Search Result

Results for "

MET phosphorylation

" in MedChemExpress (MCE) Product Catalog:

By Targets:	c-Met/HGFR (31) Akt (3) Anaplastic lymphoma kinase (ALK) (9) Apoptosis (13) Autophagy (9) c-Kit (1) Cadherin (1) Caspase (1) Checkpoint Kinase (Chk) (1) Collagen (1) EGFR (4) Endogenous Metabolite (1) Environmental Pollutants (1) ERK (3) FLT3 (1) Glutaminase (3) iGluR (3) Isotope-Labeled Compounds (4) JNK (1) Ligands for Target Protein for PROTAC (1) NF-κB (1) PAI-1 (1) PDGFR (1) Phosphatase (1) Reference Standards (5) ROS Kinase (7) TRP Channel (3) Tyrosinase (3)
By Research Areas:	Cancer (35) Cardiovascular Disease (1) Endocrinology (1) Infection (1) Metabolic Disease (5) Neurological Disease (5)

By Targets:

c-Met/HGFR (31)

Akt (3)

Anaplastic lymphoma kinase (ALK) (9)

Apoptosis (13)

Autophagy (9)

c-Kit (1)

Cadherin (1)

Caspase (1)

Checkpoint Kinase (Chk) (1)

Collagen (1)

EGFR (4)

Endogenous Metabolite (1)

Environmental Pollutants (1)

ERK (3)

FLT3 (1)

Glutaminase (3)

iGluR (3)

Isotope-Labeled Compounds (4)

JNK (1)

Ligands for Target Protein for PROTAC (1)

NF-κB (1)

PAI-1 (1)

PDGFR (1)

Phosphatase (1)

Reference Standards (5)

ROS Kinase (7)

TRP Channel (3)

Tyrosinase (3)

By Research Areas:

Cancer (35)

Cardiovascular Disease (1)

Endocrinology (1)

Infection (1)

Metabolic Disease (5)

Neurological Disease (5)

Inhibitors & Agonists

Inhibitory Antibodies

Natural
Products

Isotope-Labeled Compounds

Targets Recommended: Oxidative Phosphorylation c-Met/HGFR MetAP DYRK

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-50878

Crizotinib Maximum Cited Publications 86 Publications Verification PF-02341066	Ligands for Target Protein for PROTAC Anaplastic lymphoma kinase (ALK) c-Met/HGFR ROS Kinase	Cancer
Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and *c-Met* inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

HY-13404

Capmatinib 20+ Cited Publications INC280; INCB28060	c-Met/HGFR Apoptosis	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 .

HY-14721

Tepotinib 5+ Cited Publications EMD-1214063	c-Met/HGFR Autophagy	Cancer
Tepotinib (EMD-1214063) is an orally active and highly selective, reversible, ATP-competitive *c-Met* inhibitor with an IC₅₀ of 3 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Tepotinib inhibits c-Met phosphorylation and induces autophagy. Tepotinib has antitumor effects .

HY-109061

Lazertinib 3 Publications Verification YH25448; GNS-1480	Apoptosis Akt TRP Channel EGFR ERK	Infection Neurological Disease Metabolic Disease Cancer
Lazertinib (YH25448; GNS-1480) is an orally active, blood-brain barrier permeable third-generation EGFR tyrosine kinase inhibitor, as well as an ABCB1/ABCG2 inhibitor and a TRPA1 activator. Lazertinib exhibits IC₅₀ values of 0.4 mM and 0.2 mM against human ABCB1 and ABCG2, respectively. By inhibiting mutant EGFR signaling, EGFR phosphorylation and the downstream ERK/AKT pathway, as well as upregulating surface expression of *EGFR/MET, Lazertinib induces cell cycle arrest, apoptosis, spontaneous calcium responses, hyperexcitability of dorsal root ganglion (DRG) neurons, and TRPA1-dependent pain-like behaviors. Lazertinib competitively binds to the substrate-binding sites of ABCB1/ABCG2, stimulates their ATPase activity without altering their expression or plasma membrane localization, thereby enhancing ADCC* activity, acting as a chemosensitizer, and reversing ABCB1-mediated multidrug resistance. It exerts antitumor activity as a single agent or in combination with other drugs. Lazertinib is applicable to research related to non-small cell lung cancer, multidrug-resistant cancers, and paresthesia .

HY-P99250

Onartuzumab 2 Publications Verification METMAb	c-Met/HGFR	Cancer
Onartuzumab (MetMAb) is a unique, humanized and affinity-matured monovalent (one-armed) monoclonal antibody against the *MET* receptor. Onartuzumab potently inhibits HGF binding and receptor phosphorylation and signaling. Onartuzumab has antibody-like pharmacokinetics and antitumor activity .

HY-W015309

Decanoic acid 4 Publications Verification	Environmental Pollutants Endogenous Metabolite iGluR Glutaminase c-Met/HGFR Tyrosinase	Neurological Disease Metabolic Disease Cancer
Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of *c-Met* and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

HY-50878A

Crizotinib hydrochloride Maximum Cited Publications 86 Publications Verification PF-02341066 hydrochloride	Anaplastic lymphoma kinase (ALK) c-Met/HGFR ROS Kinase Autophagy	Cancer
Crizotinib hydrochloride (PF-02341066 hydrochloride) is an orally bioavailable, selective, and ATP-competitive dual ALK and *c-Met* inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib hydrochloride (PF-02341066 hydrochloride) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. It is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib hydrochloride (PF-02341066 hydrochloride) has effective tumor growth inhibition .

HY-18696

AMG-337 3 Publications Verification	c-Met/HGFR Caspase Apoptosis	Cancer
AMG-337 is a potent, orally active, selective MET kinase inhibitor with IC₅₀ values of 1, 1, 4.7, 5, 21.5, 1077 and >4000 nM of WT MET, H1094R MET, M1250T MET, HGF-stimulated pMET (PC3 cells) MET, V1092I MET, Y1230H MET, and D1228H MET, respectively. AMG 337 inhibits the phosphorylation of MET and downstream effectors in MET-amplified cancer cell lines, resulting in an inhibition of MET-dependent cell proliferation and induction of apoptosis .

HY-50683

JNJ-38877605 5+ Cited Publications	c-Met/HGFR	Metabolic Disease Cancer
JNJ-38877605 is an orally active ATP-competitive inhibitor of *c-Met* with an IC₅₀ of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases . JNJ-38877605 inhibits c-Met phosphorylation and regulates lipid accumulation. JNJ-38877605 can be used for tumor and metabolic disease reseach .

HY-13404C

Capmatinib dihydrochloride hydrate 20+ Cited Publications INC280 dihydrochloride hydrate; INCB-28060 dihydrochloride hydrate	c-Met/HGFR Apoptosis	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 .

HY-123856

MY10	Phosphatase NF-κB c-Met/HGFR Anaplastic lymphoma kinase (ALK)	Cardiovascular Disease Neurological Disease
MY10 is a potent and orally active receptor protein tyrosine phosphatase (RPTPβ/ζ) inhibitor. MY10 reduces NF-κB p65 expression. MY10 activates tyrosine phosphorylation of *c-Met. MY10 prevents the alcohol-induced downregulation of Ptprz1* and Alk expression. MY10 attenuates binge-like ethanol consumption and ethanol reward. MY10 can be used in the study of neurological and vascular diseases .

HY-109061B

Lazertinib mesylate 3 Publications Verification YH25448 mesylate; GNS-1480 mesylate	TRP Channel EGFR Akt ERK Apoptosis	Cancer
Lazertinib (YH25448; GNS-1480) mesylate is an orally active, blood-brain barrier permeable third-generation EGFR tyrosine kinase inhibitor, as well as an ABCB1/ABCG2 inhibitor and a TRPA1 activator. Lazertinib mesylate exhibits IC₅₀ values of 0.4 mM and 0.2 mM against human ABCB1 and ABCG2, respectively. By inhibiting mutant EGFR signaling, EGFR phosphorylation and the downstream ERK/AKT pathway, as well as upregulating surface expression of *EGFR/MET, Lazertinib mesylate induces cell cycle arrest, apoptosis, spontaneous calcium responses, hyperexcitability of dorsal root ganglion (DRG) neurons, and TRPA1-dependent pain-like behaviors. Lazertinib mesylate competitively binds to the substrate-binding sites of ABCB1/ABCG2, stimulates their ATPase activity without altering their expression or plasma membrane localization, thereby enhancing ADCC* activity, acting as a chemosensitizer, and reversing ABCB1-mediated multidrug resistance. It exerts antitumor activity as a single agent or in combination with other drugs. Lazertinib mesylate is applicable to research related to non-small cell lung cancer, multidrug-resistant cancers, and paresthesia .

HY-15735

c-Met inhibitor 1 1 Publications Verification	c-Met/HGFR	Cancer
c-Met inhibitor 1 is an orally active *c-Met* inhibitor. c-Met inhibitor 1 can inhibit *c-Met* phosphorylation with an IC₅₀ of 0.010 μM. c-Met inhibitor 1 has antitumor activity and can be used for the research of tumors such as gastric cancer, pancreatic cancer and malignant glioma .

HY-13404A

Capmatinib dihydrochloride 20+ Cited Publications INC280 dihydrochloride; INCB28060 dihydrochloride	c-Met/HGFR Apoptosis	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 .

HY-13404B

Capmatinib hydrochloride 20+ Cited Publications INC280 hydrochloride; INCB-28060 hydrochloride	c-Met/HGFR Apoptosis	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 .

HY-147259

Dalmelitinib	c-Met/HGFR	Cancer
Dalmelitinib is an orally active selective *c-Met* kinase inhibitor (IC₅₀: 2.9 nM) that binds to the ATP-binding region of c-Met. Dalmelitinib induces the phosphorylation of MET, partially or completely inhibits the phosphorylation of AKT and ERK. Dalmelitinib potently inhibits cancer cell (c-Met oncogene amplification) proliferation, and is used for the research of cancers like human non-small cell lung cancer (NSCLC) .

HY-14721R

Tepotinib (Standard) EMD-1214063 (Standard)	Reference Standards c-Met/HGFR Autophagy	Cancer
Tepotinib (Standard) is the analytical standard of Tepotinib. This product is intended for research and analytical applications. Tepotinib (EMD-1214063) is an orally active and highly selective, reversible, ATP-competitive *c-Met* inhibitor with an IC₅₀ of 3 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Tepotinib inhibits c-Met phosphorylation. Tepotinib has antitumor effects .

HY-15456

NVP-BVU972	c-Met/HGFR	Cancer
NVP-BVU972 is an selective and potent *Met* inhibitor, with an IC₅₀ of 14 nM. NVP-BVU972 also exhibits good anti-proliferative activity against *Met* with drug-resistant mutations and inhibits phosphorylation. NVP-BVU972 can be used in study of cancer .

HY-50878S

Crizotinib-d5 PF-02341066-d₅	Anaplastic lymphoma kinase (ALK) c-Met/HGFR ROS Kinase Autophagy	Cancer
Crizotinib-d₅ is the deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

HY-W266188

Decanoic acid-13C	Isotope-Labeled Compounds iGluR Tyrosinase c-Met/HGFR Glutaminase	Neurological Disease Metabolic Disease Cancer
Decanoic acid- ¹³C is the ¹³C-labeled Decanoic acid (HY-W015309). Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

HY-14721A

Tepotinib hydrochloride EMD-1214063 hydrochloride	c-Met/HGFR Autophagy	Cancer
Tepotinib (EMD-1214063) hydrochloride is an orally active and highly selective, reversible, ATP-competitive *c-Met* inhibitor with an IC₅₀ of 3 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer. Tepotinib hydrochloride inhibits c-Met phosphorylation and induces autophagy. Tepotinib hydrochloride has antitumor effects .

HY-149510

MET/PDGFRA-IN-1	c-Met/HGFR Apoptosis PDGFR	Cancer
MET/PDGFRA-IN-1 (compound 8c) is a *MET* and PDGFRA protein inhibitor (IC₅₀: 36 μM for MET). MET/PDGFRA-IN-1 inhibits MET phosphorylation and induces cell apoptosis. MET/PDGFRA-IN-1 inhibits proliferation of MET-positive cells (IC₅₀s: 15.3, 19.0, 22.0, 25.6, 21.0, 31.5 μM for AsPc-1, EBC-1, MKN-45, Mia-Paca-2, HT-29, K562 cells respectively) .

HY-165284

CM-118	c-Met/HGFR Anaplastic lymphoma kinase (ALK)	Cancer
CM-118 is a potent and selective *c-Met* and ALK inhibitor. CM-118 inhibits the HGF-induced *c-Met* phosphorylation. CM-118 inhibits phosphorylation of ALK, EML4-ALKv1, ALK F1174L, and EMl4-ALKv1 L1196M, with respective IC₅₀ values 0.92, 1.25, 1.9, and 3.5 μM. CM-118 exhibits anticancer activity against cancers dependent on the c-Met or ALK oncogenic pathways .

HY-13404R

Capmatinib (Standard) INC280 (Standard); INCB28060 (Standard)	Reference Standards c-Met/HGFR Apoptosis	Cancer
Capmatinib (Standard) is the analytical standard of Capmatinib. This product is intended for research and analytical applications. 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 .

HY-50878AS

Crizotinib-d9 hydrochloride PF-02341066-d9 hydrochloride	c-Met/HGFR Autophagy Anaplastic lymphoma kinase (ALK) ROS Kinase Isotope-Labeled Compounds	Cancer
Crizotinib-d₉ hydrochloride is deuterated labeled Crizotinib hydrochloride (HY-50878A). Crizotinib hydrochloride (PF-02341066 hydrochloride) is an orally bioavailable, selective, and ATP-competitive dual ALK and *c-Met* inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib hydrochloride (PF-02341066 hydrochloride) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. It is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib hydrochloride (PF-02341066 hydrochloride) has effective tumor growth inhibition .

HY-163006

EGFR/c-Met-IN-1	EGFR c-Met/HGFR	Cancer
EGFR/c-Met-IN-1 (compound TS-41) is a dual-target inhibitor of *EGFR/c-Met. The IC₅₀ for inhibiting EGFR ^L858R and c-Met* is 68.1 nM and 0.26 nM respectively. . EGFR/c-Met-IN-1 induces apoptosis and cell cycle arrest in A549-P cells, downregulating the phosphorylation of EGFR, c-Met, and downstream AKT. EGFR/c-Met-IN-1 inhibits tumor growth in vitro and in vivo .

HY-150582

c-Met-IN-14	c-Met/HGFR c-Kit FLT3 Apoptosis	Cancer
c-Met-IN-14 (compound 26af) is a selective inhibitor of *c-Met* kinase from N-sulfonylamidine-based derivatives, with an IC₅₀ value of 2.89 nM. c-Met-IN-14 shows anticancer activity by blocking phosphorylation of c-Met, and arrests cell cycle at G2/M phase. c-Met-IN-14 induces apoptosis of A549 cells in a dose-dependent manner .

HY-50878B

Crizotinib acetate PF-02341066 acetate	Anaplastic lymphoma kinase (ALK) ROS Kinase c-Met/HGFR	Cancer
Crizotinib (PF-02341066) acetate is an orally bioavailable, ATP-competitive ALK and *c-Met* inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib acetate inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib acetate is also a ROS1 inhibitor. Crizotinib acetate has effective tumor growth inhibition .

HY-50878R

Crizotinib (Standard) PF-02341066 (Standard)	Reference Standards Anaplastic lymphoma kinase (ALK) c-Met/HGFR ROS Kinase Autophagy	Cancer
Crizotinib (Standard) is the analytical standard of Crizotinib. This product is intended for research and analytical applications. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and *c-Met* inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

HY-50878S2

Crizotinib-d9 PF-02341066-d₉	Isotope-Labeled Compounds	Cancer
Crizotinib-d₉ (PF-02341066-d₉) is deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and *c-Met* inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

HY-50878S1

Crizotinib-d8 PF-02341066-d₈	Isotope-Labeled Compounds ROS Kinase Autophagy c-Met/HGFR Anaplastic lymphoma kinase (ALK)	Cancer
Crizotinib-d₈ (PF-02341066-d₈) is deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and *c-Met* inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

HY-13404CR

Capmatinib dihydrochloride hydrate (Standard) INC280 dihydrochloride hydrate (Standard); INCB-28060 dihydrochloride hydrate (Standard)	c-Met/HGFR Apoptosis Reference Standards	Cancer
Capmatinib (dihydrochloride hydrate) (Standard) is the analytical standard of Capmatinib (dihydrochloride hydrate). This product is intended for research and analytical applications. 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 .

HY-W015309R

Decanoic acid (Standard)	Reference Standards iGluR Tyrosinase c-Met/HGFR Glutaminase	Neurological Disease Metabolic Disease Cancer
Decanoic acid (Standard) is the analytical standard of Decanoic acid. This product is intended for research and analytical applications. Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

HY-123597

NSC 109555 DDUG; NCI C04808	Autophagy Checkpoint Kinase (Chk)	Cancer
NSC 109555 is an ATP-competitive inhibitor of checkpoint kinase 2 (Chk2; IC₅₀=200 nM in a cell-free kinase assay). It is selective for Chk2 over Chk1 and 16 kinases in a panel but does inhibit Brk, c-Met, IGFR, and LCK with IC₅₀ values of 210, 6,000, 7,400, and 7,100 nM, respectively. NSC 109555 inhibits Chk2 autophosphorylation and phosphorylation of the Chk2 substrate histone H1 in vitro (IC₅₀=240 nM). It inhibits the growth of, and induces autophagy in, L1210 leukemia cells in vitro.2 NSC 109555 (1,250 nM) potentiates gemcitabine-induced cytotoxicity in MIA PaCa-2, CFPAC-1, PANC-1, and BxPC-3 pancreatic cancer cells, as well as reduces gemcitabine-induced increases in Chk2 phosphorylation and enhances gemcitabine-induced production of reactive oxygen species (ROS) in MIA PaCa-2 cells.

HY-181993

JNK3-IN-11	JNK Cadherin Collagen PAI-1	Endocrinology
JNK3-IN-11 is a selective JNK3 inhibitor with an IC50 of 2.08 nM. JNK3-IN-11 binds to the JNK3 ATP-binding pocket, forming conserved hydrogen bonds with Met149 and a water-mediated hydrogen bond with Lys93. JNK3-IN-11 suppresses TGF-β1-induced c-Jun phosphorylation, reduces profibrotic markers COL1A1 and PAI-1, restores E-cadherin expression, and has protection against podocyte injure. JNK3-IN-11 can be used for the research of chronic kidney disease .

HY-183749

c-Met-IN-29	c-Met/HGFR Apoptosis	Cancer
c-Met-IN-29 is an orally active c-Met inhibitor with an IC₅₀ of 1.6 nM. c-Met-IN-29 binds to and functionally modulates c-Met protein, inhibiting tumor cell proliferation, migration and apoptosis. c-Met-IN-29 exhibits anti-tumor activity both in vitro and in vivo. c-Met-IN-29 can be used for the research of non-small cell lung cancer .

HY-109061A

Lazertinib mesylate hydrate YH25448 mesylate hydrate; GNS-1480 mesylate hydrate	Apoptosis Akt TRP Channel EGFR ERK	Cancer
Lazertinib (YH25448; GNS-1480) mesylate hydrate is an orally active, blood-brain barrier permeable third-generation EGFR tyrosine kinase inhibitor, as well as an ABCB1/ABCG2 inhibitor and a TRPA1 activator. Lazertinib mesylate hydrate exhibits IC₅₀ values of 0.4 mM and 0.2 mM against human ABCB1 and ABCG2, respectively. By inhibiting mutant EGFR signaling, EGFR phosphorylation and the downstream ERK/AKT pathway, as well as upregulating surface expression of *EGFR/MET, Lazertinib mesylate hydrate induces cell cycle arrest, apoptosis, spontaneous calcium responses, hyperexcitability of dorsal root ganglion (DRG) neurons, and TRPA1-dependent pain-like behaviors. Lazertinib mesylate hydrate competitively binds to the substrate-binding sites of ABCB1/ABCG2, stimulates their ATPase activity without altering their expression or plasma membrane localization, thereby enhancing ADCC* activity, acting as a chemosensitizer, and reversing ABCB1-mediated multidrug resistance. It exerts antitumor activity as a single agent or in combination with other drugs. Lazertinib mesylate hydrate is applicable to research related to non-small cell lung cancer, multidrug-resistant cancers, and paresthesia .

Cat. No.	Product Name	Target	Research Area	Image

HY-P99250

Onartuzumab 2 Publications Verification METMAb	c-Met/HGFR	Cancer
Onartuzumab (MetMAb) is a unique, humanized and affinity-matured monovalent (one-armed) monoclonal antibody against the *MET* receptor. Onartuzumab potently inhibits HGF binding and receptor phosphorylation and signaling. Onartuzumab has antibody-like pharmacokinetics and antitumor activity .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-W015309

Decanoic acid 4 Publications Verification	Structural Classification Neurological Disease Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Disease Research Fields Biological Pesticide Research Source Classification Agricultural Research	Environmental Pollutants Endogenous Metabolite iGluR Glutaminase c-Met/HGFR Tyrosinase
Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of *c-Met* and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

HY-W015309R

Decanoic acid (Standard)	Structural Classification Microorganisms Ketones, Aldehydes, Acids Endogenous metabolite Source Classification	Reference Standards iGluR Tyrosinase c-Met/HGFR Glutaminase
Decanoic acid (Standard) is the analytical standard of Decanoic acid. This product is intended for research and analytical applications. Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

Cat. No.	Product Name	Chemical Structure

HY-50878S

Crizotinib-d5
Crizotinib-d₅ is the deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

Crizotinib-d5

Crizotinib-d₅ is the deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

HY-W266188

Decanoic acid-13C
Decanoic acid- ¹³C is the ¹³C-labeled Decanoic acid (HY-W015309). Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

Decanoic acid-13C

Decanoic acid- ¹³C is the ¹³C-labeled Decanoic acid (HY-W015309). Decanoic acid is a key component of the medium-chain triglyceride (MCT) found in coconut oil. Decanoic acid is a brain-penetrant and non-competitive inhibitor of AMPA receptor showing antiseizure activity in rats. Decanoic acid reduces tyrosinase activity and inhibits melanosome maturation. Decanoic acid suppresses the phosphorylation of c-Met and induced apoptosis in hepatocellular carcinoma (HCC) cells by inhibiting the expression of various oncogenic proteins, which is promising for research in the field of mTORC1 signaling, HCC and epilepsy .

HY-50878AS

Crizotinib-d9 hydrochloride
Crizotinib-d₉ hydrochloride is deuterated labeled Crizotinib hydrochloride (HY-50878A). Crizotinib hydrochloride (PF-02341066 hydrochloride) is an orally bioavailable, selective, and ATP-competitive dual ALK and *c-Met* inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib hydrochloride (PF-02341066 hydrochloride) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. It is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib hydrochloride (PF-02341066 hydrochloride) has effective tumor growth inhibition .

Crizotinib-d9 hydrochloride

Crizotinib-d₉ hydrochloride is deuterated labeled Crizotinib hydrochloride (HY-50878A). Crizotinib hydrochloride (PF-02341066 hydrochloride) is an orally bioavailable, selective, and ATP-competitive dual ALK and c-Met inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib hydrochloride (PF-02341066 hydrochloride) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. It is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib hydrochloride (PF-02341066 hydrochloride) has effective tumor growth inhibition .

HY-50878S2

Crizotinib-d9

Crizotinib-d₉ (PF-02341066-d₉) is deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

HY-50878S1

Crizotinib-d8

Crizotinib-d₈ (PF-02341066-d₈) is deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC₅₀s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC₅₀s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition .

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