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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.
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.
SRX3177 is a potent triple inhibitor targeting CDK4/6, PI3K, and BRD4, with IC50 values of
AZD8421 is a selective CDK2 inhibitor with an IC50 of 9 nM and demonstrated selectivity over CDK1, CDK4, and CDK6. It inhibits cancer cell proliferation by blocking pRB phosphorylation, leading to cell cycle arrest and senescence. AZD8421 shows strong single-agent efficacy and synergistic effects when combined with CDK4/6 inhibitors such as Palbociclib in in vivo models of breast and ovarian cancer. Additionally, it exhibits potent activity against drug-resistant breast cancer cells, making it a promising candidate for overcoming resistance in cancer therapy.
Inixaciclib is a potent cyclin-dependent kinase (CDK) inhibitor with potential applications in anticancer research. By targeting CDKs involved in cell cycle regulation, Inixaciclib can inhibit tumor cell proliferation and is being explored as a therapeutic candidate in cancer treatment.
Cirtociclib (BLU-222) is an orally active and highly selective CDK2 inhibitor. It disrupts retinoblastoma (Rb) signaling, leading to G1 cell cycle arrest and apoptosis, particularly in CCNE1-amplified endometrial cancer cells. Cirtociclib is a promising candidate for targeted therapy in CDK2-driven malignancies.
Synonyms: SNX2-1-165; BCD-115
Senexin B (SNX2-1-165; BCD-115) is a potent, highly water-soluble, and orally bioavailable inhibitor of CDK8 and CDK19, with Kd values of 140 nM for CDK8 and 80 nM for CDK19. It is a valuable tool for studying transcriptional regulation and has potential applications in cancer and inflammatory disease research.
INX-315 is an orally active and selective CDK2 inhibitor that induces G1 phase cell cycle arrest by reducing phosphorylation of CDK2 substrates. It exhibits dose-dependent tumor growth inhibition in xenograft mouse models and holds promise as a therapeutic candidate for cancer research targeting CDK2-driven malignancies.
CP681301 is a potent CDK5 inhibitor with demonstrated antiproliferative activity. It reduces the expression of key stemness and proliferation markers—including CD133, OLIG2, SOX2, KI67, and phosphorylated CDK5—in glioma stem cells (GSCs). CP681301 also impairs self-renewal capacity in mouse glioma xenograft models and exhibits anti-tumor activity in *Drosophila*, making it a promising compound for glioma and cancer stem cell research.
Synonyms: CDK7-IN-3
SY-5609 (CDK7-IN-3) is an orally active, highly selective, and noncovalent inhibitor of CDK7, with a Kd of 0.065 nM. It demonstrates minimal activity against CDK2 (Ki = 2600 nM), CDK9 (Ki = 960 nM), and CDK12 (Ki = 870 nM), confirming its selectivity. SY-5609 induces apoptosis in tumor cells and exhibits potent antitumor activity, making it a promising candidate for targeted cancer therapy.
Synonyms: TQB3616
Culmerciclib (TQB3616) is a potent cyclin-dependent kinase (CDK)4/6 inhibitor with strong antineoplastic activity. It demonstrates significant synergistic antitumor effects in estrogen receptor (ER)-positive/HER2-negative and HER2-positive breast cancer models when combined with endocrine therapy or HER2-targeted treatments, supporting its potential for combination cancer therapy.
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: CR8; (R)-Isomer
(R)-CR8 is a second-generation analog of Roscovitine and a potent inhibitor of CDK1, CDK2, CDK5, CDK7, and CDK9. It inhibits CDK1/cyclin B (IC₅₀ = 0.09 μM), CDK2/cyclin A (0.072 μM), CDK2/cyclin E (0.041 μM), CDK5/p25 (0.11 μM), CDK7/cyclin H (1.1 μM), CDK9/cyclin T (0.18 μM), and CK1δ/ε (0.4 μM). (R)-CR8 induces apoptosis, exhibits neuroprotective effects, and functions as a molecular glue degrader that promotes the degradation of cyclin K.
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.
(S)-CR8 is a selective inhibitor of cyclin-dependent kinases (CDKs), demonstrating potent inhibitory activity with IC50 values of 0.060 μM for CDK2/cyclin E, 0.080 μM for CDK2/cyclin A, 0.11 μM for CDK9/cyclin T, 0.12 μM for CDK5/p25, and 0.15 μM for CDK1/cyclin B. This compound effectively reduces the survival of SH-SY5Y cells, with an IC50 of 0.40 μM, making it a valuable tool for studying cell cycle regulation and potential therapeutic strategies in cancer research.
Synonyms: RP107
Aloisine A is a potent cyclin-dependent kinase (CDK) inhibitor, exhibiting IC50 values of 0.15 μM for CDK1/cyclin B, 0.12 μM for CDK2/cyclin A, 0.4 μM for CDK2/cyclin E, and 0.16 μM for CDK5/p35. In addition to its CDK inhibitory effects, Aloisine A also inhibits GSK-3α and GSK-3β with IC50 values of 0.5 μM and 1.5 μM, respectively. Notably, it enhances the activity of wild-type and mutant CFTR with submicromolar affinity through a cAMP-independent mechanism, making it a valuable tool for research related to cystic fibrosis and CFTR-related disorders.
NSC693868 is a selective inhibitor of cyclin-dependent kinases CDK1 and CDK5, demonstrating IC50 values of 600 nM and 400 nM, respectively. This compound also exhibits weaker inhibition of GSK3β with an IC50 of 1 µM and does not affect CDC25 activity. NSC693868 is employed in research to elucidate the functions of CDK1 and CDK5 within various cellular signaling pathways.
Synonyms: GSK-3 Inhibitor X
(E/Z)-BIO-acetoxime is a potent and selective inhibitor of GSK-3α/β, exhibiting an IC50 of 10 nM. This compound demonstrates exceptional selectivity with over 200-fold preference against CDK5/p25, CDK2/cyclin A, and CDK1/cyclin B, with IC50 values of 2.4, 4.3, and 63 μM, respectively. Its strong inhibitory activity makes it a valuable tool for research focused on signaling pathways involved in cell proliferation, differentiation, and apoptosis.
Synonyms: GFH009; JSH-009; SLS009
Tambiciclib is a potent and selective CDK9 inhibitor with an IC50 of 1 nM, exhibiting over 200-fold selectivity against other cyclin-dependent kinases and significant selectivity over DYRK1A/B and a wide range of kinases. This compound has demonstrated effective in vitro and in vivo antileukemic activity in acute myeloid leukemia (AML) models by inhibiting RNA Polymerase II phosphorylation, leading to downregulation of MCL1 and MYC, and subsequent induction of apoptosis. Tambiciclib is suitable for research applications focused on AML and related oncological studies.
