell lines and can be used to study pancreatic cancer.

FAK-IN-2 is a potent, orally active adherens spot kinase (FAK) inhibitor (IC50: 35 nM) that exhibits antitumour effects. FAK-IN-2 covalently inhibits FAK autophosphorylation in a dose-dependent manner and also inhibits tumour cell formation and migration and induces apoptosis.

Compound 26F effectively optimizes enzyme inhibition (IC50 = 28.2 nM) while demonstrating relatively low cytotoxicity (IC50 = 3.32 μM). It induces apoptosis in MDA-MB-231 cells in a dose-dependent manner and efficiently arrests these cells in the G0/G1 phase.

Y15 (1,2,4,5-Benzenetetramine tetrahydrochlor) is a potent and specificsmall-molecule FAK scaffolding inhibitor that inhibits its autophosphorylation activity, blocks tumor growth.

Ifebemtinib (BI-853520) is an orally active and potent inhibitor of adhesion plaque kinase (FAK) (IC50=1 nM) with anti-tumour activity that inhibits globule formation and in situ tumour growth in malignant pleural mesotheliomas, and may be useful for the study of breast and ovarian cancer.

Perisulfakinin, a satiety-signaling neuropeptide, suppresses the activity of neurons that stimulate general activity [1].

Compound 1T-0216 is a blocker of AKT1-FAK interactions and reduces stimulation of FAK phosphorylation by extracellular stress in human SW620 colon cancer cells without affecting basal FAK phosphorylation.

Ifebemtinib FA (BI-853520 FA) is an orally active and potent inhibitor of adhesion patch kinase (FAK) with anticancer and antiproliferative activity for the study of ovarian and lung cancer.

AZ7550 hydrochloride (AZ7550 hydrochloride ), an active metabolite of AZD9291, inhibits the activity of IGF1R (IC50: 1.6 μM).

Compound 1T-0219 (SC) is a blocker of AKT1-FAK interaction reducing the stimulation of FAK phosphorylation in response to extracellular pressure in human SW620 colon cancer cells without affecting basal FAK phosphorylation.

Conteltinib (CT-707) is an enzyme inhibitor with antitumor activity targeting FAK, ALK, and Pyk2.Conteltinib exhibits significant inhibition of FAK, overcomes hypoxia-mediated sorafenib resistance in hepatocellular carcinoma through inhibition of YAP signaling, and can be used in advanced ALK-positive non-small-cell lung cancer and lymphoma.

Mps1-IN-1 is a potent, selective and ATP-competitive inhibitor of Mps1 kinase (IC50 : 367 nM )

FC 11 is a highly potent focal adhesion Ki nase (FAK) PROTAC®Degrader (DC50 values are 40 to 370 pM depending on cell line), which is composed of the FAK inhibitor PF 562217 joined by a linker to the cereblon-binding ligand Pomalidomide. The effects of FC 11 are reversible upon compound wash out. FC 11 also degrades autophosphorylated FAK (pFAKtyr397), displaying near complete degradation after 3 hours at 100 nM in TM3 cells.

Roslin 2 bromide (Benzylhexamethylenetetramine bromide) is a p53 reactivator that disrupts the binding of FAK and p5. Roslin 2 bromide exhibits anticancer effects.

ZINC40099027 is a specific adhesion plaque kinase (FAK) activator that promotes gastric mucosal repair in persistent aspirin-associated gastric injury through activation of adhesion plaque kinase, activates human adhesion plaque kinase by accelerating the enzyme activity of the structural domain of FAK kinase, activates cytosolic FAK, and promotes intestinal epithelial wound closure.

PF-573228 is an ATP-competitive FAK inhibitor. In a cell-free assay, the IC50 of FAK is 4 nM.

PF-431396 is a dual PYK2/FAK inhibitor (IC50: 11/2 nM).

GSK2256098 (GTPL7939) is a small molecule FAK kinase inhibitor.

NVP-TAE 226 (TAE226) is an effective FAK inhibitor (IC50: 5.5 nM) and most effective to Pyk2(IC50: 3.5 nM); 10- to 100-fold less effective against IGF-1R, InsR, c-Met, and ALK.

Defactinib (VS-6063) is an orally bioavailable, small-molecule focal adhesion kinase (FAK) inhibitor with potential antiangiogenic and antineoplastic activities.

PF-562271 is an effective ATP-competitive, reversible inhibitor of FAK(IC50=1.5 nM) and Pyk2 kinase(IC50=13 nM).

Compound 2119738-71-3 interacts with the FAK receptor.

AT-533 is a potent inhibitor of Hsp90 and HSV. AT-533 blocks the HIF-1α/VEGF/VEGFR-2 signaling pathway, leading to suppress tumor growth and angiogenesis. AT-533 also inhibits the activation of the downstream pathways, including Erk1/2, FAK, Akt/mTOR/p70S6K,. AT-533 inhibits the cell migration, invasion, and the tube formation of human umbilical vein endothelial cells (HUVECs).

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.

Azurin p28 peptide, a tumor-penetrating antitumor agent, stabilizes p53 by reducing its proteasomal degradation via the formation of a p28:p53 complex. It elicits apoptosis or cell cycle arrest and suppresses the growth of p53-positive tumors. Additionally, the peptide exhibits antiangiogenic properties by inhibiting the phosphorylation of VEGFR-2, FAK, and Akt [1] [2] [3].

VnP-16 enhances bone formation by stimulating the differentiation and activity of osteoblasts via direct β1 integrin engagement, which subsequently activates FAK [1].

PND-1186 hydrochloride (VS-4718 hydrochloride) is a highly specific, reversible and potent inhibitor of FAK (IC50: 1.5 nM), which can selectively induce apoptosis in tumor cells.

APG-2449 is an orally active inhibitor targeting ALK, ROS1, and FAK, demonstrating antitumor efficacy in mouse models of non-small cell lung cancer (NSCLC) [1].

EGFR-IN-46 is a potent dual inhibitor of EGFR (IC50: 20.17 nM) and FAK (IC50: 14.25 nM) that significantly inhibits the growth of cancer cells and induces apoptosis.

Tricin can inhibit human cytomegalovirus (HCMV) replication by inhibiting CDK9. Tricin inhibits the proliferation and invasion of C6 glioma cells via the upregulation of focal-adhesion-finase (FAK)-targeting microRNA-7.

CEP-37440 is an effective and specific Dual FAK/ALK inhibitor with IC50s of 120 nM(ALK cellular in 75% human plasma) and 2.3 nM (FAK).

Corosolic acid (Colosic acid) contains anti-angiogenic activity that can suppress FAK signaling induced by angiopoietin-1. Corosolic acid exerts anticancer activities against HCC, colon, and colorectal Y cells, by inducing apoptosis and promoting the N-terminal phosphorylation and subsequent proteasomal degradation of β-catenin.

MNS is a tyrosine kinases inhibitor, inhibits Syk, Src, p97 with IC50 of 2.5 μM, 29.3 μM and 1.7 μM, respectively.

Tos-PEG4-t-butyl ester (Tos-PEG4-Boc) is a PROTAC linker characterized by its PEG composition. This compound plays a crucial role in the synthesis of a range of PROTACs, including BI-3663, a highly selective PTK2/FAK PROTAC. It employs cereblon ligands to target E3 ligases for the degradation of PTK2, exhibiting potent inhibitory activity with an IC50 of 18 nM[1].

ALK inhibitor 1 is a selective ALK kinase inhibitor.