Name: CP-7
Brand: BOC Sciences
Rating: 5 (1 reviews)

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IUPACName

2-[4-[6-[(6-acetyl-8-cyclopentyl-5-methyl-7-oxopyrido[2,3-d]pyrimidin-2-yl)amino]pyridin-3-yl]piperazin-1-yl]-N-[2-[2-[2-[2-[[2-(2,6-dioxopiperidin-3-yl)-1,3-dioxoisoindol-4-yl]amino]ethoxy]ethoxy]ethoxy]ethyl]acetamide

Synonyms

2-(4-(6-((6-acetyl-8-cyclopentyl-5-methyl-7-oxo-7,8-dihydropyrido[2,3-d]pyrimidin-2-yl)amino)pyridin-3-yl)piperazin-1-yl)-N-(2-(2-(2-(2-((2-(2,6-dioxopiperidin-3-yl)-1,3-dioxoisoindolin-4-yl)amino)ethoxy)ethoxy)ethoxy)ethyl)acetamide; 1-Piperazineacetamide, 4-[6-[(6-acetyl-8-cyclopentyl-7,8-dihydro-5-methyl-7-oxopyrido[2,3-d]pyrimidin-2-yl)amino]-3-pyridinyl]-N-[2-[2-[2-[2-[[2-(2,6-dioxo-3-piperidinyl)-2,3-dihydro-1,3-dioxo-1H-isoindol-4-yl]amino]ethoxy]ethoxy]ethoxy]ethyl]-; 4-[6-[(6-Acetyl-8-cyclopentyl-7,8-dihydro-5-methyl-7-oxopyrido[2,3-d]pyrimidin-2-yl)amino]-3-pyridinyl]-N-[2-[2-[2-[2-[[2-(2,6-dioxo-3-piperidinyl)-2,3-dihydro-1,3-dioxo-1H-isoindol-4-yl]amino]ethoxy]ethoxy]ethoxy]ethyl]-1-piperazineacetamide

Density

1.383±0.06 g/cm3

InChI Key

UTSBHEVQCONLCR-UHFFFAOYSA-N

InChI

InChI=1S/C47H57N11O10/c1-29-34-27-51-47(54-42(34)57(31-6-3-4-7-31)45(64)40(29)30(2)59)52-37-12-10-32(26-50-37)56-18-16-55(17-19-56)28-39(61)49-15-21-67-23-25-68-24-22-66-20-14-48-35-9-5-8-33-41(35)46(65)58(44(33)63)36-11-13-38(60)53-43(36)62/h5,8-10,12,26-27,31,36,48H,3-4,6-7,11,13-25,28H2,1-2H3,(H,49,61)(H,53,60,62)(H,50,51,52,54)

SMILES

CC1=C(C(=O)N(C2=NC(=NC=C12)NC3=NC=C(C=C3)N4CCN(CC4)CC(=O)NCCOCCOCCOCCNC5=CC=CC6=C5C(=O)N(C6=O)C7CCC(=O)NC7=O)C8CCCC8)C(=O)C

Mechanism

Target: CP-7 selectively targets cyclin-dependent kinase 9 for proteasomal degradation.

Binding site: Its CDK9 ligand engages the ATP-binding catalytic pocket of CDK9.

Mechanism of action: CP-7, also reported as CP-07, is a flavonoid-based CDK9 PROTAC designed to induce selective degradation of CDK9. The compound links a CDK9-recognition element to an E3 ligase-recruiting ligand, promoting proximity-dependent ubiquitination and proteasomal clearance of CDK9 protein. Because CDK9 regulates transcriptional elongation and short-lived survival proteins, CP-7 enables evaluation of degradation-driven suppression of CDK9-dependent transcriptional programs. It is useful for studying Mcl-1 and c-Myc downregulation, prostate cancer cell models, degradation selectivity, and mechanistic differences between CDK9 inhibition and CDK9 protein depletion.

Applications

• PROTAC-Mediated Cancer Research: CP-7 is utilized in cancer research to selectively degrade oncogenic proteins, providing a novel approach to study the effects of protein knockdown on tumor cell proliferation and survival. This application aids in identifying potential therapeutic targets and understanding the molecular mechanisms driving cancer progression.

• Targeted Degradation in Neurodegenerative Studies: Researchers employ CP-7 to investigate the degradation of proteins implicated in neurodegenerative diseases. By facilitating the selective removal of pathogenic proteins, CP-7 helps elucidate disease pathways and offers insights into potential therapeutic interventions for conditions such as Alzheimer's and Parkinson's diseases.

• PROTAC-Driven Drug Resistance Exploration: CP-7 is applied in studies exploring drug resistance mechanisms by targeting and degrading proteins that confer resistance to conventional therapies. This approach assists in identifying resistance pathways and developing strategies to overcome therapeutic challenges in various disease models.

• Protein Interaction Analysis via PROTACs: CP-7 serves as a tool for dissecting protein-protein interactions by enabling the targeted degradation of specific proteins. This application allows researchers to study the dynamic roles of these interactions in cellular processes and their implications in disease states.

1. Potent and preferential degradation of CDK6 via proteolysis targeting chimera degraders.

Su, S., Yang, Z., Gao, H., Yang, H., Zhu, S., An, Z., Wang, J., Li, Q., Chandarlapaty, S., Deng, H. and Wu, W., 2019. Journal of medicinal chemistry, 62(16), pp.7575-7582.

A focused PROTAC library hijacking cancer therapeutic target CDK6 was developed. A design principle as "match/mismatch" was proposed for understanding the degradation profile differences in these PROTACs. Notably, potent PROTACs with specific and remarkable CDK6 degradation potential were generated by linking CDK6 inhibitor palbociclib and E3 ligase CRBN recruiter pomalidomide. The PROTAC strongly inhibited proliferation of hematopoietic cancer cells including multiple myeloma and robustly degraded copy-amplified/mutated forms of CDK6, indicating future potential clinical applications.

2. Homolog-Selective Degradation as a Strategy to Probe the Function of CDK6 in AML.

Brand, M., Jiang, B., Bauer, S., Donovan, K.A., Liang, Y., Wang, E.S., Nowak, R.P., Yuan, J.C., Zhang, T., Kwiatkowski, N. and Müller, A.C., 2019. Cell chemical biology, 26(2), pp.300-306.

The design of selective small molecules is often stymied by similar ligand binding pockets. Here, we report BSJ-03-123, a phthalimide-based degrader that exploits protein-interface determinants to achieve proteome-wide selectivity for the degradation of cyclin-dependent kinase 6 (CDK6). Pharmacologic CDK6 degradation targets a selective dependency of acute myeloid leukemia cells, and transcriptomics and phosphoproteomics profiling of acute degradation of CDK6 enabled dynamic mapping of its immediate role in coordinating signaling and transcription.

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Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C₁V₁ = C₂V₂