Date published: 2025-9-11

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PD-2 Inhibitors

Chemical inhibitors of PD-2 target various signaling pathways to impede its activity. Palbociclib, as a selective inhibitor of cyclin-dependent kinases CDK4 and CDK6, hampers the progression of the cell cycle, which is essential for PD-2 function. The disruption of the normal progression of the cell cycle by Palbociclib consequently leads to an indirect inhibition of PD-2, as PD-2 requires specific cell-cycle stages for its activity. Similarly, Rapamycin, by inhibiting mTOR, suppresses downstream signaling that contributes to PD-2 activity. The mTOR pathway is fundamental for various cellular processes, including those that regulate PD-2 function, and Rapamycin's interference with this pathway demonstrates an indirect method of inhibiting PD-2.

Moreover, LY294002 and Triciribine target the PI3K/Akt signaling pathway, with LY294002 directly inhibiting PI3K and Triciribine targeting Akt, thereby disrupting a critical upstream regulator of PD-2. The resultant decrease in PI3K/Akt signaling can lead to a reduction in PD-2 activity. U0126 and Selumetinib, both MEK inhibitors, and PD98059, which also targets MEK, suppress the MAPK/ERK pathway, another regulator of PD-2. With reduced activity of this pathway, PD-2 activity is diminished. SB203580 and SP600125 inhibit the p38 MAPK and JNK pathways, respectively, both of which are implicated in the regulation of PD-2. Inhibition of these kinase pathways prevents the phosphorylation events that are necessary for full PD-2 activity. Additionally, PP2 and Dasatinib, by inhibiting Src family kinases, and Sunitinib, by inhibiting receptor tyrosine kinases, block signaling routes that are requisite for PD-2's functional state. The inhibition of these kinases by PP2, Dasatinib, and Sunitinib leads to a reduction in PD-2 signaling, thereby providing further methods to functionally inhibit PD-2. Each chemical, through its respective target, orchestrates a decrease in PD-2 activity by inhibiting the specific signaling pathways or kinases that are critical for PD-2's function in the cell.

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