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Results for "

T315I

" in MedChemExpress (MCE) Product Catalog:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-101489A

    PDGFR Bcr-Abl Apoptosis Cancer
    GZD856 formic is a potent and orally active PDGFRα/β inhibitor, with IC50s of 68.6 and 136.6 nM, respectively. GZD856 formic is also a Bcr-Abl T315I inhibitor, with IC50s of 19.9 and 15.4 nM for native Bcr-Abl and the T315I mutant. GZD856 formic has antitumor activity . GZD856 (formic) is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    GZD856 formic
  • HY-153008

    Bcr-Abl Cancer
    BCR-ABL-IN-7 (compound 4) is a WT and T315I mutant ABL kinases inhibitor. BCR-ABL-IN-7 effectively inhibits activities of WT and T315I mutant ABL kinases. BCR-ABL-IN-7 can be used for the research of chronic myeloid leukemia (CML) research .
    BCR-ABL-IN-7
  • HY-101489

    PDGFR Bcr-Abl Apoptosis Cancer
    GZD856 formic is a potent and orally active PDGFRα/β inhibitor, with IC50s of 68.6 and 136.6 nM, respectively. GZD856 formic is also a Bcr-Abl T315I inhibitor, with IC50s of 19.9 and 15.4 nM for native Bcr-Abl and the T315I mutant. GZD856 formic has antitumor activity .
    GZD856
  • HY-12083

    Bcr-Abl Cancer
    PPY-A is a potent T315I mutant and wild-type Abl kinases inhibitor with IC50s of 9 and 20 nM, respectively. PPY-A inhibits Ba⁄F3 cells transformed with wild-type Abl and Abl T315I mutantl with IC50s of 390 and 180 nM, respectively. PPY-A can be used for the research of chronic myeloid leukemia (CML) .
    PPY-A
  • HY-123390

    Bcr-Abl Akt Cancer
    DB07107 is a potent agent resistant T315I mutant Bcr-Abl tyrosine kinase inhibitor. DB07107 is also a potent Akt1 inhibitor with an IC50 value of 360 nM .
    DB07107
  • HY-123450

    Bcr-Abl Apoptosis PDGFR Cancer
    S116836, a potent, orally active BCR-ABL tyrosine kinase inhibitor, blocks both wild-type as well as T315I Bcr-Abl. S116836 arrests the cells in the G0/G1 phase of cell cycle, induces apoptosis, increases ROS production, and decreases GSH production in BaF3/WT and BaF3/T315I cells. S116836 also inhibits SRC, LYN, HCK, LCK and BLK, and receptor tyrosine kinases such as FLT3, TIE2, KIT, PDGFR-β. Antitumor activies . S116836 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    S116836
  • HY-101985
    BV02
    1 Publications Verification

    Bcr-Abl Cancer
    BV02 is a potent 4-3-3 PPI (14-3-3 protein–protein interaction) inhibitor. BV02 shows cytotoxicity for hematopoietic cells expressing the IM (imatinib mesylate)-sensitive wild type Bcr-Abl and the IM-resistant T315I mutation. BV02 has the potential for the research of chronic myeloid leukemia .
    BV02
  • HY-10339
    KW-2449
    5 Publications Verification

    FLT3 FGFR Bcr-Abl Aurora Kinase Apoptosis Cancer
    KW-2449 is a multi-targeted kinase inhibitor of FLT3, ABL, ABL T315I and Aurora kinase with IC50s of 6.6, 14, 4 and 48 nM, respectively.
    KW-2449
  • HY-18819

    BCR-ABL-IN-2 is an inhibitor of BCR-ABL1 tyrosine kinase, with IC50s of 57 nM, 773 nm for ABL1 native and ABL1 T315I, respectively.
    BCR-ABL-IN-2
  • HY-160478

    Bcr-Abl Cancer
    GNF-6 (Compound 14) inhibits the gatekeeper threonine residue mutation of BCR-ABL-T315I with IC50s of 0.25 μM, 0.09 μM and 0.590 μM for c-ABL-T334I, BCR-ABL and BCR-ABL-T315I variants, respectively. GNF-6, an ATP competitive inhibitor, disrupts the assembly of the hydrophobic spine (a network of hydrophobic interactions), thereby locking the kinase in an inactive ‘DFG-out’ conformation .
    GNF-6
  • HY-119370

    Bcr-Abl Apoptosis Cancer
    CHMFL-ABL-121 is a highly potent type II ABL kinase inhibitor with IC50s of 2 nM and 0.2 nM against purified inactive ABL wt and T315I kinase protein, respectively .
    CHMFL-ABL-121
  • HY-10943
    GNF-7
    1 Publications Verification

    Bcr-Abl Ack1 Cancer
    GNF-7 is a multikinase inhibitor. GNF-7 is a Bcr-Abl inhibitor, with IC50s of 133 nM and 61 nM for Bcr-Abl WT and Bcr-Abl T315I, respectively. GNF-7 also possesses inhibitory activity against both ACK1 (activated CDC42 kinase 1) and GCK (germinal center kinase) with IC50s of 25 nM and 8 nM, respectively. GNF-7 can be used for the research of hematologic malignancies .
    GNF-7
  • HY-123159

    Aurora Kinase Cancer
    AKI603 is an inhibitor of Aurora kinase A (AurA), with an IC50 of 12.3 nM. AKI603 is developed to overcome resistance mediated by BCR-ABL-T315I mutation. AKI603 exhibits strong anti-proliferative activity in leukemic cells .
    AKI603
  • HY-50514
    AT9283
    5 Publications Verification

    JAK Aurora Kinase Bcr-Abl FLT3 Apoptosis Autophagy Cancer
    AT9283 is a multi-targeted kinase inhibitor with potent activity against Aurora A/B, JAK2/3, Abl (T315I) and Flt3 (IC50s ranging from 1 to 30 nM). AT9283 inhibits growth and survival of multiple solid tumors in vitro and in vivo .
    AT9283
  • HY-142922

    Bcr-Abl Cancer
    BCR-ABL-IN-4 is a BCR-ABL inhibitor with anticancer effects. BCR-ABL-IN-4 inhibits the cancer cell growth with IC50 values of 0.67 nM and 16 nM for K562 cells and BCR-ABL T315I transfected Ba/F3 cells, respectively (WO2021143927A1; compound 11) .
    BCR-ABL-IN-4
  • HY-10058

    JAK Aurora Kinase Bcr-Abl FLT3 Apoptosis Autophagy Cancer
    AT9283 lactic acid is a multi-targeted kinase inhibitor with potent activity against Aurora A/B, JAK2/3, Abl (T315I) and Flt3 (IC50s ranging from 1 to 30 nM). AT9283 lactic acid inhibits growth and survival of multiple solid tumors in vitro and in vivo .
    AT9283 lactic acid
  • HY-13024
    Rebastinib
    Maximum Cited Publications
    6 Publications Verification

    DCC-2036

    Bcr-Abl FLT3 Src Apoptosis Cancer
    Rebastinib (DCC-2036) is an orally active, non-ATP-competitive Bcr-Abl inhibitor for Abl1 WT and Abl1 T315I with IC50s of 0.8 nM and 4 nM, respectively. Rebastinib also inhibits SRC, KDR, FLT3, and Tie-2, and has low activity to seen towards c-Kit.
    Rebastinib
  • HY-157389

    Bcr-Abl Cancer
    AK-HW-90 (compound 2B) is a potent panBcr-Abl inhibitor with significant inhibitory activity against Imatinib (HY-15463)-resistant mutants. AK-HW-90 inhibits the resistance mutant Bcr-Abl T315I with an IC50 of 0.65 nM. AK-HW-90 has potential anticancer activity and can be used in the study of chronic myelogenous leukemia (CML) .
    AK-HW-90
  • HY-147414

    PF-114

    Bcr-Abl Cancer
    Vamotinib (PF-114) is a potent, selective and orally active tyrosine kinase inhibitor. Vamotinib inhibits the autophosphorylation of BCR/ABL and BCR/ABL-T315I. Vamotinib induces apoptosis. Vamotinib shows anti-proliferative and anti-tumor activity. Vamotinib has the potential for the research of resistant philadelphia chromosome-positive (Ph+) leukemia. Vamotinib inhibits ABL series kinases with IC50s of 0.49 nM (ABL), 0.78 nM (ABL T315I), 9.5 nM (ABL E255K), 2.0 nM (ABL F317I), 7.4 nM (ABL G250E), 1.0 nM (ABL H396P), 2.8 nM (ABL M351T), 12 nM (ABL Q252H), and 4.1 nM (ABL Y253F), respectively . Vamotinib is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    Vamotinib
  • HY-15666
    Olverembatinib
    3 Publications Verification

    GZD824; HQP1351

    Bcr-Abl Cancer
    Olverembatinib (GZD824) is a potent and orally active pan-Bcr-Abl inhibitor. Olverembatinib potently inhibits a broad spectrum of Bcr-Abl mutants. Olverembatinib strongly inhibits native Bcr-Abl and Bcr-Abl T315I with IC50s of 0.34 nM and 0.68 nM, respectively. Olverembatinib has antitumor activity . Olverembatinib is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    Olverembatinib
  • HY-15666A
    Olverembatinib dimesylate
    3 Publications Verification

    GZD824 dimesylate; HQP1351 dimesylate

    Olverembatinib (GZD824) dimesylate is a potent and orally active pan-Bcr-Abl inhibitor. Olverembatinib dimesylate potently inhibits a broad spectrum of Bcr-Abl mutants. Olverembatinib dimesylate strongly inhibits native Bcr-Abl and Bcr-Abl T315I with IC50s of 0.34 nM and 0.68 nM, respectively. Olverembatinib dimesylate has antitumor activity . Olverembatinib (dimesylate) is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    Olverembatinib dimesylate
  • HY-15814

    Bcr-Abl PDGFR c-Kit Src JAK Apoptosis Cancer
    HG-7-85-01 is a type II ATP competitive inhibitor of wild-type and gatekeeper mutations forms of Bcr-Abl, PDGFRα, Kit, and Src kinases. HG-7-85-01 inhibits T315I mutant Bcr-Abl kinase, KDR and RET with IC50s of 3 nM, 20 nM and 30 nM, and is only weak or no inhibition of other kinases (IC50>2 μM). HG-7-85-01 inhibits the cell proliferation, which is mediated by the induction of apoptosis, and inhibition of cell-cycle progression .
    HG-7-85-01
  • HY-137460

    K0706

    Bcr-Abl Cancer
    Vodobatinib (K0706) is a potent, third generation and orally active Bcr-Abl1 tyrosine kinase inhibitor with an IC50 of 7 nM. Vodobatinib exhibits activity against most BCR-ABL1 point mutants, and has no activity against BCR-ABL1T315I. Vodobatinib can be used for chronic myeloid leukemia (CML) research . Vodobatinib is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    Vodobatinib

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