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 91 - 100 of 388 results

Status:
Other

Class (Stereo):
CHEMICAL (ABSOLUTE)

Conditions:

Ergosterol (9alpha: 10beat isomer), lumisterol (9beta: 10alpha isomer), isopyrocalciferol (9beta: 10beta isomer) and pyrocalciferol (9alpha: 10alpha isomer) are all epimers of one another at C-9 and C-10. Isopyrocalciferol and pyrocalciferol are products of over-radiation of the provitamin D. These steroids don’t have biological activity since they are not steroids.
Status:
Other

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Other

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Other

Class (Stereo):
CHEMICAL (UNKNOWN)

Monastrol is a small, cell-permeable molecule that arrests cells in mitosis by specifically inhibiting Eg5, a member of the Kinesin-5 family. Monastrol has been used to probe the dynamic organization of the mitotic spindle. Monastrol inhibits both the basal and the microtubule-stimulated ATPase activity of the Eg5 motor domain. Unlike many ATPase inhibitors, monastrol does not compete with ATP binding to Eg5. Monastrol appears to inhibit microtubule-stimulated ADP release from Eg5 but does not compete with microtubule binding, suggesting that monastrol binds a novel allosteric site in the motor domain. (S)-monastrol, as compared to the (R)-enantiomer, is a more potent inhibitor of Eg5 activity in vitro and in vivo. As Monastrol, by specifically inhibiting kinesin Eg5, can cause mitotic arrest and monopolar spindle formation, it exhibits antitumor properties. Monastrol has being shown to be a potent inhibitor of pteridine reductase (PTR1) in Leishmania; it inhibits proliferation of amastigotes with an IC(50) (50% inhibitory concentration) of 10 uM in macrophage cultures infected with an L. donovani clinical isolate, with no host cytotoxicity. In experimental animals, oral administration of a 5 mg/kg dose of monastrol on two alternate days inhibits 50% of parasite growth, giving therapeutic backing to the use of monastrol as a potent antileishmanial in human VL cases.