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MDM2 phosphorylation

" in MedChemExpress (MCE) Product Catalog:

9

Inhibitors & Agonists

1

Peptides

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-123954
    BTX-A51
    1 Publications Verification

    Casein Kinase inhibitor A51

    		 Casein Kinase CDK Apoptosis Cancer
    BTX-A51 (Casein Kinase inhibitor A51) is a potent and orally active casein kinase 1α (CK1α) inhibitor. BTX-A51 induces leukemia cell apoptosis, and has potent anti-leukemic activities .
    BTX-A51
  • HY-119271
    CMLD010509

    SDS-1-021

    		 c-Myc Apoptosis Cancer
    CMLD010509 (SDS-1-021) is a highly specific inhibitor of the oncogenic translation program supporting multiple myeloma (MM)-including key oncoproteins such as MYC, MDM2, CCND1, MAF, and MCL-1. CMLD010509 (SDS-1-021) shows an IC50 below 10 nM for most MM cell lines and induces apoptosis. CMLD010509 (SDS-1-021) is a potent and selective translation inhibitor through an eIF4E phosphorylation-independent mechanism .
    CMLD010509
  • HY-123955
    Casein Kinase inhibitor A86

    		Casein Kinase CDK Apoptosis Cancer
    Casein Kinase inhibitor A86 is a potent and orally active casein kinase 1α (CK1α) inhibitor. Casein Kinase inhibitor A86 also inhibits of CDK7 (TFIIH) and CDK9 (P-TEFb). Casein Kinase inhibitor A861 induces leukemia cell apoptosis, and has potent anti-leukemic activities .
    Casein Kinase inhibitor A86
  • HY-106263B
    Tyroserleutide hydrochloride

    		PTEN PDK-1 MDM-2/p53 Apoptosis Akt Cancer
    Tyroserleutide hydrochloride is a tripeptide isolated from the degradation products of porcine spleen with antitumor activity. Tyroserleutide hydrochloride can upregulate the expression of the tumor suppressor gene PTEN and inhibit the activity of AKT and PDK1. Tyroserleutide hydrochloride inhibits tumor cell proliferation and MDM2 phosphorylation by inhibiting the PI3K/AKT pathway, and also upregulates P21, P27, P53, and induces mitochondrial damage and cell apoptosis .
    Tyroserleutide hydrochloride
  • HY-159728
    PROTAC PRMT3 degrader 1

    		PROTACs Histone Methyltransferase Apoptosis Early 2 Factor (E2F) c-Myc Cancer
    PROTAC PRMT3 degrader 1 is a selective PRMT3 PROTAC degrader with a DC50 of 2.566 μM. PROTAC PRMT3 degrader 1 forms a ternary complex with MDM2 E3 ubiquitin ligase to induce proteasomal and neddylation-dependent degradation of PRMT3. PROTAC PRMT3 degrader 1 activates intrinsic apoptosis, endoplasmic reticulum stress signaling pathways. PROTAC PRMT3 degrader 1 downregulates E2F, MYC, oxidative phosphorylation pathways. PROTAC PRMT3 degrader 1 reduces cellular asymmetric dimethylarginine (ADMA) levels. PROTAC PRMT3 degrader 1 inhibits acute leukemia cell growth. PROTAC PRMT3 degrader 1 acts with glycolysis inhibitor 2-DG to reduce ATP production, induce intrinsic apoptosis, drive synergistic antiproliferative effects. PROTAC PRMT3 degrader 1 can be used for the research of acute leukemia .
    PROTAC PRMT3 degrader 1
  • HY-119271A
    (-)-CMLD010509

    (-)-SDS-1-021

    		 c-Myc Apoptosis Cancer
    (-)-CMLD010509 ((-)-SDS-1-021) is an isomer of CMLD010509 (SDS-1-021) (HY-119271). CMLD010509 (SDS-1-021) is a highly specific inhibitor of the oncogenic translation program supporting multiple myeloma (MM)-including key oncoproteins such as MYC, MDM2, CCND1, MAF, and MCL-1. CMLD010509 (SDS-1-021) shows an IC50 below 10 nM for most MM cell lines and induces apoptosis. CMLD010509 (SDS-1-021) is a potent and selective translation inhibitor through an eIF4E phosphorylation-independent mechanism .
    (-)-CMLD010509
  • HY-159732
    PRMT3-IN-4

    		Histone Methyltransferase Cancer
    PRMT3-IN-4 (intermediate 15) is a protein arginine methyltransferase 3 (PRMT3) inhibitor. PRMT3-IN-4 is an active control for HY-19715. PRMT3-IN-4 can be used to synthesize PROTACs targeting PRMT3. PRMT3-IN-4 can be used in leukemia-related research .
    PRMT3-IN-4
  • HY-122670
    VS-II-173

    		Pim Apoptosis AMPK DYRK STAT MDM-2/p53 Cancer
    VS-II-173 is a pan-Pim kinase inhibitor with IC50 values ​​of 0.07 μM and 0.02 μM for Pim1 and Pim3, respectively, and a residual activity of 46% for Pim2 at 1 μM. VS-II-173 also inhibits kinases such as HIPK2, PRK2, RSK1, DYRK1a and AMPKα1, selectively inhibiting acute myeloid leukemia (AML) cells with significantly lower toxicity to non-malignant cells (EC50 > 30 μM). VS-II-173 weakens the phosphorylation of substrates such as Stat5 (Y694), MDM2 (S166), Bad (S112), and 4E-BP1 (T37/46) by inhibiting Pim kinase-mediated signaling pathways, blocking pro-survival signals in AML cells and inducing apoptosis. VS-II-173 synergistically enhances anti-AML activity when combined with Daunorubicin (HY-13062A). VS-II-173 can be used in AML research, especially for AML with FLT3-ITD mutations and NPM1 mutations .
    VS-II-173
  • HY-183831
    GPS167

    		MDM-2/p53 PARP Caspase Apoptosis Cancer
    GPS167 is a CLK kinase inhibitor that potently and selectively inhibits recombinant human CLK1, CLK2 and CLK4. By inhibiting CLK-mediated phosphorylation of SRSF10, GPS167 upregulates the protein-binding ability of CLK1 and CLK4 with SRSF10, downregulates oncogenic BCLAF1-L and upregulates tumor-suppressive BCLAF1-S, regulates alternative splicing of genes such as MDM2 and MDM4, stabilizes p53 protein and induces DNA damage, ultimately triggering tumor cell apoptosis. GPS167 can block the epithelial-mesenchymal transition process of tumors, activate intracellular double-stranded RNA-mediated antiviral immune responses, and produce synergistic cytotoxicity when combined with microtubule-targeting drugs. GPS167 can be used in research related to various cancers including colorectal cancer .
    GPS167

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