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AML+cell+lines

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27

Inhibitors & Agonists

1

Inhibitory Antibodies

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-15611
    KPT-185

    		CRM1 Cancer
    KPT-185 is an orally bioavailable and selective inhibitor of CRM1 and displays potent antiproliferative properties at submicromolar concentrations (IC50=100-500 nM), induces apoptosis, cell-cycle arrest, and myeloid differentiation in AML cell lines and patient blasts .
    KPT-185
  • HY-P9983
    Lintuzumab

    SGN-33; HuM-195; GLK-33 Antibody

    		 Transmembrane Glycoprotein Radionuclide-Drug Conjugates (RDCs) Inflammation/Immunology
    Lintuzumab (HUM-195) is an anti-CD33 humanized monoclonal antibody. Lintuzumab reduces the production of TNFα-induced pro-inflammatory cytokines and chemokines by AML cells. Lintuzumab promotes tumor cell killing through antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP) activities against MDR and MDR+ AML cell lines and primary AML patient samples. Lintuzumab enhances survival and reduces tumor burden in mice .
    Lintuzumab
  • HY-172581
    Clifutinib

    		FLT3 Apoptosis Ras p38 MAPK PI3K Akt JAK STAT Cancer
    Clifutinib is an orally active and selective internal tandem duplication mutation of FMS-like tyrosine kinase 3 (FLT3-ITD) inhibitor with an IC50 value of 15.1 nM. Clifutinib exerts strong antiproliferative effects on FLT3-ITD acute myeloid leukemia (AML) cell lines (MV-4-11: IC50 = 1.5 nM; MOLM-13: IC50 = 1.4 nM). Clifutinib inhibits the activity of FLT3-ITD kinase and blocks the downstream RAS/MAPK, PI3K/AKT, and JAK/STAT5 signaling pathways of FLT3. Clifutinib induces apoptosis of acute myeloid leukemia (AML) cells with FLT3-ITD mutations. Clifutinib demonstrates significant antitumor efficacy in mice bearing MV-4-11 or MOLM-13 xenografts. Clifutinib is promising for research of relapsed/refractory FLT3-ITD-positive acute myeloid leukemia .
    Clifutinib
  • HY-B1336
    Furazolidone
    3 Publications Verification

    		 Environmental Pollutants Antibiotic Bacterial Apoptosis Parasite Infection Cancer
    Furazolidone is a monoamine oxidase (MAO) inhibitor with antiproliferative, apoptosis-inducing and differentiation-promoting activities. Furazolidone may inhibit leukemia fusion protein-mediated bone marrow transformation by upregulating the stability of the tumor suppressor protein p53. Furazolidone exhibits anti-leukemic activity in acute myeloid leukemia (AML) cell lines and can be used for anti-AML research [2].
    Furazolidone
  • HY-144433
    DNMT3A-IN-1
    2 Publications Verification

    		 DNA Methyltransferase Infection
    DNMT3A-IN-1 (compound 1) is an effective and selective DNMT3A inhibitor. DNMT3A-IN-1 exhibits inhibitory activity against DNMT3A, with KI values ranging from 9.16 to 18.85 μM (AdoMet) and 11.37 to 23.34 μM (poly dI-dC). DNMT3A-IN-1 can induce apoptosis in acute myeloid leukemia (AML) cell lines (Apoptosis) .
    DNMT3A-IN-1
  • HY-148422
    Rohinitib
    1 Publications Verification

    		 Eukaryotic Initiation Factor (eIF) Apoptosis Cancer
    Rohinitib is a potent and specific eIF4A inhibitor. Rohinitib induces cell apoptosis of acute myeloid leukemia (AML) cell lines and reduces the leukemia burden of AML xenograft model. Rohinitib can be used for the research of AML .
    Rohinitib
  • HY-121725
    MM-206

    		STAT Cancer
    MM-206, a STAT3 activity inhibitor, potently inhibits the STAT3 SH2 domain-phosphopeptide interaction with IC50 of 1.2 μM. MM-206 demonstrates dose-dependent induction of apoptosis in acute myeloid leukemia (AML) cell lines .
    MM-206
  • HY-122623A
    DB818 dihydrochloride

    		Apoptosis Cancer
    DB818 dihydrochloride is the dihydrochloride salt form of DB818 (HY-122623). DB818 dihydrochloride is an inhibitor for Homeobox A9 (HOXA9). DB818 dihydrochloride reduces the formation of HOXA9-DNA complexes, inhibits the growth and induces apoptosis in AML cell lines OCI/AML3, MV4-11, and THP-1 .
    DB818 dihydrochloride
  • HY-162265A
    UCM-13369 dihydrochloride

    		Apoptosis Cancer
    UCM-13369 (Compound 4b) is a NPM1 inhibitor. UCM-13369 downregulates the pathway associated with mutant NPM1 C+, and specifically recognizes the C-end DNA-binding domain of NPM1 C+. UCM-13369 induces apoptosis in AML cell lines and primary cells. UCM-13369 can be used for leukemia research .
    UCM-13369 dihydrochloride
  • HY-142690A
    HDAC-IN-27 dihydrochloride

    		Apoptosis HDAC Cancer
    HDAC-IN-27 dihydrochloride (Compound 11h) is a potent, orally active class I HDAC-selective inhibitor with IC50 values ranging from 0.43 to 3.01 nM against HDAC1-3. HDAC-IN-27 dihydrochloride exhibits both in vivo and in vitro antitumor activity. HDAC-IN-27 dihydrochloride demonstrates significant anti-proliferative activity against acute myeloid leukemia (AML) cell lines by inducing apoptosis and histone acetylation (AcHH3 and AcHH4). HDAC-IN-27 dihydrochloride can be used for research in acute myeloid leukemia (AML) .
    HDAC-IN-27 dihydrochloride
  • HY-142690
    HDAC-IN-27

    		HDAC Apoptosis Cancer
    HDAC-IN-27 (Compound 11h) is a potent, orally active class I HDAC-selective inhibitor with IC50 values ranging from 0.43 to 3.01 nM against HDAC1-3. HDAC-IN-27 exhibits both in vivo and in vitro antitumor activity. HDAC-IN-27 demonstrates significant anti-proliferative activity against acute myeloid leukemia (AML) cell lines by inducing apoptosis and histone acetylation (AcHH3 and AcHH4). HDAC-IN-27 can be used for research in acute myeloid leukemia (AML) .
    HDAC-IN-27
  • HY-179094
    PSP-0119

    		PROTACs IRAK NF-κB Enolase Inflammation/Immunology Cancer
    PSP-0119 is a highly efficient and effective PROTAC degrader targeting IRAK4 (IC50 = 2.83 nM). PSP-0119 can inhibit IRAK4 kinase activity, NF-κβ activity, and IL-1β-induced IRAK4 phosphorylation. PSP-0119 degrades IRAK4 in FLT3-mutant AML cell lines, sparing FLT3-wild-type AML cells, FLT3-wild-type samples, and normal bone marrow. PSP-0119 downregulates alpha-enolase (eNOS) of MOLM-13 cells. PSP-0119 can be used for the study of Acute Myeloid Leukemia (AML) .
    PSP-0119
  • HY-173444
    HDAC11-IN-3

    		HDAC Transferrin Receptor Apoptosis Ferroptosis Cancer
    HDAC11-IN-3 (Compound A9) is a selective HDAC11 inhibitor (IC50: 4.1 nM). HDAC11-IN-3 has inhibitory effects on U937 and OCI-AML2 acute myeloid leukemia (AML) cell lines (IC50: 10 μM). HDAC11-IN-3 has significant anti-AML activity, inducing apoptosis, cell cycle arrest, and differentiation. HDAC11-IN-3 upregulates the iron transporters transferrin (TF) and transferrin receptor (TFRC), and activates the p62-Keap1-Nrf2-HMOX1 pathway, which together lead to increased intracellular iron levels and induce ferroptosis in AML cells. HDAC11-IN-3 can be used alone or in combination with Cytarabine (HY-13605) for AML research .
    HDAC11-IN-3
  • HY-134557
    GS87

    		GSK-3 Cancer
    GS87 is a highly specific and potent GSK3 inhibitor with IC50s of 415nM and 521nM for GSK3α and GSK3β, respectively. GS87 induces differentiation of acute myeloid leukemia (AML) cell lines by effectively activating GSK3-dependent signaling components including MAPK signaling. GS87 modulates key GSK3 target proteins involved in cell proliferation and differentiation more effectively than Lithium and SB415285 (SB). GS87 has the potential for acting as a differentiation agent for non-promyelocytic AML research .
    GS87
  • HY-155066
    FD274

    		PI3K mTOR Apoptosis Cancer
    FD274 is a highly potent PI3K/mTOR dual inhibitor with IC50s of 0.65 nM, 1.57 nM, 0.65 nM, 0.42 nM, and 2.03 nM against PI3Kα/β/γ/δ and mTOR, respectively. FD274 exhibits significant anti-proliferation of AML cell lines (HL-60 and MOLM-16). FD274 arrests HL-60 cell cycle at G1 phase and increases apoptosis. FD274 demonstrates dose-dependent inhibition of tumor growth in the HL-60 xenograft model. FD274 has the potential for acute myeloid leukemia research .
    FD274
  • HY-150025
    (4aS,8aR)-NPD-001

    		DNA Methyltransferase Apoptosis Cancer
    (4aS,8aR)-NPD-001 is a potent and allosteric inhibitor of DNMT3A. (4aS,8aR)-NPD-001 inhibits DNMT3A activity by disrupting protein-protein interactions. (4aS,8aR)-NPD-001 induces apoptosis of acute myeloid leukemia (AML) cell lines. (4aS,8aR)-NPD-001 induces differentiation of distinct AML cell lines including cells with mutated DNMT3A R882 .
    (4aS,8aR)-NPD-001
  • HY-18952A
    (Z)-SU5614

    		FLT3 Apoptosis Cancer
    (Z)-SU5614 is a potent FLT3 inhibitor and selectively induces growth arrest, apoptosis, and cell cycle arrest in Ba/F3 and AML cell lines expressing a constitutively activated FLT3 .
    (Z)-SU5614
  • HY-117690A
    dBRD9 dihydrochloride

    		PROTACs Epigenetic Reader Domain Cancer
    dBRD9 dihydrochloride is a selective BRD9 PROTAC degrader. dBRD9 dihydrochloride inhibits proliferation of AML cell lines .
    dBRD9 dihydrochloride
  • HY-162265
    UCM-13369

    		Apoptosis Cancer
    UCM-13369 (Compound 4b) is a NPM1 inhibitor. UCM-13369 downregulates the pathway associated with mutant NPM1 C+, and specifically recognizes the C-end DNA-binding domain of NPM1 C+. UCM-13369 induces apoptosis in AML cell lines and primary cells, that can be used for the research of AML .
    UCM-13369
  • HY-155529
    FD1024

    		Pim Cancer
    FD1024 is PIM inhibitor (IC50s: 1.96, 38.9, 4.17 nM for PIM1, 2, 3). FD1024 can be used for research of acute myeloid leukemia. FD1024 has strong antiproliferative activity against the tested AML cell lines, with 0.16 μM, 0.12 μM, 1.05 μM, 1.39μM for EOL-1, MV-4-11, KG-1, MOLM-16 cells. FD1024 also has antitumor efficacy in mice .
    FD1024
  • HY-132231
    FD223

    		PI3K Apoptosis Cancer
    FD223 is a potent and selective phosphoinositide 3-kinase delta (PI3Kδ) inhibitor. FD223 displays high potency (IC50=1 nM) and good selectivity over other isoforms (IC50s of 51 nM, 29 nM and 37 nM, respectively for α, β and γ). FD223 exhibits efficient inhibition of the proliferation of acute myeloid leukemia (AML) cell lines by suppressing p-AKT Ser473 thus causing G1 phase arrest during the cell cycle. FD223 has potential for the research of leukemia such as AML .
    FD223
  • HY-150797
    QA-68

    QA-68-ZU81

    		 PROTACs Epigenetic Reader Domain Inflammation/Immunology Cancer
    QA-68 (QA-68-ZU81) is an effective PROTAC-class BRD9 degrader. QA-68 can inhibit cell cycle progression and cell colony formation. QA-68 has antiproliferative activity against acute myeloid leukemia (AML) cell lines . QA-68 can be formed by a target protein ligand (red part) EA-89 (HY-170314), an E3 ubiquitin ligase ligand (blue part) Lenalidomide-I (HY-131318), and a PROTAC linker (black part) Ethyne-C2-Pip-CO-Pip-Boc (HY-170315). E3 ubiquitin ligase and linker can form Lenalidomide-ethyne-C2-Pip-CO-Pip (HY-170319).
    QA-68
  • HY-173141
    mTOR inhibitor-26

    		mTOR Cancer
    mTOR inhibitor-26 (Compound HPT-11) is an inhibitor of mTOR with an IC50 of 0.7 nM. It effectively inhibits the proliferation of AML cell lines Molm-13 and MV-4-11. mTOR inhibitor-26 exhibits antitumor activity and favorable metabolic stability, making it a promising candidate for cancer research .
    mTOR inhibitor-26
  • HY-163160
    BET-IN-23

    		Apoptosis Epigenetic Reader Domain Cancer
    Bet-in-23 (Compound 23) is a BD2-selective BET inhibitor with an IC50 of 2.9 nM. BET-IN-23 has anticancer activity and can significantly inhibit the proliferation of acute myeloid leukemia (AML) cell lines by inducing G0/G1 arrest and apoptosis in vitro .
    BET-IN-23
  • HY-155770
    FLT3-IN-20

    		FLT3 Cancer
    FLT3-IN-20 (compound 34f) is a potent FLT3 inhibitor with IC50 values of 1 and 4 nM for FLT3-D835Y and FLT3-ITD, respectively. FLT3-IN-20 has anti-proliferation efficacy in FLT3-ITD-positive AML cell lines MV4-11 and MOLM-13 (7 and 9 nM, respectively) and the MOLM-13 variant (4 nM) with the FLT3-ITD-D835Y mutation. FLT3-IN-20 can be used in research of cancer .
    FLT3-IN-20
  • HY-171334A
    P1D-34

    		PROTACs PIN1 CDK Akt c-Myc Apoptosis Reactive Oxygen Species (ROS) Cancer
    P1D-34 is a Pin1 PROTAC degrader with a DC50 value of 177 nM. P1D-34 also down-regulates Pin1 client proteins such as Cyclin D1, Rb, Mcl-1, Akt, and c-Myc. P1D-34 shows anti-proliferative activities in a panel of acute myeloid leukemia (AML) cell lines. P1D-34 induces cell DNA damage and apoptosis by releasing ROS generation. Pink: PIN1 ligand (HY-171442A), Blue: CRBN ligand (HY-14658), Black: Linker (HY-W014883) .
    P1D-34
  • HY-170576
    FLT3-IN-28

    		FLT3 STAT Apoptosis Cancer
    FLT3-IN-28 (Compound 12y) is an orally active FLT3 inhibitor with antitumor activity. FLT3-IN-28 selectively inhibits cancer cells harboring the FLT3 internal tandem duplication (ITD) mutation, with IC50 values of 85, 290, 130, 65, and 220 nM for BaF3-FLT3-ITD, BaF3-TEL-VEGFR2, MV4-11, MOLM-13, and MOLM-14 cell lines respectively (MV4-11 and MOLM-13/14 are acute myeloid leukemia (AML) cell lines carrying the FLT3-ITD mutation). Additionally, FLT3-IN-28 can downregulate the phosphorylation levels of FLT3 and STAT5 in MOLM-13 cells and induce cell cycle arrest and Apoptosis. FLT3-IN-28 has an oral bioavailability of 19.2% in SD rats and can prolong survival in a dose-dependent manner in NSG mice xenografted with MOLM-13 cells. FLT3-IN-28 holds promise for research in cancer fields related to FLT3-ITD .
    FLT3-IN-28

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