33 Results for "

FAK phosphorylation inhibitor

" in MedChemExpress (MCE) Product Catalog:
Products (33)

33 Results for "FAK phosphorylation inhibitor" in MCE Product Catalog:

66
66 Publications Verification
Cat. No.: HY-12289A
CAS No.: 1073160-26-5
Purity:  99.35%
Synonyms: VS-6063 hydrochloride; PF 04554878 hydrochloride
Target:  

FAK

Research Areas:  

Cancer

Defactinib hydrochloride (VS-6063 hydrochloride; PF 04554878 hydrochloride) is a novel FAK inhibitor, which inhibits FAK phosphorylation at the Tyr397 site in a time- and dose-dependent manner.
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29
29 Cited Publications
Cat. No.: HY-13404
CAS No.: 1029712-80-8
Purity:  99.75%
Synonyms: INC280; INCB28060
Target:  

c-Met/HGFR Apoptosis

Research Areas:  

Cancer

Capmatinib (INC280; INCB28060) is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib is largely metabolized by CYP3A4 and aldehyde oxidase .
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29
29 Cited Publications
Cat. No.: HY-13404C
CAS No.: 1865733-40-9
Purity:  99.78%
Synonyms: INC280 dihydrochloride hydrate; INCB-28060 dihydrochloride hydrate
Target:  

c-Met/HGFR Apoptosis

Research Areas:  

Cancer

Capmatinib (INC280; INCB28060) dihydrochloride hydrate is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib dihydrochloride hydrate can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib dihydrochloride hydrate potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib dihydrochloride hydrate is largely metabolized by CYP3A4 and aldehyde oxidase .
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29
29 Cited Publications
Cat. No.: HY-13404A
CAS No.: 1197376-85-4
Synonyms: INC280 dihydrochloride; INCB28060 dihydrochloride
Target:  

c-Met/HGFR Apoptosis

Research Areas:  

Cancer

Capmatinib (INC280; INCB28060) dihydrochloride is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib dihydrochloride can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib dihydrochloride potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib dihydrochloride is largely metabolized by CYP3A4 and aldehyde oxidase .
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29
29 Cited Publications
Cat. No.: HY-13404B
CAS No.: 1029714-89-3
Purity:  99.60%
Synonyms: INC280 hydrochloride; INCB-28060 hydrochloride
Target:  

c-Met/HGFR Apoptosis

Research Areas:  

Cancer

Capmatinib (INC280; INCB28060) hydrochloride is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib hydrochloride can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib hydrochloride potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib hydrochloride is largely metabolized by CYP3A4 and aldehyde oxidase .
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24
24 Cited Publications
Cat. No.: HY-B0789
CAS No.: 330161-87-0
Target:  

Src FAK Akt

Research Areas:  

Cancer

SU6656 is a Src family kinases inhibitor with IC50s of 280, 20, 130, 170 nM for Src, Yes, Lyn, and Fyn, respectively. SU6656 inhibits FAK phosphorylation at Y576/577, Y925, Y861 sites. SU6656 also inhibits p-AKT.
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4
4 Cited Publications
Cat. No.: HY-N2445
CAS No.: 37308-75-1
Flavokawain C is an orally active natural chalcone. Flavokawain C inhibits the proliferation of various cancer cells. Flavokawain C upregulates GADD153 in cancer cells, inhibits the phosphorylation of Akt and JNK, suppresses early ERK phosphorylation, activates late ERK phosphorylation, activates caspase related subtypes, induces PARP-1 cleavage, causes upregulation of p21 and p27, downregulation of mutant p53 and anti-apoptotic IAP proteins, elevates intracellular ROS levels, reduces SOD activity, and induces apoptosis. Flavokawain C downregulates FABP4, induces autophagy in cancer cells, and activates the AMPK/mTOR pathway . Flavokawain C decreases the expression of glycolysis-related proteins GLUT1 and HK2, and inhibits glycolysis in nasopharyngeal carcinoma cells. Flavokawain C inhibits the activation of the EGFR/PI3K/Akt/mTOR signaling pathway and reduces the expression of HSP90B1. Flavokawain C inhibits angiogenesis by decreasing the expression of angiogenic proteins Ang-1 and VEGF in human umbilical vein endothelial cells. Flavokawain C increases γ-H2AX levels in cells, inhibits the phosphorylation of FAK, PI3K and AKT in cells, and induces DNA damage in cells. Flavokawain C exerts anti-tumor activity in multiple tumor xenograft mouse models. Flavokawain C is applicable to research related to colorectal cancer, colon adenocarcinoma, nephroblastoma, nasopharyngeal carcinoma and liver cancer .
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1
1 Cited Publications
Cat. No.: HY-N1983
CAS No.: 38395-02-7
Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease .
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Cat. No.: HY-P1189
CAS No.: 154303-05-6
Echistatin is a naturally derived RGD-containing snake venom peptide. Echistatin exhibits an IC50 of 0.6 nM against mouse αvβ3 integrin, and acts as an antagonist against αvβ3, αIIbβ3, α5β1 integrins, pp125 FAK and paxillin. Echistatin reduces the phosphorylation of pp125 FAK and paxillin, inhibits the autophosphorylation and kinase activity of pp125 FAK, and weakens its binding to pp60src and paxillin. Echistatin disrupts the actin cytoskeleton and focal adhesions, induces melanoma cell detachment from fibronectin, and regulates cell adhesion and motility. Echistatin inhibits osteoclast maturation and migration, bone resorption, platelet aggregation, bone loss, as well as adhesion and metastasis of Lewis lung cancer cells; it also increases the number of osteoclasts and bone coverage area in mice with secondary hyperparathyroidism. Echistatin can be used in research related to melanoma, lung cancer and secondary hyperparathyroidism .
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Cat. No.: HY-P5910
CAS No.: 897026-25-4
Target:  

MDM-2/p53 Apoptosis

Research Areas:  

Cancer

Azurin p28 peptide is a tumor-penetrated antitumor peptide. Azurin p28 peptide redues proteasomal degradation of p53 through formation of a p28: p53 complex. Azurin p28 peptide induces apoptosis or cell cycle arrest. Azurin p28 peptide inhibits p53-positive tumor growths. Azurin p28 peptide shows antiangiogenic effect by inhibiting phosphorylation of VEGFR-2, FAK and Akt .
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Cat. No.: HY-103471
CAS No.: 1086639-59-9
Purity:  ≥95.0%
Target:  

FAK Interleukin Related

Research Areas:  

Cancer

Y11 inhibits the autophosphorylation of FAK1 by blocking the phosphorylation of Y397. Y11 increases the expression level of IL-6. Y11 is applicable for cancer research .
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Cat. No.: HY-120417
CAS No.: 1802937-26-3
Target:  

Src FAK

Research Areas:  

Cardiovascular Disease

JP-153 is the Src-FAK-Paxillin signaling inhibitor. JP-153 inhibits Src-dependent phosphorylation of paxillin (Y118) and downstream activation of Akt (S473). JP-153 reduces VEGF-induced migration and proliferation in retinal endothelial cells. JP-153 can be uesd for the study of neovascular eye disease .
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Cat. No.: HY-P1189A
Echistatin TFA is a naturally derived RGD-containing snake venom peptide. Echistatin TFA exhibits an IC50 of 0.6 nM against mouse αvβ3 integrin, and acts as an antagonist against αvβ3, αIIbβ3, α5β1 integrins, pp125 FAK and paxillin. Echistatin TFA reduces the phosphorylation of pp125 FAK and paxillin, inhibits the autophosphorylation and kinase activity of pp125 FAK, and weakens its binding to pp60src and paxillin. Echistatin TFA disrupts the actin cytoskeleton and focal adhesions, induces melanoma cell detachment from fibronectin, and regulates cell adhesion and motility. Echistatin TFA inhibits osteoclast maturation and migration, bone resorption, platelet aggregation, bone loss, as well as adhesion and metastasis of Lewis lung cancer cells; it also increases the number of osteoclasts and bone coverage area in mice with secondary hyperparathyroidism. Echistatin TFA can be used in research related to melanoma, lung cancer and secondary hyperparathyroidism .
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Cat. No.: HY-121811
CAS No.: 484-33-3
Purity:  99.81%
Synonyms: Lanceolatin C
Pongamol (Lanceolatin C) is an orally active flavonoid with an IC50 of 75 μM and a Ki of 58 μM against PTPase-1B, and an IC50 of 103.5 μM against intestinal α-Glycosidase. Pongamol reduces the release of IL‑1β, TNF‑α, COX‑2 and iNOS in cells, reverses the nuclear translocation of NF‑κB, and upregulates the levels of Beclin 1 and LC3 Ⅱ/LC3 Ⅰ. Pongamol promotes glucose uptake by increasing the level of GLUT4 on the surface of skeletal muscle cells. Pongamol inhibits epithelial-mesenchymal transition by suppressing the FAK/Akt-mTOR signaling pathway. Pongamol inhibits neuronal cytotoxicity, suppresses cell apoptosis and extends the lifespan of Caenorhabditis elegans by activating the MAPKs/Nrf2 signaling pathway. Pongamol exerts hypoglycemic effects in diabetic mouse models. Pongamol exhibits antibacterial activity. Pongamol alleviates oxidative stress, neuroinflammation, Aβ deposition and excessive phosphorylation of Tau Protein, and restores autophagy function in Alzheimer's disease mouse models by inhibiting the Akt/mTOR signaling pathway. Pongamol is applicable to research related to Alzheimer's disease, type 2 diabetes, non-small cell lung cancer and postprandial hyperglycemia .
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Cat. No.: HY-163709
Target:  

PROTACs FAK Akt ERK

Research Areas:  

Cancer

PROTAC FAK degrader 2 is an orally active PROTAC FAK degrader with a DC50 of 60.10 nM. PROTAC FAK degrader 2 forms a ternary complex with FAK and CRBN E3 ubiquitin ligase, driving proteasome-mediated degradation of total and phosphorylated FAK. PROTAC FAK degrader 2 inhibits phosphorylation of AKT and ERK, suppressing their downstream signaling pathways. PROTAC FAK degrader 2 reduces cancer cell viability, adhesion, migration, and invasion. PROTAC FAK degrader 2 exerts anti-tumor activity in HCT8/T tumor xenografts in mice. PROTAC FAK degrader 2 can be used for the research of breast cancer, colorectal cancer, lung cancer .
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Cat. No.: HY-P11147
CAS No.: 2319573-67-4
Research Areas:  

Cancer

IL13Rα2 D1 is an effective IL-13/IL13Rα2 signaling axis inhibitor. IL13Rα2 D1 can inhibit IL-13-induced cell adhesion, migration, invasion, and proliferation. IL13Rα2 D1 can inhibit FAK, Src, AKT, ERK1/2 phosphorylation, and MMP expression. IL13Rα2 D1 can be used for research on cancers such as colorectal cancer .
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Cat. No.: HY-176498
CAS No.: 1246952-34-0
Synonyms: BMX
NBM-T-BMX-OS01 (BMX) is a derivative of Osthole (HY-N0054). NBM-T-BMX-OS01 attenuates the phosphorylation levels of ERK and Akt in an AMPK-dependent manner. NBM-T-BMX-OS01 induces oxidative stress through the production of ROS. NBM-T-BMX-OS01 enhances Cisplatin-induced cell proliferation inhibition, colony formation inhibition, apoptosis (apoptosis) and cell cycle arrest. NBM-T-BMX-OS01 inhibits VEGF-induced phosphorylation of VEGFR2 and FAK. NBM-T-BMX-OS01 inhibits VEGF-induced endothelial cell proliferation, migration and tube formation, as well as microvessel sprouting in rat aortic rings and angiogenesis induced by colorectal cancer cells. NBM-T-BMX-OS01 inhibits the growth of subcutaneous colorectal cancer xenografts in nude mice. NBM-T-BMX-OS01 can be used in studies related to lung cancer, colorectal cancer and angiogenesis .
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Cat. No.: HY-N1983R
CAS No.: 38395-02-7
Caudatin (Standard) is the analytical standard of Caudatin (HY-N1983). This product is intended for research and analytical applications. Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease .
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Cat. No.: HY-117836
CAS No.: 1257994-15-2
Target:  

FAK

Research Areas:  

Cancer

FAK-IN-16 (compound OXA-11) is an orally active, selective focal adhesion kinase (FAK) inhibitor with an IC50 of 1.2 pM. FAK-IN-16 inhibits FAK phosphorylation at pFAK[Y397] and pFAK[Y861]. FAK-IN-16 slows tumor growth and reduces tumor vascularity, invasion. FAK-IN-16 potentiates effects of Cisplatin (HY-17394) on tumor cell proliferation and apoptosis in vitro and anti-tumor actions in mice .
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Cat. No.: HY-164527
CAS No.: 1640012-88-9
Target:  

Src FAK EGFR

Research Areas:  

Cancer

Si306 is a Src inhibitor with antitumor activity. Si306 reduces the phosphorylation of focal adhesion kinase (FAK) and the expression of epidermal growth factor receptor (EGFR), and inhibits the invasion of human glioblastoma (GBM) .
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