APRIL-TWEAK Inhibitors
Chemical inhibitors of APRIL-TWEAK target various components of the NF-κB signaling pathway, which is essential for the protein's function in cell survival and cytokine production. Thalidomide, lenalidomide, and pomalidomide, all related by their origin in the thalidomide family, disrupt this pathway by inhibiting the nuclear translocation and subsequent DNA binding of NF-κB. By halting this critical step, these inhibitors prevent the transcription of NF-κB target genes that would otherwise be activated by APRIL-TWEAK. Similarly, Bortezomib acts upstream in this pathway by preventing the degradation of IκB, the inhibitor of NF-κB. This proteasome inhibition leads to the accumulation of IκB, which sequesters NF-κB in the cytoplasm, away from the cell's genetic material where it could otherwise interact with and enhance APRIL-TWEAK's functions.
Other inhibitors such as parthenolide and Bay 11-7082 directly inhibit components of the NF-κB signaling cascade. Parthenolide targets the p65 subunit of NF-κB, preventing its nuclear translocation, while Bay 11-7082 irreversibly inhibits IκBα phosphorylation, stabilizing the NF-κB inhibitor and thus precluding NF-κB's activation. Further along this theme, (S,R)-Rolipram elevates intracellular cAMP levels, which in turn antagonize NF-κB signaling, disrupting the pathways necessary for APRIL-TWEAK function. PS-1145, IMD-0354, and TPCA-1 are more targeted in their approach, focusing on IκB kinase (IKK) inhibition, with PS-1145 and IMD-0354 selectively inhibiting IKK, and TPCA-1 specifically targeting IKK-2. By impeding IKK's role in NF-κB activation, these inhibitors prevent the downstream effects that APRIL-TWEAK would typically exert. Lastly, wedelolactone also inhibits IKK, rounding out the cadre of substances that interfere with the NF-κB pathway and consequently the functional activities of APRIL-TWEAK.
SEE ALSO...
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Thalidomide | 50-35-1 | sc-201445 sc-201445A | 100 mg 500 mg | $111.00 $357.00 | 8 | |
Thalidomide inhibits the nuclear factor kappa B (NF-κB) pathway. APRIL-TWEAK is known to be associated with the NF-κB pathway, which is critical for cell survival and cytokine production. By inhibiting NF-κB, Thalidomide can reduce the survival signals that would otherwise be enhanced by APRIL-TWEAK, thereby functionally inhibiting its activity. | ||||||
Lenalidomide | 191732-72-6 | sc-218656 sc-218656A sc-218656B | 10 mg 100 mg 1 g | $50.00 $374.00 $2071.00 | 18 | |
Lenalidomide, similar to Thalidomide, targets the NF-κB pathway. It also has been shown to inhibit the production of pro-inflammatory cytokines and to promote anti-inflammatory cytokines. Through these actions, Lenalidomide can interfere with the cellular environments that facilitate APRIL-TWEAK's functional role, leading to its functional inhibition. | ||||||
Pomalidomide | 19171-19-8 | sc-364593 sc-364593A sc-364593B sc-364593C sc-364593D sc-364593E | 5 mg 10 mg 50 mg 100 mg 500 mg 1 g | $100.00 $143.00 $312.00 $468.00 $1248.00 $1997.00 | 1 | |
Pomalidomide, an analogue of Thalidomide, acts on the same NF-κB pathway. By inhibiting NF-κB, Pomalidomide can disrupt the APRIL-TWEAK mediated activation of cells, leading to a decrease in the protein's ability to promote survival signaling, thus functionally inhibiting APRIL-TWEAK. | ||||||
Bortezomib | 179324-69-7 | sc-217785 sc-217785A | 2.5 mg 25 mg | $135.00 $1085.00 | 115 | |
Bortezomib is a proteasome inhibitor that can lead to the accumulation of IκB, an inhibitor of NF-κB. With IκB preventing NF-κB from translocating to the nucleus and binding DNA, the action of APRIL-TWEAK, which is dependent on the NF-κB signaling for some of its functions, can be functionally inhibited. | ||||||
Parthenolide | 20554-84-1 | sc-3523 sc-3523A | 50 mg 250 mg | $81.00 $306.00 | 32 | |
Parthenolide inhibits NF-κB by blocking the nuclear translocation of p65, a subunit of NF-κB. This action disrupts the signaling cascade that APRIL-TWEAK might participate in, particularly in inflammation and cell survival, therefore functionally inhibiting APRIL-TWEAK's activity. | ||||||
BAY 11-7082 | 19542-67-7 | sc-200615B sc-200615 sc-200615A | 5 mg 10 mg 50 mg | $62.00 $85.00 $356.00 | 155 | |
Bay 11-7082 is known to irreversibly inhibit IκBα phosphorylation, thereby stabilizing IκBα and inhibiting NF-κB activation. Since APRIL-TWEAK relies on NF-κB signaling for its activities, the inhibition of this pathway can lead to a functional inhibition of APRIL-TWEAK. | ||||||
IKK Inhibitor X | 431898-65-6 | sc-221742 | 5 mg | $352.00 | 3 | |
PS-1145 is a specific inhibitor of IκB kinase (IKK), which plays a crucial role in activating NF-κB. By inhibiting IKK, PS-1145 prevents the phosphorylation and degradation of IκB, thus inhibiting NF-κB activation and subsequently the function of APRIL-TWEAK as it is linked to the NF-κB signaling pathway. | ||||||
IMD 0354 | 978-62-1 | sc-203084 | 5 mg | $199.00 | 3 | |
IMD-0354 selectively inhibits IKKβ, blocking NF-κB activation. Through this action, it can inhibit the downstream effects of APRIL-TWEAK that are mediated by NF-κB signaling, leading to a decrease in APRIL-TWEAK's ability to promote cell survival and inflammation, thus functionally inhibiting the protein. | ||||||
Wedelolactone | 524-12-9 | sc-200648 sc-200648A | 1 mg 5 mg | $110.00 $337.00 | 8 | |
Wedelolactone is an inhibitor of IKK and thus NF-κB activation. By preventing the activation of NF-κB, it can suppress the functional activities of APRIL-TWEAK that are dependent on this signaling pathway, leading to its functional inhibition. | ||||||
IKK-2 Inhibitor IV | 507475-17-4 | sc-203083 | 500 µg | $133.00 | 12 | |
TPCA-1 is an inhibitor of IKK-2, which is essential for NF-κB activation. The inhibition of IKK-2 leads to reduced activity of NF-κB, and consequently, a decrease in the functional capabilitiesI apologize for any confusion, but it seems there has been a misunderstanding. You've asked for a table that includes thalidomide, lenalidomide, and pomalidomide, among other substances, in relation to their inhibitory effects on APRIL-TWEAK signaling. | ||||||