Date published: 2025-9-23

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ZNF687 Inhibitors

ZNF687 inhibitors encompass a diverse array of chemical compounds designed to indirectly suppress the functional activity of ZNF687 by targeting specific cell signaling pathways. PD 98059 and U0126, both MEK inhibitors, effectively block the MAPK/ERK pathway, which is responsible for a wide range of cellular functions, including cell cycle progression and differentiation. Inhibition of this pathway is likely to result in a reduction of ZNF687 activity, assuming ZNF687 is regulated by or associated with this pathway. Likewise, the PI3K inhibitors LY 294002 and Wortmannin lead to attenuated AKT phosphorylation and downstream signaling, which can be critical for processes that ZNF687 might influence, thus restraining ZNF687's functional activity. Rapamycin, an mTOR inhibitor, and Y-27632, a ROCK inhibitor, further contribute to the inhibition by targeting protein synthesis and cytoskeletal organization respectively, processes which might be essential for the proper functioning of ZNF687.

The inhibitory effects extend to other pathways with compounds like SB 203580, a p38 MAPK inhibitor, and SP600125, a JNK inhibitor, which modulate the MAPK signaling axis and could, in turn, reduce ZNF687 activity if there is a regulatory connection. Dasatinib, by targeting Src family kinases, could disrupt signaling pathways that might activate ZNF687, hence leading to its inhibition. GSK-3 Inhibitor XVI, by inhibiting GSK-3, could lead to the accumulation of β-catenin, a process which, if negatively correlated with ZNF687 activity, would result in its inhibition. Tyrphostin B42, a JAK2 inhibitor, and Bisindolylmaleimide I, a PKC inhibitor, further demonstrate the capacity to impede ZNF687 activity by targeting the JAK/STAT and PKC pathways, respectively, both of which could have implications for the regulation and function of ZNF687. Collectively, these inhibitors provide a comprehensive approach to diminishing the functional activity of ZNF687 through a multi-pathway strategy, although they do so indirectly by interfacing with pathways that ZNF687 is presumed to be a part of or regulated by.

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