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Pathways Recommended: MAPK/ERK Pathway
Results for "

ERK and RAS inhibitor

" in MedChemExpress (MCE) Product Catalog:

56

Inhibitors & Agonists

1

Fluorescent Dyes

1

Biochemical Assay Reagents

1

Peptides

7

Natural
Products

2

Isotope-Labeled Compounds

1

GMP Molecules

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-50846
    SCH772984
    Maximum Cited Publications
    182 Publications Verification

    		 ERK Cancer
    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-156498
    RMC-7977
    10+ Cited Publications

    		 Ras ERK Raf Ribosomal S6 Kinase (RSK) AMPK Apoptosis PARP Cancer
    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 KRAS G12C cancer models, and demonstrates good tolerability across various RAS cancer models .
    RMC-7977
  • HY-153346
    Elironrasib
    2 Publications Verification

    RMC-6291

    		 Ras ERK Apoptosis Cancer
    Elironrasib is an orally active and covalent inhibitor of KRAS G12C(ON). Elironrasib forms a tri-complex within tumor cells between KRAS G12C(ON) and cyclophilin A (CypA). Thus, Elironrasib prevents KRAS G12C(ON) from signaling via steric blockade of RAS effector binding. Elironrasib inhibits ERK signaling and induced apoptosis in KRASG12C-mutant H358 cells. Elironrasib also inhibits the proliferation of KRAS G12C mutant cells with a median IC50 of 0.11 nM .
    Elironrasib
  • 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-156002
    LUNA18

    Paluratide

    		 Ras ERK Cancer
    LUNA18 is an orally-available cyclic peptide KRAS and ERK inhibitor. LUNA18 phosphorylates ERK and AKT and decreases cell proliferation in RAS-mutated cancer cells. LUNA18 exhibits RAS signal inhibition and potent anti-cancer activities through inhibiting interaction between RAS and guanine nucleotide exchange factors (GEFs) in a mouse xenograft model. LUNA18 shows significant cellular efficacy against cell lines with KRAS genetic alterations, such as colon cancer, stomach cancer, non-small cell lung cancer and pancreaticcancer .
    LUNA18
  • HY-101494
    Temuterkib
    30+ Cited Publications

    LY3214996

    		 ERK Cancer
    Temuterkib (LY3214996) is a highly selective inhibitor of ERK1 and ERK2, with IC50 of 5 nM for both enzymes in biochemical assays. Temuterkib potently inhibits cellular p-RSK1 in BRAF and RAS mutant cancer cell lines. Temuterkib shows potent antitumor activities in cancer models with MAPK pathway alterations.
    Temuterkib
  • HY-100388
    SHP099
    70+ Cited Publications

    		 SHP2 Phosphatase Cancer
    SHP099 is an allosteric SHP2 inhibitor, with IC50s of 0.690, 1.241, 0.416, 1.968, 2.896 μM for SHP2, SHP2 D61Y, SHP2E69K, SHP2 A72V, SHP2 E76K. SHP099 inhibits cancer cell growth, such as MV4-11 and TF-1 cell (IC50: 0.32 and 1.73 μM). SHP099 inhibits RAS-ERK signaling and inhibits tumor growth .
    SHP099
  • HY-136579
    ASN007
    5 Publications Verification

    ERK-IN-3

    		 ERK Cancer
    ASN007 (ERK-IN-3) is a potent and orally active inhibitor of ERK. ASN007 inhibits ERK1/2 with low single-digit nM IC50 values. ASN007 exhibits significant anti proliferative activity against various tumor cells. ASN007 can be used for the research of cancers driven by RAS mutations .
    ASN007
  • HY-132844
    Tunlametinib

    HL-085

    		 MEK Cancer
    Tunlametinib is a highly selective, orally active MEK1/2 inhibitor (IC50=1.9 nM, MEK1). Tunlametinib blocks the RAS-RAF-MEK-ERK signaling pathway, arrests tumor cell cycle and promotes apoptosis. Tunlametinib potently inhibits the proliferation of RAS/RAF mutant cancer cells (such as BRAF V600E, KRAS G12C mutant cells). Tunlametinib shows synergistic anti-tumor effects with BRAF/KRASG12C/SHP2 inhibitors, Docetaxel (HY-B0011). Tunlametinib can be used to study targeted therapy for RAS/RAF mutation-driven malignancies (such as melanoma, colorectal cancer, and non-small cell lung cancer) .
    Tunlametinib
  • HY-N6796
    Manumycin A
    2 Publications Verification

    		 Antibiotic Exosomes Farnesyl Transferase Ras Apoptosis Phospholipase TNF Receptor Atg8/LC3 Infection Inflammation/Immunology Cancer
    Manumycin A is a polyketide antibiotic and an inhibitor of thioredoxin reductase 1 (TrxR-1). Manumycin A can inhibit the growth of breast cancer cells and exert its anti-tumor activity through LC3. Manumycin A can downregulate the release of pro-inflammatory cytokines in human monocytes stimulated by TNF α, and has potential anti-inflammatory activity. Manumycin A can inhibit the Ras/Raf/ERK1/2 signaling and hnRNP H1 in castration resistant prostate cancer cells to suppress exosome biogenesis and secretion .
    Manumycin A
  • HY-B0766
    Bicyclol

    SY801

    		 Autophagy Apoptosis HBV HCV HSP Reactive Oxygen Species (ROS) Bcl-2 Family Glutathione S-transferase p38 MAPK NF-κB Microtubule/Tubulin ERK JNK TNF Receptor Interleukin Related CDK Cyclin G-associated Kinase (GAK) mTOR P-glycoprotein Ferroptosis Infection Inflammation/Immunology Cancer
    Bicyclol (SY801) is an orally active derivative of the traditional Chinese medicine Schisandra chinensis, which has antiviral, anti-inflammatory, immunomodulatory, antioxidant, anti-steatosis, anti-fibrotic and anti-tumor activities. Bicyclol regulates the expression of heat shock proteins and plays an anti-apoptosis role in hepatocytes. Bicyclol reduces the activation of NF-κB and the levels of inflammatory factors in hepatocytes infected with hepatitis C virus (HCV) by inhibiting the activation of the ROS-MAPK-NF-κB pathway, and prevents ferroptosis in acute liver injury. Bicyclol can change the expression of Mdr-1, GSH/GST and Bcl-2, increase the intracellular concentration of anticancer drugs, and sensitize drug-resistant cells to anticancer drugs. Bicyclol inhibits the proliferation of human malignant hepatoma cells by regulating the PI3K/AKT pathway and the Ras/Raf/MEK/ERK pathway. Bicyclol can be used in the study of chronic hepatitis, acute liver injury, nonalcoholic fatty liver disease, liver fibrosis and hepatocellular carcinoma .
    Bicyclol
  • HY-141523
    Vociprotafib

    RMC-4630; SHP2-IN-7

    		 SHP2 Phosphatase Cancer
    Vociprotafib (RMC-4630) is an orally active, selective and potent phosphatase SHP2 inhibitor, which blocks activation of the RAS-RAF-MEK-ERK signaling pathway with antitumor activity. Vociprotafib accelerates the time to, and increases the magnitude of, tumor regressions in Osimertinib (HY-15772)-sensitive EGFR-mutant tumors of mice .
    Vociprotafib
  • HY-N6670
    Cefotetan

    		Antibiotic Raf ERK Ras MEK Bacterial Infection
    Cefotetan is a binding agent that targets human Raf1 kinase inhibitor protein (hRKIP). Cefotetan binds to hRKIP, reduces the binding space between hRKIP and Raf1 kinase, relieves hRKIP's inhibition of the Ras/Raf1/MEK/ERK signaling pathway, and enhances ERK phosphorylation. Cefotetan can be used to study diseases associated with dysregulated Ras/Raf1/MEK/ERK signaling pathways. Cefotetan is also a broad-spectrum antibacterial agent that disrupts cell wall synthesis by binding to bacterial penicillin-binding proteins (PBPs). It is used to study bacterial infections such as bone, skin, urinary tract, and lower respiratory tract .
    Cefotetan
  • HY-107753
    XRP44X

    		Ras Inflammation/Immunology Cancer
    XRP44X inhibits Ras-induced transcription activation with the IC50 of 10 nM. XRP44X inhibits activation of the Ras-Erk-1/2 pathway by FGF-2 . XRP44X is an inhibitor of Ras/Erk activation of Elk3 that also affects microtubules .
    XRP44X
  • HY-202699
    SHOC2-RAS PPI-IN-1

    		Ras p38 MAPK PERK MEK Cancer
    SHOC2-RAS PPI-IN-1 is a SHOC2-NRAS interaction inhibitor with IC50 of 0.048 μM and a Kd of 0.065 μM for SHOC2. SHOC2-RAS PPI-IN-1 inhibits RAS/MAPK signalling and downregulates MEK and ERK phosphorylation. SHOC2-RAS PPI-IN-1 can inhibit cells proliferation in RAS-mutant cancer models. SHOC2-RAS PPI-IN-1 can be used for the research of RAS-mutant cancers .
    SHOC2-RAS PPI-IN-1
  • HY-N9330
    Broussoflavonol F

    		Xanthine Oxidase Ras EGFR MEK PERK Apoptosis Cancer
    Broussoflavonol F is a potent dual inhibitor of the HER2-RAS-MEK-ERK signaling pathway and mushroom tyrosinase with an IC50 value of 82.3 μM. Broussoflavonol F downregulates the expression of RAS, HER2, phosphorylated BRAF, phosphorylated MEK and phosphorylated Erk proteins. Broussoflavonol F induces cell cycle arrest and apoptosis, and exhibits cytotoxicity in colon cancer cells. Broussoflavonol F inhibits endothelial proliferation, migration and tube formation, suppresses subintestinal vascular development, and reduces the mRNA levels of angiogenesis-associated genes.Broussoflavonol F can be used for colon cancer research .
    Broussoflavonol F
  • 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-N1374
    Magnolin
    2 Publications Verification

    		 ERK Inflammation/Immunology
    Magnolin, a major component of Magnolia liliiflora, inhibits the Ras/ERKs/RSK2 signaling axis by targeting the active pocket of ERK1 and ERK2 with IC50s of 87 nM and 16.5 nM, respectively.
    Magnolin
  • 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-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-136579A
    ASN007 benzenesulfonate
    5 Publications Verification

    ERK-IN-3 benzenesulfonate

    		 ERK Cancer
    ASN007 (ERK-IN-3) benzenesulfonate is a potent and orally active inhibitor of ERK. ASN007 benzenesulfonate inhibits ERK1/2 with low single-digit nM IC50 values. ASN007 benzenesulfonate exhibits significant anti proliferative activity against various tumor cells. ASN007 benzenesulfonate can be used for the research of cancers driven by RAS mutations .
    ASN007 benzenesulfonate
  • 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-120793
    CMC2.24

    TRB-N0224

    		 Ras Apoptosis MMP Inflammation/Immunology Cancer
    CMC2.24 (TRB-N0224), an orally active tricarbonylmethane agent, is effective against pancreatic tumor in mice by inhibiting Ras activation and its downstream effector ERK1/2 pathway. CMC2.24 is also a potent inhibitor of zinc-dependent MMPs with IC50s ranging from 2.0-69 μM. CMC2.24 alleviates osteoarthritis progression by restoring cartilage homeostasis and inhibiting chondrocyte apoptosis via the NF-κB/HIF-2α axis .
    CMC2.24
  • 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-159591
    YK-8S

    		Ras Akt ERK Cancer
    YK-8S is a dual-targeted K-Ras (G12D/G12C) covalent inhibitor. YK-8S shows no significant binding to wild-type K-Ras and other mutants (G12R, G13D, Q61R/K). YK-8S exhibits anti-proliferative activity against H358 (G12C) and AGS (G12D) cells. YK-8S inhibits the phosphorylation of p-AKT/p-ERK in BaF3/G12D and G12C cells. YK-8S can be used for pancreatic cancer, colorectal cancer and other tumors with high incidence of G12D .
    YK-8S
  • HY-178211
    SHY-867

    		Ras MEK ERK Akt Cancer
    SHY-867 is a pan RAS inhibitor. SHY-867 effectively prevents the binding of K-Ras proteins and other members of the Ras superfamily of small GTPases with EC50 values of 0.5-3 μM. SHY-867 effectively inhibits the phosphorylation of MEK, ERK1/2, and AKT downstream of K-Ras. SHY-867 inhibits the formation of the Ras-GTP activity complex. SHY-867 can be used to the studies of pancreatic cancer and non-small cell lung cancer .
    SHY-867
  • HY-124514
    UC-857993

    		SOS1 Ras ERK Cancer
    UC-857993 is a selective SOS1-Ras inhibitor (Kd=14.7 μM, His6-SOS1cat), suppressing catalytic activity. UC-857993 also inhibits ERK and Ras activation, suppresses the growth of mouse embryonic fibroblasts (MEFs) .
    UC-857993
  • HY-178194
    SHY-855

    		Ras MEK ERK Akt Cancer
    SHY-855 is a pan RAS inhibitor. SHY-855 effectively prevents the binding of K-Ras proteins and other members of the Ras superfamily of small GTPases with IC50 values of 0.3-5 μM. SHY-855 effectively inhibits the phosphorylation of MEK, ERK1/2, and AKT downstream of K-Ras. SHY-855 inhibits the formation of the Ras-GTP activity complex. SHY-855 can be used to the studies of pancreatic cancer and non-small cell lung cancer .
    SHY-855
  • HY-162460
    ERK1/2 inhibitor 10

    		ERK Cancer
    ERK1/2 inhibitor 10 (Compound 36c) is a potent ERK1 and ERK2 inhibitor (IC50: 0.11 and 0.08 nM respectively). ERK1/2 inhibitor 10 inhibits ERK1/2 and blocks the phosphorylation expression of their downstream substrates p90RSK and c-Myc. ERK1/2 inhibitor 10 induces cell apoptosis and incomplete autophagy-related cell death. ERK1/2 inhibitor 10 shows potent antitumor efficacy against triple-negative breast cancer and colorectal cancer models harboring BRAF and RAS mutations .
    ERK1/2 inhibitor 10
  • HY-157740
    XSJ-10

    		HDAC Cancer
    XSJ-10 is a HDAC inhibitor containing a RAS/RAF protein interfering unit, with IC50s of 0.05 and 0.04 μM in PANC-1 cells and HT-29 cells. XSJ-10 can effectively induce the apoptosis of cancer cells and suppress the tumor by strongly inhibiting the RAS-RAF-MEK-ERK signaling pathway and the acetylation level of HDAC3 .
    XSJ-10
  • HY-181067
    IK-595

    		MEK ERK Cancer
    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-149710
    POP-3MB

    		ICMT ERK Cancer
    POP-3MB (compound 1b) is an ICMT inhibitor (IC50: 2.5 μM). POP-3MB changes the subcellular localization of K-Ras and inhibits Ras activation. POP-3MB also inhibits Erk phosphorylation .
    POP-3MB
  • HY-N1374R
    Magnolin (Standard)

    		Reference Standards ERK Inflammation/Immunology
    Magnolin (Standard) is the analytical standard of Magnolin. This product is intended for research and analytical applications. Magnolin, a major component of Magnolia liliiflora, inhibits the Ras/ERKs/RSK2 signaling axis by targeting the active pocket of ERK1 and ERK2 with IC50s of 87 nM and 16.5 nM, respectively.
    Magnolin (Standard)
  • HY-164389
    SML-10-70-1

    		Ras Cancer
    SML-10-70-1 is a ligand for RAS, which covalently modifies the K-Ras G12C mutant protein, and inhibits the phosphorylation of ERK and Akt. SML-10-70-1 inhibits the proliferation of cancer cells H23, H358 and A549 with IC50 of 26.6-47.6 μM .
    SML-10-70-1
  • HY-122241
    MT477

    		PKC Cancer
    MT477 is a potent protein kinase C (PKC) inhibitor. MT477 induces apoptosis and necrosis. MT477 decreases the protein expression of Ras-GTP, p-Erk1/2, p-Elk1. MT477 shows antitumor activity .
    MT477
  • HY-170550
    KRAS G12C inhibitor 69

    		Ras ERK Cancer
    KRAS G12C inhibitor 69 (Compound K09) is the inhibitor for mutant RAS protein KRASG12C with an IC50 of 4.36 nM. KRAS G12C inhibitor 69 inhibits the ERK phosphorylation in NCI-H358 and MIA-PACA-2 with an IC50 of 12 nM and 7 nM. KRAS G12C inhibitor 69 inhibits the proliferation of cancer cell NCI-H358 and MIA-PACA-2 with IC50 of 3.15 nM and 2.33 nM .
    KRAS G12C inhibitor 69
  • HY-128393S1
    Trilinolein-13C54

    		Isotope-Labeled Compounds PI3K Akt E-Selectin Apoptosis MMP MEK ERK Cancer
    Trilinolein- 13C54 is the 13C-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 .
    Trilinolein-13C54
  • HY-128393R
    Trilinolein (Standard)

    		Reference Standards PI3K Akt E-Selectin Apoptosis MMP MEK ERK Cancer
    Trilinolein (Standard) is the analytical standard of Trilinolein (HY-128393). This product is intended for research and analytical applications. 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 (Standard)
  • HY-149539
    PLM-101

    		FLT3 RET Cancer
    PLM-101 is an orally available anticancer agent targeting FLT3 and RET with inhibitory activity against acute myeloid leukemia cells. PLM-101 inhibits RET, thereby inducing autophagic degradation of FLT3; and it inhibits the PI3K and Ras/ERK pathways, resulting in anti-leukemia activity. PLM-101 has anti-tumor efficacy in a mouse MV4-11 flank xenograft model (dose: 3, 10 mg/kg; po) and an allogeneic xenograft mouse model (dose: 40 mg/kg; po) .
    PLM-101
  • HY-100388R
    SHP099 (Standard)

    		SHP2 Reference Standards Phosphatase Cancer
    SHP099 (Standard) is the analytical standard of SHP099. This product is intended for research and analytical applications. SHP099 is an allosteric SHP2 inhibitor, with IC50s of 0.690, 1.241, 0.416, 1.968, 2.896 μM for SHP2, SHP2D61Y, SHP2E69K, SHP2A72V, SHP2E76K. SHP099 inhibits cancer cell growth, such as MV4-11 and TF-1 cell (IC50: 0.32 and 1.73 μM). SHP099 inhibits RAS-ERK signaling and inhibits tumor growth .
    SHP099 (Standard)
  • HY-119820
    Xaliproden free base

    SR57746A free base

    		 Akt Dopamine Receptor Trk Receptor 5-HT Receptor PKC JNK ERK Neurological Disease
    Xaliproden (SR57746) free base is an orally active, highly selective 5-HT1A receptor agonist. Xaliproden free base activates pertussis toxin-sensitive G protein-coupled signaling cascades, as well as the PKC, ERK1/ERK2, Akt and p21 Ras/MEK-1 pathways. Xaliproden free base 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 free base exerts neurotrophic, neuroprotective, renoprotective, anti-inflammatory, anti-apoptotic, anti-fibrotic and analgesic effects. Xaliproden free base 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 free base 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 free base
  • HY-10966R
    SB-590885 (Standard)
    5+ Cited Publications

    		 Reference Standards Raf Apoptosis Cancer
    SB-590885 (Standard) is the analytical standard of SB-590885 (HY-10966). This product is intended for research and analytical applications. 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 (Standard)
  • HY-107753R
    XRP44X (Standard)

    		Reference Standards Ras Inflammation/Immunology Cancer
    XRP44X (Standard) is the analytical standard of XRP44X (HY-107753). This product is intended for research and analytical applications. XRP44X inhibits Ras-induced transcription activation with the IC50 of 10 nM. XRP44X inhibits activation of the Ras-Erk-1/2 pathway by FGF-2 . XRP44X is an inhibitor of Ras/Erk activation of Elk3 that also affects microtubules .
    XRP44X (Standard)
  • HY-134505
    Avicin G

    		Ras Phospholipase ERK Akt Cancer
    Avicin G is a sphingomyelinase inhibitor and plasma membrane disruptor. Avicin G inhibits the enzymatic activities of neutral sphingomyelinases (SMPD2/3) and acid sphingomyelinase (SMPD1), elevates intracellular sphingomyelin levels, and alters the distribution of sphingomyelin. Avicin G interferes with the lateral segregation of GTP- and GDP-bound H-Ras, inhibits the signal output of oncogenic K-Ras and H-Ras, reduces the phosphorylation of ERK and Akt, increases lysosomal pH, and inhibits the endocytic recycling of epidermal growth factor receptor. Avicin G can be used in research related to pancreatic ductal adenocarcinoma and non-small cell lung cancer .
    Avicin G
  • HY-101494R
    Temuterkib (Standard)

    LY3214996 (Standard)

    		 ERK Reference Standards Cancer
    Temuterkib (Standard) is the analytical standard of Temuterkib (HY-101494). This product is intended for research and analytical applications. Temuterkib (LY3214996) is a highly selective inhibitor of ERK1 and ERK2, with IC50 of 5 nM for both enzymes in biochemical assays. Temuterkib potently inhibits cellular p-RSK1 in BRAF and RAS mutant cancer cell lines. Temuterkib shows potent antitumor activities in cancer models with MAPK pathway alterations.
    Temuterkib (Standard)
  • HY-175870A
    (7R)-Eras-4001

    		Ras ERK Cancer
    (7R)-Eras-4001 is an orally active KRAS mutant inhibitor with remarkable selectivity for H-RAS and N-RAS. (7R)-Eras-4001 effectively suppresses cancer cell viability by blocking downstream signaling pathways mediated by RAF family proteins, inhibiting the formation of the KRAS G12D-RAF1 RBD complex and the phosphorylation of ERK1/2. (7R)-Eras-4001 induces tumor growth inhibition and regression in a dose-dependent manner, and also reduces plasma ERK1/2 phosphorylation levels. (7R)-Eras-4001 exerts a synergistic effect with anti-PD-1 Cetuximab (HY-P9905). (7R)-Eras-4001 can be used in research on non-small cell lung cancer, pancreatic cancer, colorectal cancer, and ovarian cancer .
    (7R)-Eras-4001
  • HY-182899
    DPAP

    		PERK Ras COX PD-1/PD-L1 Apoptosis DNA/RNA Synthesis Mitochondrial Metabolism Cancer
    DPAP is a p-ERK1/2 inhibitor with an IC50 of 7.85 μM against p-ERK1/2. DPAP inhibits the expression of p-MEK1/2 and disrupts the Ras-ERK signaling pathway. DPAP inhibits the expression of COX-2 in nerve cells. DPAP damages DNA and mitochondria, induces Apoptosis via the mitochondrial pathway, and upregulates PD-L1. DPAP inhibits melanoma metastasis and angiogenesis, and inactivates spinal microglia and astrocytes. DPAP exhibits anti-melanoma activity and can be combined with anti-PD-1 monoclonal antibodies to modify anti-tumor effects. DPAP is applicable for the research of melanoma .
    DPAP
  • HY-128393S2
    Trilinolein-d5

    		Isotope-Labeled Compounds PI3K Apoptosis ERK MMP Akt MEK E-Selectin Cancer
    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 .
    Trilinolein-d5
  • HY-183365
    SL43

    		SOS1 Ras p38 MAPK ERK MEK Apoptosis Cancer
    SL43 is an orally active and potent SOS1 inhibitor with a Kd of 0.16 μM. SL43 disrupts SOS1-KRAS interaction, inhibits SOS1-mediated nucleotide exchange on KRAS mutants, and suppresses RAS-MAPK signaling. SL43 exerts antiproliferative activity against KRAS-mutant cancer cells, induces early apoptosis and G1 phase cell cycle arrest, and reduces phosphorylated MEK and ERK levels. SL43 suppresses tumor growth in a colorectal cancer xenograft model .
    SL43

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