ERK

Acenocoumarol-d₄ is deuterium labeled Acenocoumarol (HY-B1014). Acenocoumarol is an anticoagulant that functions as a Vitamin K antagonist. Acenocoumarol inhibits MAPK/ERK/JNK signaling pathway, reduces the nuclear translocation of NF-κB p65, activates Akt/GSK3β signaling pathway. Acenocoumarol induces apoptosis in cell A549, arrests cell cycle at S phase.

ROCK-IN-5 (compound I-B-37) is a potent inhibitor of ROCK, ERK, GSK, and AGC protein kinases. ROCK-IN-5 has the potential for proliferative, cardiac and neurodegenerative diseases research.

epi-Eriocalyxin A (Epieriocalyxin A), a diterpenoid isolated from Isodon eriocalyx, induces colon cancer apoptosis. epi-Eriocalyxin A also inhibits ERK1/2 and JNK activation, which suppresses Bcl-2 expression.

HYD-1 is a D-amino acid tumor cell adhesion peptide. HYD-1 contains overlapping linear peptide elements required for adhesion, migration blocking, and ERK signaling activation. HYD-1 supports adhesion of breast, prostate, ovarian, and pancreatic tumor cells, and shows no effect on tumor cell cycle distribution. HYD-1 can be used for the research of prostate cancer.

Cm-CATH2 is an antimicrobial peptide discovered from Chelonia mydas. Cm-CATH2 has a potent, broad-spectrum and rapid bactericidal ability by rapidly destroying the integrity of bacterial cell membranes. It shows strong activity against Gram-positive bacteria (such as VREF, Staphylococcus aureus), Gram-negative bacteria (such as Escherichia coli, Klebsiella pneumoniae), and fungi (such as Candida albicans) with MICs ranges from 1.17 to 18.75 μg/mL. Cm-CATH2 is also effective against various aquatic pathogenic bacteria. Cm-CATH2 not only inhibits biofilm formation but can also remove the formed biofilms. Cm-CATH2 has immunomodulatory functions and chemotactic effects on immune cells, and can inhibit the production of pro-inflammatory cytokines by macrophages stimulated by LPS (HY-D1056). Cm-CATH2 prevents the activation of NF-κB by inhibiting the degradation of IκBα, and also inhibits the phosphorylation of MAPK signaling pathways (p38, JNK, ERK). Cm-CATH2 demonstrates strong anti-infective ability in mouse peritonitis models and pneumonia models.

ERK5 ligand-1 is a is a PROTAC target protein ligand (Ligand for Target Protein for PROTAC). ERK5 ligand-1 can be used to design PROTAC, such as PROTAC ERK5 degrader-1 (HY-176528).

MK-8353 (SCH900353) hydrochloride is a potent, selective, orally active ERK1/2 inhibitor with IC₅₀ values of 23.0 nM and 8.8 nM, respectively. MK-8353 exhibits antitumor activity.

RWT9996 is a GPR17 antagonist. RWT9996 inhibits GPR17-mediated signal transduction processes, including G protein activation and β-arrestin-2 recruitment. RWT9996 inhibits MDL-29951 (HY-16312)-mediated phosphorylation of ERK1/2, phosphorylation of CREB, and accumulation of inositol phosphate (IP1) in oligodendrocyte precursor cells in vitro. RWT9996 can be used in studies related to demyelinating diseases.

Jujuboside B (Standard) is the analytical standard of Jujuboside B. This product is intended for research and analytical applications. Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway. Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM_2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.

HDB-1 is a selective inhibitor of the P2Y14 receptor (P2Y14R) with an IC₅₀ of 26 pM. HDB-1 shows no significant inhibition on P2Y1R, P2Y2R, P2Y4R, P2Y6R, and P2Y12R. HDB-1 blocks the activation of hepatic stellate cells (HSC) by inhibiting the PKA/Raf1/MEK/ERK signaling pathway mediated by P2Y14R, thereby alleviating the core pathological process of liver fibrosis. HDB-1 can be used for the study of liver fibrosis.

Aspafilioside B is a steroidal saponin. Aspafilioside B is extractable from Asparagus filicinus. Aspafilioside B activates the ERK, c-Raf and p38 MAPK signaling pathways, and upregulates H-Ras and N-Ras. Aspafilioside B mediates G2/M cell cycle arrest by altering the expression of cell cycle regulatory proteins. Aspafilioside B induces Apoptosis. Aspafilioside B increases intracellular ROS levels. Aspafilioside B is applicable to research related to hepatocellular carcinoma.

Trilinolein-d₅ is the deuterium labeled Trilinolein (HY-128393). Trilinolein is an orally active triglyceride that inhibits the PI3K/Akt, Ras/MEK/ERK signaling pathways, and MMP-2. Trilinolein can reduce oxidative stress, induce apoptosis, and inhibit cell migration. Trilinolein can be used in the research fields of cardiovascular disease, cerebrovascular disease (such as cerebral ischemia), and non-small cell lung cancer.

SF-9-2 is a PD-L1/PD-1 binding inhibitor (IC₅₀ = 24.9 nM). SF-9-2 inhibits epithelial-mesenchymal transition, migration, invasion, and proliferation of SK-N-SH cells, and also induces apoptosis and cell cycle arrest. SF-9-2 blocks PD-L1-induced SK-N-SH cell growth through the MAPK signaling pathway. SF-9-2 restores GSK-3β activity and enhances PD-L1 degradation through the ubiquitin-proteasome pathway. SF-9-2 inhibits tumor growth in the SK-N-SH NOG mouse model without significant toxicity. SF-9-2 also acts as an immune checkpoint inhibitor, blocking PD-L1 to restore T cell function. SF-9-2 can be used in neuroblastoma research.

PROTAC CB1R Degrader-1 is a potent and selective CB1R PROTAC degrader that exploits the ubiquitin-proteasome system (UPS) achieving a DC₅₀ of 3.37 μM in MCF-7 cells and showing no impact on CB2R. PROTAC CB1R Degrader-1 reduces CB1R-associated downstream signaling (p-AKT, p-ERK, BCL2, and MCM5), thereby inhibiting breast cancer cell proliferation and inducing apoptosis. PROTAC CB1R Degrader-1 can be used for breast cancer research.

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.

Pamoic acid (Standard) is the analytical standard of Pamoic acid. This product is intended for research and analytical applications. Pamoic acid (Embonic acid) is a potent GPR35 agonist with an EC₅₀ of 79 nM. Pamoic acid exhibits neuroprotective and anti-inflammatory properties.

Zoniporide mesylate (CP-597396 mesylate) is a selective Na⁺/H⁺ exchanger subtype 1 (NHE1) inhibitor with cardioprotective activity, with IC₅₀ values of 67 nM and 73 nM against rat NHE1. Zoniporide mesylate reduces intracellular Na⁺ and Ca²⁺ overload, preserves mitochondrial integrity, activates pro-survival ERK1/2 and STAT3 signaling pathways, reduces necrosis and apoptosis, and decreases neutrophil aggregation. Zoniporide mesylate is applicable to research related to myocardial ischemia-reperfusion injury and heart graft ischemia-reperfusion injury.

ETI41 is an orally active, selective TLR inhibitor that targets the nucleoside-binding Site I on TLR7 (IC₅₀ = 0.63 μM) and TLR9 (IC₅₀ = 0.16 μM), sparing surface TLRs (including TLR1/TLR2, TLR2/TLR6, TLR4 and TLR5). ETI41 potently inhibits endosomal TLR-mediated pro-inflammatory signaling with nanomolar activity in cellular, biophysical and in vivo assays. ETI41 suppresses the expression of inflammation-associated genes and effectively ameliorates symptoms in mouse models of psoriasis, and systemic lupus erythematosus (SLE). ETI41 can be used for autoimmune and inflammatory diseases research.

ERK5-IN-3 (compound 33j) is a potent and selective ERK5 (extracellular signal-related kinase 5) inhibitor, with an IC₅₀ of 6 nM. ERK5-IN-3 shows antiproliferation activity against Hela cells, with an IC₅₀ of 31 nM.

LYP-IN-5 is a lymphoid tyrosine phosphatase (LYP) inhibitor with an IC₅₀ value of 20.6 μM. LYP-IN-5 enhances the phosphorylation of ZAP70 and ERK1/2 following TCR stimulation, and promotes T cell activation. LYP-IN-5 can be used in the research of autoimmune diseases.