U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

Showing 631 - 640 of 1679 results

Status:
Other

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Other

Class (Stereo):
CHEMICAL (RACEMIC)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)



Lavendustin B is a weak tyrosine kinase inhibitor that has been used as a negative control for lavendustin A. Lavendustin A strongly inhibits epidermal growth factor receptor-associated tyrosine kinase, competes with ATP, and is noncompetitive with the peptide. Lavendustin B was previously identified as an inhibitor of HIV-1 integrase (IN) interaction with its cognate cellular cofactor, lens epithelium-derived growth factor (LEDGF/p75).
Lavendustin C or HDBA (2-hyroxyl-5-(2,5-dihydroxybenzylamino) benzoic acid) is the active pharmacophore of lavendustin A, a tyrosine kinase inhibitor isolated from a butyl acetate extract of Streptomyces griseolavendus.
Chronic myelogenous leukemia (CML) is a hematological malignancy caused by a chromosomal rearrangement that generates a fusion protein, Bcr-Abl, with deregulated tyrosine kinase activity. GNF-5, an analogue of GNF-2 with improved pharmacokinetic properties, is an allosteric inhibitor of Bcr-Abl that enters the myristate binding pocket at the base of the C-lobe in the Abl kinase domain. When used in combination with the ATP-competitive inhibitors imatinib or nilotinib, suppressed the emergence of resistance mutations in vitro, displayed additive inhibitory activity in biochemical and cellular assays against T315I mutant human Bcr-Abl and displayed in vivo efficacy against this recalcitrant mutant in a murine bone-marrow transplantation model. Findings in streptozotocin treated mice (diabetes model) demonstrated that GNF-5 prevented the loss of beta cells and the increase in blood glucose as well as increased insulin protein levels when compared with control mice. In addition GNF-5 inhibited the development of airway hyperresponsiveness and airway remodeling in mouse model of asthma.