CDK1
CDK1 (cyclin-dependent kinase 1) is a highly conserved serine/threonine kinase that functions as a central regulator of eukaryotic cell-cycle progression through cyclin-dependent substrate phosphorylation, particularly during G2/M transition and mitosis[1][2]. Mechanistically, CDK1 forms active complexes with cyclins and coordinates centrosome dynamics, chromosome segregation, spindle organization, and mitotic progression through phosphorylation-dependent signaling networks[2][3]. CDK1 also regulates translational control during mitosis by directly phosphorylating key components of the protein synthesis machinery, including 4E-BP1, thereby linking cell-cycle progression with cellular growth programs[4][5]. In disease models, aberrant CDK1 activity contributes to tumor-cell proliferation, and elevated dependence on CDK1-mediated mitotic signaling has supported its investigation as a therapeutic target across multiple malignancies[6][7]. Compared with related cyclin-dependent kinase isoforms, CDK1 is distinguished by its indispensable role in driving mitotic entry and execution, making it a critical node for cell-cycle control and experimental interrogation of mitotic mechanisms[1][2]. For experimental applications, the ATP-competitive inhibitor RO-3306 is widely used to achieve reversible CDK1 suppression, inducing G2/M arrest and enabling mechanistic studies of mitotic regulation, DNA-damage responses, apoptosis, and cancer-cell vulnerability[6][8]. Furthermore, pharmacological inhibition of CDK1 blocks phosphorylation-dependent oncogenic functions of downstream substrates, including SET isoform 1, which regulates mitotic fidelity, cell migration, invasion, and tumor growth in cellular and xenograft models[3][6].
References:
- [1]. Wikipedia.
- [2]. Łukasik P, et al. Cyclin-Dependent Kinases (CDK) and Their Role in Diseases Development-Review. Int J Mol Sci. 2021 Mar 13;22(6):2935. [Content Brief]
- [3]. Yin L, et al. Cyclin-dependent kinase 1-mediated phosphorylation of SET at serine 7 is essential for its oncogenic activity. Cell Death Dis. 2019 May 16;10(6):385. [Content Brief]
- [4]. Jin Z, et al. Compartmentation of Metabolism of the C12-, C9-, and C5-n-dicarboxylates in Rat Liver, Investigated by Mass Isotopomer Analysis: ANAPLEROSIS FROM DODECANEDIOATE. J Biol Chem. 2015 Jul 24;290(30):18671-7. [Content Brief]
- [5]. Velásquez C, et al. Mitotic protein kinase CDK1 phosphorylation of mRNA translation regulator 4E-BP1 Ser83 may contribute to cell transformation. Proc Natl Acad Sci U S A. 2016 Jul 26;113(30):8466-71. [Content Brief]
- [6]. Kojima K, et al. Cyclin-dependent kinase 1 inhibitor RO-3306 enhances p53-mediated Bax activation and mitochondrial apoptosis in AML. Cancer Sci. 2009 Jun;100(6):1128-36. [Content Brief]
- [7]. Shi Z, et al. From Structure Modification to Drug Launch: A Systematic Review of the Ongoing Development of Cyclin-Dependent Kinase Inhibitors for Multiple Cancer Therapy. J Med Chem. 2022 May 12;65(9):6390-6418. [Content Brief]
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CDK1 Related Products (198)
Related Products (198)
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Recombinant Proteins (9)
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Antibodies (3)
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XL495
0 ImagesCat. No.: HY-182906CAS No.: 3040320-93-9XL495 is an potent, selective and orally active PKMYT1 inhibitor. XL495 inhibits CDK1 Thr14 phosphorylation and induces KAP1 Ser824 phosphorylation in xenograft tumors. XL495 reduces tumor growth in colorectal and breast cancer xenograft models, and achieves tumor regression with DNA-damaging agents in colorectal cancer xenograft models. XL495 can be used for the research of cancer, such as breast cancer and colorectal cancer.
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CDK4/6-IN-3
0 ImagesCat. No.: HY-126244CAS No.: 2366237-37-6CDK4/6-IN-3 is a brain-penetrant CDK4/CDK6 inhibitor with Kis of <0.3 nM and 2.2 nM, respectively. CDK4/6-IN-3 inhibits CDK1 with a Ki of 110 nM. CDK4/6-IN-3 can be used for the treatment of glioblastoma.
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Riviciclib
0 ImagesCat. No.: HY-16559ACAS No.: 920113-02-6Synonyms: P276-00 free baseRiviciclib (P276-00 free base) is a potent cyclin-dependent kinase (CDK) inhibitor, which inhibits CDK9-cyclinT1, CDK4-cyclin D1, and CDK1-cyclinB with IC50s of 20 nM, 63 nM, and 79 nM, respectively. Riviciclib shows antitumor activity on cisplatin-resistant cells.
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CDK9-IN-45
0 ImagesCat. No.: HY-179023CDK9-IN-45 (Compound B11) is a highly selective CDK9 inhibitor with IC50 values for CDK9 and CDK1 of 7.13 and 489.5 nM respectively. CDK9-IN-45 exhibits a potent inhibitory effect on colorectal cancer cells. CDK9-IN-45 induces cell apoptosis and leads to significant accumulation of ROS. CDK9-IN-45 activates Caspase-3, downregulates Mcl-1, XIAP, and c-Myc. CDK9-IN-45 can be used for research on colorectal cancer.
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CDK4-IN-7
0 ImagesCat. No.: HY-184444CAS No.: 3113087-01-4CDK4-IN-7 is a CDK4 inhibitor with an IC50 of 26 nM. CDK4-IN-7 shows selectivity for CDK1, with an IC50 of 4.2262 μM. CDK4-IN-7 can be used in cancer research.
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CDKI-83
0 ImagesCat. No.: HY-123034CAS No.: 1189558-88-0CDKI-83 is a potent CDK9 and CDK1 inhibitor with Ki values of 21 nM and 72 nM for CDK9/T1 and CDK1/B, respectively. CDKI-83 demonstrates effective anti-proliferative activity in human tumour cell lines with a GI50<1 μM. CDKI-83 effectively induces apoptosis in A2780 human ovarian cancer cells. CDKI-83 reduces phosphorylation at Ser-2 of RNA polymerase II (RNAPII) by inhibiting cellular CDK9 activity, and down-regulates Mcl-1 and Bcl-2. CDKI-83 has the potential for anti-cancer research.
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Aloisine A
0 ImagesCat. No.: HY-112363CAS No.: 496864-16-5Synonyms: RP107Aloisine A (RP107) is a a potent cyclin-dependent kinase (CDK) inhibitor with IC50s of 0.15 μM, 0.12 μM, 0.4 μM, 0.16 μM for CDK1/cyclin B, CDK2/cyclin A, CDK2/cyclin E, CDK5/p35, respectively. Aloisine A ininhibits GSK-3α (IC50=0.5 μM) and GSK-3β (IC50=1.5 μM). Aloisine A stimulates wild-type CFTR and mutated CFTR, with submicromolar affinity by a cAMP-independent mechanism. Aloisine A has the potential for CFTR-related diseases, including cystic fibrosis research.
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LZ9
0 ImagesCat. No.: HY-170306CAS No.: 844441-29-8LZ9 is a ATP-competitive CDK1 and CDK2 inhibitor. LZ9 has the potential for the research of colorectal cancer (CRC).
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M1-20
0 ImagesCat. No.: HY-P11028M1-20 is a CDK1 inhibitor. M1-20 promotes CDK1 ubiquitination by CUL4-DDB1-DCAF1 complexes and degradation through the proteasome pathway. M1-20 abolishes the formation of CDK1/CCNB1 complexes. M1-20 has significant anticancer activity of spontaneous breast cancer in FVB/N MMTV-PyVT mice model.
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Cyproheptadine-d3
0 ImagesCat. No.: HY-B1622SCAS No.: 2712455-05-3Cyproheptadine-d3 is the d3-labeled Cyproheptadine (HY-B1622). Cyproheptadine acts as a p38 MAP kinase activator, CHK2 activator, histamine H1 receptor inhibitor and serotonin receptor inhibitor. Cyproheptadine mediates cell cycle arrest via G1 phase arrest, G1/S transition arrest, G0/G1 phase arrest, reduced expression of cyclins D1/D2/D3, upregulated expression of HBP1, p16, p21, p27, and decreased phosphorylation of retinoblastoma protein. Cyproheptadine induces Apoptosis by increasing PARP and cleaved PARP, as well as activating the mitochondrial caspase pathway. Cyproheptadine inhibits tumor growth with extremely low toxicity to normal cells. Cyproheptadine can be used in research related to hepatocellular carcinoma, multiple myeloma and acute myeloid leukemia.
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Calactin
0 ImagesCat. No.: HY-167237CAS No.: 20304-47-6Calactin is a glycoside that can be isolated from Asclepias curassavica L.. Calactin activates caspase-3, caspase-8, caspase-9, and phosphorylates ERK. Calactin induces DNA damage, apoptosis, PARP cleavage, G2/M phase cell cycle arrest, shifts Bax/Bcl-2 expression, and shows anti-proliferation effects in leukemia cells. Calactin can be used for the research of leukemia.
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CKD-712
0 ImagesCat. No.: HY-114214CAS No.: 626252-75-3CKD-712 is an orally active multi-target tetrahydroisoquinoline derivatived and a potent inhibitor of the NF-κB pathway. CKD-712 selectively inhibits MMP-9 with no effect on MMP-2, downregulates the expression of TNF-α, IL-6, cyclin A, cyclin B, CDK-1 and other proteins, and activates the PI3K/Akt signaling pathway. CKD-712 blocks the activation and nuclear translocation of NF-κB, downregulates inflammatory factors and pro-tumor metastatic proteins, and induces G2/M phase arrest in tumor cells and thereby inhibits the invasion of cancer cells. CKD-712 can be used for the research of sepsis, myocardial ischemia-reperfusion injury and non-small cell lung cancer.
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TrkA Inhibitor
0 ImagesCat. No.: HY-112471CAS No.: 388626-12-8TrkA Inhibitor (Compound 18) is a CDK2 inhibitor with an IC50 of 0.69 μM over CDK1. TrkA Inhibitor can be used for chemotherapy-induced alopecia research.
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CDC20/HSP90-IN-1
0 ImagesCat. No.: HY-179012CDC20/HSP90-IN-1 (Compound 2b) is a Cdc20/Hsp90 inhibitor with a Kd of 16.2 μM for Cdc20 and a Kd of 0.241 μM for Hsp90α. CDC20/HSP90-IN-1 exerts potent antitumor activity through reducing p53-mediated Cdc20, upregulating Bim, downregulating Cyclin B1 expression, and disturbing B-Raf and AKT pathways via destroying Hsp90 chaperone function. CDC20/HSP90-IN-1 overcomes Vemurafenib (HY-12057)-induced resistant melanoma.
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BLINK11
0 ImagesCat. No.: HY-173347BLINK11 is a BBB-penetrant CDK5 inhibitor. BLINK11 lowers CDK5 activity for both complexes CDK5/p35 (IC50 = 17.09 nM) and CDK5/p25 (IC50 = 14.69 nM). BLINK11 offers anti-diabetic and neuroprotective benefits. BLINK11 lowers blood glucose, enhances cognition, and reduces neurodegeneration in T2D mice.
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CDK4/6/HDAC-IN-1
0 ImagesCat. No.: HY-170651CDK4/6/HDAC-IN-1 (Compound N14) is a dual-targeting inhibitor of CDK4/6 and HDAC (IC50: CDK4 = 7.23 nM, CDK6 = 13.20 nM, HDAC1 = 55.66 nM, HDAC6 = 48.38 nM). CDK4/6/HDAC-IN-1 induces cell Apoptosis and G0/G1 phase arrest through HDAC-p21-CDK signaling pathway. CDK4/6/HDAC-IN-1 inhibits hepatocellular carcinoma.
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CDK/HDAC-IN-2
0 ImagesCat. No.: HY-146276CAS No.: 2580938-58-3CDK/HDAC-IN-2 is a potent HDAC/CDK dual inhibitor with IC50 of 6.4, 0.25, 45, >1000, 8.63, 0.30, >1000 nM for HDAC1, HDAC2, HDAC3, HDAC6,8, CDK1, CDK2, CDK4,6,7, respectively. CDK/HDAC-IN-2 shows excellent antiproliferative activities. CDK/HDAC-IN-2 induces apoptosis and cell cycle arrest at G2/M phase. CDK/HDAC-IN-2 shows potent antitumor efficacy.
