Cdk1/Cdk2 Inhibitors
Cyclin-dependent kinases (CDKs) are a family of protein kinases first discovered for their role in regulating the cell cycle. Among them, CDK1 and CDK2 are pivotal in controlling cell cycle progression and have been extensively studied for their functional roles in cellular biology. CDK1, also known as CDC2, is essential for the control of the cell cycle at the G2/M transition. It forms a complex with cyclin B, which is necessary for the initiation of mitosis. The activation of CDK1 induces numerous cellular events required for mitotic progression, including chromosome condensation, nuclear envelope breakdown, and spindle formation. On the other hand, CDK2 associates with cyclins E and A and is primarily active during the S phase and G2. It is critical for the control of the cell cycle at the G1/S transition, initiating DNA replication, and is involved in centrosome duplication during the S phase. The regulation of CDK1 and CDK2 activities is intricately controlled by various mechanisms, including the binding of cyclins, phosphorylation by specific kinases, and the action of CDK inhibitors. The proper functioning of these kinases is crucial for cell cycle control, and their dysregulation is often associated with uncontrolled cell proliferation and tumorigenesis.
Inhibition of CDK1 and CDK2 is a complex process that involves several mechanisms. One common method is the use of small molecules that bind to the ATP-binding site of these kinases, blocking their catalytic activity. This competitive inhibition disrupts the phosphorylation of specific substrates required for cell cycle progression, thereby arresting the cell cycle. Another mechanism involves the modulation of regulatory proteins that control CDK activity. For instance, the activation of CDK1 and CDK2 is regulated by their association with cyclins and by phosphorylation at specific sites. Inhibitors can modulate the interaction between CDKs and cyclins or affect the phosphorylation state of CDKs, thereby altering their activity. Additionally, the endogenous CDK inhibitors, such as the CIP/KIP family, play a vital role in the regulation of CDK activity. These inhibitors can bind to CDK-cyclin complexes, inhibiting their activity and thus providing a natural regulatory mechanism for cell cycle control.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Dinaciclib | 779353-01-4 | sc-364483 sc-364483A | 5 mg 25 mg | $242.00 $871.00 | 1 | |
Dinaciclib is a potent pan-CDK inhibitor with significant activity against CDK1 and CDK2. It functions by competitively binding to the ATP-binding sites of these kinases, thereby blocking their kinase activity. This inhibition disrupts the phosphorylation of critical substrates required for cell cycle progression, leading to cell cycle arrest and apoptosis in cancer cells. | ||||||
Flavopiridol | 146426-40-6 | sc-202157 sc-202157A | 5 mg 25 mg | $78.00 $254.00 | 41 | |
Flavopiridol is a broad-spectrum CDK inhibitor targeting CDK1 and CDK2 among others. It binds competitively to the ATP-binding pocket, inhibiting kinase activity. This action prevents the phosphorylation of key proteins involved in cell cycle regulation, particularly affecting the transition from G1 to S phase and the progression through S phase. | ||||||
R547 | 741713-40-6 | sc-364596 sc-364596A | 2 mg 5 mg | $375.00 $395.00 | ||
R547 is a selective inhibitor of CDK1 and CDK2. It binds to the ATP-binding site of these kinases, effectively blocking their phosphorylation activity. This inhibition leads to the disruption of cell cycle progression, especially at the G1/S and G2/M phases. | ||||||
RO-3306 | 872573-93-8 | sc-358700 sc-358700A sc-358700B | 1 mg 5 mg 25 mg | $65.00 $160.00 $320.00 | 37 | |
RO-3306 is a potent and selective inhibitor of CDK1. Its mechanism involves the binding to the ATP-binding site of CDK1, inhibiting its kinase activity. This selective inhibition results in the arrest of the cell cycle at the G2/M phase, which is crucial for mitosis. | ||||||
CVT-313 | 199986-75-9 | sc-221445 sc-221445A sc-221445B | 1 mg 5 mg 50 mg | $102.00 $408.00 $2550.00 | 17 | |
CVT-313 selectively inhibits CDK2 by binding to its ATP-binding pocket, preventing its kinase activity. This selective inhibition leads to a blockade of the cell cycle progression at the S phase, as CDK2 is essential for the initiation and progression through this phase. | ||||||
AT7519 | 844442-38-2 | sc-364416 sc-364416A sc-364416B sc-364416C | 5 mg 10 mg 100 mg 1 g | $207.00 $246.00 $1025.00 $3065.00 | 1 | |
AT7519 acts as a pan-CDK inhibitor, effectively targeting CDK1, CDK2, CDK4, and CDK9. It binds to the ATP-binding sites of these kinases, inhibiting their activity. | ||||||
Roscovitine | 186692-46-6 | sc-24002 sc-24002A | 1 mg 5 mg | $92.00 $260.00 | 42 | |
Roscovitine inhibits CDK1/CDK2 by competitively binding to their ATP-binding sites. This inhibition prevents the phosphorylation of key regulatory proteins involved in the cell cycle, DNA repair, and transcription, leading to cell cycle arrest and apoptosis. | ||||||
Cdc7/Cdk9 Inhibitor | 845714-00-3 | sc-311303 | 5 mg | $270.00 | 1 | |
Cdc7/Cdk9 Inhibitor (PHA-767491)c binds to the ATP-binding pocket of these kinases, thereby blocking their catalytic activity. This inhibition disrupts the normal cell cycle progression, particularly affecting the G1/S and G2/M transitions, and is being investigated for its anticancer potential. | ||||||
Indirubin-3′-monoxime | 160807-49-8 | sc-202660 sc-202660A sc-202660B | 1 mg 5 mg 50 mg | $77.00 $315.00 $658.00 | 1 | |
Indirubin-3'-oxime exhibits inhibitory effects on CDK1 and CDK2 by binding to their ATP-binding sites. This binding disrupts the kinase activity, leading to an interruption in the cell cycle, particularly at the G1/S and G2/M phases. | ||||||
BMS-265246 | 582315-72-8 | sc-364440 sc-364440A | 5 mg 10 mg | $304.00 $555.00 | ||
BMS-265246 functions as a selective inhibitor of CDK1 and CDK2. Its mechanism of action includes the binding to the ATP-binding pockets of these kinases, thereby inhibiting their activity. This results in cell cycle arrest, particularly affecting the G1/S and G2/M transitions | ||||||