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Pathways Recommended: MAPK/ERK Pathway Neuronal Signaling PI3K/Akt/mTOR JAK/STAT Signaling
Results for "

ERK/AKT signaling pathways

" in MedChemExpress (MCE) Product Catalog:

120

Inhibitors & Agonists

2

Screening Libraries

1

Fluorescent Dyes

1

Biochemical Assay Reagents

6

Peptides

2

Inhibitory Antibodies

40

Natural
Products

9

Isotope-Labeled Compounds

1

GMP Molecules

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N0265
    Asperosaponin VI
    3 Publications Verification

    Akebia saponin D

    		 Caspase Apoptosis PERK p38 MAPK Akt HIF/HIF Prolyl-Hydroxylase PPAR Cardiovascular Disease Neurological Disease
    Asperosaponin VI is a saponin component from Dipsacus asper. Asperosaponin VI induces osteoblast differentiation through the BMP-2/p38 and ERK1/2 signaling pathways. Asperosaponin VI protects against hypoxia-induced cardiomyocyte apoptosis by activating the PI3K/Akt and CREB pathways. Additionally, Asperosaponin VI also has antidepressant and wound-healing-promoting activities .
    Asperosaponin VI
  • HY-N0371
    Pachymic acid
    5 Publications Verification

    3-O-Acetyltumulosic acid

    		 Akt ERK Cancer
    Pachymic acid is a lanostrane-type triterpenoid from P. cocos. Pachymic acid inhibits Akt and ERK signaling pathways.
    Pachymic acid
  • HY-N0104
    Curcumol
    5+ Cited Publications

    (-)-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-N6973
    Boldine
    1 Publications Verification

    		 RANKL/RANK Apoptosis Inflammation/Immunology Cancer
    Boldine is an apomorphine isoquinoline alkaloid extracted from the root of the pheasant pepper (Litsea cubeba). Boldine is an oral effective antioxidant, anti-inflammatory, antitumor agent, and can inhibit osteoclast formation. Boldine induces apoptosis of human bladder cancer cells by regulating ERK, AKT and GSK-3β. Boldine ameliorates bone destruction by down-regulating the OPG/RANKL/RANK signaling pathway. It can be used in rheumatoid arthritis research .
    Boldine
  • HY-109041
    Razuprotafib
    4 Publications Verification

    AKB-9778

    		 Phosphatase Tie Inflammation/Immunology
    Razuprotafib (AKB-9778) is a potent and selective inhibitor of the catalytic activity of VE-PTP (vascular endothelial protein tyrosine phosphatase) with an IC50of 17 pM. Razuprotafib promotes TIE2 activation, enhances ANG1-induced TIE2 activation, and stimulates phosphorylation of signaling molecules in the TIE2 pathway, including AKT, eNOS, and ERK. Razuprotafib inhibits the structurally related phosphatase PTP1B with an IC50 of 780 nM. Razuprotafib shows excellent selectivity for VE-PTP versus a variety of phosphatases, with the exception of HPTPη (IC50=36 pM) and HPTPγ (100 pM) .
    Razuprotafib
  • HY-W008947
    SEW​2871
    5+ Cited Publications

    		 LPL Receptor ERK Akt Neurological Disease Metabolic Disease Inflammation/Immunology
    SEW2871 is an orally active, potent, highly selective S1P1 (sphingosine-1-phosphate type 1 receptor) agonist, with an EC50 of 13.8 nM. SEW2871 activates ERK, Akt, and Rac signaling pathways and induces S1P1 internalization and recycling. SEW2871 reduces lymphocyte numbers in blood. SEW2871 can be used for the research of diabetes, Alzheimer’s disease, liver fibrosis, and inflammatory responses .
    SEW​2871
  • HY-N0103
    Sophocarpine
    Maximum Cited Publications
    11 Publications Verification

    		 Autophagy Apoptosis NF-κB PI3K Akt MEK ERK PTEN Cardiovascular Disease Inflammation/Immunology Cancer
    Sophocarpine is a PTEN activator and an inhibitor of PI3K/Akt, MEK/ERK, and NF-κB signaling pathways. Sophocarpine upregulates PTEN expression and inhibits PI3K/Akt phosphorylation, arrests tumor cell cycle and induces apoptosis. Sophocarpine inhibits MEK/ERK phosphorylation and VEGF secretion, reducing tumor cell migration. Sophocarpine can also inhibit NF-κB activation and p38 and JNK phosphorylation, reduce the expression of inflammatory factors such as iNOS and COX-2, and activate the Nrf2/HO-1 pathway to reduce oxidative stress. Sophocarpine has anti-tumor, anti-inflammatory, antioxidant and anti-apoptotic effects, and can be used in the research of cancers such as glioblastoma and colorectal cancer, inflammation-related diseases, and Doxorubicin (HY-15142A)-induced cardiac damage .
    Sophocarpine
  • 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-109556
    Insulin Detemir

    		Akt ERK Metabolic Disease
    Insulin Detemir is an artificial insulin, shows effect on controlling blood sugar levels. Insulin Detemir stimulates GLP-1 secretion as a consequence of enhanced Gcg expression by a mechanism involving activation of Akt- and/or extracellular signal-regulated kinase (ERK)-dependent-cat and CREB signaling pathways. Insulin Detemir can be used for type 2 diabetes research .
    Insulin Detemir
  • 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-12494
    LDC1267
    5+ Cited Publications

    		 TAM Receptor FLT3 Neurological Disease Cancer
    LDC1267 is a AXL/TAM/FLT3 inhibitor with IC50 values of 42 nM, 130 nM, and 63 nM against AXL, MERTK, and TYRO3, respectively. LDC1267 blocks GAS6-induced AXL phosphorylation and the downstream AKT/ERK1/2 signaling pathway. LDC1267 inhibits cancer cell proliferation, colony formation, and glioblastoma cell invasion, without causing obvious impairment of cytotoxic autophagic flux. LDC1267 exerts a synergistic effect when used in combination with Imatinib (HY-15463) in chronic myeloid leukemia models. LDC1267 can be widely applied in studies related to glioblastoma and chronic myeloid leukemia .
    LDC1267
  • HY-N0231
    Bavachalcone
    2 Publications Verification

    Broussochalcone B

    		 Bacterial Antibiotic NF-κB PERK Akt Autophagy Apoptosis Infection Neurological Disease Inflammation/Immunology Cancer
    Bavachalcone is a potent inducer of apoptosis. Bavachalcone exerts anticancer activity by promoting autophagy and apoptosis in HepG2 cells. Bavachalcone acts as an anti-neuroinflammatory and antidepressant through the NF-κB pathway. Bavachalcone inhibits osteoclasts by interfering with ERK and Akt signaling pathways and the expression of c-Fos and NFATc1. Bavachalcone exhibits a significant inhibitory effect on baculovirus-expressed BACE-1 in vitro .
    Bavachalcone
  • 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-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-N7110
    6-Hydroxyflavone
    2 Publications Verification

    		 Akt ERK JNK GABA Receptor Neurological Disease Metabolic Disease Inflammation/Immunology
    6-Hydroxyflavone is an orally effective flavonoid compound. 6-Hydroxyflavone can inhibit LPS (HY-D1056) -induced NO production and has anti-inflammatory effects. 6-Hydroxyflavone promotes osteoblast differentiation by activating AKT, ERK 1/2 and JNK signaling pathways. 6-Hydroxyflavone has an inhibitory effect on bovine hemoglobin (BHb) glycosylation. 6-Hydroxyflavone has a kidney protective effect. In addition, 6-Hydroxyflavone enhances GABA-induced current through the Benzodiazepine sites of γ-aminobutyric acid (GABAA) receptors. 6-Hydroxyflavone shows a clear preference for α2 - and α3 - subtypes, which play an anti-anxiety role .
    6-Hydroxyflavone
  • 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-101364
    CHPG
    4 Publications Verification

    		 mGluR NF-κB ERK Akt Cardiovascular Disease Inflammation/Immunology
    CHPG is a selective mGluR5 agonist, and attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells . CHPG protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways .
    CHPG
  • 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-17587
    4-Methylbenzylidene camphor
    2 Publications Verification

    4-MBC; Enzacamene

    		 Apoptosis PI3K Akt ERK Metabolic Disease
    4-Methylbenzylidene camphor (4-MBC) is an endocrine disrupter that produces estrogen-like effects. 4-Methylbenzylidene camphor decreases the proliferation of human trophoblast cells and induces apoptosis. 4-Methylbenzylidene camphor activates PI3K/AKT and ERK1/2 signaling pathways and elevates intracellular ROS production. 4-Methylbenzylidene camphor is a ultraviolet (UV) filter and may hamper normal placental formation during early pregnancy .
    4-Methylbenzylidene camphor
  • HY-128393
    Trilinolein
    1 Publications Verification

    		 PI3K Akt E-Selectin Apoptosis MMP MEK ERK Cancer
    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 .
    Trilinolein
  • HY-168438
    ERBB agonist-1
    1 Publications Verification

    		 EGFR Akt ERK Cardiovascular Disease
    ERBB agonist-1 (Compound EF-1) is an agonist for ERBB4, that activates the ERBB4 signaling pathway by inducing dimerization of the ERBB4 receptor with an EC50 of 10.5 μM. ERBB agonist-1 induces phosphorylation of Akt and ERK1/2, reduces the collagen expression in cardiac fibroblasts, inhibits H2O2-induced cardiomyocyte death and Ang II (HY-13948)-induced cardiomyocyte hypertrophy. ERBB agonist-1 prevents fibrosis and exhibits cardioprotective efficacy in mouse models .
    ERBB agonist-1
  • 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-B0380A
    Trimebutine maleate

    		Opioid Receptor Toll-like Receptor (TLR) Calcium Channel Potassium Channel IRAK ERK JNK NF-κB Akt Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Trimebutine maleate is a multi-target inhibitor and opioid receptor agonist with antimuscarinic activity. Trimebutine maleate inhibits L-type Ca 2+ channels and large-conductance calcium-activated potassium channels (BKCa channels), thereby inhibiting extracellular calcium influx and potassium ion efflux. Trimebutine maleate also targets Toll-like receptors, inhibits Toll-like receptor 2/4/7/8/9 signals, and inhibits LPS-induced IRAK1 activation, as well as ERK1/2, JNK and NF-κB activation, thereby exerting anti-inflammatory effects. Trimebutine maleate also induces tumor cell apoptosis by inhibiting the AKT/ERK pathway. Trimebutine maleate also inhibits excessive contraction of smooth muscle and can be used in the study of gastrointestinal disorders such as irritable bowel syndrome (IBS) .
    Trimebutine maleate
  • HY-B0380
    Trimebutine

    		Opioid Receptor Toll-like Receptor (TLR) Calcium Channel Potassium Channel IRAK ERK JNK NF-κB Akt Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Trimebutine is a multi-target inhibitor and opioid receptor agonist with antimuscarinic activity. Trimebutine inhibits L-type Ca 2+ channels and large-conductance calcium-activated potassium channels (BKCa channels), thereby inhibiting extracellular calcium influx and potassium ion efflux. Trimebutine also targets Toll-like receptors, inhibits Toll-like receptor 2/4/7/8/9 signals, and inhibits LPS-induced IRAK1 activation, as well as ERK1/2, JNK and NF-κB activation, thereby exerting anti-inflammatory effects. Trimebutine also induces tumor cell apoptosis by inhibiting the AKT/ERK pathway. Trimebutine also inhibits excessive contraction of smooth muscle and can be used in the study of gastrointestinal disorders such as irritable bowel syndrome (IBS) .
    Trimebutine
  • HY-14604
    Xaliproden hydrochloride
    1 Publications Verification

    SR57746A; SR57746 hydrochloride

    		 5-HT Receptor Dopamine Receptor Trk Receptor PKC ERK Akt JNK Neurological Disease Metabolic Disease
    Xaliproden (SR57746) hydrochloride (SR57746A) is an orally active, highly selective 5-HT1A receptor agonist. Xaliproden hydrochloride activates pertussis toxin-sensitive G protein-coupled signaling cascades, as well as the PKC, ERK1/ERK2, Akt and p21 Ras/MEK-1 pathways. Xaliproden hydrochloride also downregulates the JNK/p66/c-Jun signaling pathway, induces phosphorylation of the shc adaptor protein, regulates extracellular dopamine and 5-HT levels, and induces [ 35S]GTPγS labeling in rat brain structures rich in 5-HT1A receptors. Xaliproden hydrochloride exerts neurotrophic, neuroprotective, renoprotective, anti-inflammatory, anti-apoptotic, anti-fibrotic and analgesic effects. Xaliproden hydrochloride also enhances NGF-induced neurite outgrowth, promotes motor neuron survival, attenuates renal tubular injury and inhibits chemotherapy-induced mechanical allodynia, without activating or altering NGF-induced TrkA receptor activation. Xaliproden hydrochloride can be used in the research of motor neuron disease, diabetic nephropathy, chemotherapy-induced peripheral neuropathy, amyotrophic lateral sclerosis, Alzheimer's disease, acute tonic nociceptive pain, inflammatory pain, depression and anxiety .
    Xaliproden hydrochloride
  • HY-19820A
    NSC45586 sodium
    1 Publications Verification

    		 Akt Ser/Thr Protease Apoptosis MMP Cardiovascular Disease Neurological Disease Inflammation/Immunology
    NSC45586 sodium is an inhibitor of PHLPP. NSC45586 sodium targets the PP2C phosphatase domains of PHLPP1 and PHLPP2, blocks the phosphatase activity of PHLPP, increases the expression level of FOXO1 in the nucleus, and reduces the protein expression of PHLPP1. NSC45586 sodium activates the AKT survival signaling pathway, enhances IGF-1-induced AKT activation, and inhibits the phosphorylation of AKT/ERK under basal conditions. NSC45586 sodium reduces staurosporine-induced neuronal death, preserves notochord cell morphology and KRT19 expression, inhibits cell apoptosis (apoptosis), improves the viability and proliferation of nucleus pulposus cells, upregulates the expression of ACAN/SOX9, and downregulates the expression of MMP13. NSC45586 sodium binds tightly to bovine serum albumin (bovine serum albumin), and exerts a more significant effect on nucleus pulposus in male individuals. NSC45586 sodium can be used in studies related to global cerebral ischemia and intervertebral disc degeneration .
    NSC45586 sodium
  • HY-N2445
    Flavokawain C
    4 Publications Verification

    		 Apoptosis Akt JNK PERK Caspase PARP MDM-2/p53 IAP Reactive Oxygen Species (ROS) SOD FABP Autophagy AMPK mTOR GLUT EGFR PI3K HSP VEGFR FAK Cancer
    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 .
    Flavokawain C
  • HY-101364A
    CHPG sodium salt
    4 Publications Verification

    		 mGluR NF-κB ERK Akt Neurological Disease Inflammation/Immunology
    CHPG sodium salt is a selective mGluR5 agonist, and attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells . CHPG sodium salt protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways. .
    CHPG sodium salt
  • 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-N7043
    Isosilybin A
    2 Publications Verification

    		 Apoptosis PPAR NF-κB p38 MAPK ERK Androgen Receptor Inflammation/Immunology Cancer
    Isosilybin A is a PPARγ agonist that can be isolated from silymarin. Isosilybin A activates extrinsic and intrinsic pathways of apoptosis through targeting of the Akt-NF-kB-AR axis. Isosilybin A can relieve the inflammatory response in the rosacea model via inhibiting Erk and p38 signaling pathways and M1 macrophage polarization, with its targets related to RELA and VEGFA. Isosilybin A has anti-prostate cancer (PCA) activity [1][2][3].
    Isosilybin A
  • 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-150795
    SY-LB-35

    		TGF-beta/Smad PI3K Akt ERK JNK Others
    SY-LB-35 is a potent bone morphogenetic protein (BMP) receptor agonist. SY-LB-35 can stimulate significant increases in cell number and cell viability in the C2C12 myoblast cell line, and causes shifts towards the S and G2/M phases of the cell cycle. SY-LB-35 stimulates canonical Smad and non-canonical PI3K/Akt, ERK, p38 and JNK intracellular signaling pathways .
    SY-LB-35
  • 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-148877
    AT-533

    		HSP HSV HIF/HIF Prolyl-Hydroxylase VEGFR NF-κB ERK Akt FAK Infection Inflammation/Immunology Cancer
    AT-533 is a potent Hsp90 and HSV inhibitor. AT-533 suppresses tumor growth and angiogenesis by blocking the HIF-1α/VEGF/VEGFR-2 signaling pathway. AT-533 also inhibits the activation of the downstream pathways, including Akt/mTOR/p70S6K, Erk1/2 and FAK. AT-533 inhibits the tube formation, cell migration, and invasion of human umbilical vein endothelial cells (HUVECs) .
    AT-533
  • 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-N4309
    Lotusine

    		Amylases Glycosidase Neurological Disease Metabolic Disease Cancer
    Lotusine is an orally active signaling pathway modulator and enzyme inhibitor, with an IC50 of 30.60 μg/mL against α-amylase and an IC50 of 36.15 μg/mL against α-glucosidase. Lotusine inhibits the EGFR-Akt-ERK signaling pathway by reducing the levels of phosphorylated EGFR, Akt and ERK. Lotusine induces apoptosis, triggers G0/G1 cell cycle arrest and inhibits cancer cell proliferation. Lotusine reduces lipid peroxidation and increases the activities of SOD, CAT and GPx. Lotusine is applicable to researches related to non-small cell lung cancer, type 2 diabetes and autism spectrum disorder .
    Lotusine
  • HY-15872
    FTI-277

    		Farnesyl Transferase Ras ERK mTOR Caspase Apoptosis Akt PI3K Bacterial Cardiovascular Disease Neurological Disease Cancer
    FTI-277 is a farnesyltransferase (FTase) inhibitor. FTI-277 inhibits Ras farnesylation, blocks the phosphorylation of downstream ERK1/2 and mTOR, and reduces membrane-bound active N-ras protein. FTI-277 activates caspase 3, upregulates Bim expression, induces cell apoptosis, suppresses regulatory T cell expansion, enhances macrophage phagocytosis, and improves bacterial clearance. FTI-277 activates the PI3K/Akt signaling pathway, inhibits osteoblast differentiation, and reduces the proliferation ability of neuroblastoma cells. FTI-277 can be used in research related to head and neck squamous cell carcinoma, neuroblastoma, sepsis, and vascular calcification .
    FTI-277
  • HY-110038
    FTI-277 TFA

    		Farnesyl Transferase Ras ERK mTOR Apoptosis Caspase Akt PI3K Bacterial Cardiovascular Disease Neurological Disease Cancer
    FTI-277 TFA is a farnesyltransferase (FTase) inhibitor. FTI-277 TFA inhibits Ras farnesylation, blocks the phosphorylation of downstream ERK1/2 and mTOR, and reduces membrane-bound active N-ras protein. FTI-277 TFA activates caspase 3, upregulates Bim expression, induces cell apoptosis, suppresses regulatory T cell expansion, enhances macrophage phagocytosis, and improves bacterial clearance. FTI-277 TFA activates the PI3K/Akt signaling pathway, inhibits osteoblast differentiation, and reduces the proliferation ability of neuroblastoma cells. FTI-277 TFA can be used in research related to head and neck squamous cell carcinoma, neuroblastoma, sepsis, and vascular calcification .
    FTI-277 TFA
  • HY-W130965
    1-Formyl-beta-carboline

    		Influenza Virus Akt Infection
    1-Formyl-beta-carboline is an alkaloid with inhibitory activity against Newcastle disease virus (NDV). 1-Formyl-beta-carboline can effectively inhibit different genotypes of NDV with IC50 values within 10 μM, and its inhibition rate is more than 90% at a concentration of 20 μM. 1-Formyl-beta-carboline mainly exerts its effects by inhibiting the adsorption and entry processes in the NDV life cycle. 1-Formyl-beta-carboline has been identified as a novel HN inhibitor that can directly interact with the NDV HN protein and affect the adsorption of NDV. 1-Formyl-beta-carboline also inhibits the entry of NDV by inhibiting the PI3K/Akt signaling pathway rather than the ERK pathway .
    1-Formyl-beta-carboline
  • HY-N0265R
    Asperosaponin VI (Standard)

    Akebia saponin D (Standard)

    		 Reference Standards Caspase Apoptosis PERK Akt p38 MAPK HIF/HIF Prolyl-Hydroxylase PPAR Cardiovascular Disease Neurological Disease
    Asperosaponin VI (Standard) is the analytical standard of Asperosaponin VI. This product is intended for research and analytical applications. Asperosaponin VI is a saponin component from Dipsacus asper. Asperosaponin VI induces osteoblast differentiation through the BMP-2/p38 and ERK1/2 signaling pathways. Asperosaponin VI protects against hypoxia-induced cardiomyocyte apoptosis by activating the PI3K/Akt and CREB pathways. Additionally, Asperosaponin VI also has antidepressant and wound-healing-promoting activities .
    Asperosaponin VI (Standard)
  • HY-169212
    I194496

    		PI3K Annexin A ERK VEGFR STAT Raf FAK Akt Ras Cancer
    I194496 is a potent cystathionine γ-lyase (CSE) inhibitor, with an IC50 of 0.79 mM. I194496 can inhibit the growth of human TNBC cells via the dual targeting PI3K/Akt and Ras/Raf/ERK pathway and suppress the metastasis of human TNBC cells via down-regulating Anxa2/STAT3 and VEGF/FAK/Paxillin signaling pathways .
    I194496
  • 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-N0103A
    Sophocarpine monohydrate
    Maximum Cited Publications
    11 Publications Verification

    		 Autophagy Apoptosis NF-κB PI3K Akt MEK ERK Cardiovascular Disease Inflammation/Immunology Cancer
    Sophocarpine monohydrate is a PTEN activator and an inhibitor of PI3K/Akt, MEK/ERK, and NF-κB signaling pathways. Sophocarpine monohydrate upregulates PTEN expression and inhibits PI3K/Akt phosphorylation, arrests tumor cell cycle and induces apoptosis. Sophocarpine monohydrate inhibits MEK/ERK phosphorylation and VEGF secretion, reducing tumor cell migration. Sophocarpine monohydrate can also inhibit NF-κB activation and p38 and JNK phosphorylation, reduce the expression of inflammatory factors such as iNOS and COX-2, and activate the Nrf2/HO-1 pathway to reduce oxidative stress. Sophocarpine monohydrate has anti-tumor, anti-inflammatory, antioxidant and anti-apoptotic effects, and can be used in the research of cancers such as glioblastoma and colorectal cancer, inflammation-related diseases, and Doxorubicin (HY-15142A)-induced cardiac damage .
    Sophocarpine monohydrate
  • 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-N6926
    1,3,5-Tricaffeoylquinic acid

    		HIV Apoptosis Caspase VEGFR ERK PI3K Akt mTOR PARP Infection Cancer
    1,3,5-Tricaffeoylquinic acid acts as an angiogenesis inhibitor and apoptosis inducer, and exhibits anti-HIV activity. 1,3,5-Tricaffeoylquinic acid inhibits the phosphorylation of VEGFR2, ERK, PI3K, Akt and mTOR in the angiogenesis signaling pathway. 1,3,5-Tricaffeoylquinic acid regulates apoptosis-related proteins, upregulates the levels of activated caspase-8, Bax, activated PARP and caspase-3/9, while downregulates the level of Bcl-2. 1,3,5-Tricaffeoylquinic acid inhibits tube formation and shows cytotoxicity against ovarian cancer cells. 1,3,5-Tricaffeoylquinic acid can be used in studies related to ovarian cancer .
    1,3,5-Tricaffeoylquinic acid
  • HY-173571
    TK-685

    		SHP2 Apoptosis Cancer
    TK-685 is an orally active, selective, and allosteric SHP2 inhibitor with an IC50 of 2.1 nM. TK-685 inhibits esophageal cancer cell proliferation and induced apoptosis by targeting SHP2-mediated AKT and ERK signaling pathways .
    TK-685
  • HY-N10133
    Licoflavanone

    3′-Prenylnaringenin

    		 Bacterial mTOR Akt PI3K NF-κB Caspase JNK ERK COX NO Synthase Apoptosis Others
    Licoflavanone (3′-Prenylnaringenin) is a flavanone with antioxidant, anti-inflammatory and anticancer activities. Licoflavanone can be isolated from the leaf extract of Glycyrrhiza glabra. Licoflavanone downregulates the mTOR/PI3K/AKT signaling pathway to inhibit the proliferation, migration and invasion of cancer cells, while activates Bax, Bad and multiple caspase enzymes to induce apoptosis. Its anti-inflammatory effect is manifested by reducing the nuclear translocation of NF-κB, decreasing the phosphorylation levels of p38, JNK and ERK1/2, thereby inhibiting the expression of nitric oxide, proinflammatory cytokines, COX-2 and iNOS. Licoflavanone is used in studies on nasopharyngeal carcinoma and related mechanisms .
    Licoflavanone
  • HY-174306
    MARY1

    		5-HT Receptor PGC-1α Akt PI3K Ras MEK ERK Metabolic Disease
    MARY1 is a selective 5-HT2BR antagonist with an IC50 of 380 nM and a Ki of 764 nM (human 5-HT2BR). MARY1 induces renal mitochondrial biogenesis (MB) and enhances renal mitochondrial function by increasing mitochondrial respiratory capacity, mitochondrial protein levels, and mitochondrial number in renal proximal tubular cells (RPTCs). MARY1 induces MB through 5-HT2BR and dual PI3K/AKT and RAS/MEK/ERK cell signaling pathways in RPTCs. MARY1 can be used to study renal diseases associated with metabolic and mitochondrial dysfunction .
    MARY1
  • HY-163709
    PROTAC FAK degrader 2

    		PROTACs FAK Akt ERK 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 .
    PROTAC FAK degrader 2
  • 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

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