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CDK inhibitors block cyclin-dependent kinases (CDKs), the serine/threonine kinases that drive the cell cycle. Each CDK becomes active only when bound to a cyclin partner, and successive cyclin-CDK complexes order DNA replication and mitosis. CDK4 and CDK6 pair with D-type cyclins to control progression through G1, while CDK1 governs entry into mitosis. Palbociclib and abemaciclib are selective CDK4/6 inhibitors used to study G1 arrest and retinoblastoma protein phosphorylation. Dinaciclib and seliciclib act on several family members, including CDK2, CDK5 and CDK9, which also links them to transcription research. Ro 3306 inhibits CDK1 and is used to hold cells reversibly at the G2/M boundary for synchronization experiments.
THAL-SNS-032 is a selective CDK9 degrader PROTAC consisting of a CDK-binding SNS-032 ligand linked to a thalidomide derivative that binds the E3 ubiquitin ligase Cereblon (CRBN).
JH-XI-10-02 is a potent and selective degrader of CDK8, with an IC50 of 159 nM, based on PROTAC.
PROTAC CDK9 Degrader-1 is a selective CDK9 degrader.
BSJ-03-123 is a potent and novel CDK6-selective small-molecule degrader (PROTAC).
TL12-186 is a cereblon-dependent PROTAC degrader with broad-spectrum activity against multiple kinases, including CDKs, BTK, FLT3, Aurora kinases, TEC, ULK, and ITK. It inhibits CDK2/cyclin A and CDK9/cyclin T1 with IC₅₀ values of 73 nM and 55 nM, respectively, making it a valuable tool for studying kinase-driven signaling pathways and cancer biology.
BSJ-03-204 is a potent and selective PROTAC degrader targeting CDK4 and CDK6, constructed by linking Palbociclib to a cereblon ligand. It exhibits IC₅₀ values of 26.9 nM for CDK4/D1 and 10.4 nM for CDK6/D1, without inducing degradation of IKZF1 or IKZF3. BSJ-03-204 demonstrates strong anti-cancer activity and is a valuable tool for cell cycle and oncology research.
BSJ-04-132 is a potent and selective Ribociclib-based PROTAC degrader targeting CDK4, constructed using ligands for cereblon and CDK. It exhibits IC₅₀ values of 50.6 nM for CDK4/D1 and 30 nM for CDK6/D1, while sparing CDK6 and IKZF1/3 from degradation. BSJ-04-132 demonstrates anti-cancer activity and is a valuable tool for cell cycle and oncology research.
PROTAC CDK2/9 Degrader-1 (Compound F3) is a potent dual PROTAC degrader targeting CDK2 (DC₅₀ = 62 nM) and CDK9 (DC₅₀ = 33 nM), constructed by linking a CDK inhibitor to a cereblon ligand. It effectively inhibits PC-3 prostate cancer cell proliferation (IC₅₀ = 0.12 µM) by inducing cell cycle arrest in the S and G2/M phases, making it a valuable tool for cancer and cell cycle research.
BSJ-4-116 is a PROTAC molecule derived from a modified form of the multi-kinase degrader TL12-186, linked to a cereblon ligand and E3 ligase ligand intermediate. It induces time- and concentration-dependent degradation of CDK12 in Jurkat T cells and downregulates genes involved in DNA double-strand break repair at 50 nM. BSJ-4-116 also inhibits MOLT-4 leukemia cell growth in a cereblon-dependent manner, supporting its application in cancer and DNA repair research.
PROTAC CDK12/13 Degrader-1 (7f) TFA is a highly selective dual degrader of CDK12 and CDK13, with DC₅₀ values of 2.2 nM and 2.1 nM, respectively. It exhibits strong antiproliferative activity and is a valuable tool for investigating cell cycle regulation and therapeutic strategies in breast cancer research.
BSJ-03-204 triTFA is a potent and selective PROTAC degrader targeting CDK4/6, constructed using ligands for cereblon and CDK. Based on Palbociclib, it exhibits IC₅₀ values of 26.9 nM for CDK4/D1 and 10.4 nM for CDK6/D1. BSJ-03-204 triTFA does not induce IKZF1/3 degradation and shows anti-cancer activity, making it a valuable tool for cell cycle and oncology research.
XY028-133 (Example 14) is a PROTAC-based degrader targeting CDK4/6, composed of ligands for von Hippel-Lindau (VHL) and CDK. It induces selective degradation of CDK4/6 and exhibits anti-tumor activity, making it a useful tool for cell cycle and cancer research.
LL-K8-22 is a potent, selective, and durable PROTAC degrader targeting the CDK8–cyclin C complex, with DC₅₀ values of 2.52 μM and 2.64 μM, respectively. It suppresses STAT1 Ser727 phosphorylation and inhibits E2F- and MYC-driven oncogenic transcriptional programs. LL-K8-22 shows potential for use in triple-negative breast cancer (TNBC) research and related therapeutic studies.
PROTAC CDK12/13 Degrader-1 (7f) is a highly selective dual degrader targeting CDK12 and CDK13, with DC₅₀ values of 2.2 nM and 2.1 nM, respectively. It exhibits potent anti-proliferative activity and serves as a valuable tool for investigating transcriptional regulation and therapeutic strategies in breast cancer research.
PP-C8 is a potent and selective PROTAC degrader targeting the CDK12–Cyclin K complex. It induces efficient degradation of CDK12 and Cyclin K with DC₅₀ values of 416 nM and 412 nM, respectively. In preclinical models, PP-C8 exhibits strong synergistic antiproliferative effects when combined with PARP inhibitors, particularly in triple-negative breast cancer (TNBC), highlighting its potential as a therapeutic strategy for enhancing DNA damage response–targeted treatments.
LL-K12-18 is a two-site molecular glue that enhances the protein-protein interaction between CDK12 and DDB1, stabilizing the complex and promoting cyclin K degradation with an EC50 of 0.37 nM. It exhibits potent transcriptional repression and anti-proliferative activity in tumor cells, making it a valuable tool for cancer research.
YJ1206 is an orally active and selective PROTAC degrader targeting CDK12 and CDK13, with an IC50 of 12.55 nM in VCaP cells. It induces DNA damage, promotes apoptosis, and leads to tumor regression in orthotopic WA74 patient-derived xenograft (PDX) models of resistant prostate cancer. Additionally, YJ1206 enhances antitumor efficacy when used in combination with AKT pathway inhibitors, highlighting its potential for combination therapy in advanced prostate cancer.
Synonyms: (S,R,S)-AHPC-Me-PEG2-dabrafenib
DD-03-156 is a potent and selective degrader of CDK17 and LIMK2. It exhibits high selectivity and potency, making it a strong candidate for the development of a chemical probe targeting CDK17 degradation.
YX-2-107 is a CDK6-degrading PROTAC with an IC50 of 4.4 nM, designed for selective degradation of CDK6. This compound effectively inhibits retinoblastoma (RB) phosphorylation and reduces FOXM1 expression in vitro. YX-2-107 has potential applications in research related to Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), demonstrating its ability to attenuate disease progression in rat models.
CPS2 is a highly potent and selective PROTAC that irreversibly degrades cyclin-dependent kinase 2 (CDK2) with an IC50 of 24 nM. This compound is valuable for exploring the role of CDK2 in cell cycle regulation and has applications in the study of acute myeloid leukemia. Its unique mechanism provides a powerful tool for researchers investigating targeted protein degradation in cancer therapies.
CP-10 is a PROTAC designed to selectively target and degrade cyclin-dependent kinase 6 (CDK6) through its binding to Cereblon. Demonstrating a DC50 of 2.1 nM, this compound effectively inhibits the proliferation of various hematopoietic cancer cell lines, including multiple myeloma, and is capable of degrading both mutated and overexpressed forms of CDK6. Its specific activity makes CP-10 a valuable tool for research into CDK6-related malignancies and potential therapeutic strategies.
SNX7886 is a potent PROTAC degrader targeting CDK8 and CDK19. It effectively induces degradation of CDK8 and CDK19, achieving up to 90% and 80% degradation, respectively, in 293 cells. This compound is valuable for research applications in understanding the role of CDK8/19 in various biological processes and cancer pathways.
DB1113 is a bifunctional compound designed for targeted protein degradation of various kinases. It effectively induces degradation of ABL1, ABL2, BLK, CDK4, CDK11B, EPHA3, MAPK7, RIPK1, and others, facilitating the investigation of kinase-related signaling pathways. DB1113 is suitable for research focusing on diseases or disorders associated with dysregulated kinase activity, providing a valuable tool for exploring therapeutic interventions in cancer and other conditions.
Synonyms: CDK4/6-IN-11
BSJ-02-162 is a potent PROTAC degrader targeting CDK4/6 through the utilization of a thalidomide-based E3 ligase ligand and a selective CDK4/6 inhibitor. This compound effectively recruits ubiquitin ligases to facilitate the targeted degradation of CDK4/6, thereby modulating cellular responses to cell cycle regulation. BSJ-02-162 is designed for research applications exploring cancer therapies and the mechanisms of protein homeostasis within tumor cells.
CDK2 degrader 1 is a selective molecular glue degrader targeting cyclin-dependent kinase 2 (CDK2). It effectively induces ubiquitination and proteasomal degradation of CDK2 by binding to cereblon, achieving a Dmax greater than 80% and a Ki greater than 1 μM. This compound is utilized in cancer research, providing insights into tumor biology and potential therapeutic strategies.
