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AKT+inhibitor

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75

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-10358
    MK-2206 dihydrochloride
    Maximum Cited Publications
    462 Publications Verification

    MK-2206 (2HCl)

    		 Bcl-2 Family Apoptosis mTOR Akt GSK-3 Cardiovascular Disease Inflammation/Immunology Cancer
    MK-2206 dihydrochloride (MK-2206 2HCl) is an orally active pan-AKT inhibitor, with IC50 values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 dihydrochloride inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 dihydrochloride induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 dihydrochloride causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 dihydrochloride can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .
    MK-2206 dihydrochloride
  • HY-15186
    Ipatasertib
    55+ Cited Publications

    GDC-0068; RG7440

    		 Organoid Akt Apoptosis Cancer
    Ipatasertib (GDC-0068) is an orally active, highly selective and ATP-competitive pan-Akt inhibitor with IC50 values of 5, 18, 8 nM for Akt1/2/3, respectively. Ipatasertib synchronously activates FoxO3a and NF-κB through inhibition of Akt leading to p53-independent activation of PUMA. Ipatasertib also induces apoptosis in cancer cells and inhibits tumor growth in xenograft mouse models .
    Ipatasertib
  • HY-108232
    MK-2206
    Maximum Cited Publications
    462 Publications Verification

    		 Bcl-2 Family Apoptosis mTOR Akt GSK-3 Metabolic Disease Inflammation/Immunology Cancer
    MK-2206 is an orally active pan-AKT inhibitor, with IC50 values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .
    MK-2206
  • HY-10355
    AKT inhibitor VIII
    55+ Cited Publications

    AKTi-1/2

    		 Akt Apoptosis Metabolic Disease Cancer
    AKT inhibitor VIII (AKTi-1/2) is a cell-permeable quinoxaline compound that has been shown to potently, selectively, allosterically, and reversibly inhibit Akt1, Akt2, and Akt3 activity with IC50s of 58 nM, 210 nM, and 2119 nM, respectively.
    AKT inhibitor VIII
  • HY-15965
    Uprosertib
    15+ Cited Publications

    GSK2141795

    		 Akt Cancer
    Uprosertib (GSK2141795) is a potent and selective pan-Akt inhibitor with IC50 values of 180/328/38 nM for Akt1/Akt2/Akt3, respectively.
    Uprosertib
  • HY-19719
    Miransertib
    15+ Cited Publications

    ARQ-092

    		 Akt Parasite Infection Cancer
    Miransertib (ARQ-092) is a potent, orally active, selective and allosteric Akt inhibitor with IC50s of 2.7 nM, 14 nM and 8.1 nM for Akt1, Akt2, Akt3, respectively. Miransertib is also a potent the AKT1-E17K mutant protein inhibitor and has the potential for PI3K/AKT-driven tumors and Proteus syndrome research . Miransertib is effective against Leishmania .
    Miransertib
  • HY-10249
    GSK-690693
    40+ Cited Publications

    		 Akt AMPK Autophagy Cancer
    GSK-690693 is an ATP-competitive pan-Akt inhibitor with IC50s of 2 nM, 13 nM, 9 nM for Akt1, Akt2 and Akt3, respectively. GSK-690693 is also an AMPK inhibitor, affects Unc-51-like autophagy activating kinase 1 (ULK1) activity and robustly inhibits STING-dependent IRF3 activation .
    GSK-690693
  • HY-133120
    INY-03-041
    1 Publications Verification

    		 PROTACs Akt Cancer
    INY-03-041 is a potent, highly selective and PROTAC-based pan-AKT degrader consisting of the ATP-competitive AKT inhibitor Ipatasertib (HY-15186) conjugated to Lenalidomide (HY-A0003, Cereblon ligand). INY-03-041 inhibits AKT1, AKT2 and AKT3 with IC50s of 2.0, 6.8 and 3.5 nM, respectively .
    INY-03-041
  • HY-50909
    Perifosine
    15+ Cited Publications

    KRX-0401; NSC 639966; D21266

    		 Akt Autophagy Apoptosis Cancer
    Perifosine is an oral Akt inhibitor which inhibits proliferation of different tumor cell lines with IC50s of 0.6-8.9 μM.
    Perifosine
  • HY-10425
    Rizavasertib
    10+ Cited Publications

    A-443654

    		 Akt Cancer
    A-443654 is a pan-Akt inhibitor and has equal potency against Akt1, Akt2, or Akt3 within cells (Ki=160 pM) .
    Rizavasertib
  • HY-101984
    N6,N6-Dimethyladenosine
    4 Publications Verification

    		 Nucleoside Antimetabolite/Analog Adenosine Receptor Akt SARS-CoV Infection Cancer
    N6,N6-Dimethyladenosine, a modified ribonucleoside, is an endogenous A3 adenosine receptor ligand. N6,N6-Dimethyladenosine is an AKT inhibitor with antitumor effects. N6, N6-Dimethyladenosine targets SARS-CoV-2 entry protein ADAM17. N6, N6-Dimethyladenosine robustly inhibits AKT signaling in a variety of non-small cell lung cancer cell lines .
    N6,N6-Dimethyladenosine
  • HY-151504
    Engasertib
    2 Publications Verification

    ALM301

    		 Akt Cancer
    Engasertib is an orally active highly specific AKT inhibitor with IC50 values of 0.13 µM, 0.09 µM and 2.75 µM for AKT1, AKT2 and AKT3, respectively. Engasertib inhibits AKT phosphorylation and modulates downstream signalling in vitro. Engasertib can inhibit cancer cell proliferation and tumor growth .
    Engasertib
  • HY-19934
    Pifusertib

    TAS-117

    		 Akt Apoptosis Autophagy Cancer
    Pifusertib (TAS-117) is a potent, selective, orally active allosteric Akt inhibitor (with IC50s of 4.8, 1.6, and 44 nM for Akt1, 2, and 3, respectively). Pifusertib triggers anti-myeloma activities and enhances fatal endoplasmic reticulum (ER) stress induced by proteasome inhibition. Pifusertib induces apoptosis and autophagy .
    Pifusertib
  • HY-N0534
    Vitexin-2"-O-rhamnoside

    		DNA/RNA Synthesis Apoptosis PI3K Akt Caspase SOD Interleukin Related Cardiovascular Disease Inflammation/Immunology Cancer
    Vitexin-2"-O-rhamnoside is an orally active flavonoid glycoside. Vitexin-2"-O-rhamnoside inhibits Apoptosis, increases the phosphorylation levels of PI3K/Akt, inhibits caspase-3, SOD activity, and promotes cytokine (IL-2, IL-6, and IL-12) secretion. Vitexin-2"-O-rhamnoside strongly inhibits DNA synthesis in MCF-7 cells with an IC50 of 17.5 μM. Vitexin-2"-O-rhamnoside enhances immune function and improves the absorption of active compounds. Vitexin-2"-O-rhamnoside has antioxidant activity. Vitexin-2"-O-rhamnoside is used in the study of cardiovascular disease and immune-related diseases .
    Vitexin-2
  • HY-19832
    SC66
    5 Publications Verification

    		 MOFs Akt Apoptosis Cancer
    SC66 is an Akt inhibitor, reduces cell viability in a dose- and time-dependent manner, inhibits colony formation and induces apoptosis in hepatocellular carcinoma (HCC) cells.
    SC66
  • HY-15186A
    Ipatasertib dihydrochloride
    55+ Cited Publications

    GDC-0068 dihydrochloride; RG-7440 dihydrochloride

    		 Organoid Akt Cancer
    Ipatasertib dihydrochloride (GDC-0068 dihydrochloride) is a highly selective and ATP-competitive pan-Akt inhibitor with IC50s of 5, 18 and 8 nM for Akt1, Akt2 and Akt3, respectively.
    Ipatasertib dihydrochloride
  • HY-40351
    4-Chloro-7H-pyrrolo[2,3-d]pyrimidine

    		Drug Intermediate Others
    4-Chloro-7H-pyrrolo[2,3-d]pyrimidine is a nitrogen-containing heterocyclic organic synthesis intermediate that can be used for the synthesis of JAK and PKB/Akt inhibitors .
    4-Chloro-7H-pyrrolo[2,3-d]pyrimidine
  • HY-132302
    Hu7691

    		Akt PKA PKC ROCK Ribosomal S6 Kinase (RSK) SGK Cancer
    Hu7691 is an orally active, selective Akt inhibitor with IC50s of 4.0 nM, 97.5 nM, 28 nM for Akt1, Akt2 and Akt3, respectively. Hu7691 inhibits tumor growth and enables decrease of cutaneous toxicity in mice .
    Hu7691
  • HY-75813
    2-Aminonicotinaldehyde

    		Biochemical Assay Reagents Akt 5-HT Receptor Neurological Disease Cancer
    2-Aminonicotinaldehyde is a synthetic intermediate. 2-Aminonicotinaldehyde can be used for the synthesis of 5-HT3 receptor antagonists, AKT inhibitors, and other compounds. 2-Aminonicotinaldehyde is applicable to research on depression and cancers (including hepatocellular carcinoma) .
    2-Aminonicotinaldehyde
  • HY-19934A
    Pifusertib hydrochloride

    TAS-117 hydrochloride

    		 Akt Apoptosis Autophagy Cancer
    Pifusertib (TAS-117) hydrochloride is a potent, selective, orally active allosteric Akt inhibitor (with IC50s of 4.8, 1.6, and 44 nM for Akt1, 2, and 3, respectively). Pifusertib hydrochloride triggers anti-myeloma activities and enhances fatal endoplasmic reticulum (ER) stress induced by proteasome inhibition. Pifusertib hydrochloride induces apoptosis and autophagy .
    Pifusertib hydrochloride
  • HY-15673
    KP372-1
    3 Publications Verification

    		 Quinone Reductase Akt Reactive Oxygen Species (ROS) Apoptosis Cancer
    KP372-1 is an Akt inhibitor that inhibits proliferation and induces apoptosis and anoikis. KP372-1 is also an NQO1 redox cycling agent that causes DNA damage (including DNA breakage) by generating ROS. KP372-1 can be used in cancer research (such as head and neck squamous cell carcinoma (HNSCC) and pancreatic cancer) .
    KP372-1
  • HY-19719A
    Miransertib hydrochloride
    15+ Cited Publications

    ARQ-092 hydrochloride

    		 Akt Parasite Infection Cancer
    Miransertib hydrochloride (ARQ-092 hydrochloride) is a potent, orally active, selective and allosteric Akt inhibitor with IC50s of 2.7 nM, 14 nM and 8.1 nM for Akt1, Akt2, Akt3, respectively. Miransertib hydrochloride is also a potent the AKT1-E17K mutant protein inhibitor and has the potential for PI3K/AKT-driven tumors and Proteus syndrome research . Miransertib hydrochloride is effective against Leishmania .
    Miransertib hydrochloride
  • HY-N2907
    Atranorin

    		Wnt Ras Endogenous Metabolite Bacterial Fungal PD-1/PD-L1 Tim3 Akt AP-1 STAT Infection Neurological Disease Inflammation/Immunology Cancer
    Atranorin is a secondary metabolite of lichens and AKT inhibitor. Atranorin possesses multiple activities such as antibacterial, anti-inflammatory, antioxidant, anti-glycation, analgesic, and anti-tumor effects. Atranorin has IC50 values for scavenging DPPH and ABTS free radicals of 117 μM and less than 10 μM, respectively. Additionally, Atranorin also exhibits effects in promoting wound healing. Atranorin can be used in the research of various diseases, including myelodysplastic syndromes, tumors, and inflammatory conditions .
    Atranorin
  • HY-107586
    Demethylasterriquinone B1

    DAQ B1; L-783281; Dimethylasterriquinone

    		 Insulin Receptor Akt NO Synthase NADPH Oxidase JAK STAT FOXO DNA/RNA Synthesis ERK Flavivirus Cardiovascular Disease Infection Metabolic Disease Inflammation/Immunology
    Demethylasterriquinone B1 (DAQ B1; L-783281) is an orally active insulin receptor (insulin receptor) agonist and AKT activator. By activating AKT, Demethylasterriquinone B1 upregulates the expression and activity of eNOS to increase NO production, while downregulating the expression of the NADPH oxidase subunit p22phox to reduce oxidative stress and improve vascular endothelial dysfunction in hypertensive rats. Demethylasterriquinone B1 combind with an AKT inhibitor targets the insulin signaling pathway to activate two antiviral pathways, RNA interference and JAK/STAT, in mosquitoes, thereby reducing Zika virus infection .
    Demethylasterriquinone B1
  • HY-14971
    (E)-Akt inhibitor-IV
    3 Publications Verification

    (E)-AKTIV

    		 Akt Cancer
    (E)-Akt inhibitor-IV ((E)-AKTIV) is a PI3K-Akt inhibitor, with potent cytotoxic .
    (E)-Akt inhibitor-IV
  • HY-19982
    AKT-IN-6
    2 Publications Verification

    		 Akt Cancer
    AKT-IN-6 (Example 13) is a potent Akt inhibitor. AKT-IN-6 inhibits Akt1, Akt2 and Akt3 with IC50s < 500nM, respectively. (patent WO2013056015A1).
    AKT-IN-6
  • HY-10721
    PF-AKT400

    AKT protein kinase inhibitor

    		 Akt Cancer
    PF-AKT400 is a broadly selective, potent, ATP-competitive Akt inhibitor, displays 900-fold greater selectivity for PKBα (IC50=0.5 nM) than PKA (IC50=450 nM).
    PF-AKT400
  • HY-14971A
    AKT inhibitor IV
    2 Publications Verification

    AKTIV

    		 Akt Cancer
    Akt inhibitor-IV (AKTIV) acts as a PI3K-Akt inhibitor at the E isomer (HY-14971), with potent cytotoxicity .
    AKT inhibitor IV
  • HY-18296
    AKT-IN-1
    5 Publications Verification

    		 Akt Cancer
    AKT-IN-1 is an allosteric AKT inhibitor with an IC50 of 1.042 μM.
    AKT-IN-1
  • HY-100654
    10-DEBC hydrochloride

    		Akt Bacterial Infection Inflammation/Immunology
    10-DEBC hydrochloride is a selective Akt inhibitor, with an IC50 of 1.28 μM. 10-DEBC hydrochloride is a novel anti-TB compound .
    10-DEBC hydrochloride
  • HY-15369
    FPA-124

    		Akt Apoptosis Cancer
    FPA-124, a cell-permeable copper complex, is a selective Akt inhibitor with an IC50 of 0.1 μM. FPA-124 interacts with both the pleckstrin homology (PH) and the kinase domains of Akt. FPA-124 induces apoptosis .
    FPA-124
  • HY-133120A
    INY-03-041 trihydrochloride
    1 Publications Verification

    		 PROTACs Akt Cancer
    INY-03-041 trihydrochloride is a potent, highly selective and PROTAC-based pan-AKT degrader consisting of the ATP-competitive AKT inhibitor Ipatasertib (HY-15186) conjugated to Lenalidomide (HY-A0003). INY-03-041 trihydrochloride inhibits AKT1, AKT2 and AKT3 with IC50s of 2.0, 6.8 and 3.5 nM, respectively .
    INY-03-041 trihydrochloride
  • HY-126257
    AKT-IN-3

    		Akt Apoptosis Cancer
    AKT-IN-3 (compound E22) is a potent, orally active low hERG blocking Akt inhibitor, with 1.4 nM, 1.2 nM and 1.7 nM for Akt1, Akt2 and Akt3, respectively. AKT-IN-3 (compound E22) also exhibits good inhibitory activity against other AGC family kinases, such as PKA, PKC, ROCK1, RSK1, P70S6K, and SGK. AKT-IN-3 (compound E22) induces apoptosis and inhibits metastasis of cancer cells .
    AKT-IN-3
  • HY-101984R
    N6,N6-Dimethyladenosine (Standard)

    		Reference Standards Nucleoside Antimetabolite/Analog Adenosine Receptor Akt SARS-CoV Infection Cancer
    N6,N6-Dimethyladenosine (Standard) is the analytical standard of N6,N6-Dimethyladenosine (HY-101984). This product is intended for research and analytical applications. N6,N6-Dimethyladenosine, a modified ribonucleoside, is an endogenous A3 adenosine receptor ligand. N6,N6-Dimethyladenosine is an AKT inhibitor with antitumor effects. N6, N6-Dimethyladenosine targets SARS-CoV-2 entry protein ADAM17. N6, N6-Dimethyladenosine robustly inhibits AKT signaling in a variety of non-small cell lung cancer cell lines.
    N6,N6-Dimethyladenosine (Standard)
  • HY-149842
    AKT-IN-18

    		Akt Apoptosis Cancer
    AKT-IN-18, an inhibitor of Akt, inhibits Akt with an IC50 of 69.45 μΜ in A549 cells. AKT-IN-18 induces apoptosis and can be used in non-small cell lung cancer study .
    AKT-IN-18
  • HY-147768
    PI3K/AKT-IN-2

    		PI3K Akt Microtubule/Tubulin MMP Apoptosis Cancer
    PI3K/AKT-IN-2 (Compound 12c) is a PI3K and AKT inhibitor. PI3K/AKT-IN-2 blocks the epithelial-mesenchymal transition (EMT) and induces apoptosis. PI3K/AKT-IN-2 inhibits the polymerization of tubulin .
    PI3K/AKT-IN-2
  • HY-10357
    MK-2206 free base

    		Akt mTOR Apoptosis GSK-3 Bcl-2 Family Metabolic Disease Inflammation/Immunology Cancer
    MK-2206 free base is an orally active pan-AKT inhibitor, with IC50 values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 free base inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 free base induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 free base causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 free base can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .
    MK-2206 free base
  • HY-153640
    AKT-IN-14

    		Akt Cancer
    AKT-IN-14 (Example 2) is a potent AKTinhibitor with the IC50 values of <0.01 nM, 1.06 nM and 0.66 nM for AKT1, AKT2, AKT3, respectively. AKT-IN-14 can be used in cancer research .
    AKT-IN-14
  • HY-15965A
    Uprosertib hydrochloride

    GSK2141795 hydrochloride

    		 Akt Cancer
    Uprosertib hydrochloride (GSK2141795 hydrochloride) is a potent and selective pan-Akt inhibitor with IC50 values of 180/328/38 nM for Akt1/Akt2/Akt3, respectively.
    Uprosertib hydrochloride
  • HY-133850
    10-DEBC

    		Pim Cancer
    10-DEBC is a selective Akt inhibitor. 10-DEBC shows strong inhibitory activity against Moloney murine leukemia virus (Pim) kinase-1 (IC50=1.28 μM) .
    10-DEBC
  • HY-132302A
    Hu7691 free base

    		Akt PKA PKC ROCK Ribosomal S6 Kinase (RSK) SGK Cancer
    Hu7691 free base is an orally active, selective Akt inhibitor with IC50s of 4.0 nM, 97.5 nM, 28 nM for Akt1, Akt2 and Akt3, respectively. Hu7691 free base inhibits tumor growth and enables decrease of cutaneous toxicity in mice .
    Hu7691 free base
  • HY-173273
    YJZ5118

    		CDK Apoptosis DNA/RNA Synthesis Akt Cancer
    YJZ5118 is a selective CDK12/CDK13 inhibitor with IC50 values of 39.5 nM and 26.4 nM. YJZ5118 suppresses transcription of DNA damage response genes and induces DNA damage in tumor cells. YJZ5118 inhibits proliferation and triggers apoptosis. YJZ5118 inhibits RNA polymerase II Ser2 phosphorylation and increases Akt pathway activity. YJZ5118 exhibits synergistic effects with Akt inhibitors. YJZ5118 can be used for the research of cancer, such as prostate cancer .
    YJZ5118
  • HY-N2907R
    Atranorin (Standard)

    		Wnt Reference Standards Ras Endogenous Metabolite Bacterial Fungal PD-1/PD-L1 Tim3 Akt AP-1 STAT Infection Neurological Disease Inflammation/Immunology Cancer
    Atranorin (Standard) is the analytical standard of Atranorin (HY-N2907). This product is intended for research and analytical applications. Atranorin is a secondary metabolite of lichens and AKT inhibitor. Atranorin possesses multiple activities such as antibacterial, anti-inflammatory, antioxidant, anti-glycation, analgesic, and anti-tumor effects. Atranorin has IC50 values for scavenging DPPH and ABTS free radicals of 117 μM and less than 10 μM, respectively. Additionally, Atranorin also exhibits effects in promoting wound healing. Atranorin can be used in the research of various diseases, including myelodysplastic syndromes, tumors, and inflammatory conditions .
    Atranorin (Standard)
  • HY-153640A
    AKT-IN-14 free base

    		Akt Cancer
    AKT-IN-14 (Example 2) free baseis a potent AKTinhibitor with the IC50 values of <0.01 nM, 1.06 nM and 0.66 nM for AKT1, AKT2, AKT3, respectively. AKT-IN-14 free basecan be used in cancer research .
    AKT-IN-14 free base
  • HY-P10049
    TAT-TCL1-Akt-in

    		Akt Cancer
    TAT-TCL1-Akt-in is an Akt inhibitor .
    TAT-TCL1-Akt-in
  • HY-16034
    AKT-IN-20

    		Akt Cancer
    AKT-IN-20 is an AKT inhibitor, and can be used for research of cancer
    AKT-IN-20
  • HY-161704
    AKT-IN-23

    		Akt Cancer
    AKT-IN-23 is an AKT inhibitor. AKT-IN-23 can be used in cancer research .
    AKT-IN-23
  • HY-164414
    CCT129254

    AT 11854

    		 Akt Cancer
    CCT129254 is a potent Akt inhibitor. CCT129254 reduces the motility of melanoma cells in vivo .
    CCT129254
  • HY-112148
    AKT-IN-2

    		Akt Cancer
    AKT-IN-2 is a potent, selective and orally bioavailable AKT inhibitor with an IC50 of 5 nM for AKT1 .
    AKT-IN-2
  • HY-138767
    AKT-IN-5

    		Akt Cancer
    AKT-IN-5 (Example 8) is a Akt inhibitor with IC50 values of 450 nM and 400 nM for Akt1 and Akt2, respectively .
    AKT-IN-5

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