1. Signaling Pathways
  2. MAPK/ERK Pathway
    Stem Cell/Wnt
  3. ERK

ERK

Extracellular signal regulated kinases

ERKs (Extracellular-signal-regulated kinases) are widely expressed protein kinase intracellular signalling molecules that are involved in functions including the regulation of meiosis, mitosis, and postmitotic functions in differentiated cells. Many different stimuli, including growth factors, cytokines, virus infection, ligands for heterotrimeric G protein-coupled receptors, transforming agents, and carcinogens, activate the ERK pathway. In the MAPK/ERK pathway, Ras activates c-Raf, followed by mitogen-activated protein kinase kinase (abbreviated as MKK, MEK, or MAP2K) and then MAPK1/2 (below). Ras is typically activated by growth hormones through receptor tyrosine kinases and GRB2/SOS, but may also receive other signals. ERKs are known to activate many transcription factors, such as ELK1, and some downstream protein kinases. Disruption of the ERK pathway is common in cancers, especially Ras, c-Raf and receptors such as HER2.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-18723
    Yoda 1
    Activator 99.97%
    Yoda 1 is a potent and selective Piezo1 agonist. Yoda 1 activates purified Piezo1 channels. Yoda 1 potently inhibits macropinocytosis induced by epidermal growth factor (EGF). Yoda 1 enhances Ca2+ influx followed by activation of the calcium-activated potassium channel KCa3.1 and inhibition of Rac1 activation.
    Yoda 1
  • HY-10201
    Sorafenib
    Inhibitor 99.85%
    Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
    Sorafenib
  • HY-12028
    PD98059
    Inhibitor 99.94%
    PD98059 is a potent and selective MEK inhibitor with an IC50 of 5 µM. PD98059 binds to the inactive form of MEK, thereby preventing the activation of MEK1 (IC50 of 2-7 µM) and MEK2 (IC50 of 50 µM) by upstream kinases. PD98059 is a ERK1/2 signaling inhibitor. PD98059 is a ligand for the aryl hydrocarbon receptor (AHR), and suppresses TCDD binding (IC50 of 4 μM) and AHR transformation (IC50 of 1 μM). PD98059 also inhibits Mycobacterium bovis Bacillus CalmetteGuerin (BCG)-induced autophagy.
    PD98059
  • HY-50846
    SCH772984
    Inhibitor 99.83%
    SCH772984 is a highly selective and ATP-competitive ERK inhibitor, with IC50s of 4 and 1 nM for ERK1 and ERK2, respectively. SCH772984 has antitumor activity in MAPK inhibitor-na?ve and MAPK inhibitor-resistant cells containing BRAF or RAS mutations.
    SCH772984
  • HY-50876
    Daporinad
    Inhibitor 99.91%
    Daporinad (FK866) is a non-competitive inhibitor of nicotinamide phosphoribosyltransferase (Nampt), with a Ki value of 0.3 nM. Daporinad depletes NAD+ and ATP levels, inhibits mTORC1 and MAPK/ERK pathways, and activates TFEB to induce autophagy. Daporinad causes the depletion of the endoplasmic reticulum Ca²⁺ pool, ultimately weakening the mitogen-induced Ca²⁺ signal and the activation and function of T cells. Daporinad induces cell cycle arrest and apoptosis, and inhibits cell proliferation. Daporinad can be used for the study of myeloma, liver cancer, and immunosuppression.
    Daporinad
  • HY-153793A
    Alcudacigib TFA
    Inhibitor 99.72%
    Alcudacigib (ASP1570; DGKζ-IN-1) TFA is an orally active diacylglycerol kinase ζ (DGKζ) inhibitor, with an IC50 of 4.7 nM against human DGKζ and an IC50 of 3.0 nM against mouse DGKζ. Alcudacigib TFA selectively inhibits the kinase activity of DGKζ and induces proteasome-dependent degradation of DGKζ protein. Alcudacigib TFA enhances the anti-tumor functions of T cells and NK cells. Alcudacigib TFA can be used for the research of advanced/metastatic solid tumors.
    Alcudacigib TFA
  • HY-181067
    IK-595
    Inhibitor 98.55%
    IK-595 is a MEK1/MEK2 inhibitor with high affinity (7.39 nM).IK-595 blocks EGF-induced ERK1/2 phosphorylation in AsPC-1 cells with IC50 value of 0.1 nM. IK-595 has oral activity and blood-brain barrier penetration. IK-595 can be used for the research of Ras/MAPK pathway-altered cancers.
    IK-595
  • HY-P11474
    FZ1 peptide
    Activator 99.92%
    FZ1 peptide is an integrin αvβ3 agonist. FZ1 peptide binds to integrin αvβ3, effectively activates FAK, FAK-dependent AKT and ERK1/2 signaling pathways. FZ1 peptide enhances VEGFC-induced endothelial angiogenesis, accelerates diabetic skin wound healing.
    FZ1 peptide
  • HY-19696
    Tauroursodeoxycholate
    Inhibitor 99.93%
    Tauroursodeoxycholate (Tauroursodeoxycholic acid) is an orally active endoplasmic reticulum (ER) stress inhibitor. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3 and caspase-12. Tauroursodeoxycholate also inhibits ERK.
    Tauroursodeoxycholate
  • HY-D0886
    β-Glycerophosphate disodium salt pentahydrate
    Activator 99.99%
    β-Glycerophosphate disodium salt pentahydrate is a bioactive endogenous metabolite and a phosphatase inhibitor. β-Glycerophosphate disodium salt pentahydrate plays an important role in inducing and maintaining osteoblast differentiation, mineral metabolism and signal transduction, and can be used as a drug carrier to form heat-sensitive hydrogels. β-Glycerophosphate disodium salt hydrate accelerates the calcification of vascular smooth muscle cells.
    β-Glycerophosphate disodium salt pentahydrate
  • HY-N0431
    Astragaloside IV
    Inhibitor 99.93%
    Astragaloside IV, an active component isolated from Astragalus membranaceus, suppresses the activation of ERK1/2 and JNK, and downregulates matrix metalloproteases (MMP)-2, (MMP)-9 in MDA-MB-231 breast cancer cells.
    Astragaloside IV
  • HY-156498
    RMC-7977
    Inhibitor 99.48%
    RMC-7977 is an orally active triple-complex RAS inhibitor that can simultaneously bind to cyclophilin A (CYPA) (Kd = 195 nM) and KRAS (G12V) (Kd = 292 μM). It exhibits broad-spectrum inhibitory activity against KRAS, NRAS, and HRAS proteins and their various wild-type and mutant variants. RMC-7977 induces apoptosis by inhibiting the phosphorylation of ERK, CRAF, and RSK, as well as increasing PARP cleavage. This leads to tumor regression, reduces resistance in KRASG12C cancer models, and demonstrates good tolerability across various RAS cancer models.
    RMC-7977
  • HY-15816
    Ulixertinib
    Inhibitor 99.95%
    Ulixertinib (BVD-523; VRT752271) is a potent, orally active, highly selective, ATP-competitive and reversible covalent inhibitor of ERK1/2 kinases, with an IC50 of <0.3 nM against ERK2. Ulixertinib (BVD-523; VRT752271) inhibits the phosphorylated ERK2 (pERK) and downstream kinase RSK (pRSK) in an A375 melanoma cell line.
    Ulixertinib
  • HY-100489
    TBHQ
    Activator 99.88%
    TBHQ (tert-Butylhydroquinone) is a widely used Nrf2 activator, protects against Doxorubicin (DOX)-induced cardiotoxicity through activation of Nrf2. TBHQ (tert-Butylhydroquinone) is also an ERK activator; rescues Dehydrocorydaline (DHC)-induced cell proliferation inhibitionin melanoma.
    TBHQ
  • HY-N0003
    Honokiol
    Activator 99.90%
    Honokiol is a bioactive, biphenolic phytochemical that possesses potent antioxidative, anti-inflammatory, antiangiogenic, and anticancer activities by targeting a variety of signaling molecules. It inhibits the activation of Akt. Honokiol can readily cross the blood brain barrier.
    Honokiol
  • HY-108635
    C16-PAF
    Activator 99.86%
    C16-PAF (PAF (C16)), a phospholipid mediator, is a platelet-activating factor and ligand for PAF G-protein-coupled receptor (PAFR). C16-PAF exhibits anti-apoptotic effect and inhibits caspase-dependent death by activating the PAFR. C16-PAF is a potent MAPK and MEK/ERK activator. C16-PAF induces increased vascular permeability.
    C16-PAF
  • HY-13749
    Sitagliptin
    Inhibitor 99.94%
    Sitagliptin (MK-0431) is an orally active and highly selective DPP4 inhibitor with an IC50 value of 19 nM. Sitagliptin blocks the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) by competing inhibition mechanism (Kᵢ = 1 nM), thereby increasing the level of active incretin. Sitagliptin can also directly stimulate the secretion of GLP-1 by intestinal L cells by activating the cAMP/PKA and ERK1/2 pathways, and this effect is independent of DPP-4. Sitagliptin shows protective effects on pancreatic islet grafts in 1-type diabetes models. Sitagliptin can be used for the study of 1-type and 2-type diabetes.
    Sitagliptin
  • HY-19696A
    Tauroursodeoxycholate sodium
    Inhibitor 98.40%
    Tauroursodeoxycholate (Tauroursodeoxycholic acid; TUDCA) sodium is an endoplasmic reticulum (ER) stress inhibitor. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3 and caspase-12. Tauroursodeoxycholate also inhibits ERK.
    Tauroursodeoxycholate sodium
  • HY-126304
    β-Glycerophosphate disodium salt hydrate
    Activator 99.92%
    β-Glycerophosphate disodium salt pentahydrate is a bioactive endogenous metabolite and a phosphatase inhibitor. β-Glycerophosphate disodium salt pentahydrate plays an important role in inducing and maintaining osteoblast differentiation, mineral metabolism and signal transduction, and can be used as a drug carrier to form heat-sensitive hydrogels. β-Glycerophosphate disodium salt hydrate accelerates the calcification of vascular smooth muscle cells.
    β-Glycerophosphate disodium salt hydrate
  • HY-139414
    Lysophosphatidylcholines
    99.9%
    Lysophosphatidylcholines is an orally active lysolipid and a component of oxidized low density lipoprotein (LDL). Lysophosphatidylcholines induces cell injury, the production of IL-1β and apoptosis. Lysophosphatidylcholines has a proactive effect on sepsis.
    Lysophosphatidylcholines
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