Cdc45 inhibitors represent a unique class of compounds that, though not directly targeting Cdc45, modulate its activity by influencing various cellular processes and signaling pathways. These inhibitors generally exert their effects by disrupting key steps in DNA replication, cell cycle progression, or DNA damage response mechanisms, processes in which Cdc45 plays a pivotal role. For instance, compounds like Aphidicolin, Camptothecin, and Gemcitabine target different stages of DNA replication. Aphidicolin inhibits DNA polymerases, while Camptothecin stabilizes the DNA-topoisomerase I complex, and Gemcitabine incorporates into DNA, causing chain termination. Each of these actions results in replication stress or disruption, indirectly necessitating the involvement of Cdc45, which is integral to the formation and progression of replication forks. By hampering the normal process of DNA synthesis, these compounds indirectly influence Cdc45's function in the replication machinery.
In addition to replication-focused inhibitors, other compounds in this class target cell cycle regulators and DNA damage response pathways. For example, Palbociclib, a CDK4/6 inhibitor, halts cell cycle progression, indirectly reducing the demand for Cdc45 in DNA replication. Similarly, inhibitors like VE-821, KU-55933, and AZD7762 target ATR, ATM, and CHK1/CHK2 kinases, respectively. These kinases are key players in orchestrating the cellular response to DNA damage and replication stress. By inhibiting these kinases, the compounds increase replication stress or disrupt cell cycle checkpoints, leading to a heightened dependence on Cdc45 for maintaining replication fidelity and genomic stability. In conclusion, the class of Cdc45 inhibitors encompasses a diverse range of compounds that, though not directly targeting Cdc45, indirectly modulate its activity through various biochemical pathways. These inhibitors are characterized by their ability to induce replication stress, disrupt cell cycle progression, or impair DNA damage response mechanisms, thereby influencing the functional role of Cdc45 in DNA replication and genomic stability maintenance.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Aphidicolin | 38966-21-1 | sc-201535 sc-201535A sc-201535B | 1 mg 5 mg 25 mg | $82.00 $300.00 $1082.00 | 30 | |
Aphidicolin, a tetracyclic diterpene antibiotic, is known to inhibit DNA polymerase alpha and delta. This inhibition disrupts DNA replication, a process where Cdc45 plays a critical role. By blocking DNA synthesis, Aphidicolin indirectly impacts Cdc45 activity, as Cdc45 is essential for the initiation and progression of DNA replication forks. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $57.00 $182.00 $92.00 | 21 | |
Camptothecin, a topoisomerase I inhibitor, impedes the ability of topoisomerase I to relieve DNA supercoiling during replication. Since Cdc45 is involved in replication fork stability and progression, the stabilization of topoisomerase I-DNA cleavage complexes by Camptothecin indirectly affects Cdc45's role in DNA replication. | ||||||
Olaparib | 763113-22-0 | sc-302017 sc-302017A sc-302017B | 250 mg 500 mg 1 g | $206.00 $299.00 $485.00 | 10 | |
Olaparib, a PARP inhibitor, impairs the repair of single-strand DNA breaks, which can indirectly necessitate the involvement of replication machinery, including Cdc45. As Cdc45 is integral in replication fork progression, the increase in replication stress due to PARP inhibition potentially enhances the reliance on Cdc45 function. | ||||||
Palbociclib | 571190-30-2 | sc-507366 | 50 mg | $315.00 | ||
PD 0332991, a CDK4/6 inhibitor, indirectly affects Cdc45 by inhibiting cyclin-dependent kinases that are crucial for cell cycle progression. The inhibition of CDK4/6 leads to cell cycle arrest, reducing the demand for replication machinery, including Cdc45. | ||||||
Hydroxyurea | 127-07-1 | sc-29061 sc-29061A | 5 g 25 g | $76.00 $255.00 | 18 | |
Hydroxyurea inhibits ribonucleotide reductase, leading to a depletion of deoxyribonucleotide triphosphates (dNTPs), essential substrates for DNA synthesis. This depletion indirectly affects Cdc45's function in replication by reducing the availability of necessary substrates, thereby impacting replication fork progression where Cdc45 is involved. | ||||||
2′-Deoxy-2′,2′-difluorocytidine | 95058-81-4 | sc-275523 sc-275523A | 1 g 5 g | $56.00 $128.00 | ||
2'-Deoxy-2',2'-difluorocytidine is a nucleoside analog that gets incorporated into DNA, leading to chain termination during replication. | ||||||
Flavopiridol | 146426-40-6 | sc-202157 sc-202157A | 5 mg 25 mg | $78.00 $254.00 | 41 | |
Flavopiridol is a potent inhibitor of cyclin-dependent kinases (CDKs). By inhibiting CDKs, it leads to cell cycle arrest, particularly at the G1 phase. This arrest reduces the requirement for DNA replication machinery, including Cdc45, thus indirectly affecting its activity as part of the replication complex. | ||||||
VE 821 | 1232410-49-9 | sc-475878 | 10 mg | $360.00 | ||
VE-821 is an ATR kinase inhibitor. ATR is involved in the response to DNA damage and replication stress. Inhibition of ATR by VE-821 can increase replication stress, potentially leading to a greater dependency on replication machinery, including Cdc45, for DNA repair and replication fork stability. | ||||||
UCN-01 | 112953-11-4 | sc-202376 | 500 µg | $246.00 | 10 | |
UCN-01 (7-Hydroxystaurosporine) is a potent inhibitor of protein kinase C and several other kinases. By inhibiting these kinases, UCN-01 can disrupt various signaling pathways, including those related to cell cycle control and DNA damage response, potentially affecting the regulation and activity of Cdc45 as part of the replication machinery. | ||||||
ATM Kinase Inhibitor | 587871-26-9 | sc-202963 | 2 mg | $108.00 | 28 | |
ATM Kinase Inhibitor plays a critical role in the response to DNA double-strand breaks and replication stress. Inhibition of ATM can lead to increased replication stress, which may indirectly increase the reliance on Cdc45 for managing DNA replication and repair processes. | ||||||