KKL 顾客使用本产品发表的 0 篇科研文献

HSP90

51 nM (IC50, MDA-MB-468 cells)

Zelavespib is an effective Hsp90 inhibitor with an IC50 of 51 nM in MDA-MB-468 cells. Zelavespib inhibits the growth of various tumor cells, such as MDA-MB-468, MDA-MB-231, and HCC-1806 cells, with IC50 values of 65 ± 8 nM, 140 ± 5 nM, and 87 ± 3 nM, respectively. This inhibition is associated with G2-M blockade. Zelavespib (10-1000 nM) can induce significant apoptosis in triple negative breast cancer (TNBC). Zelavespib (0.5, 1 μM) also downregulates oncogenes involved in TNBC invasion potential [1].

Zelavespib (0.5 μM) can reduce and deplete BCR signaling kinase. Zelavespib (0.25-10 μM) exhibits cytotoxicity towards CLL cells, but has minimal impact on PBMCs or resting B cells. In addition, Zelavespib (0-1 μM) reduces CLL activity by inducing mitochondrial apoptosis and antagonizes survival signals from the CLL microenvironment at 0.5 μM.

Zelavespib (0.05 μM) induces apoptosis in MDA-MB-231, BT-474, and MCF7 cells, and TNF - α can enhance this induction effect. Zelavespib (0.05 μM) can degrade IKK β and downregulate NF - κ B transcriptional activity induced by TNF - α treatment.

Zelavespib (75 mg/kg, intraperitoneal injection) caused tumor accumulation, prolonged downregulation of anti-tumor driving molecules, and completed and retained the response at non-toxic doses in MDA-MB-468 tumor bearing mice.

Zelavespib (75 mg/kg, 3 x weeks, intraperitoneal injection) can inhibit tumor growth, which is related to the downregulation of various Hsp90 regulated malignant motor proteins.