cdk2 in 4

CDK2-IN-4 is a potent and selective inhibitor of CDK2 with an IC50 of 44 nM for CDK2 cyclin A. It shows 2,000-fold selectivity over CDK1 cyclin B with IC50 of 86 uM.

CDK2 4-IN-2 (compound 56) serves as a dual inhibitor for CDK2 and CDK4, exhibiting an IC50 of less than 100 nM. It is applicable in cancer research.

EGFR CDK2-IN-4 (compound 4c) is a dual inhibitor targeting EGFR and CDK-2, with IC50 values of 89.6 nM for EGFR and 165.4 nM for CDK-2. It induces apoptosis and S phase cell cycle arrest in MCF-7 cells, showing significant anti-cancer activity with an IC50 of 2.74 μM against MCF-7 cells [1].

CDK2 4-IN-1 (compound B-4a) serves as both a CDK2 4 inhibitor and a microtubule polymerization inhibitor, making it useful in cancer research.

GSK-3 inhibitor 4 is an orally active and brain-permeable compound that acts as a triple inhibitor of GSK-3, CDK2, and CDK5, with IC50 values of 0.56 nM (GSK-3β), 0.45 nM (GSK-3α), 0.47 μM (CDK2), and 0.68 μM (CDK5). It effectively reduces Tau protein levels and can be used in the study of Alzheimer's disease.

IMPDH2-IN-4 (compound 2d) is a Mycophenolic acid analog and a selective IMPDH2 inhibitor with a Ki of 1.8 μM. It exhibits potent cytotoxic activity against osteosarcoma cancer cell lines. Additionally, IMPDH2-IN-4 demonstrates high affinity for VEGFR-2, CDK2, and IMPDH.

CDK2-IN-39 (compound 4) is a CDK2 inhibitor.

NUAK1-IN-2 (Compound 24) is an inhibitor of NUAK1 with an IC50 of 3.162 nM, as well as an inhibitor of CDK2 4 6. It is applicable in research related to cancer, neurodevelopmental disorders, and Alzheimer's disease.

GSK269962A hydrochloride (GSK 269962 hydrochloride) is a potent and selective ROCK inhibitor with anti-inflammatory and vasodilatory effects, inhibits ROCK1 and ROCK2, and can be used in the study of acute myeloid leukemias.

CDK12-IN-4, a pyrazolotriazine compound, exhibits potent inhibition of CDK12 by achieving an IC50 value of 0.641 μM, utilizing high ATP levels (2 mM). Notably, CDK12-IN-4 does not impact CDK2 Cyclin E (IC50 > 20 μM) or CDK9 Cyclin T1 (IC50 > 20 μM) under the influence of high ATP (2 mM) levels (WO2021116178A1).

CDK1 2 4-IN-1 (compound 3a) is a potent CDK inhibitor with IC50 values of 1.47, 0.78, and 0.87 μM for CDK1, CDK2, and CDK4, respectively. It can be used in cancer research to arrest the cell cycle at the G2 M phase and induce apoptosis, elevating Bax, caspase-3, and P53 levels while decreasing Bcl-2 levels [1].

CDK HDAC-IN-1 exhibits potent inhibitory activity towards CDK2 4 6 and HDAC6, with IC50 values of 60.9 ± 2.9 nM, 276 ± 22.3 nM, 27.2 ± 4.2 nM, and 128.6 ± 0.4 nM, respectively.

CDK-IN-9 (compound 24) is a potent inhibitor of CDK and acts on CDK2 E (IC50: 4 nM). It functions as a molecular gel that induces interaction between CDK12 and DDB1, and can dephosphorylate retinoblastoma protein and RNA polymerase II, thereby inducing apoptosis.

CDK1-IN-4 (10d) is a selective CDK1 inhibitor that acts on CDK1 (IC50: 44.52 nM), CDK2 (IC50: 624.93 nM), and CDK5 (IC50: 135.22 nM). It affects the cell cycle, inhibiting the growth of cancer cells, and can be used in cancer research.

CGP74514A is a CDK1 inhibitor with potential anticancer activity. In U937 cells, CGP74514A - induced apoptosis (5 microM) became apparent within 4 hr and approached 100% by 24 hr. The pan- caspase inhibitor Boc-fmk and the caspase-8 inhibitor lETD-fmk opposed CGP74514A -induced caspase-9 activation and PARP degradation, but not cytochrome c or Smac DIABLO release. CGP74514A -mediated apoptosis was substantially blocked by ectopic expression of full-length Bel- 2, a loop-deleted mutant Bcl-2, and Bcl-x(L). CGP74514A treatment (5 microM; 18 hr) resulted in increased p21(CIP1) expression, p27(KIP1) degradation, diminished E2F1 expression, and dephosphorylation of p34(CDC2). It also induced early (i.e., within 2 hr) inhibition of CDK1 activity and dephosphorylation of pRb, followed by pRb degradation, but did not block pRb phosphorylation at CDK2- and CDK4- specific sites. These findings indicate that the selective CDK1 inhibitor, CGP74514A , induces complex changes in cell cycle......

1. Ginsenoside Rg5 could be a beneficial agent for the treatment of Alzheimer's disease. 2. Ginsenoside Rg5 suppresses LPS-induced nitric oxide (NO) production and proinflammatory TNF-α secretion. 3. Ginsenoside Rg5 can ameliorate lung inflammation possib

CDK7-IN-20 is a potent, selective, and irreversible inhibitor of Cyclin-Dependent Kinase 7 (CDK7) with an IC50 value of 4 nM, exhibiting over 206-fold selectivity against related kinases [CDK1, CDK2, CDK3, CDK5, CDK6, CDK9, and CDK12]. It holds potential for research into autosomal dominant polycystic kidney disease (ADPKD).

Multi-kinase-IN-4 (compound 5d) is a multi-targeted kinase inhibitor effective against VEGFR2, EGFR, HER2, and CDK2, with IC50 values of 0.33, 0.22, 0.18, and 2.09 μM, respectively. It shows broad-spectrum anti-cancer activity in HepG2, MCF-7, MDA-231, and HeLa cell lines (IC50: 1.94–7.1 µM) and exhibits lower toxicity in WI-38 cells (IC50 = 40.85 µM). Additionally, it induces apoptosis, causes S-phase cell cycle arrest in HepG2 cells, and holds potential for cancer research [1].

CDK2-IN-18 (compound 8q) serves as a powerful inhibitor of CDK 2 E and CDK 4 D1, showing IC50 values of 8 nM and 46 nM, respectively. It effectively inhibits tumor cell proliferation [1].

PI3K AKT-IN-4 (compound 3), a diterpenoid extracted from the roots and rhizomes of Salvia castanea Dielsf., exhibits antitumor properties by inhibiting cell viability and proliferation (IC 50 =4.72 μM) and promoting apoptosis in Hep3B cells. This compound obstructs the G0 G1 phase of the cell cycle, triggers mitochondrial dysfunction, and induces oxidative stress. Moreover, PI3K AKT-IN-4 combats hepatocellular carcinoma through the inhibition of the PI3K-Akt signaling pathway and by interacting with PARP1 and CDK2 targets.