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(4- (7- (3,5- dimethyloxyphenyl)- 1H- pyrazolo(3,4)pyridin- 6- yl)- 4- fluoro)benzene

a protein kinase inhibitor; structure in first source

Also Known As:

APcK110

Networked: 1 relevant articles (0 outcomes, 0 trials/studies)

Bio-Agent Context: Research Results

Heterocyclic Compounds: 198
- 1-Ring Heterocyclic Compounds
  - Azoles: 2138
    - Pyrazoles: 61
      - (4-(7-(3,5-dimethyloxyphenyl)-1H-pyrazolo(3,4)pyridin-6-yl)-4-fluoro)benzene: 1
  - Pyridines: 88
    - (4-(7-(3,5-dimethyloxyphenyl)-1H-pyrazolo(3,4)pyridin-6-yl)-4-fluoro)benzene: 1

Experts

1.	Albitar, Maher: 1 article (05/2009)
2.	Bornmann, William: 1 article (05/2009)
3.	Estrov, Zeev: 1 article (05/2009)
4.	Faderl, Stefan: 1 article (05/2009)
5.	Harris, David: 1 article (05/2009)
6.	Hazan-Halevy, Inbal: 1 article (05/2009)
7.	Kantarjian, Hagop M: 1 article (05/2009)
8.	Liu, Zhiming: 1 article (05/2009)
9.	Maxwell, David: 1 article (05/2009)
10.	Pal, Ashutosh: 1 article (05/2009)

Related Diseases

1.	Acute Myeloid Leukemia (Acute Myelogenous Leukemia) 05/01/2009 - "Kit inhibitor APcK110 induces apoptosis and inhibits proliferation of acute myeloid leukemia cells." 05/01/2009 - "We investigated the activity and mechanism of action of APcK110, a novel Kit inhibitor, in the mastocytosis cell line HMC1.2 (KITV560G and KITD816V), acute myeloid leukemia (AML) lines OCIM2 and OCI/AML3 (both wild-type), and primary samples from patients with AML. "
2.	Mastocytosis 05/01/2009 - "We investigated the activity and mechanism of action of APcK110, a novel Kit inhibitor, in the mastocytosis cell line HMC1.2 (KITV560G and KITD816V), acute myeloid leukemia (AML) lines OCIM2 and OCI/AML3 (both wild-type), and primary samples from patients with AML. " 05/01/2009 - "Although APcK110 activity may partly depend on cytokine responsiveness (e.g., SCF) and not exclusively KIT mutation status, it remains a potent inhibitor of AML and mastocytosis cell lines and primary AML samples. " 05/01/2009 - "We show that (a) APcK110 inhibits proliferation of the mastocytosis cell line HMC1.2 and the SCF-responsive cell line OCI/AML3 in a dose-dependent manner; (b) APcK110 is a more potent inhibitor of OCI/AML3 proliferation than the clinically used Kit inhibitors imatinib and dasatinib and at least as potent as cytarabine; (c) APcK110 inhibits the phosphorylation of Kit, Stat3, Stat5, and Akt in a dose-dependent fashion, showing activity of APcK110 on Kit and its downstream signaling pathways; (d) APcK110 induces apoptosis by cleavage of caspase-3 and poly(ADP-ribose) polymerase; and (e) APcK110 inhibits proliferation of primary AML blasts in a clonogenic assay but does not affect proliferation of normal colony-forming cells. "

Related Drugs and Biologics

1.	Caspase 3 (Caspase-3)
2.	Cytokines
3.	Poly(ADP-ribose) Polymerases (Poly ADP Ribose Polymerase)
4.	Cytarabine (Cytosar-U)
5.	Dasatinib (BMS 354825)
6.	Imatinib Mesylate (Gleevec)