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Pathways Recommended: MAPK/ERK Pathway Neuronal Signaling JAK/STAT Signaling
Results for "

MAPK/ERK signaling pathway

" in MedChemExpress (MCE) Product Catalog:

87

Inhibitors & Agonists

2

Screening Libraries

5

Fluorescent Dyes

4

Biochemical Assay Reagents

6

Peptides

2

Inhibitory Antibodies

29

Natural
Products

8

Isotope-Labeled Compounds

4

GMP Molecules

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-50876
    Daporinad
    60+ Cited Publications

    FK866; APO866

    		 NAMPT Autophagy Apoptosis mTOR p38 MAPK ERK Cancer
    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-15244
    Alpelisib
    Maximum Cited Publications
    125 Publications Verification

    BYL-719

    		 PI3K Apoptosis Cancer
    Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
    Alpelisib
  • HY-10966
    SB-590885
    5+ Cited Publications

    		 Raf Apoptosis Neurological Disease Metabolic Disease Cancer
    SB-590885 is a BRAF/c-Raf kinase inhibitor that selectively targets B-Raf, and it amplifies the ERK/MAPK signaling pathway in RAS-activated cells. SB-590885 effectively inhibits the malignant proliferation, transformation and tumorigenicity of oncogenic B-Raf cells; it also induces the proliferation of erythroid progenitor cells, delays their differentiation and promotes hemoglobin synthesis, thereby improving ineffective erythropoiesis and reducing apoptosis. SB-590885 exerts a synergistic effect with TGF-β inhibitors and glucocorticoids, significantly promoting the formation of erythroid colonies in cells from patients with Diamond-Blackfan anemia (DBA). SB-590885 is mainly used in relevant studies on DBA, cisplatin-induced myelosuppression-related anemia, and pan-cancers such as melanoma and colorectal cancer .
    SB-590885
  • HY-N0104
    Curcumol
    Maximum Cited Publications
    9 Publications Verification

    (-)-Curcumol

    		 Apoptosis Cancer
    Curcumol ((-)-Curcumol), a bioactive sesquiterpenoid, possesses numerous pharmacological activities like anticancer, antimicrobial, antifungal, antiviral, and antiinflammatory. Curcumol is a potent inducer of apoptosis in numerous cancer cells via targeting key signaling pathways as MAPK/ERK, PI3K/Akt and NF-κB which are generally deregulated in several cancers .
    Curcumol
  • HY-N0498
    Nitidine chloride
    4 Publications Verification

    		 Parasite Apoptosis STAT Topoisomerase ERK FAK p38 MAPK NF-κB Inflammation/Immunology Cancer
    Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway, also has anti-inflammatory activity. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway .
    Nitidine chloride
  • HY-P10408
    Candidalysin

    		EGFR MMP Calcium Channel NOD-like Receptor (NLR) ERK p38 MAPK Infection Inflammation/Immunology
    Candidalysin is a cytolytic peptide toxin secreted by the fungus Candida albicans. Candidalysin drives epithelial immune responses by activating the EGFR-MAPK signaling pathway, inducing MMP expression and calcium influx, and regulating the c-Fos transcription factor and MKP1 via p38 MAPK and ERK1/2 respectively. Candidalysin is essential for mucosal and systemic infections, activating NLRP3 to promote inflammatory responses, neutrophil recruitment, and Th17 immunity. Candidalysin activates LDH causing membrane damage and exhibiting cytotoxicity
    Candidalysin
  • HY-119272
    EF24
    2 Publications Verification

    		 ERK Caspase NF-κB Apoptosis p38 MAPK Reactive Oxygen Species (ROS) Inflammation/Immunology Cancer
    EF24, a curcumin analogue, is an NF-kB inhibitor with great anti-tumor efficacy and oral bioavailability via deactivation of the MAPK/ERK signaling pathway in oral squamous cell carcinoma (OSCC). EF24 is active against melanoma and breast cancer cell lines with GI50 values of 0.7 μM and 0.8 μM, respectively. EF24 induces cell cycle arrest and apoptosis in MDA-MB-231 human breast cancer cells and DU-145 human prostate cancer cells. EF24 increases the levels of activated caspase 3 and 9, and decreases the phosphorylated forms of MEK1 and ERK .
    EF24
  • HY-N1419
    Vaccarin
    1 Publications Verification

    		 AMPK Akt ERK p38 MAPK NF-κB Nuclear Factor of activated T Cells (NFAT) JNK Cardiovascular Disease Metabolic Disease
    Vaccarin is an orally active flavonoid glycoside with multiple biological functions. Vaccarin promotes neovascularization by activating AKT and ERK. Vaccarin activates the AMPK signaling pathway to improve insulin resistance and steatosis. Vaccarin is a MAPK, NF-κB, and NFAT inhibitor, effectively blocking RANKL-induced osteoclastogenesis .
    Vaccarin
  • HY-D0168
    Orcinol

    3,5-Dihydroxytoluene

    		 Fluorescent Dye Tyrosinase p38 MAPK ERK Metabolic Disease Cancer
    Orcinol (3,5-Dihydroxytoluene) is an organic compound used in biological dyeing and proteomics research. Orcinol inhibits melanogenesis in B16F10 cells by upregulating the MAPK/ERK signaling pathway, and suppresses the expression of MITF, tyrosinase (TYR), TRP1, and DCT. Orcinol exhibits certain DPPH radical scavenging activity. In addition, Orcinol can alter nitrogen balance in animals. Orcinol holds promise for research in cancer and metabolic diseases .
    Orcinol
  • HY-W010201
    Citronellol
    2 Publications Verification

    (±)-Citronellol; (±)-β-Citronellol

    		 Environmental Pollutants Necroptosis Autophagy Fungal Reactive Oxygen Species (ROS) ERK Atg8/LC3 TNF Receptor Apoptosis PI3K p62 Cardiovascular Disease Neurological Disease Cancer
    Citronellol ((±)-Citronellol) is an orally active inducer of apoptosis. Citronellol can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol can induce necroptosis in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis .
    Citronellol
  • HY-N0493
    Pectolinarigenin
    2 Publications Verification

    		 COX Lipoxygenase NF-κB p38 MAPK ERK HIF/HIF Prolyl-Hydroxylase Keap1-Nrf2 PI3K Apoptosis Autophagy Neurological Disease Inflammation/Immunology Cancer
    Pectolinarigenin is an orally active dual inhibitor of COX-2/5-LOX with anti-inflammatory, antioxidant, antitumor and neuroprotective activities. Pectolinarigenin exerts neuroprotective and anti-inflammatory effects on astrocyte inflammation via the NFκB and MAPK pathways. Pectolinarigenin inhibits LPS-induced phosphorylation of ERK1/2, N-FκB and p38MAPK, directly inhibits the enzymatic activity or binding of COX-2, 5-LOX and HIF-1α, and reduces the level of XIAP. Pectolinarigenin modifies Keap1 to promote nuclear accumulation of Nrf2, induces ARE-mediated antioxidant enzyme expression, and possesses direct free radical scavenging activity. Pectolinarigenin reduces the release of NO, proinflammatory mediators and leukotrienes, and increases the level of IL-10. Pectolinarigenin induces G2/M cell cycle arrest, apoptosis (Apoptosis) and autophagy (Autophagy) via the PI3K/AKT/mTOR signaling pathway. Pectolinarigenin reduces renal crystal deposition and inhibits melanin synthesis. Pectolinarigenin inhibits inflammation and alleviates allergy in mouse models of inflammation. Pectolinarigenin alleviates renal injury, inflammation and oxidative stress in mice by inhibiting HIF-1α activity. Pectolinarigenin can be used for the research of neurodegenerative diseases, inflammatory/allergic diseases, calcium oxalate nephrocalcinosis, gastric cancer, melasma, post-inflammatory diseases and chloasma .
    Pectolinarigenin
  • HY-144903
    Migoprotafib

    GDC-1971

    		 SHP2 Phosphatase p38 MAPK ERK Cancer
    Migoprotafib (GDC-1971) (compound 199) is a SHP2 inhibitor. Migoprotafib inhibits the MAPK/ERK signaling pathway, and exhibits antitumor activity .
    Migoprotafib
  • HY-N0852
    Benzoylpaeoniflorin

    		p38 MAPK NF-κB Interleukin Related JNK PERK CXCR Cardiovascular Disease Inflammation/Immunology
    Benzoylpaeoniflorin is an orally active monoterpene glycoside compound. Benzoylpaeoniflorin exerts anti-inflammatory, anti-allergic, psoriasis-improving and sepsis-improving effects by inhibiting signaling pathways such as TNF/NF-κB and MAPK, as well as regulating immune homeostasis. Benzoylpaeoniflorin can be used in research related to immune, allergic and inflammatory diseases .
    Benzoylpaeoniflorin
  • HY-111940
    LUT014

    		Raf p38 MAPK ERK Inflammation/Immunology
    LUT014 is a topical inhibitor targeting BRAF that cannot pass through the blood-brain barrier. LUT014 inhibits BRAF kinase and abnormally activates the MAPK/ERK signaling pathway, promoting the proliferation of epidermal keratinocytes, repairing skin barrier damage caused by radiation damage, and alleviating inflammatory responses. LUT014 is independent of RAS signaling and accelerates the repair and regeneration of damaged skin cells. LUT014 can be used to study radiation dermatitis, especially skin damage caused by breast cancer radiotherapy .
    LUT014
  • HY-15001G
    Stemregenin 1

    SR1

    		 Aryl Hydrocarbon Receptor Cancer
    Stemregenin 1 (SR1) (GMP) is a GMP-grade Stemregenin 1 (HY-15001). GMP-grade small molecules can be used as adjuvants in cell therapy. Stemregenin 1 is a potent aryl hydrocarbon receptor (AhR) antagonist with an IC50 of 127 nM. Stemregenin 1 (GMP) can competitively bind to AhR and inhibit its nuclear translocation, inhibiting osteoclastogenesis and promoting hematopoietic progenitor cell expansion by blocking the AhR-c-src-NF-κB/p-ERK MAPK-NFATc1 signaling pathway. Stemregenin 1 (GMP) can be used for the study of osteoporosis, in vitro expansion of hematopoietic stem cells, and the study of the mechanism of bone metabolic diseases .
    Stemregenin 1
  • HY-N0819
    Raddeanin A
    1 Publications Verification

    		 Apoptosis PI3K Akt ERK mTOR Wnt β-catenin Wee1 JNK VEGFR CDK Neurological Disease Inflammation/Immunology Cancer
    Raddeanin A is an oleanane-type triterpenoid saponin with oral activity. Raddeanin A inhibits SRC, mTOR, JNK, VEGFR2, NLRP3 inflammasome, Wnt/β-catenin, Wee1, PI3K/AKT signaling pathway, MAPK/ERK signaling pathway, AR-FL, AR-Vs, and downregulates the expression of p-PI3K and p-AKT. Raddeanin A inhibits osteoclast formation, bone resorption, osteolysis, cancer cell invasion, migration, proliferation, angiogenesis and epithelial-mesenchymal transition, while induces apoptosis, cell cycle arrest, ROS production, immunogenic cell death and dendritic cell maturation. Raddeanin A improves blood-retinal barrier function, alleviates inflammation, regulates the tumor microenvironment, and enhances the activity of anti-PD-1 antibody. Raddeanin A is applicable to the research of breast cancer-associated osteolysis, human osteosarcoma, colorectal cancer, glioblastoma, Alzheimer's disease, cholangiocarcinoma, melanoma, non-small cell lung cancer, castration-resistant prostate cancer and multiple myeloma .
    Raddeanin A
  • HY-N0660
    Jujuboside B

    		Apoptosis PARP Caspase AMPK Autophagy VEGFR Keap1-Nrf2 STING 11β-HSD Ferroptosis PI3K Akt p38 MAPK ERK Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    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, PM2.5-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 .
    Jujuboside B
  • HY-N0863
    Methyl protodioscin

    NSC-698790; Smilax saponin B

    		 Bcl-2 Family Apoptosis Akt c-Myc ERK p38 MAPK JNK FOXO Cancer
    Methyl protodioscin (NSC-698790; Smilax saponin B) is a multi-target, selective, steroidal diglycoside inhibitor with antitumor activity that induces cell cycle arrest. The mechanism of action of Methyl protodioscin is complex, involving the induction of G2/M cell cycle arrest, regulation of the Bcl-2/Bax apoptotic pathway, inhibition of the Akt1/c-Myc axis and MAPK/ERK signaling, while simultaneously downregulating ADAM15 and inducing FOXO1 to reduce cholesterol synthesis. It also inhibits the JNK/c-Jun pathway, reducing the production of inflammatory factors (IL-6, TNF-α). Methyl protodioscin exhibits significant antitumor (inhibiting proliferation, migration, invasion, and inducing apoptosis), anti-inflammatory, and anti-restenosis activities. Methyl protodioscin can be used in research on lung cancer, prostate cancer, pancreatic cancer, and other tumors, as well as inflammatory diseases such as airway inflammation and enteritis .
    Methyl protodioscin
  • HY-W923189
    Neral

    		Interleukin Related COX TNF Receptor NOD-like Receptor (NLR) NO Synthase PERK p38 MAPK Reactive Oxygen Species (ROS) Caspase Autophagy Herbicide Inflammation/Immunology Cancer
    Neral is a plant-derived anti-inflammatory, antioxidant and anticancer agent. Neral inhibits the phosphorylation of ERK1/2, p38 MAPK and IκB in macrophages induced by LPS (HY-D1056), suppresses the secretion of TNF-α and IL-6, as well as the expression of pro-IL-1β, iNOS and COX-2 in cells, and reduces the production of ROS in cells. Neral inhibits the activation of the NLRP3 inflammasome, and decreases the activation of caspase-1 and the secretion of IL-1β in mouse macrophages. Neral induces autophagy, and exhibits antiproliferative activity both in in vitro breast cancer cell models and mouse xenograft models. Neral regulates brassinosteroid, jasmonic acid and ethylene signaling pathways, and induces the expression of AP2/ERF-ERF and bHLH family genes in rice roots. Neral acts as a herbicide safener, alleviates the damage induced by Fenoxaprop-P-ethyl (HY-B2013), and promotes the elongation of rice roots. Neral can be used in research related to breast cancer, inflammatory and immune system diseases, and herbicide safeners .
    Neral
  • HY-15244A
    Alpelisib hydrochloride
    Maximum Cited Publications
    125 Publications Verification

    BYL-719 hydrochloride

    		 PI3K Apoptosis Cancer
    Alpelisib (BYL-719) hydrochloride is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib hydrochloride also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib hydrochloride not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib hydrochloride can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
    Alpelisib hydrochloride
  • HY-B1014
    Acenocoumarol

    		VD/VDR p38 MAPK JNK ERK NF-κB Akt GSK-3 PKA Apoptosis Cardiovascular Disease Inflammation/Immunology Cancer
    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 .
    Acenocoumarol
  • HY-N2963
    Broussonin E
    2 Publications Verification

    		 ERK p38 MAPK JAK STAT TNF Receptor Interleukin Related COX Arginase Inflammation/Immunology
    Broussonin E is a phenolic compound and shows anti-inflammatory activity. Broussonin E can suppress inflammation by modulating macrophages activation statevia inhibiting the ERK and p38 MAPK and enhancing JAK2-STAT3 signaling pathway. Broussonin E can be used for the research of inflammation-related diseases such as atherosclerosis .
    Broussonin E
  • HY-P991413
    ZEB85

    		Trk Receptor ERK Akt p38 MAPK Neurological Disease Inflammation/Immunology
    ZEB85 is a human monoclonal antibody (mAb) targeting TrkB. ZEB85 activates TrkB and its downstream cascades, including the ERK, PLCγ, AKT, MAPK signaling pathways and cFOS expression, and enhances neuronal activity. ZEB85 prevents β-amyloid toxicity in cultured hippocampal neurons. ZEB85 is applicable to the research of Alzheimer's disease (AD) .
    ZEB85
  • HY-N2375
    L-Quebrachitol

    		Wnt β-catenin p38 MAPK Metabolic Disease
    L-Quebrachitol is a methoxy analog of inositol that can be isolated from plants. L-Quebrachitol has free-radical scavenging, gastroprotection, anti-platelet aggregation and anti-diabetic activity. L-Quebrachitol promotes osteoblastogenesis by uppregulation of BMP-2, runt-related transcription factor-2 (Runx2), MAPK (ERK, JNK, p38α), and Wnt/β-catenin signaling pathway .
    L-Quebrachitol
  • HY-148385
    Ganglioside GM2

    		Endogenous Metabolite Integrin FAK Src ERK p38 MAPK Neurological Disease Cancer
    Ganglioside GM2 is a human tumor antigen predominantly found in human tumor cells and fetal brain tissue. As a sialylated glycosphingolipid, Ganglioside GM2 is involved in processes such as cell signaling, adhesion, and motility. Ganglioside GM2 abnormal expression and accumulation are associated with tumors and neurodegenerative disorders. Ganglioside GM2 promotes tumor cell migration and invasion by directly binding to the integrin β1 receptor, activating the FAK/Src/Erk-MAPK signaling pathway, and inducing actin cytoskeleton remodeling .
    Ganglioside GM2
  • HY-P4322
    H-Ile-Lys-Val-Ala-Val-OH
    1 Publications Verification

    		 ERK Akt Neurological Disease Cancer
    H-Ile-Lys-Val-Ala-Val-OH is one of the most potent active sites of laminin-1. H-Ile-Lys-Val-Ala-Val-OH promotes cell adhesion, neurite outgrowth, and tumor growth. H-Ile-Lys-Val-Ala-Val-OH stimulates BMMSC population growth and proliferation by activating MAPK/ERK1/2 and PI3K/Akt signalling pathways .
    H-Ile-Lys-Val-Ala-Val-OH
  • HY-N4322
    Decursinol angelate
    1 Publications Verification

    		 PKC Inflammation/Immunology Cancer
    Decursinol angelate acts as a PKC activator and GDH inhibitor, with an IC50 of 1.432 μM against human GDH. Decursinol angelate activates PKC, downregulates PKCα and PKCβII isoforms, and exerts cytotoxic activity against cancer cells. Decursinol angelate binds to GDH and inhibits its enzymatic activity. Decursinol angelate inhibits VEGF-induced autophosphorylation of VEGFR2, downstream p42/44 ERK and JNK-MAPK signaling pathways, as well as the angiogenesis process. Decursinol angelate is applicable to research related to cancer and leukemia .
    Decursinol angelate
  • HY-G0007
    Omeprazole sulfone
    2 Publications Verification

    Omeprazole sulphone

    		 Drug Metabolite Cytochrome P450 Aryl Hydrocarbon Receptor Inflammation/Immunology
    Omeprazole sulfone (Omeprazole sulphone) is one of the major circulating metabolites of Omeprazole (HY-B0113) in vivo, and belongs to class 4 non-mutagenic impurities. Omeprazole sulfone does not bind to the aryl hydrocarbon receptor (AhR), nor does it induce the expression of CYP1A1 or CYP1A2. However, Omeprazole sulfone promotes the migration of gastric epithelial cells under basal conditions and reverses the inhibitory effect of Indomethacin (HY-14397) on cell migration. Omeprazole sulfone does not promote cell proliferation, nor does it upregulate COX-2 expression or activate signaling pathways such as ERK, P38 MAPK and PI3K. Omeprazole sulfone maintains basal ulcer healing under non-acid-dependent conditions and can be used in studies related to gastric ulcer repair .
    Omeprazole sulfone
  • HY-N0363
    (+)-Columbianetin
    2 Publications Verification

    (S)-Columbianetin

    		 ERK JNK Collagen TGF-beta/Smad p38 MAPK Reactive Oxygen Species (ROS) Others
    (+)-Columbianetin ((S)-Columbianetin) acts as an inhibitor of JNK/ERK. (+)-Columbianetin inhibits UVA-induced phosphorylation of JNK and ERK, reduces the production of MMP-1, reverses UVA-induced Collagen (HY-NP003) degradation, and alleviates UVA-mediated inhibition of Smad2/3 phosphorylation and translocation. (+)-Columbianetin regulates the AP-1 and ASK1-MAPK signaling pathways, inhibits the production of ROS and blocks sub-G1 cell cycle arrest. (+)-Columbianetin is applicable to research related to skin aging .
    (+)-Columbianetin
  • HY-12716A
    BRL-44408 maleate

    		Adrenergic Receptor ERK p38 MAPK Dopamine Receptor Cardiovascular Disease Neurological Disease
    BRL-44408 maleate is a selective, blood-brain barrier-permeable α2A-adrenergic receptor antagonist with a Ki value of 8.56 nM against human targets. BRL-44408 maleate exhibits activities such as antidepressant, analgesic effects and attenuation of sepsis-induced acute lung injury by regulating the release of neurotransmitters such as norepinephrine and dopamine, or inhibiting signaling pathways including ERK1/2, p38MAPK and p65. BRL-44408 maleate can be used in studies related to acute respiratory distress syndrome, depression and visceral pain .
    BRL-44408 maleate
  • HY-N0910
    Notoginsenoside Ft1
    1 Publications Verification

    		 PI3K mTOR Akt Apoptosis p38 MAPK ERK Transmembrane Glycoprotein Glutathione Reductase (GR) Estrogen Receptor/ERR Calcium Channel Ferroptosis G protein-coupled Bile Acid Receptor 1 FXR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Notoginsenoside Ft1 is an orally active bioactive saponin. Notoginsenoside Ft1 inhibits the PI3K/AKT/mTOR signaling pathway, activates the p38 MAPK and ERK1/2 signaling pathways, and increases the proportion of CD8 + T cells, thereby inducing apoptosis and lysosomal cell death in various cancer cells, and promoting angiogenesis. Notoginsenoside Ft1 causes vasodilation by activating glucocorticoid receptors (GR) and estrogen receptor beta (ERβ) in endothelial cells. Notoginsenoside Ft1 increases intracellular Ca 2+ accumulation, reduces cAMP levels by activating a signaling network mediated through P2Y12 receptors, and promotes platelet aggregation, thereby exerting a procoagulant effect. Notoginsenoside Ft1 inhibits ferroptosis (ferroptosis) in renal tubular epithelial cells by activating the TGR5 receptor, thereby demonstrating a renal protective effect. Notoginsenoside Ft1 acts as a TGR5 agonist and an FXR antagonist to combat obesity and insulin resistance .
    Notoginsenoside Ft1
  • HY-N2902
    Artocarpin

    		Reactive Oxygen Species (ROS) Cancer
    Artocarpin is an orally active apoptosis inducer. Artocarpin targets NF-κB, Erk1/2, p38 MAPK, AktS473, p53, Akt 1 kinase and Akt 2 kinase. Artocarpin induces reactive oxygen species (ROS) production, mediates p53-dependent and p53-independent apoptotic signaling pathways, induces G1-phase cell cycle arrest, and triggers autophagic cell death. Artocarpin exerts cytotoxic and bactericidal effects on cancer cells, reduces bacterial load, and exhibits anti-inflammatory, analgesic and anti-angiogenic activities .
    Artocarpin
  • HY-Y1322
    Triphenyl phosphate

    		Environmental Pollutants Mitophagy Apoptosis NF-κB p38 MAPK ERK JNK PI3K Akt Monoamine Oxidase Reactive Oxygen Species (ROS) PPAR Indoleamine 2,3-Dioxygenase (IDO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring .
    Triphenyl phosphate
  • HY-N8303
    Gardenin A

    		ERK PAK Neurological Disease Inflammation/Immunology
    Gardenin A is an orally active and synthetic PMF analogue with the neurotrophic effect for neurite outgrowth and neuronal differentiation. Gardenin A promotes neuritogenesis via activating MAPK/ERK, PKC, and PKA, but not TrkA, CREB signaling pathways. Gardenin A also has sedative, anxiolytic, antidepressant, and anticonvulsant effects .
    Gardenin A
  • HY-164350
    KRAS inhibitor-27

    		Ras ERK p38 MAPK Cancer
    KRAS inhibitor-27 (Compound 15h) is the inhibitor for KRAS. KRAS inhibitor-27 inhibits KRAS G12D/G12V mutated cells AsPC-1, SW620 and KRAS wildtype cell HT-29 with IC50 of 378, 0.6 and 3230 nM, respectively. KRAS inhibitor-27 inhibits ERK phosphorylation (IC50 in cell AsPC-1 and SW620 is 0.6 nM and 1 nM), reduces the expression of DUSP4, thereby inhibiting MAPK signaling pathway .
    KRAS inhibitor-27
  • HY-117548
    UNC1062
    2 Publications Verification

    		 TAM Receptor Apoptosis p38 MAPK ERK PI3K Akt JAK STAT Cardiovascular Disease Cancer
    UNC1062 is a highly selective tyrosine kinase (MERTK) inhibitor with an IC50 of 1.1 nM (Morrison Ki = 0.33 nM). UNC1062 exhibits good selectivity for the TAM family (TYRO3 IC50 = 60 nM, AXL IC50 = 85 nM). UNC1062 exhibits significant anti-proliferative effects and induces apoptosis in various cancer models (such as melanoma, gastric cancer, and acute myeloid leukemia). UNC1062 inhibits multiple pathways, including MAPK/ERK, PI3K/AKT and JAK/STAT and affects the motility of head and neck squamous cell carcinoma (HNSCC) cells through the RhoA signaling pathway. UNC1062 inhibits macrophage efferocytosis, and it suitable for research on atherosclerosis .
    UNC1062
  • HY-126858
    Ambuic acid

    (+)-Ambuic acid

    		 ERK JNK NO Synthase COX Infection Inflammation/Immunology
    Ambuic acid exhibits antimicrobial activity against Staphylococcus aureus, with IC50 of 43.9 μM for strain ATCC 6538. Ambuic acid is an inhbitor for the biosynthesis of cyclic peptide quorum sensing molecules (quormones) in gram-positive bacteria. Ambuic acid exhibits anti-inflammatory activity through ERK/JNK/MAPK signaling pathway .
    Ambuic acid
  • HY-N6576
    Hellebrigenin

    		p38 MAPK ERK JNK IAP PARP Apoptosis Caspase Cancer
    Hellebrigenin is an inhibitor that selectively targets the MAPK signaling pathway (ERK, p38, JNK) and XIAP, and can inhibit Akt expression and phosphorylation. Hellebrigenin can activate endogenous apoptosis pathways (such as mitochondrial membrane potential disruption, Caspase family activation, PARP cleavage), downregulate anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulate pro-apoptotic proteins (Bax, Bak). Hellebrigenin can also induce DNA double-strand breaks to activate the ATM pathway. Hellebrigenin can inhibit tumor cell proliferation and clone formation, and is mainly used in the study of oral squamous cell carcinoma, liver cancer and other cancers .
    Hellebrigenin
  • HY-176192
    SMU-14a

    		Toll-like Receptor (TLR) NF-κB p38 MAPK ERK IKK TNF Receptor Interleukin Related Inflammation/Immunology
    SMU-14a is a selective Toll-like receptor 3 (TLR3) inhibitor wirh an IC50 of 0.18 μM. SMU-14a reduces phosphorylation of p65, ERK, and TBK1 via NF-κB, MAPK, and IRF3 signaling pathways. SMU-14a inhibits IL-6 secretion in mouse peritoneal macrophages, downregulates TNF-α in human peripheral blood monocytes and decreases serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. SMU-14a can be used for the research of acute hepatitis .
    SMU-14a
  • HY-W010201R
    Citronellol (Standard)
    2 Publications Verification

    (±)-Citronellol (Standard); (±)-β-Citronellol (Standard)

    		 Reactive Oxygen Species (ROS) Reference Standards ERK PI3K TNF Receptor Atg8/LC3 p62 Apoptosis Necroptosis Autophagy Fungal Cardiovascular Disease Neurological Disease Cancer
    Citronellol (Standard) is the analytical standard of Citronellol. Citronellol (Standard) is an orally active inducer of apoptosis. Citronellol (Standard) can prevent oxidative stress, mitochondrial dysfunction, and apoptosis in the SH-SY5Y cell Parkinson's disease model induced by 6-OHDA by regulating the ROS-NO, MAPK/ERK, and PI3K/Akt signaling pathways. Citronellol (Standard) can induce necroptosis in human lung cancer cells through the TNF-α pathway and accumulation of ROS. Citronellol (Standard) can reduce the levels of LC-3 and p62 to regulate the autophagy pathway, inhibit oxidative stress and neuroinflammation, and thus have neuroprotective effects on Parkinson's rats. Citronellol (Standard) exhibits anti-fungal activity against Trichophyton rubrum by inhibiting ergosterol synthesis .
    Citronellol (Standard)
  • HY-145025
    ERK1/2 inhibitor 3

    		ERK Inflammation/Immunology Cancer
    ERK1/2 inhibitor 3 is a potent inhibitor of ERK1/2. Mitogen-activated protein kinase (MAPK) plays an extremely important role in the signal transduction pathway, and extracellular signal regulated kinase (ERK) is a member of the MAPK family. ERK1/2 inhibitor 3 has the potential for the research or prevention of cancer, inflammation or other proliferative diseases (extracted from patent WO2021218912A1, compound 1) .
    ERK1/2 inhibitor 3
  • HY-136778
    INH2BP

    		PARP Reactive Oxygen Species (ROS) Bcl-2 Family Caspase ERK p38 MAPK Cardiovascular Disease
    INH2BP is a poly(ADP-ribose) polymerase (PARP) inhibitor with antioxidant and anti-apoptotic activities. INH2BP reduces the production of intracellular reactive oxygen species (ROS), modulates the expression of apoptosis-related proteins such as Bax, Bcl-2 and cleaved caspase-3 and enhances cell survival through the activation of the ERK1/2 and p38 MAPK signaling pathways. INH2BP is promising for research of cardiovascular diseases .
    INH2BP
  • HY-12716
    BRL-44408

    		Adrenergic Receptor p38 MAPK Dopamine Receptor ERK Cardiovascular Disease Neurological Disease
    BRL-44408 is a selective, blood-brain barrier-permeable α2A-adrenergic receptor antagonist with a Ki value of 8.56 nM against human targets. BRL-44408 exhibits activities such as antidepressant, analgesic effects and attenuation of sepsis-induced acute lung injury by regulating the release of neurotransmitters such as norepinephrine and dopamine, or inhibiting signaling pathways including ERK1/2, p38MAPK and p65. BRL-44408 can be used in studies related to acute respiratory distress syndrome, depression and visceral pain .
    BRL-44408
  • HY-120505
    ITZ-1

    		ERK p38 MAPK Inflammation/Immunology
    ITZ-1 is an orally active and selective extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinase (MAPK) pathway inhibitor with an IC50 of 0.51 μM for inhibiting interleukin-1β (IL-1β)-induced matrix metalloproteinase-13 (MMP-13) production. ITZ-1 reduces MMP-13 expression and suppresses nitric oxide (NO)-induced chondrocyte apoptosi. ITZ-1 is promising for research of osteoarticular diseases .
    ITZ-1
  • HY-Y1322S
    Triphenyl phosphate-d15

    Celluflex TPP-d15; DHPF 005-d15; Disflamol TP-d15; Disflamoll TP-d15; NSC 57868-d15; Phenyl phosphate ((PhO)3PO)-d15; Phoscon FR 903N-d15

    		 Isotope-Labeled Compounds Environmental Pollutants ERK Indoleamine 2,3-Dioxygenase (IDO) p38 MAPK NF-κB Akt Monoamine Oxidase Mitophagy Reactive Oxygen Species (ROS) JNK PI3K PPAR Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Triphenyl phosphate-d15 is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.
    Triphenyl phosphate-d15
  • HY-119420
    Acetoxycycloheximide

    		Antibiotic Apoptosis Caspase JNK p38 MAPK TNF Receptor ERK NF-κB Mitochondrial Metabolism Inflammation/Immunology Cancer
    Acetoxycycloheximide is an antibiotic with antitumor activity. Acetoxycycloheximide a protein synthesis inhibitor. Acetoxycycloheximide significantly induces activation of procaspase-3 and subsequent apoptosis mediated by the Cytochrome c from mitochondria via activation of JNK pathway. Acetoxycycloheximide triggers the downregulation of cell surface TNF-R1 via the activation of ERK and p38 MAPK, thereby preventing activation of the NF-κB signaling pathway by TNF-α. Acetoxycycloheximide is much more toxic to female rats than to males. Acetoxycycloheximide can be used for inflammatory and immune diseases and cancers research .
    Acetoxycycloheximide
  • HY-145026
    ERK1/2 inhibitor 4

    		ERK Inflammation/Immunology Cancer
    ERK1/2 inhibitor 5 is a potent inhibitor of ERK1/2. Mitogen-activated protein kinase (MAPK) plays an extremely important role in the signal transduction pathway, and extracellular signal regulated kinase (ERK) is a member of the MAPK family. ERK1/2 inhibitor 5 has the potential for the research or prevention of cancer, inflammation or other proliferative diseases (extracted from patent WO2020238776A1) .
    ERK1/2 inhibitor 4
  • HY-145027
    ERK1/2 inhibitor 5

    		ERK Cancer
    ERK1/2 inhibitor 5 is a potent inhibitor of ERK1/2. Mitogen-activated protein kinase (MAPK) plays an extremely important role in the signal transduction pathway, and extracellular signal regulated kinase (ERK) is a member of the MAPK family. ERK1/2 inhibitor 5 has the potential for the research or prevention of cancer, inflammation or other proliferative diseases (extracted from patent WO2020238776A1) .
    ERK1/2 inhibitor 5
  • HY-120406
    PLS-123

    		Btk Akt mTOR p38 MAPK ERK CCR Apoptosis Cancer
    LPS-123 is a covalently irreversible BTK inhibitor with an IC50 of < 5 nM. LPS-123 simultaneously inhibits the catalytic activity of BTK at Tyr551 and its self-activation at Tyr223. LPS-123 inhibits phosphorylation of the AKT/mTOR and MAPK signaling pathways, activation of PLCγ2, ERK1/2, p38, AKT, and mTOR, and blocks the production of CCL3 and CCL4 chemokines. LPS-123 exhibits significant anti-proliferative activity against various B-cell lymphoma cell lines and effectively induces apoptosis via a caspase-dependent pathway. LPS-123 also demonstrates significant antitumor activity in the OCI-Ly7 xenograft model. LPS-123 can be used for lymphoma research .
    PLS-123
  • HY-178391
    SMU-037

    		ROS Kinase p38 MAPK ERK Apoptosis Cancer
    SMU-037 is an orally active and selective ROS1 inhibitor that demonstrates potent activity (IC₅₀ = 6.8 nM) and possesses the ability to penetrate the blood-brain barrier. SMU-037 shows ~25-fold selectivity over ALK, and superior sensitivity against the G2032R mutation. SMU-037 attenuates phosphorylation of ROS1 and downstream MAPK-ERK signaling pathway, leading to cell cycle arrest and apoptosis. SMU-037 effectively suppresses tumor progression in both xenograft and intracranial mouse models. SMU-037 can be used for non-small cell lung cancer (NSCLC) research .
    SMU-037

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