p63 Inhibitors
p63 inhibitors represent a diverse class of chemical compounds designed to modulate the activity of p63, a transcription factor belonging to the p53 family with crucial roles in cellular development, differentiation, and apoptosis. These inhibitors can be broadly categorized into direct and indirect inhibitors, each with distinct mechanisms of action. While there are limited direct inhibitors of p63, several compounds indirectly modulate p63 through various pathways, providing insights into strategies for targeting p63-mediated cellular processes. Nutlin-3, PRIMA-1, and RITA, known for their effects on p53, indirectly influence p63 due to shared structural homology between p53 and p63. These compounds impact p63 by promoting the refolding and activation of mutant p53, leading to the restoration of its transcriptional activity. Additionally, NSC 319726 directly inhibits the p63-TAp63 interaction, disrupting p63's transcriptional activity by preventing its interaction with its coactivator. Indirect inhibitors such as Selinexor and Cisplatin influence p63 by modulating cellular stress responses. Selinexor inhibits XPO1, leading to the nuclear accumulation of p63, while Cisplatin induces DNA damage, activating stress responses interconnected with p63-mediated cellular processes.
Compounds like SB 216763 and 5-Azacytidine indirectly modulate p63 through the Wnt/β-catenin pathway and epigenetic regulation, respectively. SB 216763 inhibits GSK-3, leading to Wnt pathway activation, and 5-Azacytidine influences p63 by altering DNA methylation patterns. TPCK indirectly stabilizes p63 by inhibiting the proteasome, disrupting its degradation. Topotecan induces DNA damage, activating stress responses interconnected with p63-mediated cellular processes. Furthermore, XL413 indirectly modulates p63 by inhibiting CDC7, leading to cell cycle arrest. As p63 is implicated in cell cycle regulation, XL413's impact on the cell cycle can influence p63-mediated cellular processes. In summary, while direct inhibitors of p63 are limited, these compounds provide valuable tools for understanding and modulating p63 activity, offering insights for interventions in diseases where dysregulation of p63 is implicated. The diverse mechanisms of action showcased by these inhibitors highlight the complex regulatory network governing p63-mediated cellular processes
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
(–)-Nutlin-3 | 675576-98-4 | sc-222086 sc-222086A | 1 mg 5 mg | $122.00 $219.00 | 2 | |
Nutlin-3 is a small molecule inhibitor of the p53-MDM2 interaction. While p63 shares structural homology with p53 and interacts with MDM2, Nutlin-3 indirectly inhibits p63 by preventing MDM2-mediated degradation of p53. By disrupting the p53-MDM2 interaction, Nutlin-3 stabilizes p53 and indirectly impacts p63, as the two proteins share common regulatory pathways. This inhibition can lead to alterations in cellular processes governed by p63, such as cell cycle regulation and apoptosis. | ||||||
KPT 330 | 1393477-72-9 | sc-489062 | 5 mg | $173.00 | ||
Selinexor is a selective inhibitor of XPO1 (Exportin-1), a nuclear export protein. While not directly targeting p63, Selinexor indirectly modulates p63 by inhibiting its nuclear export. XPO1 is involved in shuttling proteins out of the nucleus, and Selinexor's blockade of XPO1 can lead to the nuclear accumulation of p63. This altered subcellular localization can impact p63-mediated transcriptional activities, influencing cellular processes such as proliferation and differentiation. | ||||||
NSC 319726 | 71555-25-4 | sc-477736 | 10 mg | $159.00 | ||
NSC 319726 is a small molecule inhibitor that disrupts the interaction between p63 and its transcriptional coactivator TAp63. By interfering with this protein-protein interaction, NSC 319726 inhibits the transcriptional activity of p63, leading to modulation of downstream target genes involved in cell cycle regulation and apoptosis. | ||||||
Cisplatin | 15663-27-1 | sc-200896 sc-200896A | 100 mg 500 mg | $138.00 $380.00 | 101 | |
Cisplatin is a platinum-containing chemotherapeutic agent that can indirectly impact p63 through DNA damage-induced stress responses. While not a direct inhibitor, Cisplatin induces DNA damage, activating cellular stress responses that can influence p63 activity. DNA damage response pathways, such as ATM/ATR signaling, are interconnected with p63-mediated cellular processes. | ||||||
SB-216763 | 280744-09-4 | sc-200646 sc-200646A | 1 mg 5 mg | $71.00 $202.00 | 18 | |
SB 216763 is a small molecule inhibitor of GSK-3 (Glycogen Synthase Kinase-3). While not directly targeting p63, SB 216763 indirectly influences p63 through the Wnt/β-catenin signaling pathway. GSK-3 is a negative regulator of the Wnt pathway, and its inhibition by SB 216763 leads to the activation of Wnt signaling. As Wnt signaling is interconnected with p63-mediated cellular processes, SB 216763's impact on the Wnt pathway can modulate p63 activity . | ||||||
5-Azacytidine | 320-67-2 | sc-221003 | 500 mg | $280.00 | 4 | |
5-Azacytidine is a nucleoside analog that incorporates into DNA and acts as a DNA methyltransferase inhibitor. While not directly targeting p63, 5-Azacytidine can indirectly modulate p63 activity by influencing DNA methylation patterns. Aberrant DNA methylation is associated with altered gene expression, including genes regulated by p63. | ||||||
Topotecan | 123948-87-8 | sc-338718 | 100 mg | $582.00 | ||
Topotecan is a topoisomerase I inhibitor used in cancer therapy. While not a direct p63 inhibitor, Topotecan indirectly modulates p63 by inducing DNA damage through inhibition of topoisomerase I. DNA damage response pathways activated by Topotecan are interconnected with p63-mediated cellular processes. | ||||||
XL413 | 1169562-71-3 | sc-474909 | 5 mg | $275.00 | ||
XL413 is a small molecule inhibitor of CDC7, a kinase involved in DNA replication initiation. While not directly targeting p63, XL413 indirectly influences p63 by disrupting the cell cycle. CDC7 is essential for the initiation of DNA replication, and its inhibition by XL413 leads to cell cycle arrest. | ||||||