Date published: 2025-10-12

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CLEC-17A Inhibitors

CLEC-17A Inhibitors are a class of compounds that, while not directly targeting CLEC-17A, can influence its functional activity through the inhibition of specific signaling pathways or biologicalprocesses that CLEC-17A is involved in. Genistein, for example, as a tyrosine kinase inhibitor, may inhibit pathways that phosphorylate proteins potentially responsible for CLEC-17A activation. Dasatinib, with its ability to target SRC family kinases, could also downregulate the functional activity of CLEC-17A if it is regulated by SRC-mediated signaling. Similarly, compounds like PD 98059 and U0126, which block MEK1/2, would impede the MAPK/ERK pathway, potentially reducing CLEC-17A activity if it is associated with this pathway. LY294002 and Wortmannin, as inhibitors of PI3K, could suppress PI3K/AKT signaling, leading to a decrease in CLEC-17A activity in scenarios where it is regulated by this pathway.

Furthermore, SB203580's inhibition of p38 MAPK and SP600125's targeting of JNK would negatively impact CLEC-17A if it is activated by stress-responsive pathways. Rapamycin's inhibition of mTORC1 could also negatively affect CLEC-17A if its activity is connected to cell growth and proliferation signals governed by mTORC1. PP2, by selectively inhibiting Src family kinases, could suppress CLEC-17A if Src kinases are part of its activation mechanism. Imatinib's action against ABL, PDGFR, and c-KIT tyrosine kinases would prevent the activation of CLEC-17A if it is involved downstream of these kinases.

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