2. Signaling Pathways
  3. Cell Cycle/DNA Damage
  4. CDK
  5. CDK14 Isoform

CDK14

CDK14 (cyclin-dependent kinase 14, also known as PFTAIRE1/PFTK1) is a serine/threonine kinase that functions in cell-cycle regulation through association with cyclins and participates in the G2/M transition of mitosis.[1][2] Mechanistically, CDK14 forms an active complex with Cyclin Y and phosphorylates the Wnt co-receptor LRP6, thereby promoting canonical Wnt/β-catenin signaling and facilitating progression into mitosis.[2][2] Through regulation of Wnt pathway activity, CDK14 contributes to cell proliferation, stem-cell maintenance, and tissue development.[2][2] In disease contexts, elevated CDK14 activity has been linked to tumor progression, and experimental depletion or inhibition of CDK14 suppresses mammary stem-cell regeneration, triple-negative breast cancer growth, and metastatic potential through attenuation of Wnt/β-catenin signaling.[2] Genetic studies further demonstrate that Cdk14 deficiency impairs epithelial and endothelial cell proliferation, induces G2/M cell-cycle arrest, and exacerbates lung injury responses in mouse models, highlighting its role in tissue repair and regeneration.[3] Compared with other cyclin-dependent kinases, CDK14 belongs to the CDK5 subfamily and is distinguished by its Cyclin Y-dependent regulation of LRP6 phosphorylation and canonical Wnt signaling.[3] For experimental applications, the covalent CDK14 inhibitor FMF-04-159-2 has been used to reduce Wnt signaling, suppress triple-negative breast cancer progression, and decrease pathological α-synuclein accumulation in cellular and animal models of synucleinopathy, supporting CDK14 as a pharmacologically tractable research target.[2][4]

CDK14 Related Products (6):

Cat. No. Product Name Effect Purity
  • HY-X0009
    Tambiciclib
    		Inhibitor 99.21%
    Tambiciclib (GFH009, JSH-009) is an orally active, highly potent and selective CDK9 inhibitor (IC50 = 1 nM), demonstrating >200-fold selectivity over other CDKs, >100-fold selectivity over DYRK1A/B, and excellent selectivity over 468 kinases/mutants. Tambiciclib demonstrates potent in vitro and in vivo antileukemic efficacy in acute myeloid leukemia (AML) mouse models by inhibiting RNA Pol II phosphorylation, downregulating MCL1 and MYC, and inducing apoptosis. Tambiciclib can be used for AML research.
  • HY-127104
    FMF-04-159-2
    		Inhibitor 99.64%
    FMF-04-159-2 is a covalent CDK14 inhibitor. FMF-04-159-2 inhibits CDK14 and CDK2 with IC50s of 39.6 nM and 256 nM in NanoBRET assay, respectively.
  • HY-X0150
    JSH-150
    		Inhibitor 98.36%
    JSH-150 is a highly selective and potent CDK9 inhibitor with an IC50 of 1 nM.
  • HY-137342
    SB1-G-187
    		Degrader 98.70%
    SB1-G-187 is a multi-target kinase PROTAC degrader with activity against various kinases including GCK, YES1, IRAK1 and LYN. SB1-G-187 induces degradation of target kinases via a p97-dependent pathway, and forms ternary complexes with CRBN and specific functional kinases. SB1-G-187 can be used in tumor-related research. (Pink: multi-target kinase ligand (HY-125142); Blue: CRBN ligand (HY-A0003); Black: linker).
  • HY-X0009A
    Tambiciclib dimaleate
    		Inhibitor 99.53%
    Tambiciclib (GFH009, JSH-009) dimaleate is an orally active, highly potent and selective CDK9 inhibitor (IC50 = 1 nM), demonstrating >200-fold selectivity over other CDKs, >100-fold selectivity over DYRK1A/B, and excellent selectivity over 468 kinases/mutants. Tambiciclib dimaleate demonstrates potent in vitro and in vivo antileukemic efficacy in acute myeloid leukemia (AML) mouse models by inhibiting RNA Pol II phosphorylation, downregulating MCL1 and MYC, and inducing apoptosis. Tambiciclib dimaleate can be used for AML research.
  • HY-160213
    JA397
    		Inhibitor
    JA397, a chemical probe, is a potent and selective inhibitor for the TAIRE family with cellular activity ranging from IC50 values of 21 nM to 307 nM.